PMC:7445716 / 71119-71122 JSON TXT

Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases Abstract Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain–Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11–max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues. Introduction Coronavirus disease 2019 (COVID-19) pandemic has rapidly spread around the world from Jan-2020, with more than 14,000,000 cases confirmed so far [1]. Although primary affecting the respiratory system, central and peripheral neurological manifestations associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been increasingly reported [2–4]. In detail, several pieces of evidence suggested an association between SARS-CoV-2 infection and the development of Guillain–Barré Syndrome (GBS) [5–56]. GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]. With this background, our systematic review aimed to provide a comprehensive and updated overview of all case reports and series of COVID-19-related GBS to identify predominant clinical, laboratory, and neurophysiological patterns and to discuss the possible underlying pathophysiology. Methods We performed a systematic review according to the SALSA (Search, Appraisal, Synthesis, and Analysis) analytic framework [65]. We screened in PubMed and Google Scholar databases for all case descriptions of GBS associated with COVID-19 that were published from January 1st 2020 up to July 20th 2020. Keywords (including all commonly used abbreviations of these terms) used in the search strategy were as follows: [“acute autoimmune neuropathy” OR “acute inflammatory demyelinating polyneuropathy” OR “acute inflammatory demyelinating polyradiculoneuropathy,” OR “acute inflammatory polyneuropathy” OR “Demyelinating Polyradiculoneuropathy” OR “Guillain–Barre Syndrome” OR “Guillain–Barre” OR ““Miller–Fisher” OR “Bickerstaff encephalitis” OR “AIDP” OR “AMAN” OR “AMSAN” OR polyneuritis cranialis] AND [“COVID-19” OR “Wuhan coronavirus” OR “novel coronavirus” OR “novel coronavirus 2019” OR “SARS” OR “SARS-CoV-2”]. Suitable references were also identified in the authors’ archives of scientific literature on GBS. We restricted our search to studies published in English, Spanish, or Italian. Publications that were not peer-reviewed were excluded from this study. PRISMA criteria were applied. For each case, we extracted data concerning demographic and clinical variables, results of diagnostic investigations, and outcome. If the GBS clinical variant [57] or the electrophysiological subtype [61] was not explicitly reported in the paper, we reconstructed it, when possible, from reported details. We also classified the diagnostic certainty of all cases according to the Brighton Criteria [66]. Searches were performed by SAR, AA, and MF. The selection of relevant articles was shared with all authors. For statistical analysis, we used IBM SPSS Statistics version 21 (IBM, Armonk, NY, USA). Based on the distribution of values, continuous data were expressed as mean ± standard deviation or as median and interquartile range (IQR). Depending on the number of groups and data distribution, we applied the t test, the Mann–Whitney U test or the Kruskal–Wallis test (followed by Dunn–Bonferroni post hoc test). All reported p values were adjusted for multiple comparisons. We adopted the Chi-square test for categorical variables. Differences were considered statistically significant at p < 0.05. For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients. Results Our literature search identified 101 papers, including 37 case reports, 12 case series, 3 reviews with case reports, 42 reviews, 4 letters, 1 original article, 1 point of view, and 1 brief report. Four and one patients were excluded from the analysis because of a missing laboratory-proven SARS-CoV-2 infection or an ambiguous GBS diagnosis [disease course resembling chronic inflammatory demyelinating neuropathy (CIDP)], respectively. A total of 52 studies were included in the final analysis (total patients = 73) [5–56]. All data concerning the analyzed patients are reported in Table 1. For one case [20], most clinical and diagnostic details were not reported; therefore, many of our analyses were limited to 72 patients. Epidemiological distribution and demographic characteristics of the patients To date, GBS cases (n = 73) were reported from all continents except Australia. In details, patients were originally from Italy (n = 20), Iran (n = 10), Spain (n = 9), USA (n = 8), United Kingdom (n = 5), France (n = 4), Switzerland (n = 4), Germany (n = 3), Austria (n = 1), Brazil (n = 1), Canada (n = 1), China (n = 1), India (n = 1), Morocco (n = 1), Saudi Arabia (n = 1), Sudan (n = 1), The Netherlands (n = 1), and Turkey (n = 1) (Table 1, Fig. 1). The mean age at onset was 55 ± 17 years (min 11–max 94), including four pediatric cases [21, 27, 35, 41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643). Comorbidities were variably reported with no prevalence of a particular disease. Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America Clinical picture, diagnosis, and therapy of COVID-19 All reported GBS cases (n = 72) except two were symptomatic for COVID-19 with various severity. Most common manifestations of COVID-19 included fever (73.6%, 53/72), cough (72.2%, 52/72), dyspnea and/or pneumonia (63.8%, 46/72), hypo-/ageusia (22.2%, 16/72), hypo-/anosmia (20.8%, 15/72), and diarrhea (18.1%, 13/72). One of the two asymptomatic subjects never developed fever, respiratory symptoms, or pneumonia [10], whereas the other patient showed an asymptomatic pneumonia at chest computed tomography (CT) [12]. In all but six patients with available data [22, 24, 36, 44, 45, 52], SARS-CoV-2 RT-PCR with naso- or oropharyngeal swab or fecal exam was positive at first or following tests. Nevertheless, these six patients tested positive at SARS-CoV-2 serology. In four patients, the laboratory exam for the diagnostic confirmation was not specified [20, 40]. Typical “ground glass” aspects at chest-CT or similar findings at CT, Magnetic Resonance Imaging (MRI) or X-ray compatible with COVID-19 interstitial pneumonia were reported in 40 cases. The detailed therapies for COVID-19 are described in Table 1. Clinical features of GBS spectrum In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1). Results of electrophysiological, CSF, biochemical, and neuroimaging investigations Detailed electroneurography results were reported in 84.9% (62/73) of the cases. Specifically, 77.4% (48/62) cases showed a pattern compatible with a demyelinating polyradiculoneuropathy. In contrast, axonal damage was prominent in 14.5% (9/62). In a minority of the patients (8.1%), a mixed pattern was reported (5/62). Regarding CSF analysis (full results were available in 59 out of 73 cases), the classical albuminocytological dissociation (cell count < 5/µl with elevated CSF proteins) was detected in 71.2% of the cases (42/59) with a median CSF protein of 100.0 mg/dl (min: 49, max: 317 mg/dl). Mild pleocytosis (i.e., cell count ≥ 5/µl), with a maximum cell count of 13/µl, was evident in 5/59 cases (8.5%). Furthermore, CSF SARS-CoV-2 RNA was undetectable in all tested patients (n = 31) (Table 1). Detailed blood haematological and biochemical examinations showed variably leucocytosis (n = 4), leucopenia (n = 17), thrombocytosis (n = 3), thrombocytopenia (n = 5), and increased levels of C-reactive protein (CRP) (n = 22), erythrocyte sedimentation rate (n = 4), d-Dimer (n = 5), fibrinogen (n = 3), ferritin (n = 3), LDH (n = 7), IL-6 (n = 4), IL-1 (n = 3), IL-8 (n = 3), and TNF-α (n = 3) (Table 1). Furthermore, anti-GD1b and anti-GM1 antibodies were positive in one patient with MFS [23] and in one with classic sensorimotor GBS [13], respectively, whereas 33 cases tested negative (one in equivocal range) for anti-ganglioside antibodies. Cranial and spinal MRI scans were performed in a minority of the patients (23/73, 31.5%). Five patients (three cases with AIDP [9, 12, 25], one case with MFS [30], and one case with bilateral facial palsy with paresthesia [52]) showed cranial nerve contrast enhancement in the context of correspondent cranial nerve palsies. Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18, 46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9, 27, 31, 36, 37, 42, 52] and two cases [17, 46], respectively (Table 1). Distribution of clinical and electrophysiological variants and diagnosis of GBS From the clinical point of view, most examined patients presented with a classic sensorimotor variant (70.0%, 51/73), whereas Miller Fisher syndrome, GBS/MFS overlap variants (including polyneuritis cranialis), bilateral facial palsy with paresthesia, pure motor, and paraparetic were described in seven, two, five, four, and one patients, respectively. In three cases, no clinical variant could be established using the reported details (Table 1). In the examined population, 81.8% subjects fulfilled electrophysiological criteria for AIDP (45/55), 12.7% (7/55) for AMSAN, and 5.4% (3/55) for AMAN subtypes. Finally, a specific electrophysiological subtype was not attributable in 18 patients due to the lack of detailed information. The diagnosis of GBS was established based on clinical, CSF, and electrophysiological findings in 44/73 (60.3%) patients, clinical, and electrophysiological data in 18/73 (24.7%) cases, clinical, and CSF data in 8/73 (11.0%), and only clinical findings in 3/73 (4.1%) patients. Indeed, the highest level of diagnostic certainty (level one) was confirmed in 44/73 cases (60.3%). Level two and three were obtained in 24/73 cases (32.9%) and 5/73 (6.8%), respectively (Table 1). Management of GBS and patient outcomes All cases with available therapy data (n = 70) except ten [13, 15, 23, 25, 26, 33, 35–37, 41] were treated with intravenous immunoglobulin (IVIG) (Table 1). Conversely, plasma exchange and steroid therapy were performed in ten (four of them received also IVIG) and two cases, respectively. In two patients, no therapy was given. Mechanical or non-invasive ventilation was implemented in 21.4% (15/70) and 7.1% (5/70) patients due to worsening of GBS or COVID-19, respectively. At further observation (n = 68), 72.1% (49/68) patients demonstrated clinical improvement with partial or complete remission, 10.3% (7/68) cases showed no improvement, 11.8% (8/68) still required critical care treatment, and 5.8% (4/68) died (Table 1). Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66] Interestingly, patients with no improvement or poor outcome (n = 19) showed a slightly higher (but not significant) frequency of clinical history and/or a radiological picture of COVID-19 pneumonia (14/19, 73.7%) compared to those with a favorable prognosis (29/48, 60.4%, p = 0.541). Moreover, the former group of patients was significantly older (mean 62.7 ± 17.8 years, p = 0.011), but with comparable distribution of sex (p = 0.622) and electrophysiological subtypes (p = 0.144) and similar latency between COVID-19 and GBS (p = 0.588) and nadir (p = 0.825), compared to the latter (mean age 51.8 ± 16.6 years). The same findings were confirmed even after excluding cases with no improvement from the analysis (to prevent a possible bias related to the short follow-up time). Discussion COVID-19 pandemic prompts all efforts for the early recognition and treatment of its manifestations. In analogy to other viruses, belonging or not to the coronavirus family [63, 67], neurologic complications in COVID-19 are emerging as one of the most significant clinical chapters of this pandemic. In this regard, peripheral and central nervous system damage in COVID-19 has been postulated to be the consequence of two different mechanisms: 1) hematogenous (infection of endothelial cells or leucocytes) or trans-neuronal (via olfactory tract or other cranial nerves) dissemination to central nervous system in relation with viral neurotropism, and 2) abnormal immune-mediated response causing secondary neurological involvement [62, 68, 69]. The first mechanism is supposed to be responsible for the most common neurological symptoms developed by patients with COVID-19 (e.g., hypogeusia, hyposmia, headache, vertigo, and dizziness). In contrast, the second can lead to severe complications during or after the course of the illness, either dysimmune (e.g., myelitis, encephalitis, GBS) or induced by cytokine overproduction (hypercoagulable state and cerebrovascular events) [68, 69]. In the present systematic review, we reviewed clinical features, results of diagnostic investigations, and outcome in 73 cases of COVID-19-associated GBS spectrum [5–56]. In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70, 71]. However, pediatric cases with GBS have been increasingly reported in the literature [21, 27, 35, 41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus–GBS [72]. This finding may also reflect the gender epidemiology of SARS-CoV-2. In this regard, males typically show a worse COVID-19 outcome compared to the females [70, 71], possibly due to a generally shorter life expectancy or to higher circulating Angiotensin-Converting-Enzyme 2 (ACE2) levels, the cellular receptor for SARS-CoV-2, in the former compared to the latter [71]. Moreover, given that GBS is a rare disease [57] the epidemiological distribution of the reported cases seems to reflect current worldwide outbreaks, with Europe being the “hottest” spot in March–May 2020 and USA together with Asia in the following period [73, 74]. On another issue, despite a few GBS cases seemed to have a para-infectious profile [10, 37, 38, 40, 55, 56] as described for Zika virus [75], all other reported patients developed neurological symptoms with a typical latency after COVID-19 (median time 14 days). This feature, together with the frequently reported negative nasopharyngeal swab at GBS onset [22, 24, 36, 44, 45, 52] and clinical improvement after IVIG therapy, seems to support the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [76, 77]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.) in GBS tested cases may reinforce the hypothesis of a systemic inflammatory storm in COVID-19 [76, 77]. However, given the limited data, we could not perform an accurate analysis of the distribution and, eventually, prognostic value of inflammatory markers in COVID-19-associated GBS. Moreover, we cannot exclude that in cases with GBS developing before or together with COVID-19 symptoms, the disease might have progressed sub-clinically in the early phase to manifest afterwards with its typical systemic clinical picture. Indeed, two cases [10, 12], who tested positive for SARS-CoV-2, never developed COVID-19 respiratory or systemic symptoms and one of them showed an asymptomatic pneumonia at chest-CT [12]. However, only more extensive epidemiological and translational studies, with the aim to compare the characteristics of GBS associated or not with COVID-19, could clarify these issues. In our population, most common clinical manifestations and distribution of clinical variants resemble those of classic GBS confirming the predominance of the sensorimotor syndrome compared to MFS and other rare variants [57–59, 66]. Similarly, the results of CSF analysis reflected typical neurochemical findings in non-COVID-19 GBS. In the latter, elevated CSF proteins and pleocytosis were described in about 50–80% [57, 78] and 11–15% cases, respectively [58, 79, 80], largely overlapping with the percentages in our cohort. In this regard, the mostly normal cell count, together with the absence of SARS-CoV-2 RNA in all tested CSF samples [6–9, 12–14, 16, 21–24, 31, 33, 36, 42, 44, 52, 55], makes the possibility of a direct invasion from SARS-CoV-2 into the nerve roots with intrathecal viral replication less probable. However, a possible bias might rely on the lack of systematic data concerning the latency between symptom onset and CSF sampling in COVID-19 GBS cases. On another issue, in a further case of MFS associated withCOVID-19, who came to our attention, we observed the absence of intrathecal synthesis of SARS-CoV-2 antibodies together with a massive increase of CSF phosphorylated neurofilament heavy chain (pNfH) and serum neurofilament light chain (NfL) proteins, supporting the role of neurochemical markers as easily implementable tools for the detection of nervous system affection in COVID-19-related diseases [81, 82]. At variance with CSF findings, we found a discrepancy concerning MRI findings between classic GBS and COVID-19-related GBS. Specifically, while most cases of the former group showed typically spinal root enhancement at MRI [83], in the latter group, in analogy with Zika-associated GBS, the same finding was less frequently reported [84]. However, caution should be warranted in the interpretation of these results, given that MRI findings might have been underestimated, due to lack of a sufficient number of exams in the context of pandemic-imposed restrictions in the routine clinical setting. Regarding the distribution of GBS electrophysiological variants, our analysis showed that COVID-19-associated GBS manifests prevalently with AIDP and, to a lesser extent, with AMSAN and AMAN, in line with classic GBS in Western countries [66, 85]. Conversely, the observation of positive anti-GD1b antibodies in one COVID-19-related MFS patient and negative anti-ganglioside antibodies in other five cases appear in discordance with the high prevalence (≈ 90%) of anti-GQ1b antibodies among non-COVID-19 MFS cases [86], and may suggest different immune-mediated mechanisms. However, these results could not be generalized until a wider population would be tested. In analogy to classic GBS, approximately one-fifth of COVID-19-associated GBS subjects required mechanical ventilation during hospitalisation [87]. In this regard, cases with no improvement or unfavorable outcome showed, in comparison to those with a good prognosis, an older age, confirming similar findings both in classic GBS [58, 88] and in COVID-19 [89], and a slightly higher frequency (without reaching a statistical significance) of past or concurrent COVID-19 pneumonia. However, given the short follow-up time in most cases, we could not reach a definite conclusion on the impact of past or concurrent COVID-19 restrictive syndrome due to pneumonia on the prognosis of GBS patients. Future prospective studies are needed to clarify this issue. Moreover, given that also preceding diarrhea (mostly caused by Campylobacter Jejuni infection) is a strong negative prognostic factor in classic GBS [57, 88], further prospective studies are needed to compare the severity of GBS related to COVID-19 to that associated with C. jejuni. Finally, in the context of respiratory failure and ventilation associated with COVID-19, the differential diagnosis should always take into consideration critical illness neuropathy and myopathy, which tend to develop later during the critical course [90]. Despite these findings, approximately one-third of COVID-19-related GBS patients showed no clinical and/or radiological evidence of pneumonia, providing evidence that GBS may also develop in the context of a paucisymptomatic or even asymptomatic COVID-19. However, given that among the GBS population only two asymptomatic COVID-19 patients were reported to date, we may speculate that, in most cases, a certain degree of lung injury (even minimal) or at least hematic dissemination (e.g., fever underlying significant viral load) is necessary to trigger the immuno-mediated process through lymphocytic recognition of self-antigens or molecular mimicry. Major strengths of our review are the inclusion of a high number of patients, together with an in-depth analysis of the clinical and diagnostic features of COVID-19-associated GBS. We are aware that selection bias might have occurred, given that most reported cases to date have been described mostly in Europe (47 out of 73) and during COVID-19 highest spreading. Therefore, future extensive epidemiological studies are necessary to ascertain the nature of the association between COVID-19 and GBS (causal or coincidental). Moreover, we cannot exclude the possibility that at least some of the cases represent instances of CIDP, given the frequent absence of a follow-up longer than 2 months. On another issue, the low but possible evidence of an epidemiological link between vaccines and GBS development [57, 58] should aware the clinicians of the possible occurrence of GBS after COVID-19 vaccination in the long-term future. In conclusion, based on the systematic review of 73 cases, we showed that the clinical picture of COVID-19-associated GBS seems to resemble that of classic GBS or Zika-associated GBS. Moreover, the chronological evolution, the response to IVIG, and the absence of SARS-CoV-2 RNA in CSF may suggest a prominent post-infectious immune-mediated mechanism rather than a para-infectious one. Although most cases were symptomatic for COVID-19, the preliminary report of a few patients without respiratory or systemic symptoms raises a significant healthcare issue, namely the importance of SARS-CoV-2 testing in all patients with suspected GBS during the pandemic, with the aim to provide an eventual rapid case isolation. Nevertheless, only further analyses on more comprehensive cohorts could help in clarifying better all these issues. Acknowledgements Open Access funding provided by Projekt DEAL. This work was in part supported by a COVID-19 grant from the state Baden-Württemberg. Authors’ contributions Conceptualization: all authors; methodology, formal analysis, and investigation: Samir Abu-Rumeileh, Ahmed Abdelhak, and Matteo Foschi; writing—original draft preparation: all authors; figure preparation: Matteo Foschi; writing—review and editing: all authors; supervision: Markus Otto and Hayrettin Tumani. Compliance with ethical standards Conflicts of interest The authors declare that they have no conflict of interest related to the content of this article. Ethical standard For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.

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article-title	Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases
abstract	Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain–Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11–max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.
p	Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain–Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11–max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.
body	Introduction Coronavirus disease 2019 (COVID-19) pandemic has rapidly spread around the world from Jan-2020, with more than 14,000,000 cases confirmed so far [1]. Although primary affecting the respiratory system, central and peripheral neurological manifestations associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been increasingly reported [2–4]. In detail, several pieces of evidence suggested an association between SARS-CoV-2 infection and the development of Guillain–Barré Syndrome (GBS) [5–56]. GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]. With this background, our systematic review aimed to provide a comprehensive and updated overview of all case reports and series of COVID-19-related GBS to identify predominant clinical, laboratory, and neurophysiological patterns and to discuss the possible underlying pathophysiology. Methods We performed a systematic review according to the SALSA (Search, Appraisal, Synthesis, and Analysis) analytic framework [65]. We screened in PubMed and Google Scholar databases for all case descriptions of GBS associated with COVID-19 that were published from January 1st 2020 up to July 20th 2020. Keywords (including all commonly used abbreviations of these terms) used in the search strategy were as follows: [“acute autoimmune neuropathy” OR “acute inflammatory demyelinating polyneuropathy” OR “acute inflammatory demyelinating polyradiculoneuropathy,” OR “acute inflammatory polyneuropathy” OR “Demyelinating Polyradiculoneuropathy” OR “Guillain–Barre Syndrome” OR “Guillain–Barre” OR ““Miller–Fisher” OR “Bickerstaff encephalitis” OR “AIDP” OR “AMAN” OR “AMSAN” OR polyneuritis cranialis] AND [“COVID-19” OR “Wuhan coronavirus” OR “novel coronavirus” OR “novel coronavirus 2019” OR “SARS” OR “SARS-CoV-2”]. Suitable references were also identified in the authors’ archives of scientific literature on GBS. We restricted our search to studies published in English, Spanish, or Italian. Publications that were not peer-reviewed were excluded from this study. PRISMA criteria were applied. For each case, we extracted data concerning demographic and clinical variables, results of diagnostic investigations, and outcome. If the GBS clinical variant [57] or the electrophysiological subtype [61] was not explicitly reported in the paper, we reconstructed it, when possible, from reported details. We also classified the diagnostic certainty of all cases according to the Brighton Criteria [66]. Searches were performed by SAR, AA, and MF. The selection of relevant articles was shared with all authors. For statistical analysis, we used IBM SPSS Statistics version 21 (IBM, Armonk, NY, USA). Based on the distribution of values, continuous data were expressed as mean ± standard deviation or as median and interquartile range (IQR). Depending on the number of groups and data distribution, we applied the t test, the Mann–Whitney U test or the Kruskal–Wallis test (followed by Dunn–Bonferroni post hoc test). All reported p values were adjusted for multiple comparisons. We adopted the Chi-square test for categorical variables. Differences were considered statistically significant at p < 0.05. For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients. Results Our literature search identified 101 papers, including 37 case reports, 12 case series, 3 reviews with case reports, 42 reviews, 4 letters, 1 original article, 1 point of view, and 1 brief report. Four and one patients were excluded from the analysis because of a missing laboratory-proven SARS-CoV-2 infection or an ambiguous GBS diagnosis [disease course resembling chronic inflammatory demyelinating neuropathy (CIDP)], respectively. A total of 52 studies were included in the final analysis (total patients = 73) [5–56]. All data concerning the analyzed patients are reported in Table 1. For one case [20], most clinical and diagnostic details were not reported; therefore, many of our analyses were limited to 72 patients. Epidemiological distribution and demographic characteristics of the patients To date, GBS cases (n = 73) were reported from all continents except Australia. In details, patients were originally from Italy (n = 20), Iran (n = 10), Spain (n = 9), USA (n = 8), United Kingdom (n = 5), France (n = 4), Switzerland (n = 4), Germany (n = 3), Austria (n = 1), Brazil (n = 1), Canada (n = 1), China (n = 1), India (n = 1), Morocco (n = 1), Saudi Arabia (n = 1), Sudan (n = 1), The Netherlands (n = 1), and Turkey (n = 1) (Table 1, Fig. 1). The mean age at onset was 55 ± 17 years (min 11–max 94), including four pediatric cases [21, 27, 35, 41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643). Comorbidities were variably reported with no prevalence of a particular disease. Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America Clinical picture, diagnosis, and therapy of COVID-19 All reported GBS cases (n = 72) except two were symptomatic for COVID-19 with various severity. Most common manifestations of COVID-19 included fever (73.6%, 53/72), cough (72.2%, 52/72), dyspnea and/or pneumonia (63.8%, 46/72), hypo-/ageusia (22.2%, 16/72), hypo-/anosmia (20.8%, 15/72), and diarrhea (18.1%, 13/72). One of the two asymptomatic subjects never developed fever, respiratory symptoms, or pneumonia [10], whereas the other patient showed an asymptomatic pneumonia at chest computed tomography (CT) [12]. In all but six patients with available data [22, 24, 36, 44, 45, 52], SARS-CoV-2 RT-PCR with naso- or oropharyngeal swab or fecal exam was positive at first or following tests. Nevertheless, these six patients tested positive at SARS-CoV-2 serology. In four patients, the laboratory exam for the diagnostic confirmation was not specified [20, 40]. Typical “ground glass” aspects at chest-CT or similar findings at CT, Magnetic Resonance Imaging (MRI) or X-ray compatible with COVID-19 interstitial pneumonia were reported in 40 cases. The detailed therapies for COVID-19 are described in Table 1. Clinical features of GBS spectrum In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1). Results of electrophysiological, CSF, biochemical, and neuroimaging investigations Detailed electroneurography results were reported in 84.9% (62/73) of the cases. Specifically, 77.4% (48/62) cases showed a pattern compatible with a demyelinating polyradiculoneuropathy. In contrast, axonal damage was prominent in 14.5% (9/62). In a minority of the patients (8.1%), a mixed pattern was reported (5/62). Regarding CSF analysis (full results were available in 59 out of 73 cases), the classical albuminocytological dissociation (cell count < 5/µl with elevated CSF proteins) was detected in 71.2% of the cases (42/59) with a median CSF protein of 100.0 mg/dl (min: 49, max: 317 mg/dl). Mild pleocytosis (i.e., cell count ≥ 5/µl), with a maximum cell count of 13/µl, was evident in 5/59 cases (8.5%). Furthermore, CSF SARS-CoV-2 RNA was undetectable in all tested patients (n = 31) (Table 1). Detailed blood haematological and biochemical examinations showed variably leucocytosis (n = 4), leucopenia (n = 17), thrombocytosis (n = 3), thrombocytopenia (n = 5), and increased levels of C-reactive protein (CRP) (n = 22), erythrocyte sedimentation rate (n = 4), d-Dimer (n = 5), fibrinogen (n = 3), ferritin (n = 3), LDH (n = 7), IL-6 (n = 4), IL-1 (n = 3), IL-8 (n = 3), and TNF-α (n = 3) (Table 1). Furthermore, anti-GD1b and anti-GM1 antibodies were positive in one patient with MFS [23] and in one with classic sensorimotor GBS [13], respectively, whereas 33 cases tested negative (one in equivocal range) for anti-ganglioside antibodies. Cranial and spinal MRI scans were performed in a minority of the patients (23/73, 31.5%). Five patients (three cases with AIDP [9, 12, 25], one case with MFS [30], and one case with bilateral facial palsy with paresthesia [52]) showed cranial nerve contrast enhancement in the context of correspondent cranial nerve palsies. Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18, 46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9, 27, 31, 36, 37, 42, 52] and two cases [17, 46], respectively (Table 1). Distribution of clinical and electrophysiological variants and diagnosis of GBS From the clinical point of view, most examined patients presented with a classic sensorimotor variant (70.0%, 51/73), whereas Miller Fisher syndrome, GBS/MFS overlap variants (including polyneuritis cranialis), bilateral facial palsy with paresthesia, pure motor, and paraparetic were described in seven, two, five, four, and one patients, respectively. In three cases, no clinical variant could be established using the reported details (Table 1). In the examined population, 81.8% subjects fulfilled electrophysiological criteria for AIDP (45/55), 12.7% (7/55) for AMSAN, and 5.4% (3/55) for AMAN subtypes. Finally, a specific electrophysiological subtype was not attributable in 18 patients due to the lack of detailed information. The diagnosis of GBS was established based on clinical, CSF, and electrophysiological findings in 44/73 (60.3%) patients, clinical, and electrophysiological data in 18/73 (24.7%) cases, clinical, and CSF data in 8/73 (11.0%), and only clinical findings in 3/73 (4.1%) patients. Indeed, the highest level of diagnostic certainty (level one) was confirmed in 44/73 cases (60.3%). Level two and three were obtained in 24/73 cases (32.9%) and 5/73 (6.8%), respectively (Table 1). Management of GBS and patient outcomes All cases with available therapy data (n = 70) except ten [13, 15, 23, 25, 26, 33, 35–37, 41] were treated with intravenous immunoglobulin (IVIG) (Table 1). Conversely, plasma exchange and steroid therapy were performed in ten (four of them received also IVIG) and two cases, respectively. In two patients, no therapy was given. Mechanical or non-invasive ventilation was implemented in 21.4% (15/70) and 7.1% (5/70) patients due to worsening of GBS or COVID-19, respectively. At further observation (n = 68), 72.1% (49/68) patients demonstrated clinical improvement with partial or complete remission, 10.3% (7/68) cases showed no improvement, 11.8% (8/68) still required critical care treatment, and 5.8% (4/68) died (Table 1). Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66] Interestingly, patients with no improvement or poor outcome (n = 19) showed a slightly higher (but not significant) frequency of clinical history and/or a radiological picture of COVID-19 pneumonia (14/19, 73.7%) compared to those with a favorable prognosis (29/48, 60.4%, p = 0.541). Moreover, the former group of patients was significantly older (mean 62.7 ± 17.8 years, p = 0.011), but with comparable distribution of sex (p = 0.622) and electrophysiological subtypes (p = 0.144) and similar latency between COVID-19 and GBS (p = 0.588) and nadir (p = 0.825), compared to the latter (mean age 51.8 ± 16.6 years). The same findings were confirmed even after excluding cases with no improvement from the analysis (to prevent a possible bias related to the short follow-up time). Discussion COVID-19 pandemic prompts all efforts for the early recognition and treatment of its manifestations. In analogy to other viruses, belonging or not to the coronavirus family [63, 67], neurologic complications in COVID-19 are emerging as one of the most significant clinical chapters of this pandemic. In this regard, peripheral and central nervous system damage in COVID-19 has been postulated to be the consequence of two different mechanisms: 1) hematogenous (infection of endothelial cells or leucocytes) or trans-neuronal (via olfactory tract or other cranial nerves) dissemination to central nervous system in relation with viral neurotropism, and 2) abnormal immune-mediated response causing secondary neurological involvement [62, 68, 69]. The first mechanism is supposed to be responsible for the most common neurological symptoms developed by patients with COVID-19 (e.g., hypogeusia, hyposmia, headache, vertigo, and dizziness). In contrast, the second can lead to severe complications during or after the course of the illness, either dysimmune (e.g., myelitis, encephalitis, GBS) or induced by cytokine overproduction (hypercoagulable state and cerebrovascular events) [68, 69]. In the present systematic review, we reviewed clinical features, results of diagnostic investigations, and outcome in 73 cases of COVID-19-associated GBS spectrum [5–56]. In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70, 71]. However, pediatric cases with GBS have been increasingly reported in the literature [21, 27, 35, 41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus–GBS [72]. This finding may also reflect the gender epidemiology of SARS-CoV-2. In this regard, males typically show a worse COVID-19 outcome compared to the females [70, 71], possibly due to a generally shorter life expectancy or to higher circulating Angiotensin-Converting-Enzyme 2 (ACE2) levels, the cellular receptor for SARS-CoV-2, in the former compared to the latter [71]. Moreover, given that GBS is a rare disease [57] the epidemiological distribution of the reported cases seems to reflect current worldwide outbreaks, with Europe being the “hottest” spot in March–May 2020 and USA together with Asia in the following period [73, 74]. On another issue, despite a few GBS cases seemed to have a para-infectious profile [10, 37, 38, 40, 55, 56] as described for Zika virus [75], all other reported patients developed neurological symptoms with a typical latency after COVID-19 (median time 14 days). This feature, together with the frequently reported negative nasopharyngeal swab at GBS onset [22, 24, 36, 44, 45, 52] and clinical improvement after IVIG therapy, seems to support the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [76, 77]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.) in GBS tested cases may reinforce the hypothesis of a systemic inflammatory storm in COVID-19 [76, 77]. However, given the limited data, we could not perform an accurate analysis of the distribution and, eventually, prognostic value of inflammatory markers in COVID-19-associated GBS. Moreover, we cannot exclude that in cases with GBS developing before or together with COVID-19 symptoms, the disease might have progressed sub-clinically in the early phase to manifest afterwards with its typical systemic clinical picture. Indeed, two cases [10, 12], who tested positive for SARS-CoV-2, never developed COVID-19 respiratory or systemic symptoms and one of them showed an asymptomatic pneumonia at chest-CT [12]. However, only more extensive epidemiological and translational studies, with the aim to compare the characteristics of GBS associated or not with COVID-19, could clarify these issues. In our population, most common clinical manifestations and distribution of clinical variants resemble those of classic GBS confirming the predominance of the sensorimotor syndrome compared to MFS and other rare variants [57–59, 66]. Similarly, the results of CSF analysis reflected typical neurochemical findings in non-COVID-19 GBS. In the latter, elevated CSF proteins and pleocytosis were described in about 50–80% [57, 78] and 11–15% cases, respectively [58, 79, 80], largely overlapping with the percentages in our cohort. In this regard, the mostly normal cell count, together with the absence of SARS-CoV-2 RNA in all tested CSF samples [6–9, 12–14, 16, 21–24, 31, 33, 36, 42, 44, 52, 55], makes the possibility of a direct invasion from SARS-CoV-2 into the nerve roots with intrathecal viral replication less probable. However, a possible bias might rely on the lack of systematic data concerning the latency between symptom onset and CSF sampling in COVID-19 GBS cases. On another issue, in a further case of MFS associated withCOVID-19, who came to our attention, we observed the absence of intrathecal synthesis of SARS-CoV-2 antibodies together with a massive increase of CSF phosphorylated neurofilament heavy chain (pNfH) and serum neurofilament light chain (NfL) proteins, supporting the role of neurochemical markers as easily implementable tools for the detection of nervous system affection in COVID-19-related diseases [81, 82]. At variance with CSF findings, we found a discrepancy concerning MRI findings between classic GBS and COVID-19-related GBS. Specifically, while most cases of the former group showed typically spinal root enhancement at MRI [83], in the latter group, in analogy with Zika-associated GBS, the same finding was less frequently reported [84]. However, caution should be warranted in the interpretation of these results, given that MRI findings might have been underestimated, due to lack of a sufficient number of exams in the context of pandemic-imposed restrictions in the routine clinical setting. Regarding the distribution of GBS electrophysiological variants, our analysis showed that COVID-19-associated GBS manifests prevalently with AIDP and, to a lesser extent, with AMSAN and AMAN, in line with classic GBS in Western countries [66, 85]. Conversely, the observation of positive anti-GD1b antibodies in one COVID-19-related MFS patient and negative anti-ganglioside antibodies in other five cases appear in discordance with the high prevalence (≈ 90%) of anti-GQ1b antibodies among non-COVID-19 MFS cases [86], and may suggest different immune-mediated mechanisms. However, these results could not be generalized until a wider population would be tested. In analogy to classic GBS, approximately one-fifth of COVID-19-associated GBS subjects required mechanical ventilation during hospitalisation [87]. In this regard, cases with no improvement or unfavorable outcome showed, in comparison to those with a good prognosis, an older age, confirming similar findings both in classic GBS [58, 88] and in COVID-19 [89], and a slightly higher frequency (without reaching a statistical significance) of past or concurrent COVID-19 pneumonia. However, given the short follow-up time in most cases, we could not reach a definite conclusion on the impact of past or concurrent COVID-19 restrictive syndrome due to pneumonia on the prognosis of GBS patients. Future prospective studies are needed to clarify this issue. Moreover, given that also preceding diarrhea (mostly caused by Campylobacter Jejuni infection) is a strong negative prognostic factor in classic GBS [57, 88], further prospective studies are needed to compare the severity of GBS related to COVID-19 to that associated with C. jejuni. Finally, in the context of respiratory failure and ventilation associated with COVID-19, the differential diagnosis should always take into consideration critical illness neuropathy and myopathy, which tend to develop later during the critical course [90]. Despite these findings, approximately one-third of COVID-19-related GBS patients showed no clinical and/or radiological evidence of pneumonia, providing evidence that GBS may also develop in the context of a paucisymptomatic or even asymptomatic COVID-19. However, given that among the GBS population only two asymptomatic COVID-19 patients were reported to date, we may speculate that, in most cases, a certain degree of lung injury (even minimal) or at least hematic dissemination (e.g., fever underlying significant viral load) is necessary to trigger the immuno-mediated process through lymphocytic recognition of self-antigens or molecular mimicry. Major strengths of our review are the inclusion of a high number of patients, together with an in-depth analysis of the clinical and diagnostic features of COVID-19-associated GBS. We are aware that selection bias might have occurred, given that most reported cases to date have been described mostly in Europe (47 out of 73) and during COVID-19 highest spreading. Therefore, future extensive epidemiological studies are necessary to ascertain the nature of the association between COVID-19 and GBS (causal or coincidental). Moreover, we cannot exclude the possibility that at least some of the cases represent instances of CIDP, given the frequent absence of a follow-up longer than 2 months. On another issue, the low but possible evidence of an epidemiological link between vaccines and GBS development [57, 58] should aware the clinicians of the possible occurrence of GBS after COVID-19 vaccination in the long-term future. In conclusion, based on the systematic review of 73 cases, we showed that the clinical picture of COVID-19-associated GBS seems to resemble that of classic GBS or Zika-associated GBS. Moreover, the chronological evolution, the response to IVIG, and the absence of SARS-CoV-2 RNA in CSF may suggest a prominent post-infectious immune-mediated mechanism rather than a para-infectious one. Although most cases were symptomatic for COVID-19, the preliminary report of a few patients without respiratory or systemic symptoms raises a significant healthcare issue, namely the importance of SARS-CoV-2 testing in all patients with suspected GBS during the pandemic, with the aim to provide an eventual rapid case isolation. Nevertheless, only further analyses on more comprehensive cohorts could help in clarifying better all these issues.
sec	Introduction Coronavirus disease 2019 (COVID-19) pandemic has rapidly spread around the world from Jan-2020, with more than 14,000,000 cases confirmed so far [1]. Although primary affecting the respiratory system, central and peripheral neurological manifestations associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been increasingly reported [2–4]. In detail, several pieces of evidence suggested an association between SARS-CoV-2 infection and the development of Guillain–Barré Syndrome (GBS) [5–56]. GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]. With this background, our systematic review aimed to provide a comprehensive and updated overview of all case reports and series of COVID-19-related GBS to identify predominant clinical, laboratory, and neurophysiological patterns and to discuss the possible underlying pathophysiology.
title	Introduction
p	Coronavirus disease 2019 (COVID-19) pandemic has rapidly spread around the world from Jan-2020, with more than 14,000,000 cases confirmed so far [1]. Although primary affecting the respiratory system, central and peripheral neurological manifestations associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been increasingly reported [2–4]. In detail, several pieces of evidence suggested an association between SARS-CoV-2 infection and the development of Guillain–Barré Syndrome (GBS) [5–56].
p	GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64].
p	With this background, our systematic review aimed to provide a comprehensive and updated overview of all case reports and series of COVID-19-related GBS to identify predominant clinical, laboratory, and neurophysiological patterns and to discuss the possible underlying pathophysiology.
sec	Methods We performed a systematic review according to the SALSA (Search, Appraisal, Synthesis, and Analysis) analytic framework [65]. We screened in PubMed and Google Scholar databases for all case descriptions of GBS associated with COVID-19 that were published from January 1st 2020 up to July 20th 2020. Keywords (including all commonly used abbreviations of these terms) used in the search strategy were as follows: [“acute autoimmune neuropathy” OR “acute inflammatory demyelinating polyneuropathy” OR “acute inflammatory demyelinating polyradiculoneuropathy,” OR “acute inflammatory polyneuropathy” OR “Demyelinating Polyradiculoneuropathy” OR “Guillain–Barre Syndrome” OR “Guillain–Barre” OR ““Miller–Fisher” OR “Bickerstaff encephalitis” OR “AIDP” OR “AMAN” OR “AMSAN” OR polyneuritis cranialis] AND [“COVID-19” OR “Wuhan coronavirus” OR “novel coronavirus” OR “novel coronavirus 2019” OR “SARS” OR “SARS-CoV-2”]. Suitable references were also identified in the authors’ archives of scientific literature on GBS. We restricted our search to studies published in English, Spanish, or Italian. Publications that were not peer-reviewed were excluded from this study. PRISMA criteria were applied. For each case, we extracted data concerning demographic and clinical variables, results of diagnostic investigations, and outcome. If the GBS clinical variant [57] or the electrophysiological subtype [61] was not explicitly reported in the paper, we reconstructed it, when possible, from reported details. We also classified the diagnostic certainty of all cases according to the Brighton Criteria [66]. Searches were performed by SAR, AA, and MF. The selection of relevant articles was shared with all authors. For statistical analysis, we used IBM SPSS Statistics version 21 (IBM, Armonk, NY, USA). Based on the distribution of values, continuous data were expressed as mean ± standard deviation or as median and interquartile range (IQR). Depending on the number of groups and data distribution, we applied the t test, the Mann–Whitney U test or the Kruskal–Wallis test (followed by Dunn–Bonferroni post hoc test). All reported p values were adjusted for multiple comparisons. We adopted the Chi-square test for categorical variables. Differences were considered statistically significant at p < 0.05. For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.
title	Methods
p	We performed a systematic review according to the SALSA (Search, Appraisal, Synthesis, and Analysis) analytic framework [65]. We screened in PubMed and Google Scholar databases for all case descriptions of GBS associated with COVID-19 that were published from January 1st 2020 up to July 20th 2020. Keywords (including all commonly used abbreviations of these terms) used in the search strategy were as follows: [“acute autoimmune neuropathy” OR “acute inflammatory demyelinating polyneuropathy” OR “acute inflammatory demyelinating polyradiculoneuropathy,” OR “acute inflammatory polyneuropathy” OR “Demyelinating Polyradiculoneuropathy” OR “Guillain–Barre Syndrome” OR “Guillain–Barre” OR ““Miller–Fisher” OR “Bickerstaff encephalitis” OR “AIDP” OR “AMAN” OR “AMSAN” OR polyneuritis cranialis] AND [“COVID-19” OR “Wuhan coronavirus” OR “novel coronavirus” OR “novel coronavirus 2019” OR “SARS” OR “SARS-CoV-2”]. Suitable references were also identified in the authors’ archives of scientific literature on GBS. We restricted our search to studies published in English, Spanish, or Italian. Publications that were not peer-reviewed were excluded from this study. PRISMA criteria were applied. For each case, we extracted data concerning demographic and clinical variables, results of diagnostic investigations, and outcome. If the GBS clinical variant [57] or the electrophysiological subtype [61] was not explicitly reported in the paper, we reconstructed it, when possible, from reported details. We also classified the diagnostic certainty of all cases according to the Brighton Criteria [66]. Searches were performed by SAR, AA, and MF. The selection of relevant articles was shared with all authors.
p	For statistical analysis, we used IBM SPSS Statistics version 21 (IBM, Armonk, NY, USA). Based on the distribution of values, continuous data were expressed as mean ± standard deviation or as median and interquartile range (IQR). Depending on the number of groups and data distribution, we applied the t test, the Mann–Whitney U test or the Kruskal–Wallis test (followed by Dunn–Bonferroni post hoc test). All reported p values were adjusted for multiple comparisons. We adopted the Chi-square test for categorical variables. Differences were considered statistically significant at p < 0.05.
p	For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.
sec	Results Our literature search identified 101 papers, including 37 case reports, 12 case series, 3 reviews with case reports, 42 reviews, 4 letters, 1 original article, 1 point of view, and 1 brief report. Four and one patients were excluded from the analysis because of a missing laboratory-proven SARS-CoV-2 infection or an ambiguous GBS diagnosis [disease course resembling chronic inflammatory demyelinating neuropathy (CIDP)], respectively. A total of 52 studies were included in the final analysis (total patients = 73) [5–56]. All data concerning the analyzed patients are reported in Table 1. For one case [20], most clinical and diagnostic details were not reported; therefore, many of our analyses were limited to 72 patients. Epidemiological distribution and demographic characteristics of the patients To date, GBS cases (n = 73) were reported from all continents except Australia. In details, patients were originally from Italy (n = 20), Iran (n = 10), Spain (n = 9), USA (n = 8), United Kingdom (n = 5), France (n = 4), Switzerland (n = 4), Germany (n = 3), Austria (n = 1), Brazil (n = 1), Canada (n = 1), China (n = 1), India (n = 1), Morocco (n = 1), Saudi Arabia (n = 1), Sudan (n = 1), The Netherlands (n = 1), and Turkey (n = 1) (Table 1, Fig. 1). The mean age at onset was 55 ± 17 years (min 11–max 94), including four pediatric cases [21, 27, 35, 41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643). Comorbidities were variably reported with no prevalence of a particular disease. Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America Clinical picture, diagnosis, and therapy of COVID-19 All reported GBS cases (n = 72) except two were symptomatic for COVID-19 with various severity. Most common manifestations of COVID-19 included fever (73.6%, 53/72), cough (72.2%, 52/72), dyspnea and/or pneumonia (63.8%, 46/72), hypo-/ageusia (22.2%, 16/72), hypo-/anosmia (20.8%, 15/72), and diarrhea (18.1%, 13/72). One of the two asymptomatic subjects never developed fever, respiratory symptoms, or pneumonia [10], whereas the other patient showed an asymptomatic pneumonia at chest computed tomography (CT) [12]. In all but six patients with available data [22, 24, 36, 44, 45, 52], SARS-CoV-2 RT-PCR with naso- or oropharyngeal swab or fecal exam was positive at first or following tests. Nevertheless, these six patients tested positive at SARS-CoV-2 serology. In four patients, the laboratory exam for the diagnostic confirmation was not specified [20, 40]. Typical “ground glass” aspects at chest-CT or similar findings at CT, Magnetic Resonance Imaging (MRI) or X-ray compatible with COVID-19 interstitial pneumonia were reported in 40 cases. The detailed therapies for COVID-19 are described in Table 1. Clinical features of GBS spectrum In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1). Results of electrophysiological, CSF, biochemical, and neuroimaging investigations Detailed electroneurography results were reported in 84.9% (62/73) of the cases. Specifically, 77.4% (48/62) cases showed a pattern compatible with a demyelinating polyradiculoneuropathy. In contrast, axonal damage was prominent in 14.5% (9/62). In a minority of the patients (8.1%), a mixed pattern was reported (5/62). Regarding CSF analysis (full results were available in 59 out of 73 cases), the classical albuminocytological dissociation (cell count < 5/µl with elevated CSF proteins) was detected in 71.2% of the cases (42/59) with a median CSF protein of 100.0 mg/dl (min: 49, max: 317 mg/dl). Mild pleocytosis (i.e., cell count ≥ 5/µl), with a maximum cell count of 13/µl, was evident in 5/59 cases (8.5%). Furthermore, CSF SARS-CoV-2 RNA was undetectable in all tested patients (n = 31) (Table 1). Detailed blood haematological and biochemical examinations showed variably leucocytosis (n = 4), leucopenia (n = 17), thrombocytosis (n = 3), thrombocytopenia (n = 5), and increased levels of C-reactive protein (CRP) (n = 22), erythrocyte sedimentation rate (n = 4), d-Dimer (n = 5), fibrinogen (n = 3), ferritin (n = 3), LDH (n = 7), IL-6 (n = 4), IL-1 (n = 3), IL-8 (n = 3), and TNF-α (n = 3) (Table 1). Furthermore, anti-GD1b and anti-GM1 antibodies were positive in one patient with MFS [23] and in one with classic sensorimotor GBS [13], respectively, whereas 33 cases tested negative (one in equivocal range) for anti-ganglioside antibodies. Cranial and spinal MRI scans were performed in a minority of the patients (23/73, 31.5%). Five patients (three cases with AIDP [9, 12, 25], one case with MFS [30], and one case with bilateral facial palsy with paresthesia [52]) showed cranial nerve contrast enhancement in the context of correspondent cranial nerve palsies. Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18, 46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9, 27, 31, 36, 37, 42, 52] and two cases [17, 46], respectively (Table 1). Distribution of clinical and electrophysiological variants and diagnosis of GBS From the clinical point of view, most examined patients presented with a classic sensorimotor variant (70.0%, 51/73), whereas Miller Fisher syndrome, GBS/MFS overlap variants (including polyneuritis cranialis), bilateral facial palsy with paresthesia, pure motor, and paraparetic were described in seven, two, five, four, and one patients, respectively. In three cases, no clinical variant could be established using the reported details (Table 1). In the examined population, 81.8% subjects fulfilled electrophysiological criteria for AIDP (45/55), 12.7% (7/55) for AMSAN, and 5.4% (3/55) for AMAN subtypes. Finally, a specific electrophysiological subtype was not attributable in 18 patients due to the lack of detailed information. The diagnosis of GBS was established based on clinical, CSF, and electrophysiological findings in 44/73 (60.3%) patients, clinical, and electrophysiological data in 18/73 (24.7%) cases, clinical, and CSF data in 8/73 (11.0%), and only clinical findings in 3/73 (4.1%) patients. Indeed, the highest level of diagnostic certainty (level one) was confirmed in 44/73 cases (60.3%). Level two and three were obtained in 24/73 cases (32.9%) and 5/73 (6.8%), respectively (Table 1). Management of GBS and patient outcomes All cases with available therapy data (n = 70) except ten [13, 15, 23, 25, 26, 33, 35–37, 41] were treated with intravenous immunoglobulin (IVIG) (Table 1). Conversely, plasma exchange and steroid therapy were performed in ten (four of them received also IVIG) and two cases, respectively. In two patients, no therapy was given. Mechanical or non-invasive ventilation was implemented in 21.4% (15/70) and 7.1% (5/70) patients due to worsening of GBS or COVID-19, respectively. At further observation (n = 68), 72.1% (49/68) patients demonstrated clinical improvement with partial or complete remission, 10.3% (7/68) cases showed no improvement, 11.8% (8/68) still required critical care treatment, and 5.8% (4/68) died (Table 1). Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66] Interestingly, patients with no improvement or poor outcome (n = 19) showed a slightly higher (but not significant) frequency of clinical history and/or a radiological picture of COVID-19 pneumonia (14/19, 73.7%) compared to those with a favorable prognosis (29/48, 60.4%, p = 0.541). Moreover, the former group of patients was significantly older (mean 62.7 ± 17.8 years, p = 0.011), but with comparable distribution of sex (p = 0.622) and electrophysiological subtypes (p = 0.144) and similar latency between COVID-19 and GBS (p = 0.588) and nadir (p = 0.825), compared to the latter (mean age 51.8 ± 16.6 years). The same findings were confirmed even after excluding cases with no improvement from the analysis (to prevent a possible bias related to the short follow-up time).
title	Results
p	Our literature search identified 101 papers, including 37 case reports, 12 case series, 3 reviews with case reports, 42 reviews, 4 letters, 1 original article, 1 point of view, and 1 brief report. Four and one patients were excluded from the analysis because of a missing laboratory-proven SARS-CoV-2 infection or an ambiguous GBS diagnosis [disease course resembling chronic inflammatory demyelinating neuropathy (CIDP)], respectively. A total of 52 studies were included in the final analysis (total patients = 73) [5–56]. All data concerning the analyzed patients are reported in Table 1. For one case [20], most clinical and diagnostic details were not reported; therefore, many of our analyses were limited to 72 patients.
sec	Epidemiological distribution and demographic characteristics of the patients To date, GBS cases (n = 73) were reported from all continents except Australia. In details, patients were originally from Italy (n = 20), Iran (n = 10), Spain (n = 9), USA (n = 8), United Kingdom (n = 5), France (n = 4), Switzerland (n = 4), Germany (n = 3), Austria (n = 1), Brazil (n = 1), Canada (n = 1), China (n = 1), India (n = 1), Morocco (n = 1), Saudi Arabia (n = 1), Sudan (n = 1), The Netherlands (n = 1), and Turkey (n = 1) (Table 1, Fig. 1). The mean age at onset was 55 ± 17 years (min 11–max 94), including four pediatric cases [21, 27, 35, 41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643). Comorbidities were variably reported with no prevalence of a particular disease. Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America
title	Epidemiological distribution and demographic characteristics of the patients
p	To date, GBS cases (n = 73) were reported from all continents except Australia. In details, patients were originally from Italy (n = 20), Iran (n = 10), Spain (n = 9), USA (n = 8), United Kingdom (n = 5), France (n = 4), Switzerland (n = 4), Germany (n = 3), Austria (n = 1), Brazil (n = 1), Canada (n = 1), China (n = 1), India (n = 1), Morocco (n = 1), Saudi Arabia (n = 1), Sudan (n = 1), The Netherlands (n = 1), and Turkey (n = 1) (Table 1, Fig. 1). The mean age at onset was 55 ± 17 years (min 11–max 94), including four pediatric cases [21, 27, 35, 41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643). Comorbidities were variably reported with no prevalence of a particular disease. Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America
figure	Fig. 1 Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America
label	Fig. 1
caption	Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America
p	Temporal and spatial distribution of reported cases with COVID-19-associated Guillain–Barré syndrome in literature from 1st January until 20th July 2020. The x-axis shows the number of described patients. The y-axis illustrates the countries of provenience of the cases. In each line, different colours represent the months of April, May, June, and July (* until 20th July) 2020, in which the cases were published. Abbreviations: UK, United Kingdom, USA, United States of America
sec	Clinical picture, diagnosis, and therapy of COVID-19 All reported GBS cases (n = 72) except two were symptomatic for COVID-19 with various severity. Most common manifestations of COVID-19 included fever (73.6%, 53/72), cough (72.2%, 52/72), dyspnea and/or pneumonia (63.8%, 46/72), hypo-/ageusia (22.2%, 16/72), hypo-/anosmia (20.8%, 15/72), and diarrhea (18.1%, 13/72). One of the two asymptomatic subjects never developed fever, respiratory symptoms, or pneumonia [10], whereas the other patient showed an asymptomatic pneumonia at chest computed tomography (CT) [12]. In all but six patients with available data [22, 24, 36, 44, 45, 52], SARS-CoV-2 RT-PCR with naso- or oropharyngeal swab or fecal exam was positive at first or following tests. Nevertheless, these six patients tested positive at SARS-CoV-2 serology. In four patients, the laboratory exam for the diagnostic confirmation was not specified [20, 40]. Typical “ground glass” aspects at chest-CT or similar findings at CT, Magnetic Resonance Imaging (MRI) or X-ray compatible with COVID-19 interstitial pneumonia were reported in 40 cases. The detailed therapies for COVID-19 are described in Table 1.
title	Clinical picture, diagnosis, and therapy of COVID-19
p	All reported GBS cases (n = 72) except two were symptomatic for COVID-19 with various severity. Most common manifestations of COVID-19 included fever (73.6%, 53/72), cough (72.2%, 52/72), dyspnea and/or pneumonia (63.8%, 46/72), hypo-/ageusia (22.2%, 16/72), hypo-/anosmia (20.8%, 15/72), and diarrhea (18.1%, 13/72). One of the two asymptomatic subjects never developed fever, respiratory symptoms, or pneumonia [10], whereas the other patient showed an asymptomatic pneumonia at chest computed tomography (CT) [12]. In all but six patients with available data [22, 24, 36, 44, 45, 52], SARS-CoV-2 RT-PCR with naso- or oropharyngeal swab or fecal exam was positive at first or following tests. Nevertheless, these six patients tested positive at SARS-CoV-2 serology. In four patients, the laboratory exam for the diagnostic confirmation was not specified [20, 40]. Typical “ground glass” aspects at chest-CT or similar findings at CT, Magnetic Resonance Imaging (MRI) or X-ray compatible with COVID-19 interstitial pneumonia were reported in 40 cases. The detailed therapies for COVID-19 are described in Table 1.
sec	Clinical features of GBS spectrum In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1).
title	Clinical features of GBS spectrum
p	In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1).
sec	Results of electrophysiological, CSF, biochemical, and neuroimaging investigations Detailed electroneurography results were reported in 84.9% (62/73) of the cases. Specifically, 77.4% (48/62) cases showed a pattern compatible with a demyelinating polyradiculoneuropathy. In contrast, axonal damage was prominent in 14.5% (9/62). In a minority of the patients (8.1%), a mixed pattern was reported (5/62). Regarding CSF analysis (full results were available in 59 out of 73 cases), the classical albuminocytological dissociation (cell count < 5/µl with elevated CSF proteins) was detected in 71.2% of the cases (42/59) with a median CSF protein of 100.0 mg/dl (min: 49, max: 317 mg/dl). Mild pleocytosis (i.e., cell count ≥ 5/µl), with a maximum cell count of 13/µl, was evident in 5/59 cases (8.5%). Furthermore, CSF SARS-CoV-2 RNA was undetectable in all tested patients (n = 31) (Table 1). Detailed blood haematological and biochemical examinations showed variably leucocytosis (n = 4), leucopenia (n = 17), thrombocytosis (n = 3), thrombocytopenia (n = 5), and increased levels of C-reactive protein (CRP) (n = 22), erythrocyte sedimentation rate (n = 4), d-Dimer (n = 5), fibrinogen (n = 3), ferritin (n = 3), LDH (n = 7), IL-6 (n = 4), IL-1 (n = 3), IL-8 (n = 3), and TNF-α (n = 3) (Table 1). Furthermore, anti-GD1b and anti-GM1 antibodies were positive in one patient with MFS [23] and in one with classic sensorimotor GBS [13], respectively, whereas 33 cases tested negative (one in equivocal range) for anti-ganglioside antibodies. Cranial and spinal MRI scans were performed in a minority of the patients (23/73, 31.5%). Five patients (three cases with AIDP [9, 12, 25], one case with MFS [30], and one case with bilateral facial palsy with paresthesia [52]) showed cranial nerve contrast enhancement in the context of correspondent cranial nerve palsies. Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18, 46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9, 27, 31, 36, 37, 42, 52] and two cases [17, 46], respectively (Table 1).
title	Results of electrophysiological, CSF, biochemical, and neuroimaging investigations
p	Detailed electroneurography results were reported in 84.9% (62/73) of the cases. Specifically, 77.4% (48/62) cases showed a pattern compatible with a demyelinating polyradiculoneuropathy. In contrast, axonal damage was prominent in 14.5% (9/62). In a minority of the patients (8.1%), a mixed pattern was reported (5/62). Regarding CSF analysis (full results were available in 59 out of 73 cases), the classical albuminocytological dissociation (cell count < 5/µl with elevated CSF proteins) was detected in 71.2% of the cases (42/59) with a median CSF protein of 100.0 mg/dl (min: 49, max: 317 mg/dl). Mild pleocytosis (i.e., cell count ≥ 5/µl), with a maximum cell count of 13/µl, was evident in 5/59 cases (8.5%). Furthermore, CSF SARS-CoV-2 RNA was undetectable in all tested patients (n = 31) (Table 1).
p	Detailed blood haematological and biochemical examinations showed variably leucocytosis (n = 4), leucopenia (n = 17), thrombocytosis (n = 3), thrombocytopenia (n = 5), and increased levels of C-reactive protein (CRP) (n = 22), erythrocyte sedimentation rate (n = 4), d-Dimer (n = 5), fibrinogen (n = 3), ferritin (n = 3), LDH (n = 7), IL-6 (n = 4), IL-1 (n = 3), IL-8 (n = 3), and TNF-α (n = 3) (Table 1).
p	Furthermore, anti-GD1b and anti-GM1 antibodies were positive in one patient with MFS [23] and in one with classic sensorimotor GBS [13], respectively, whereas 33 cases tested negative (one in equivocal range) for anti-ganglioside antibodies.
p	Cranial and spinal MRI scans were performed in a minority of the patients (23/73, 31.5%). Five patients (three cases with AIDP [9, 12, 25], one case with MFS [30], and one case with bilateral facial palsy with paresthesia [52]) showed cranial nerve contrast enhancement in the context of correspondent cranial nerve palsies. Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18, 46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9, 27, 31, 36, 37, 42, 52] and two cases [17, 46], respectively (Table 1).
sec	Distribution of clinical and electrophysiological variants and diagnosis of GBS From the clinical point of view, most examined patients presented with a classic sensorimotor variant (70.0%, 51/73), whereas Miller Fisher syndrome, GBS/MFS overlap variants (including polyneuritis cranialis), bilateral facial palsy with paresthesia, pure motor, and paraparetic were described in seven, two, five, four, and one patients, respectively. In three cases, no clinical variant could be established using the reported details (Table 1). In the examined population, 81.8% subjects fulfilled electrophysiological criteria for AIDP (45/55), 12.7% (7/55) for AMSAN, and 5.4% (3/55) for AMAN subtypes. Finally, a specific electrophysiological subtype was not attributable in 18 patients due to the lack of detailed information. The diagnosis of GBS was established based on clinical, CSF, and electrophysiological findings in 44/73 (60.3%) patients, clinical, and electrophysiological data in 18/73 (24.7%) cases, clinical, and CSF data in 8/73 (11.0%), and only clinical findings in 3/73 (4.1%) patients. Indeed, the highest level of diagnostic certainty (level one) was confirmed in 44/73 cases (60.3%). Level two and three were obtained in 24/73 cases (32.9%) and 5/73 (6.8%), respectively (Table 1).
title	Distribution of clinical and electrophysiological variants and diagnosis of GBS
p	From the clinical point of view, most examined patients presented with a classic sensorimotor variant (70.0%, 51/73), whereas Miller Fisher syndrome, GBS/MFS overlap variants (including polyneuritis cranialis), bilateral facial palsy with paresthesia, pure motor, and paraparetic were described in seven, two, five, four, and one patients, respectively. In three cases, no clinical variant could be established using the reported details (Table 1). In the examined population, 81.8% subjects fulfilled electrophysiological criteria for AIDP (45/55), 12.7% (7/55) for AMSAN, and 5.4% (3/55) for AMAN subtypes. Finally, a specific electrophysiological subtype was not attributable in 18 patients due to the lack of detailed information. The diagnosis of GBS was established based on clinical, CSF, and electrophysiological findings in 44/73 (60.3%) patients, clinical, and electrophysiological data in 18/73 (24.7%) cases, clinical, and CSF data in 8/73 (11.0%), and only clinical findings in 3/73 (4.1%) patients. Indeed, the highest level of diagnostic certainty (level one) was confirmed in 44/73 cases (60.3%). Level two and three were obtained in 24/73 cases (32.9%) and 5/73 (6.8%), respectively (Table 1).
sec	Management of GBS and patient outcomes All cases with available therapy data (n = 70) except ten [13, 15, 23, 25, 26, 33, 35–37, 41] were treated with intravenous immunoglobulin (IVIG) (Table 1). Conversely, plasma exchange and steroid therapy were performed in ten (four of them received also IVIG) and two cases, respectively. In two patients, no therapy was given. Mechanical or non-invasive ventilation was implemented in 21.4% (15/70) and 7.1% (5/70) patients due to worsening of GBS or COVID-19, respectively. At further observation (n = 68), 72.1% (49/68) patients demonstrated clinical improvement with partial or complete remission, 10.3% (7/68) cases showed no improvement, 11.8% (8/68) still required critical care treatment, and 5.8% (4/68) died (Table 1). Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66] Interestingly, patients with no improvement or poor outcome (n = 19) showed a slightly higher (but not significant) frequency of clinical history and/or a radiological picture of COVID-19 pneumonia (14/19, 73.7%) compared to those with a favorable prognosis (29/48, 60.4%, p = 0.541). Moreover, the former group of patients was significantly older (mean 62.7 ± 17.8 years, p = 0.011), but with comparable distribution of sex (p = 0.622) and electrophysiological subtypes (p = 0.144) and similar latency between COVID-19 and GBS (p = 0.588) and nadir (p = 0.825), compared to the latter (mean age 51.8 ± 16.6 years). The same findings were confirmed even after excluding cases with no improvement from the analysis (to prevent a possible bias related to the short follow-up time).
title	Management of GBS and patient outcomes
p	All cases with available therapy data (n = 70) except ten [13, 15, 23, 25, 26, 33, 35–37, 41] were treated with intravenous immunoglobulin (IVIG) (Table 1). Conversely, plasma exchange and steroid therapy were performed in ten (four of them received also IVIG) and two cases, respectively. In two patients, no therapy was given. Mechanical or non-invasive ventilation was implemented in 21.4% (15/70) and 7.1% (5/70) patients due to worsening of GBS or COVID-19, respectively. At further observation (n = 68), 72.1% (49/68) patients demonstrated clinical improvement with partial or complete remission, 10.3% (7/68) cases showed no improvement, 11.8% (8/68) still required critical care treatment, and 5.8% (4/68) died (Table 1). Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66]
table-wrap	Table 1 Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66]
label	Table 1
caption	Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases
p	Summary of clinical findings, results of diagnostic investigations, and outcome in 73 GBS cases
table	Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface) Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
tr	Article Country Age Sex GBS clinical picture COVID-19 clinical picture Previous comorbidities GBS diagnosis Level of diagnostic certaintyb GBS variant
th	Article
th	Country
th	Age
th	Sex
th	GBS clinical picture
th	COVID-19 clinical picture
th	Previous comorbidities
th	GBS diagnosis
th	Level of diagnostic certaintyb
th	GBS variant
tr	Days between COVID-19 symptoms and GBS onset Onset Disease course Autonomic disturbances Respiratory symptoms/failure Time to Nadira
th	Days between COVID-19 symptoms and GBS onset
th	Onset
th	Disease course
th	Autonomic disturbances
th	Respiratory symptoms/failure
th	Time to Nadira
tr	Agosti et al. [5] Italy 68 M 5 days after LL weakness Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia NA No NA Dry cough associated with fever, dysgeusia, and hyposmia Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm Clinical + CSF + electrophysiology 1 Pure motor
td	Agosti et al. [5]
td	Italy
td	68
td	M
td	5 days after
td	LL weakness
td	Bilateral facial palsy, progressive symmetric ascending flaccid tetraparesis, achilles tendon areflexia
td	NA
td	No
td	NA
td	Dry cough associated with fever, dysgeusia, and hyposmia
td	Dyslipidemia, benign prostatic hypertrophy, hypertension, abdominal aortic aneurysm
td	Clinical + CSF + electrophysiology
td	1
td	Pure motor
tr	Alberti et al. [6] Italy 71 M 4 days after (no resolution of pneumonia) LL paraesthesia Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea None Yes (concurrent pneumonia) 4 days after symptoms onset (24 h after the admission) Fever (low grade), dyspnea, pneumonia Hypertension, treated abdominal aortic aneurysm, treated lung cancer Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Alberti et al. [6]
td	Italy
td	71
td	M
td	4 days after (no resolution of pneumonia)
td	LL paraesthesia
td	Ascendant weakness, flaccid tetraparesis, hypoesthesia and paraesthesia in the 4 limbs, generalized areflexia, dyspnea
td	None
td	Yes (concurrent pneumonia)
td	4 days after symptoms onset (24 h after the admission)
td	Fever (low grade), dyspnea, pneumonia
td	Hypertension, treated abdominal aortic aneurysm, treated lung cancer
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Arnaud et al. [7] France 64 M 23 days after Fast progressive LL weakness Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia None No 4 days after symptoms onset Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia DM type 2 Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Arnaud et al. [7]
td	France
td	64
td	M
td	23 days after
td	Fast progressive LL weakness
td	Generalized areflexia, severe flaccid proximal paraparesis, decreased proprioceptive length-dependent sensitivity and LL pinprick and light touch hypoesthesia
td	None
td	No
td	4 days after symptoms onset
td	Fever, cough, diarrhea, dyspnea, severe interstitial pneumonia
td	DM type 2
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Assini et al. [8] Italy 55 M 20 days after Bilateral eyelid ptosis, dysphagia, dysphonia Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect None Yes (concurrent pneumonia) NA Fever, anosmia, ageusia, cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor overlapping with Miller-Fisher
td	Assini et al. [8]
td	Italy
td	55
td	M
td	20 days after
td	Bilateral eyelid ptosis, dysphagia, dysphonia
td	Masseter weakness, tongue protusion (bilateral hypoglossal nerve paralysis), UL and LL hyporeflexia without muscle weakness, soft palate elevation defect
td	None
td	Yes (concurrent pneumonia)
td	NA
td	Fever, anosmia, ageusia, cough, pneumonia
td	NA
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor overlapping with Miller-Fisher
tr	Assini et al. [8] Italy 60 M 20 days after Distal tetraparesis with right foot drop, autonomic disturbances UL and LL distal weakness, right foot drop, generalized areflexia Gastroplegia, paralytic ileus, loss of blood pressure control Yes (concurrent pneumonia) NA Fever, severe interstitial pneumonia NA Clinical + electrophysiology 2 Pure motor
td	Assini et al. [8]
td	Italy
td	60
td	M
td	20 days after
td	Distal tetraparesis with right foot drop, autonomic disturbances
td	UL and LL distal weakness, right foot drop, generalized areflexia
td	Gastroplegia, paralytic ileus, loss of blood pressure control
td	Yes (concurrent pneumonia)
td	NA
td	Fever, severe interstitial pneumonia
td	NA
td	Clinical + electrophysiology
td	2
td	Pure motor
tr	Bigaut et al. [9] France 43 M 21 days after UL and LL paraesthesia, distal LL weakness Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia None No 2 days after symptoms onset Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Bigaut et al. [9]
td	France
td	43
td	M
td	21 days after
td	UL and LL paraesthesia, distal LL weakness
td	Extension to midthigh and tips of the finger with ataxia, right peripheral facial nerve palsy, generalized areflexia
td	None
td	No
td	2 days after symptoms onset
td	Cough, asthenia, myalgia in legs, followed by acute anosmia and ageusia with diarrhea, mild interstitial pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Bigaut et al. [9] France 70 F 10 days after Acute proximal tetraparesis, distal forelimb and perioral paraesthesia Respiratory weakness, loss of ambulation None Yes 3 days after symptoms onset Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia Obesity Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Bigaut et al. [9]
td	France
td	70
td	F
td	10 days after
td	Acute proximal tetraparesis, distal forelimb and perioral paraesthesia
td	Respiratory weakness, loss of ambulation
td	None
td	Yes
td	3 days after symptoms onset
td	Anosmia, ageusia, diarrhea, asthenia, myalgia, moderate interstitial pneumonia
td	Obesity
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Bracaglia et al. [10] Italy 66 F Unknown (due to asymptomatic infection) Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia None No NA Asymptomatic None Clinical + electrophysiology 2 Classic sensorimotor
td	Bracaglia et al. [10]
td	Italy
td	66
td	F
td	Unknown (due to asymptomatic infection)
td	Acute proximal and distal tetraparesis, lumbar pain and distal tingling sensation
td	Loss of ambulation, difficulty in speeching and swallowing, generalized areflexia
td	None
td	No
td	NA
td	Asymptomatic
td	None
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Camdessanche et al. [11] France 64 M 11 days after UL and LL paraesthesia Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia None Yes 3 days after symptoms onset Fever (high grade), cough, pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Camdessanche et al. [11]
td	France
td	64
td	M
td	11 days after
td	UL and LL paraesthesia
td	Ascendent weakness, flaccid tetraparesis, generalized areflexia, dysphagia
td	None
td	Yes
td	3 days after symptoms onset
td	Fever (high grade), cough, pneumonia
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Chan et al. [12] Canada 58 M 20 days after home isolation for suspected contact Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia NA None No NA Asymptomatic, interstitial pneumonia None Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia
td	Chan et al. [12]
td	Canada
td	58
td	M
td	20 days after home isolation for suspected contact
td	Bilateral facial weakness, dysarthria, feet paraesthesia, LL areflexia
td	NA
td	None
td	No
td	NA
td	Asymptomatic, interstitial pneumonia
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Bilateral facial palsy with paraesthesia
p	Bilateral facial palsy
p	with paraesthesia
tr	Chan et al. [13] USA 68 M 18 days after Gait disturbance, hands and feet paraesthesia LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness None No 8 days after the onset of symptoms Fever and upper respiratory symptoms NA Clinical + CSF 2 Classic sensorimotor
td	Chan et al. [13]
td	USA
td	68
td	M
td	18 days after
td	Gait disturbance, hands and feet paraesthesia
td	LL proximal weakness, absent vibratory and proprioceptive sense at the toes, UL hyporeflexia, LL areflexia, unsteady gait with inability to toe or heel walk, bilateral facial weakness, dysphagia, dysarthria, neck flexion weakness
td	None
td	No
td	8 days after the onset of symptoms
td	Fever and upper respiratory symptoms
td	NA
td	Clinical + CSF
td	2
td	Classic sensorimotor
tr	Chan et al. [13] USA 84 M 16 days after Hands and feet paraesthesia, progressive gait disturbance Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure Yes (not specified autonomic dysfunction) Yes 25 days after the onset of symptoms Fever NA Clinical + CSF 2 Classic sensorimotor
td	Chan et al. [13]
td	USA
td	84
td	M
td	16 days after
td	Hands and feet paraesthesia, progressive gait disturbance
td	Bilateral facial weakness, progressive arm weakness, neuromuscular respiratory failure
td	Yes (not specified autonomic dysfunction)
td	Yes
td	25 days after the onset of symptoms
td	Fever
td	NA
td	Clinical + CSF
td	2
td	Classic sensorimotor
tr	Coen et al. [14] Switzerland 70 M 6 days after Paraparesis, distal allodynia Generalized areflexia Difficulties in voiding and constipation No NA Dry cough, myalgia, fatigue None Clinical + CSF + 0electrophysiology 1 Classic sensorimotor
td	Coen et al. [14]
td	Switzerland
td	70
td	M
td	6 days after
td	Paraparesis, distal allodynia
td	Generalized areflexia
td	Difficulties in voiding and constipation
td	No
td	NA
td	Dry cough, myalgia, fatigue
td	None
td	Clinical + CSF + 0electrophysiology
td	1
td	Classic sensorimotor
tr	Ebrahimzadeh et al. [15] Iran 46 M 18 days after Pain and numbness in distal LL and UL extremities, ascending weakness in legs Mild peripheral right facial nerve palsy, generalized areflexia None No 7 days after symptoms onset Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms) None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Ebrahimzadeh et al. [15]
td	Iran
td	46
td	M
td	18 days after
td	Pain and numbness in distal LL and UL extremities, ascending weakness in legs
td	Mild peripheral right facial nerve palsy, generalized areflexia
td	None
td	No
td	7 days after symptoms onset
td	Low-grade fever, sore thorat, dry cough and mild dyspnea, bilateral interstitial pneumonia (concurrent with neurological symptoms)
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Ebrahimzadeh et al. [15] Iran 65 M 10 days after Progressive ascending LL and UL extremities weakness and paraesthesia Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia None No 14 days after symptoms onset History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms) Hypertension Clinical + electrophysiology 2 Classic sensorimotor
td	Ebrahimzadeh et al. [15]
td	Iran
td	65
td	M
td	10 days after
td	Progressive ascending LL and UL extremities weakness and paraesthesia
td	Proximal and distal UL and LL weakness, UL hyporeflexia and LL areflexia
td	None
td	No
td	14 days after symptoms onset
td	History of COVID-19 (symptoms not specified), fine crackles in both lungs (concurrent with neurological symptoms)
td	Hypertension
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	El Otmani et al. [16] Morocco 70 F 3 days after Weakness and paraesthesia in the 4 limbs Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign None No NA Dry cough, pneumonia Rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	El Otmani et al. [16]
td	Morocco
td	70
td	F
td	3 days after
td	Weakness and paraesthesia in the 4 limbs
td	Tetraparesis, hypotonia, generalized areflexia, bilateral positive Lasègue sign
td	None
td	No
td	NA
td	Dry cough, pneumonia
td	Rheumatoid arthritis
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Esteban Molina et al. [17] Spain 55 F 14 days after Paraesthesia and weakness in the 4 limbs Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia None Yes 3 days after symptoms onset (48 h after the admission) Fever, dry cough and dyspnoea, pneumonia Dyslipidemia Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Esteban Molina et al. [17]
td	Spain
td	55
td	F
td	14 days after
td	Paraesthesia and weakness in the 4 limbs
td	Lumbar pain, dysphagia, tetraplegia, general areflexia, bilateral facial palsy, lingual and perioral paraesthesia
td	None
td	Yes
td	3 days after symptoms onset (48 h after the admission)
td	Fever, dry cough and dyspnoea, pneumonia
td	Dyslipidemia
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Farzi et al. [18] Iran 41 M 10 days after Paraesthesia of the feet Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position None No 7 days after symptoms onset Cough, dyspnea and fever DM type II Clinical + electrophysiology 2 Classic sensorimotor
td	Farzi et al. [18]
td	Iran
td	41
td	M
td	10 days after
td	Paraesthesia of the feet
td	Tetraparesis, areflexia at the LL and hyporeflexia at the UL, stocking-and-glove hypesthesia and reduced sense of vibration and position
td	None
td	No
td	7 days after symptoms onset
td	Cough, dyspnea and fever
td	DM type II
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Fernández–Domínguez et al. [19] Spain 74 F 15 days after Gait ataxia and generalized areflexia NA NA No NA Respiratory symptoms (not further detailed) Hypertension and follicular lymphoma Clinical + CSF 2 Miller Fisher variant
td	Fernández–Domínguez et al. [19]
td	Spain
td	74
td	F
td	15 days after
td	Gait ataxia and generalized areflexia
td	NA
td	NA
td	No
td	NA
td	Respiratory symptoms (not further detailed)
td	Hypertension and follicular lymphoma
td	Clinical + CSF
td	2
td	Miller Fisher variant
tr	Finsterer et al. [20] India 20 M 5 days after NA NA NA NA NA NA NA Clinical + electrophysiology 2 NA
td	Finsterer et al. [20]
td	India
td	20
td	M
td	5 days after
td	NA
td	NA
td	NA
td	NA
td	NA
td	NA
td	NA
td	Clinical + electrophysiology
td	2
td	NA
tr	Frank et al. [21] Brazil 15 M > 5 days after Paraparesis, pain in the LL Rapidly progressive ascending tetraparesis, areflexia NA No NA Fever, intense sweating NA Clinical + electrophysiology 2 Classic sensorimotor
td	Frank et al. [21]
td	Brazil
td	15
td	M
td	> 5 days after
td	Paraparesis, pain in the LL
td	Rapidly progressive ascending tetraparesis, areflexia
td	NA
td	No
td	NA
td	Fever, intense sweating
td	NA
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Gigli et al. [22] Italy 53 M NA Paraesthesia, gait ataxia NA NA NA NA Fever, diarrhea NA Clinical + CSF + electrophysiology 1 NA
td	Gigli et al. [22]
td	Italy
td	53
td	M
td	NA
td	Paraesthesia, gait ataxia
td	NA
td	NA
td	NA
td	NA
td	Fever, diarrhea
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	NA
tr	Gutiérrez-Ortiz et al. [23] Spain 50 M 3 days after Vertical diplopia, perioral paraesthesia, gait ataxia Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia None No NA Fever, cough, malaise, headache, low back pain, anosmia, ageusia Bronchial asthma Clinical + CSF 2 Miller Fisher variant
td	Gutiérrez-Ortiz et al. [23]
td	Spain
td	50
td	M
td	3 days after
td	Vertical diplopia, perioral paraesthesia, gait ataxia
td	Right internuclear ophthalmoparesis and right fascicular oculomotor palsy, ataxia, generalized areflexia
td	None
td	No
td	NA
td	Fever, cough, malaise, headache, low back pain, anosmia, ageusia
td	Bronchial asthma
td	Clinical + CSF
td	2
td	Miller Fisher variant
tr	Gutiérrez-Ortiz et al. [23] Spain 39 M 3 days after Diplopia (bilateral abducens palsy) Generalized areflexia None No NA Diarrhea, low-grade fever None Clinical + CSF 2 Polyneuritis cranialis (GBS–Miller Fisher Interface)
td	Gutiérrez-Ortiz et al. [23]
td	Spain
td	39
td	M
td	3 days after
td	Diplopia (bilateral abducens palsy)
td	Generalized areflexia
td	None
td	No
td	NA
td	Diarrhea, low-grade fever
td	None
td	Clinical + CSF
td	2
td	Polyneuritis cranialis (GBS–Miller Fisher Interface)
tr	Helbok et al. [24] Austria 68 M 14 days after Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia Ascending weakness, flaccid tetraparesis, generalized areflexia NA Yes 2 days after symptoms onset (24 h after the admission) Fever, dry cough, myalgia, anosmia and ageusia. None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Helbok et al. [24]
td	Austria
td	68
td	M
td	14 days after
td	Hypoaesthesia and paraesthesia in the LL, proximal weakness, areflexia, stand ataxia
td	Ascending weakness, flaccid tetraparesis, generalized areflexia
td	NA
td	Yes
td	2 days after symptoms onset (24 h after the admission)
td	Fever, dry cough, myalgia, anosmia and ageusia.
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Hutchins et al. [25] USA 21 M 16 days after Right-sided facial numbness and weakness Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia NA No 3 days after symptoms onset Fever, cough, dyspnoea, diarrhea, nausea, headache Hypertension, prediabetes, and class I obesity Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia
td	Hutchins et al. [25]
td	USA
td	21
td	M
td	16 days after
td	Right-sided facial numbness and weakness
td	Bilateral facial palsy, severe dysarthria, bilateral LL weakness , bilateral UL paraesthesia, areflexia
td	NA
td	No
td	3 days after symptoms onset
td	Fever, cough, dyspnoea, diarrhea, nausea, headache
td	Hypertension, prediabetes, and class I obesity
td	Clinical + CSF + electrophysiology
td	1
td	Bilateral facial palsy with paraesthesia
tr	Juliao Caamaño et al. [26] Spain 61 M 10 days after Facial diplegia No progression None No 1 day after symptoms onset Fever and cough None Clinical + electrophysiology 3 Bilateral facial nerve palsy
td	Juliao Caamaño et al. [26]
td	Spain
td	61
td	M
td	10 days after
td	Facial diplegia
td	No progression
td	None
td	No
td	1 day after symptoms onset
td	Fever and cough
td	None
td	Clinical + electrophysiology
td	3
td	Bilateral facial nerve palsy
tr	Khalifa et al. [27] Kingdom of Saudi Arabia 11 M 20 days after Gait ataxia, areflexia and paraesthesia in the LL Gradual motor improvement, persistent hyporeflexia NA No NA Acute upper respiratory tract infection, low-grade fever, dry cough. NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Khalifa et al. [27]
td	Kingdom of Saudi Arabia
td	11
td	M
td	20 days after
td	Gait ataxia, areflexia and paraesthesia in the LL
td	Gradual motor improvement, persistent hyporeflexia
td	NA
td	No
td	NA
td	Acute upper respiratory tract infection, low-grade fever, dry cough.
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Kilinc et al. [28] The Netherlands 50 M 24 days after Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia Progression of limb weakness and inability to walk NA No 11 days after symptoms onset Dry cough None Clinical + electrophysiology 2 Classic sensorimotor
td	Kilinc et al. [28]
td	The Netherlands
td	50
td	M
td	24 days after
td	Facial diplegia, symmetrical proximal weakness, paraesthesia of distal extremities, gait ataxia, areflexia
td	Progression of limb weakness and inability to walk
td	NA
td	No
td	11 days after symptoms onset
td	Dry cough
td	None
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Lampe et al. [29] Germany 65 M 2 days after Acute right UL and LL weakness causing recurrent falls Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia None No 3 days after symptoms onset Fever and dry cough None Clinical + CSF + electrophysiology 1 Pure motor
td	Lampe et al. [29]
td	Germany
td	65
td	M
td	2 days after
td	Acute right UL and LL weakness causing recurrent falls
td	Right UL paresis, slight paraparesis more pronounced on the right side, generalized hyporeflexia
td	None
td	No
td	3 days after symptoms onset
td	Fever and dry cough
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Pure motor
tr	Lantos et al. [30] USA 36 M 4 days after Opthalmoparesisa and hypoesthesia below knee Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia None No NA Fever, chills, and myalgia None Clinical 3 Miller Fisher variant
td	Lantos et al. [30]
td	USA
td	36
td	M
td	4 days after
td	Opthalmoparesisa and hypoesthesia below knee
td	Progressive ophthalmoparesis (including initial left III cranial nerve and eventual bilateral VI cranial nerve palsies), ataxia, and hyporeflexia
td	None
td	No
td	NA
td	Fever, chills, and myalgia
td	None
td	Clinical
td	3
td	Miller Fisher variant
tr	Lascano et al. [31] Switzerland 52 F 15 days after (no resolution of pneumonia) Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia Constipation, abdominal pain Yes 4 days after symptoms onset Dry cough, dysgeusia, cacosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Lascano et al. [31]
td	Switzerland
td	52
td	F
td	15 days after (no resolution of pneumonia)
td	Back pain, diarrhea, rapidly progressive tetraparesis, distal paraesthesia
td	Worsening of proximal weakness (tetraplegia), generalized areflexia, ataxia
td	Constipation, abdominal pain
td	Yes
td	4 days after symptoms onset
td	Dry cough, dysgeusia, cacosmia
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Lascano et al. [31] Switzerland 63 F 7 days after (no resolution of pneumonia) Limb weakness, pain on the left calf Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia None No 5 days after symptoms onset Dry cough, shivering, breathing difficulties, chest pain, odynophagia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor
td	Lascano et al. [31]
td	Switzerland
td	63
td	F
td	7 days after (no resolution of pneumonia)
td	Limb weakness, pain on the left calf
td	Moderate tetraparesis, LL and left UL areflexia, distal hypoesthesia and paraesthesia
td	None
td	No
td	5 days after symptoms onset
td	Dry cough, shivering, breathing difficulties, chest pain, odynophagia
td	DM type 2
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Lascano et al. [31] Switzerland 61 F 22 days after LL weakness, dizziness, dysphagia Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes) None Yes 4 days after symptoms onset Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Lascano et al. [31]
td	Switzerland
td	61
td	F
td	22 days after
td	LL weakness, dizziness, dysphagia
td	Moderate tetraparesis, bilateral facial palsy, lower limb allodynia, severe hypopallesthesia, areflexia (except for bicipital tendon reflexes)
td	None
td	Yes
td	4 days after symptoms onset
td	Productive cough, headaches, fever, myalgia, diarrhea, nausea, vomiting, weight loss, recurrent episodes of transient loss of consciousness
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Manganotti et al. [32] Italy 50 F 16 days after Diplopia and facial paraesthesia Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch None Yes (concurrent pneumonia) NA Fever, cough, ageusia, bilateral pneumonia None Clinical + CSF 2 Miller Fisher variant
td	Manganotti et al. [32]
td	Italy
td	50
td	F
td	16 days after
td	Diplopia and facial paraesthesia
td	Ataxia, diplopia in vertical and lateral gaze, left upper arm dysmetria, generalized areflexia, mild lower facial defects, and mild hypoesthesia in the left mandibular and maxillary branch
td	None
td	Yes (concurrent pneumonia)
td	NA
td	Fever, cough, ageusia, bilateral pneumonia
td	None
td	Clinical + CSF
td	2
td	Miller Fisher variant
tr	Manganotti et al. [33] Italy 72 M 18 days after Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side NA NA No NA Fever, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Manganotti et al. [33]
td	Italy
td	72
td	M
td	18 days after
td	Tetraparesis UL > LL, LL paraesthesia , generalized areflexia, facial weakness on the right side
td	NA
td	NA
td	No
td	NA
td	Fever, dyspnea, hyposmia and ageusia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Manganotti et al. [33] Italy 72 M 30 days after Tetraparesis LL > UL, paraesthesia, global areflexia NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + electrophysiology 1 Classic sensorimotor
td	Manganotti et al. [33]
td	Italy
td	72
td	M
td	30 days after
td	Tetraparesis LL > UL, paraesthesia, global areflexia
td	NA
td	NA
td	No
td	NA
td	Fever, cough, dyspnea, hyposmia and ageusia
td	NA
td	Clinical + electrophysiology
td	1
td	Classic sensorimotor
tr	Manganotti et al. [33] Italy 49 F 14 days after Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness NA NA No NA Fever, cough, dyspnea, hyposmia and ageusia NA Clinical + CSF + electrophysiology 1 Miller Fisher variant
td	Manganotti et al. [33]
td	Italy
td	49
td	F
td	14 days after
td	Ophthalmoplegia, limb ataxia, generalized areflexia, diplopia, facial hypoesthesia, facial weakness
td	NA
td	NA
td	No
td	NA
td	Fever, cough, dyspnea, hyposmia and ageusia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Miller Fisher variant
tr	Manganotti et al. [33] Italy 94 M 33 days after LL weakness, generalized hyporeflexia NA NA No NA Fever, cough, gastrointestinal symptoms NA Clinical + electrophysiology 2 Classic sensorimotor
td	Manganotti et al. [33]
td	Italy
td	94
td	M
td	33 days after
td	LL weakness, generalized hyporeflexia
td	NA
td	NA
td	No
td	NA
td	Fever, cough, gastrointestinal symptoms
td	NA
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Manganotti et al. [33] Italy 76 M 22 days after Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia NA NA No NA Fever, cough, dysuria, hyposmia, ageusia NA Clinical + CSF + electrophysiology 1 Pure motor
td	Manganotti et al. [33]
td	Italy
td	76
td	M
td	22 days after
td	Quadriparesis UL > LL, generalized areflexia, facial weakness, transient diplopia
td	NA
td	NA
td	No
td	NA
td	Fever, cough, dysuria, hyposmia, ageusia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Pure motor
tr	Marta-Enguita et al. [34] Spain 76 F 8 days after Back pain and progressive tetraparesis with distal-onset paraesthesia Progressive with dysphagia and cranial nerves involvement, generalized areflexia NA Yes 10 days after symptom onset Cough and fever without dyspnea None Clinical 3 NA
td	Marta-Enguita et al. [34]
td	Spain
td	76
td	F
td	8 days after
td	Back pain and progressive tetraparesis with distal-onset paraesthesia
td	Progressive with dysphagia and cranial nerves involvement, generalized areflexia
td	NA
td	Yes
td	10 days after symptom onset
td	Cough and fever without dyspnea
td	None
td	Clinical
td	3
td	NA
tr	Mozhdehipanah et al. [35] Iran 38 M 16 days after Progressive LL paraesthesia, facial diplegia, lobal areflexia Mild LL weakness , bulbar symptoms developed Blood pressure instability, tachycardia No 8 days after symptoms onset Upper respiratory infection (no further details) NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia
td	Mozhdehipanah et al. [35]
td	Iran
td	38
td	M
td	16 days after
td	Progressive LL paraesthesia, facial diplegia, lobal areflexia
td	Mild LL weakness , bulbar symptoms developed
td	Blood pressure instability, tachycardia
td	No
td	8 days after symptoms onset
td	Upper respiratory infection (no further details)
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Bilateral facial palsy with paraesthesia
tr	Mozhdehipanah et al. [35] Iran 14 F NA Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia NA NA No NA Upper respiratory infection (no further details) NA Clinical + CSF 2 Classic sensorimotor
td	Mozhdehipanah et al. [35]
td	Iran
td	14
td	F
td	NA
td	Ascending quadriparesis, UL hyporeflexia, LL areflexia, distal hypoesthesia, ataxia
td	NA
td	NA
td	No
td	NA
td	Upper respiratory infection (no further details)
td	NA
td	Clinical + CSF
td	2
td	Classic sensorimotor
tr	Mozhdehipanah et al. [35] Iran 44 F 26 days after Weakness of LL Tetraparesis, generalized areflexia, symmetrical hypoesthesia NA Yes NA Dry cough, fever, myalgia, progressive dyspnea COPD Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Mozhdehipanah et al. [35]
td	Iran
td	44
td	F
td	26 days after
td	Weakness of LL
td	Tetraparesis, generalized areflexia, symmetrical hypoesthesia
td	NA
td	Yes
td	NA
td	Dry cough, fever, myalgia, progressive dyspnea
td	COPD
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Mozhdehipanah et al. [35] Iran 66 F 30 days after Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia NA No No NA Fever, dry cough, severe myalgia DM, hypertension, and rheumatoid arthritis Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Mozhdehipanah et al. [35]
td	Iran
td	66
td	F
td	30 days after
td	Progressive UL and LL weakness, generalized areflexia, symmetrical hypoesthesia
td	NA
td	No
td	No
td	NA
td	Fever, dry cough, severe myalgia
td	DM, hypertension, and rheumatoid arthritis
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Naddaf et al. [36] USA 58 F 17 days after Progressive paraparesis, imbalance, severe lower thoracic pain without radiation Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait None No NA Fever, dysgeusia without anosmia, bilateral interstitial pneumonia None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Naddaf et al. [36]
td	USA
td	58
td	F
td	17 days after
td	Progressive paraparesis, imbalance, severe lower thoracic pain without radiation
td	Mild neck flexion weakness, mild/moderate distal UL and proximal and distal LL weakness, UL hyporeflexia, LL areflexia, moderately severe length-dependent sensory loss in the feet, ataxic gait
td	None
td	No
td	NA
td	Fever, dysgeusia without anosmia, bilateral interstitial pneumonia
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Oguz-Akarsu et al. [37] Turkey 53 F Concurrent pneumonia Dysarthria, progressive LL weakness and numbness Ataxia, generalized areflexia None No NA Mild fever (37.5 °C), pneumonia None Clinical + electrophysiology 2 Classic sensorimotor
td	Oguz-Akarsu et al. [37]
td	Turkey
td	53
td	F
td	Concurrent pneumonia
td	Dysarthria, progressive LL weakness and numbness
td	Ataxia, generalized areflexia
td	None
td	No
td	NA
td	Mild fever (37.5 °C), pneumonia
td	None
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Ottaviani et al. [38] Italy 66 F 7 days after (concurrent pneumonia) Flaccid paraparesis, no sensory symptoms Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia NA Yes 13 days after symptoms onset Fever and cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Ottaviani et al. [38]
td	Italy
td	66
td	F
td	7 days after (concurrent pneumonia)
td	Flaccid paraparesis, no sensory symptoms
td	Progressively developed proximal weakness in all limbs, dysesthesia, and unilateral facial palsy, generalized areflexia
td	NA
td	Yes
td	13 days after symptoms onset
td	Fever and cough, pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Padroni et al. [39] Italy 70 F 23 days after UL and LL paraesthesia, gait difficulties, asthenia Ascendant weakness, tetraparesis, generalized areflexia None Yes 6 days after symptoms onset Fever (38.5 °C), dry cough, pneumonia None Clinical + CSF + Electrophysiology 1 Classic sensorimotor
td	Padroni et al. [39]
td	Italy
td	70
td	F
td	23 days after
td	UL and LL paraesthesia, gait difficulties, asthenia
td	Ascendant weakness, tetraparesis, generalized areflexia
td	None
td	Yes
td	6 days after symptoms onset
td	Fever (38.5 °C), dry cough, pneumonia
td	None
td	Clinical + CSF + Electrophysiology
td	1
td	Classic sensorimotor
tr	Paterson et al. [40] UK 42 M 13 day after Distal limb numbness and weakness, dysphagia Tetraparesis, generalized areflexia, sensory loss NA Yes 16 days after symptom onset Cough, fever dyspnea, diarrhea, anosmia None Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Paterson et al. [40]
td	UK
td	42
td	M
td	13 day after
td	Distal limb numbness and weakness, dysphagia
td	Tetraparesis, generalized areflexia, sensory loss
td	NA
td	Yes
td	16 days after symptom onset
td	Cough, fever dyspnea, diarrhea, anosmia
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Paterson et al. [40] UK 60 M 1 day before Distal limb numbness and weakness Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness Yes Yes 5 days after symptom onset Headache, ageusia, anosmia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Paterson et al. [40]
td	UK
td	60
td	M
td	1 day before
td	Distal limb numbness and weakness
td	Tetraparesis, generalized areflexia, sensory loss, dysautonomia, facial and bulbar weakness
td	Yes
td	Yes
td	5 days after symptom onset
td	Headache, ageusia, anosmia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Paterson et al. [40] UK 38 M 21 day after Distal limb numbness, weakness, clumsiness Mild distal weakness, sensory ataxia None No NA Cough, diarrhea NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Paterson et al. [40]
td	UK
td	38
td	M
td	21 day after
td	Distal limb numbness, weakness, clumsiness
td	Mild distal weakness, sensory ataxia
td	None
td	No
td	NA
td	Cough, diarrhea
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Paybast et al. [41] Iran 38 M 21 days after Acute progressive ascending paraesthesia of distal LL Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex Tachycardia and blood pressure instability No 3 days after symptoms onset Symptoms of upper respiratory tract infection Hypertension Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Paybast et al. [41]
td	Iran
td	38
td	M
td	21 days after
td	Acute progressive ascending paraesthesia of distal LL
td	Quadriparesthesia, bilateral facial droop with drooling of saliva and slurred speech, generalized areflexia, swallowing inability, bilaterally absent gag reflex
td	Tachycardia and blood pressure instability
td	No
td	3 days after symptoms onset
td	Symptoms of upper respiratory tract infection
td	Hypertension
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Paybast et al. [41] Iran 14 F 21 days after Progressive ascending quadriparesthesia, mild LL weakness Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia None No 2 days after symptoms onset Symptoms of upper respiratory tract infection None Clinical + CSF 2 Classic sensorimotor
td	Paybast et al. [41]
td	Iran
td	14
td	F
td	21 days after
td	Progressive ascending quadriparesthesia, mild LL weakness
td	Mild proximal and distal LL weakness, hypoactive deep tendon reflexes in UL and absent in LL, decreased light touch, position, and vibration sensation in all distal limbs up to ankle and elbow joints, gait ataxia
td	None
td	No
td	2 days after symptoms onset
td	Symptoms of upper respiratory tract infection
td	None
td	Clinical + CSF
td	2
td	Classic sensorimotor
tr	Pfefferkorn et al. [42] Germany 51 M 14 days after UL and LL weakness, acral paraesthesia Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis None Yes 15 days after symptoms onset Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Pfefferkorn et al. [42]
td	Germany
td	51
td	M
td	14 days after
td	UL and LL weakness, acral paraesthesia
td	Tetraparesis, generalized areflexia, deterioration to an almost complete peripheral locked-in syndrome with tetraplegia, complete sensory loss at 4 limbs, bilateral facial and hypoglossal paresis
td	None
td	Yes
td	15 days after symptoms onset
td	Fluctuating fever, flu-like symptoms with marked fatigue and dry cough, pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Rana et al. [43] USA 54 M 14 days after LL paresthesias of LL Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis Resting tachycardia and urinary retention Yes NA Rhinorrhea, odynophagia, fever, chills, and night sweats Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection Clinical + electrophysiology 2 Miller Fisher variant
td	Rana et al. [43]
td	USA
td	54
td	M
td	14 days after
td	LL paresthesias of LL
td	Ascending tetraparesis, general areflexia, burning sensation diplopia, facial diplegia, mild ophthalmoparesis
td	Resting tachycardia and urinary retention
td	Yes
td	NA
td	Rhinorrhea, odynophagia, fever, chills, and night sweats
td	Hypertension, hyperlipidemia, restless leg syndrome, and chronic back pain, concurrent C. Difficile infection
td	Clinical + electrophysiology
td	2
td	Miller Fisher variant
tr	Reyes-Bueno et al. [44] Spain 50 F 15 days after Root-type pain in all four limbs, dorsal and lumbar back pain LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia Dry mouth, diarrhea and unstable blood pressure No 12 days after symptoms onset Diarrhea, odynophagia and cough NA Clinical + CSF + electrophysiology 1 Miller Fisher variant
td	Reyes-Bueno et al. [44]
td	Spain
td	50
td	F
td	15 days after
td	Root-type pain in all four limbs, dorsal and lumbar back pain
td	LL Weakness, ataxia, diplopia, bilateral facial palsy, generalized areflexia
td	Dry mouth, diarrhea and unstable blood pressure
td	No
td	12 days after symptoms onset
td	Diarrhea, odynophagia and cough
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Miller Fisher variant
tr	Riva et al. [45] Italy 60+ M 17 days after Progressive limb weakness and distal paresthesia at four limbs Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia None No 10 days after symptoms onset Fever, headache, myalgia, anosmia and ageusia NA Clinical + electrophysiology 2 Classic sensorimotor
td	Riva et al. [45]
td	Italy
td	60+
td	M
td	17 days after
td	Progressive limb weakness and distal paresthesia at four limbs
td	Ascending paraparesis with involvement of the cranial nerves (facial diplegia), generalized areflexia
td	None
td	No
td	10 days after symptoms onset
td	Fever, headache, myalgia, anosmia and ageusia
td	NA
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Sancho-Saldaña et al. [46] Spain 56 F 15 days after Unsteadiness and paraesthesia in both hands Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis No Yes 3 days after symptoms onset Fever, dry cough and dyspnea, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Sancho-Saldaña et al. [46]
td	Spain
td	56
td	F
td	15 days after
td	Unsteadiness and paraesthesia in both hands
td	Lumbar pain and ascending weakness, global areflexia, bilateral facial nerve palsy, oropharyngeal weakness and severe proximal tetraparesis
td	No
td	Yes
td	3 days after symptoms onset
td	Fever, dry cough and dyspnea, pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Scheidl et al. [47] Germany 54 F 11 days after Proximal weakness of LL, numbness of 4 limbs Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia None No 12 days after symptoms onset Temporary ageusia, None Clinical + CSF + electrophysiology 1 Paraparetic variant
td	Scheidl et al. [47]
td	Germany
td	54
td	F
td	11 days after
td	Proximal weakness of LL, numbness of 4 limbs
td	Initial worsening of the paraparesis with rapid improvement upon initiation of the treatment, areflexia
td	None
td	No
td	12 days after symptoms onset
td	Temporary ageusia,
td	None
td	Clinical + CSF + electrophysiology
td	1
td	Paraparetic variant
tr	Sedaghat et al. [48] Iran 65 M 14 days after LL distal weakness Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia None No 4 days after symptoms onset Fever, cough and sometimes dyspnea, pneumonia DM type 2 Clinical + electrophysiology 2 Classic sensorimotor
td	Sedaghat et al. [48]
td	Iran
td	65
td	M
td	14 days after
td	LL distal weakness
td	Ascending weakness, tetraparesis, facial bilateral palsy, generalized areflexia, LL distal hypoesthesia and hypopallesthesia
td	None
td	No
td	4 days after symptoms onset
td	Fever, cough and sometimes dyspnea, pneumonia
td	DM type 2
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Sidig et al. [49] Sudan 65 M 5 days after Numbness and weakness in both UL and LL Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia Urinary incontinence Yes NA Low-grade fever, sore throat, dry cough, headache and generalized fatigability DM and Hypertension Clinical + electrophysiology 2 Classic sensorimotor
td	Sidig et al. [49]
td	Sudan
td	65
td	M
td	5 days after
td	Numbness and weakness in both UL and LL
td	Ascending weakness, bilateral facial paraesthesia and palsy, clumsiness of UL, tetraparesis, slight palatal muscle weakness, areflexia
td	Urinary incontinence
td	Yes
td	NA
td	Low-grade fever, sore throat, dry cough, headache and generalized fatigability
td	DM and Hypertension
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Su et al. [50] USA 72 M 6 days after Proximal UL and LL weakness Progression with worsening of the paresis, areflexia, hypoesthesia Hypotension alternating with hypertension and tachycardia Yes 8 days after symptoms onset Mild diarrhea, anorexia and chills without fever or respiratory symptoms Coronary artery disease, hypertension and alcohol abuse Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Su et al. [50]
td	USA
td	72
td	M
td	6 days after
td	Proximal UL and LL weakness
td	Progression with worsening of the paresis, areflexia, hypoesthesia
td	Hypotension alternating with hypertension and tachycardia
td	Yes
td	8 days after symptoms onset
td	Mild diarrhea, anorexia and chills without fever or respiratory symptoms
td	Coronary artery disease, hypertension and alcohol abuse
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Tiet et al. [51] United Kingdom 49 M 21 days after Distal LL paraesthesia LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia None No 4 days after symptoms onset Shortness of breath, headache and cough Sinusitis Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Tiet et al. [51]
td	United Kingdom
td	49
td	M
td	21 days after
td	Distal LL paraesthesia
td	LL and UL weakness, facial diplegia, distal reduced sensation to pinprick and vibration sense, LL dysesthesia, generalized areflexia
td	None
td	No
td	4 days after symptoms onset
td	Shortness of breath, headache and cough
td	Sinusitis
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Toscano et al. [52] Italy 77 F 7 days after UL and LL paraesthesia Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness None Yes NA Fever, cough, ageusia, pneumonia Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Toscano et al. [52]
td	Italy
td	77
td	F
td	7 days after
td	UL and LL paraesthesia
td	Flaccid tetraplegia, areflexia, facial weakness, dysphagie, tongue weakness
td	None
td	Yes
td	NA
td	Fever, cough, ageusia, pneumonia
td	Previous ischemic stroke, diverticulosis, arterial hypertension, atrial fibrillation
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Toscano et al. [52] Italy 23 M 10 days after Facial diplegia LL paraesthesia, generalized areflexia, sensory ataxia None No 2 days after symptoms onset Fever, pharyngitis NA Clinical + CSF + electrophysiology 1 Bilateral facial palsy with paraesthesia
td	Toscano et al. [52]
td	Italy
td	23
td	M
td	10 days after
td	Facial diplegia
td	LL paraesthesia, generalized areflexia, sensory ataxia
td	None
td	No
td	2 days after symptoms onset
td	Fever, pharyngitis
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Bilateral facial palsy with paraesthesia
tr	Toscano et al. [52] Italy 55 M 10 days after Neck pain, Paresthesias in the 4 limbs, LL weakness Flaccid tetraparesis, areflexia, facial weakness None Yes NA Fever, cough, pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Toscano et al. [52]
td	Italy
td	55
td	M
td	10 days after
td	Neck pain, Paresthesias in the 4 limbs, LL weakness
td	Flaccid tetraparesis, areflexia, facial weakness
td	None
td	Yes
td	NA
td	Fever, cough, pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Toscano et al. [52] Italy 76 M 5 days after Lumbar pain, LL weakness Flaccid tetraparesis, generalized areflexia, ataxia None No 4 days after symptoms onset Cough and hyposmia NA Clinical + CSF+ Electrophysiology 1 Classic sensorimotor
td	Toscano et al. [52]
td	Italy
td	76
td	M
td	5 days after
td	Lumbar pain, LL weakness
td	Flaccid tetraparesis, generalized areflexia, ataxia
td	None
td	No
td	4 days after symptoms onset
td	Cough and hyposmia
td	NA
td	Clinical + CSF+ Electrophysiology
p	Clinical + CSF+
p	Electrophysiology
td	1
td	Classic sensorimotor
tr	Toscano et al. [52] Italy 61 M 7 days after LL weakness and paraesthesia Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia None Yes NA Cough, ageusia and anosmia, pneumonia NA Clinical + CSF+ electrophysiology 1 Classic sensorimotor
td	Toscano et al. [52]
td	Italy
td	61
td	M
td	7 days after
td	LL weakness and paraesthesia
td	Ascending weakness, tetraplegia, facial weakness, areflexia, dysphagia
td	None
td	Yes
td	NA
td	Cough, ageusia and anosmia, pneumonia
td	NA
td	Clinical + CSF+ electrophysiology
td	1
td	Classic sensorimotor
tr	Velayos Galán et al. [53] Spain 43 M 10 days after Distal weakness and numbness of the 4 limbs, gait ataxia Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia NA No 2 days after admission Cough, pneumonia NA Clinical + electrophysiology 2 Classic sensorimotor
td	Velayos Galán et al. [53]
td	Spain
td	43
td	M
td	10 days after
td	Distal weakness and numbness of the 4 limbs, gait ataxia
td	Progression of the weakness with bilateral facial paresis and dysphagia, generalized areflexia
td	NA
td	No
td	2 days after admission
td	Cough, pneumonia
td	NA
td	Clinical + electrophysiology
td	2
td	Classic sensorimotor
tr	Virani et al. [54] USA 54 M 8 days after LL weakness, numbness Ascending weakness, tetraparesis, areflexia Urinary retention Yes Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset) Fever (102 F), dry cough, pneumonia Clostridium difficile colitis 2 days before GBS onset Clinical 3 Classic sensorimotor
td	Virani et al. [54]
td	USA
td	54
td	M
td	8 days after
td	LL weakness, numbness
td	Ascending weakness, tetraparesis, areflexia
td	Urinary retention
td	Yes
td	Shortly after presentation in the outpatient clinic (after 2 days of symptoms onset)
td	Fever (102 F), dry cough, pneumonia
td	Clostridium difficile colitis 2 days before GBS onset
td	Clinical
td	3
td	Classic sensorimotor
tr	Webb et al. [55] United Kingdom 57 6 days after Ataxia, progressive limb weakness and foot dysaesthesia, Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia None Yes 3 days after symptoms onset Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia Untreated hypertension and psoriasis Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Webb et al. [55]
td	United Kingdom
td	57
td	6 days after
td	Ataxia, progressive limb weakness and foot dysaesthesia,
td	Tetraparesis, generalized areflexia, hypoesthesia in the 4 limbs, hypopallesthesia in LL, dysphagia
td	None
td	Yes
td	3 days after symptoms onset
td	Mild cough and headache, myalgia and malaise, slight fever, diarrhea, pneumonia
td	Untreated hypertension and psoriasis
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
tr	Zhao et al. [56] China 61 F 8 days before LL weakness Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia None No 4 days after symptoms onset Fever (38·2 °C), dry cough pneumonia NA Clinical + CSF + electrophysiology 1 Classic sensorimotor
td	Zhao et al. [56]
td	China
td	61
td	F
td	8 days before
td	LL weakness
td	Ascending weakness, tetraparesis, areflexia, LL distal hypoesthesia
td	None
td	No
td	4 days after symptoms onset
td	Fever (38·2 °C), dry cough pneumonia
td	NA
td	Clinical + CSF + electrophysiology
td	1
td	Classic sensorimotor
table	Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome GBS COVID-19 Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days) Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance. Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol, Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness. Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms
tr	Article COVID-19 diagnosis Blood findings Auto-antibodies and screening for most common GBS causes CSF findings Electrophysiology: Neuropathy type and GBS electrophysiologic subtype MRI (brain and spinal) Management and therapy Outcome
th	Article
th	COVID-19 diagnosis
th	Blood findings
th	Auto-antibodies and screening for most common GBS causes
th	CSF findings
th	Electrophysiology: Neuropathy type and GBS electrophysiologic subtype
th	MRI (brain and spinal)
th	Management and therapy
th	Outcome
tr	GBS COVID-19
th	GBS
th	COVID-19
tr	Agosti et al. [5] RT-PCR + chest CT Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L) Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis Increased total protein (98 mg/dl), cell count: 2/106 L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Antiviral drugs (not specifically mentioned) Improvement, discharged home after 30 days
td	Agosti et al. [5]
td	RT-PCR + chest CT
td	Thrombocytopenia (101 × 109 /L, reference value: 125–300 × 109 /L), lymphocytopenia (0.48 × 109 /L, reference value: 1.1–3.2 × 109 /L)
td	Negative ANA, anti-DNA, c-ANCA, p-ANCA, negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, HSV 1 and 2, VZV, influenza virus A and B, HIV, normal B12 and serum protein electrophoresis
td	Increased total protein (98 mg/dl), cell count: 2/106 L
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	Antiviral drugs (not specifically mentioned)
td	Improvement, discharged home after 30 days
tr	Alberti et al. [6] RT-PCR + chest CT NA NA Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Lopinavir/ritonavir, hydroxychloroquine 24 h after admission, death because of respiratory failure
td	Alberti et al. [6]
td	RT-PCR + chest CT
td	NA
td	NA
td	Increased total protein (54 mg/dl), 9 cells/µl, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days) + mechanical invasive ventilation
td	Lopinavir/ritonavir, hydroxychloroquine
td	24 h after admission, death because of respiratory failure
tr	Arnaud et al. [7] RT-PCR + chest CT NA Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquin, cefotaxime, azithromycine Progressive improvement
td	Arnaud et al. [7]
td	RT-PCR + chest CT
td	NA
td	Negative anti-ganglioside and antineural antibodies, negative Campylobacter Jejuni, HIV, syphilis, CMV, EBV serology
td	Increased total protein (1.65 g/L), no pleyocitosis, negative oligoclonal bands, negative SARS-CoV-2 PCR, negative EBV and CMV RT-PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquin, cefotaxime, azithromycine
td	Progressive improvement
tr	Assini et al. [8] RT-PCR Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL) NA Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Demyelinating with sural sparing AIDP Brain: no pathological findings IVIG 400 mg/kg (5 days) Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation 5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength
td	Assini et al. [8]
td	RT-PCR
td	Lymphocytopenia, increased LDH and inflammation markers; low serum albumin (2.9 mg/dL)
td	NA
td	Normal total protein level, increased IgG/albumin ratio (233), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF)
td	Demyelinating with sural sparing AIDP
p	Demyelinating with sural sparing
p	AIDP
td	Brain: no pathological findings
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, arbidol, ritonavir and lopinavir + mechanical invasive ventilation
td	5 days after IVIG, improvement of swallowing, speech, tongue motility, eyelid ptosis and strength
tr	Assini et al. [8] RT-PCR + chest CT Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL) Negative anti-ganglioside antibodies Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF) Motor sensory axonal, muscular neurogenic changes AMSAN NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation 5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop
td	Assini et al. [8]
td	RT-PCR + chest CT
td	Lymphocytopenia, increased LDH and GGT, leucocytosis, low serum albumin (2.6 mg/dL)
td	Negative anti-ganglioside antibodies
td	Normal total protein level, increased IgG/albumin ratio (170), negative SARS-CoV-2 PCR, presence of oligoclonal bands (both in serum and CSF)
td	Motor sensory axonal, muscular neurogenic changes AMSAN
p	Motor sensory axonal, muscular neurogenic changes
p	AMSAN
td	NA
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, antiretroviral therapy, tocilizumab + tracheostomy and assisted ventilation
td	5 days after IVIG, improvement of vegetative symptoms, persistence of hyporeflexia and right foot drop
tr	Bigaut et al. [9] RT-PCR + chest CT Normal blood count, negative CRP Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves) IVIG 400 mg/kg (5 days) + non-invasive ventilation NA Progressive improvement
td	Bigaut et al. [9]
td	RT-PCR + chest CT
td	Normal blood count, negative CRP
td	Negative anti-ganglioside antibodies, negative HIV, Lyme and syphilis serology
td	Increased total protein (0.95 g/L), cell count: 1 × 106/L, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Spinal: Radiculitis and plexitis on both brachial and lumbar plexus; multiple cranial neuritis (in III, VI, VII, and VIII nerves)
td	IVIG 400 mg/kg (5 days) + non-invasive ventilation
td	NA
td	Progressive improvement
tr	Bigaut et al. [9] RT-PCR + chest CT Increased CRP Negative anti-ganglioside antibodies Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg (5 days) NA Slow progressive improvement
td	Bigaut et al. [9]
td	RT-PCR + chest CT
td	Increased CRP
td	Negative anti-ganglioside antibodies
td	Increased total protein (1.6 g/L), cell count: 6 × 106/L, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	NA
td	Slow progressive improvement
tr	Bracaglia et al. [10] RT-PCR (normal chest CT) Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9) Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia. Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5% Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, ritonavir, darunavir Improvement of UL and LL weakness, development of facial diplegia
td	Bracaglia et al. [10]
td	RT-PCR (normal chest CT)
td	Elevated CPK (461 U/L, normal < 145), CRP 5,65 mg/dL (normal < 0.5), lymphocyto- penia (0·68 × 109/L, normal 1·10–4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), elevation of IL-6 (11 pg/mL, normal < 5.9)
td	Negative anti-ganglioside antibodies; negative microbiologic testing on CSF and serum for HSV1-2, EBV, VZV, CMV, HIV, Mycoplasma Pneumoniae and Borrelia.
td	Increased total protein (245 mg/dL) and increased cell count: 13 cells/mm3, polymorphonucleate 61.5%
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, ritonavir, darunavir
td	Improvement of UL and LL weakness, development of facial diplegia
tr	Camdessanche et al. [11] RT-PCR + chest CT NA Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E Increased total protein (1.66 g/L), normal cell count Demyelinating AIDP NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days NA
td	Camdessanche et al. [11]
td	RT-PCR + chest CT
td	NA
td	Negative anti-gangliosides antibodies; negative screening for Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, CMV, EBV, HSV1-2, VZV, Influenza virus A & B, HIV, and hepatitis E
td	Increased total protein (1.66 g/L), normal cell count
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days) + mechanical invasive ventilation
td	Oxygen therapy, paracetamol, low molecular weight heparin, lopinavir/ritonavir 400/100 mg twice a day for 10 days
td	NA
tr	Chan et al. [12] RT-PCR + chest CT Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L) NA Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR Demyelinating AIDP Brain: bilateral intracranial facial nerve enhancement IVIG 400 mg/kg (5 days) Empiric azithromycin and ceftriaxone Slight improvement of facial weakness, unchanged paraesthesia
td	Chan et al. [12]
td	RT-PCR + chest CT
td	Persistent thrombocytosis (maximum PC 688 ×109/L), elevated d-dimer (1.47 mg/L)
td	NA
td	Increased total protein (1.00 g/L), cell count: 4 × 106/L (normal), negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: bilateral intracranial facial nerve enhancement
td	IVIG 400 mg/kg (5 days)
td	Empiric azithromycin and ceftriaxone
td	Slight improvement of facial weakness, unchanged paraesthesia
tr	Chan et al. [13] RT-PCR NA Negative anti-gangliosides antibodies Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR NA Lumbosacral spine: no pathological findings 5 sessions of plasmapheresis NA Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset
td	Chan et al. [13]
td	RT-PCR
td	NA
td	Negative anti-gangliosides antibodies
td	Increased total protein (226 mg/dL), leucocytes: 3 cells/mm3, glucose: 56 mg/dL, negative SARS-CoV-2 PCR
td	NA
td	Lumbosacral spine: no pathological findings
td	5 sessions of plasmapheresis
td	NA
td	Resolution of dysphagia, ambulation with minimal assistance 28 days after symptoms onset
tr	Chan et al. [13] RT-PCR NA Elevated GM2 IgG/IgM antibodies Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR NA NA Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG NA Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator
td	Chan et al. [13]
td	RT-PCR
td	NA
td	Elevated GM2 IgG/IgM antibodies
td	Increased total protein (67 mg/dL), leucocytes: 1 cells/mm3, glucose 58 mg/dL, negative SARS-CoV-2 PCR
td	NA
td	NA
td	Mechanical invasive ventilation + 5 sessions of plasmapheresis (without benefit on ventilation) + IVIG
td	NA
td	Persistence of quadriparesis with intermittent autonomic dysfunction, slowly weaned from the ventilator
tr	Coen et al. [14] RT-PCR + serology Normal (not specified) Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) NA Rapid improvement. From day 11 from hospitalisation Rehabilitation
td	Coen et al. [14]
td	RT-PCR + serology
td	Normal (not specified)
td	Negative anti-gangliosides antibodies; negative meningitis/encephalitis panel
td	Albuminocytological dissociation, no intrathecal IgG synthesis, negative SARS-CoV-2 PCR
td	Demyelinating with sural sparing AIDP
p	Demyelinating with sural sparing
p	AIDP
td	Brain: NA Spinal: no pathological findings
p	Brain: NA
p	Spinal: no pathological findings
td	IVIG 400 mg/kg (5 days)
td	NA
td	Rapid improvement. From day 11 from hospitalisation Rehabilitation
p	Rapid improvement. From day 11 from hospitalisation
p	Rehabilitation
tr	Ebrahimzadeh et al. [15] RT-PCR + chest CT Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings None Hydroxychloroquine for 5 days Improvement of muscle strength to near normal after 16 days
td	Ebrahimzadeh et al. [15]
td	RT-PCR + chest CT
td	Normal CRP (5 mg/L), normal serum protein immunoelectrophoresis
td	Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL
td	Increased total protein (78 mg/dL), normal cell count (erythrocyte = 0/mm3, leukocyte = 4/mm3), normal glucose (70 mg/dL)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings Spinal: no pathological findings
p	Brain: no pathological findings
p	Spinal: no pathological findings
td	None
td	Hydroxychloroquine for 5 days
td	Improvement of muscle strength to near normal after 16 days
tr	Ebrahimzadeh et al. [15] RT-PCR + chest CT Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL NA Demyelinating AIDP NA IVIG NA Improvement of muscle strength in all extremities after 14 days
td	Ebrahimzadeh et al. [15]
td	RT-PCR + chest CT
td	Slightly elevated CRP (34 mg/L), normal serum protein immunoelectrophoresis
td	Negative anti-GQ1b antibodies, negative screening for Campylobacter jejuni, HIV, EBV, CMV, influenza virus (type A and B), HCV, non-reactive VDRL
td	NA
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG
td	NA
td	Improvement of muscle strength in all extremities after 14 days
tr	El Otmani et al. [16] RT-PCR + chest CT Lymphocytopenia (520/ml) NA Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2 Motor sensory axonal AMSAN NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day At week 1 from admission no significant neurological improvement
td	El Otmani et al. [16]
td	RT-PCR + chest CT
td	Lymphocytopenia (520/ml)
td	NA
td	Increased total protein (1 g/L), normal cell count, negative PCR assay for SARS-CoV-2
p	Increased total protein (1 g/L), normal cell count, negative PCR assay for
p	SARS-CoV-2
td	Motor sensory axonal AMSAN
p	Motor sensory axonal
p	AMSAN
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine 600 mg/day; azithromycin 500 mg at the first day, then 250 mg per day
td	At week 1 from admission no significant neurological improvement
tr	Esteban Molina et al. [17] RT-PCR + chest X-ray Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl Negative bacteriological and viral tests Increased total protein (86 mg/dL), cell count: 3x106/L Demyelinating AIDP Brain: leptomeningeal enhancement in midbrain and cervical spine IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, azithromycin, ceftriaxon Motor improvement but persistence of paraesthesia
td	Esteban Molina et al. [17]
td	RT-PCR + chest X-ray
td	Leucocyte 7400/mm3, lymphocyte 2400/mm3. Hb 14 g/dl. PC 408,000/mm3, d-Dimer 556 ng/ml. Ferritin 544 ng/ml, CRP 2.04 mg/dl, Fibrinogen 6.8 g/dl
td	Negative bacteriological and viral tests
td	Increased total protein (86 mg/dL), cell count: 3x106/L
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: leptomeningeal enhancement in midbrain and cervical spine
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine, azithromycin, ceftriaxon
td	Motor improvement but persistence of paraesthesia
tr	Farzi et al. [18] RT-PCR + chest CT Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h NA NA Demyelinating AIDP NA IVIG (2 g/kg over 5 days) Lopinavir/ritonavir and hydroxychloroquine Improvement after 3 days, favorable outcome
td	Farzi et al. [18]
td	RT-PCR + chest CT
td	Lymphopenia (WBC:5.9 × 109/L, neutrophils: 85%, lymphocyte:15%), elevated levels of CRP, ESR 69 mm/h
td	NA
td	NA
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG (2 g/kg over 5 days)
td	Lopinavir/ritonavir and hydroxychloroquine
td	Improvement after 3 days, favorable outcome
tr	Fernández–Domínguez et al. [19] RT-PCR NA Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies Increased total protein (110 mg/dL), albuminocytological dissociation Demyelinating NA Brain: no pathological findings IVIG 20 g/day (5 days) Hydroxychloroquine, lopinavir/ritonavir NA
td	Fernández–Domínguez et al. [19]
td	RT-PCR
td	NA
td	Negative anti-GD1b antibodies, negative other anti-ganglioside antibodies
td	Increased total protein (110 mg/dL), albuminocytological dissociation
td	Demyelinating NA
p	Demyelinating
p	NA
td	Brain: no pathological findings
td	IVIG 20 g/day (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir
td	NA
tr	Finsterer et al. [20] NA NA NA NA Axonal AMAN NA IVIG NA Recovery
td	Finsterer et al. [20]
td	NA
td	NA
td	NA
td	NA
td	Axonal AMAN
p	Axonal
p	AMAN
td	NA
td	IVIG
td	NA
td	Recovery
tr	Frank et al. [21] RT-PCR, + serology (IgG and IgM) WBC and CRP normal Negative hepatitis B and C, HIV and VDRL tests Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus Axonal AMAN Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg/day (5 days) Methylprednisolone, azithromycin, albendazole Some improvement, weakness persisted
td	Frank et al. [21]
td	RT-PCR, + serology (IgG and IgM)
td	WBC and CRP normal
td	Negative hepatitis B and C, HIV and VDRL tests
td	Two CSF analysis 2 weeks apart, both showing normal cell count and CSF biochemistry, negative SARS-CoV-2 PCR, negative PCR for HSV1, HSV2, CMV, EBV, VZV; Zika virus; Dengue virus and Chikungunya virus
td	Axonal AMAN
p	Axonal
p	AMAN
td	Brain: no pathological findings Spinal: no pathological findings
p	Brain: no pathological findings
p	Spinal: no pathological findings
td	IVIG 400 mg/kg/day (5 days)
td	Methylprednisolone, azithromycin, albendazole
td	Some improvement, weakness persisted
tr	Gigli et al. [22] Chest CT + serology (negative RT-PCR) NA Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab) Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR Demyelinating AIDP NA NA NA NA
td	Gigli et al. [22]
td	Chest CT + serology (negative RT-PCR)
td	NA
td	Negative anti-ganglioside antibodies, negative PCR for influenza A and B viruses (nasal swab)
td	Increased total protein (192.8 mg/L), leucocytes: 2.6 cells/µL, positive Ig for SARS-CoV-2, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	NA
td	NA
td	NA
tr	Gutiérrez-Ortiz et al. [23] RT-PCR Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR NA NA IVIG 400 mg/kg (5 days) NA After 2 weeks from admission complete resolution except anosmia, ageusia
td	Gutiérrez-Ortiz et al. [23]
td	RT-PCR
td	Lymphocytes 1000 cells/UI, CRP 2.8 mg/dl
td	Positive anti-GD1b antibodies, other anti-ganglioside antibodies negative
td	Increased total protein (80 mg/dl), no leucocytes, glucose 62 mg/dl, negative SARS-CoV-2 PCR
p	Increased total protein (80 mg/dl), no leucocytes, glucose
p	62 mg/dl, negative SARS-CoV-2 PCR
td	NA
td	NA
td	IVIG 400 mg/kg (5 days)
td	NA
td	After 2 weeks from admission complete resolution except anosmia, ageusia
tr	Gutiérrez-Ortiz et al. [23] RT-PCR Leucopenia (3100 cells/µl) NA Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR NA NA None Paracetamol 2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes
td	Gutiérrez-Ortiz et al. [23]
td	RT-PCR
td	Leucopenia (3100 cells/µl)
td	NA
td	Increased total protein (62 mg/dl), WBC: 2/μl (all monocytes), glucose: 50 mg/dl, negative SARS-CoV-2 PCR
td	NA
td	NA
td	None
td	Paracetamol
td	2 weeks later complete neurological recovery with no ageusia, complete eye movements, and normal deep tendon reflexes
tr	Helbok et al. [24] Chest CT + serology (repeated negative RT-PCR) WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood) Demyelinating with sural sparing AIDP Spinal: no pathological findings IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation None Improvement of muscle forces with recovery of mobility without significant help after 8 weeks
td	Helbok et al. [24]
td	Chest CT + serology (repeated negative RT-PCR)
td	WBC 8.1G/L (normal: 4.0–10.0G/L), CRP 2.3 mg/dL, (normal: 0.0–0.5 mg/dL), fibrinogen level 650 mg/dL (normal: 210–400 mg/dL), LDH 276 U/L (normal: 100–250 U/L), erythrocyte sedimentation rate 55 mm/1 h
td	Negative PCR for CMV, EBV, influenza virus A/B, Respiratory Syncytial Virus and IgM antibodies for Chlamydia pneumoniae and Mycoplasma pneumoniae
td	Increased total protein (64 mg/dl), cell count: 2 cells/mm3, serum/ CSF glucose ratio of 0.83, negative SARS-CoV-2 PCR, positive anti-SARS-CoV-2 antibodies (not determined if intrathecal synthesis or passive transfer from blood)
td	Demyelinating with sural sparing AIDP
p	Demyelinating with sural sparing
p	AIDP
td	Spinal: no pathological findings
td	IVIG 30 g + plasma exchange (4 cycles) + mechanical invasive ventilation
td	None
td	Improvement of muscle forces with recovery of mobility without significant help after 8 weeks
tr	Hutchins et al. [25] RT-PCR + chest CT Lymphopenia (absolute lymphocyte count of 0.7 K/mm3) Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test) Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes Mixed demyelinating and axonal EMG subtype unknown Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings Plasma exchange (5 cycles) NA Discharged to inpatient rehabilitation
td	Hutchins et al. [25]
td	RT-PCR + chest CT
td	Lymphopenia (absolute lymphocyte count of 0.7 K/mm3)
td	Serum HSV IgG and IgM. Respiratory viral panel PCR negative Negative GM1, GD1b, and GQ1b IgG and IgM), aquaporin-4 receptor (IgG), HIV 1/2, HSV 1/2 (IgG and IgM), CMV (IgM), Mycoplasma pneumoniae (IgG and IgM), Borrelia burgdorferi (IgG and IgM), Bartonella species (IgG and IgM), and syphilis (Venereal Disease Research Laboratory test)
td	Increased total protein (49 mg/dL), normal glucose levels (65 mg/dL), no leukocytes
td	Mixed demyelinating and axonal EMG subtype unknown
td	Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve Spinal: no pathological findings
p	Brain: enhancement of the facial and abducens nerves bilaterally, as well as the right oculomotor nerve
p	Spinal: no pathological findings
td	Plasma exchange (5 cycles)
td	NA
td	Discharged to inpatient rehabilitation
tr	Juliao Caamaño et al. [26] RT-PCR NA NA Normal total protein (44 mg/dL), no pleocytosis Absent blink-reflex EMG subtype unknown Brain: no pathological findings Oral prednisolone Hydroxychloroquine and lopinavir/ritonavir for 14 days Minimal improvement of muscle weakness after 2 weeks
td	Juliao Caamaño et al. [26]
td	RT-PCR
td	NA
td	NA
td	Normal total protein (44 mg/dL), no pleocytosis
td	Absent blink-reflex EMG subtype unknown
p	Absent blink-reflex
p	EMG subtype unknown
td	Brain: no pathological findings
td	Oral prednisolone
td	Hydroxychloroquine and lopinavir/ritonavir for 14 days
td	Minimal improvement of muscle weakness after 2 weeks
tr	Khalifa et al. [27] RT-PCR + chest X-ray + chest CT WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49) Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43 Cell count: 5 mm3, increased total protein (316.7 mg/dL) Demyelinating AIDP Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots IVIG 1 g/kg (2 days) Paracetamol, azithromycin, hydroxychloroquine Discharge to home after 15 days with clinical and electrophysiological improvement
td	Khalifa et al. [27]
td	RT-PCR + chest X-ray + chest CT
td	WBC 5.5 × 103, PC 356 × 103, CRP 0.5 mg/dL (normal 0.0–0.5), serum ferritin 87.3 ng/ml (normal 12.0–150.0), elevated d-Dimer levels 0.72 mg/L (0.00–0.49)
td	Negative screening for: influenza A and B viruses; influenza A virus subtypes H1, H3, and H5 including subtype H5N1 of the Asian lineage; parainfluenza virus types 1, 2, 3, and 4; respiratory syncytial virus types A and B; adenovirus; metapneumovirus; rhinovirus; enterovirus; Coronavirus 229E, HKU1, NL63, and OC43
td	Cell count: 5 mm3, increased total protein (316.7 mg/dL)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings Spinal: enhancement of the cauda equina nerve roots
p	Brain: no pathological findings
p	Spinal: enhancement of the cauda equina nerve roots
td	IVIG 1 g/kg (2 days)
td	Paracetamol, azithromycin, hydroxychloroquine
td	Discharge to home after 15 days with clinical and electrophysiological improvement
tr	Kilinc et al. [28] Fecal PCR + serology NA Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV Normal cell count, normal proteins Predominantly demyelinating AIDP Brain: no pathological findings IVIG 2 g/kg (5 days) None Persistence of mild symptoms at the discharge (after 14 days)
td	Kilinc et al. [28]
td	Fecal PCR + serology
td	NA
td	Negative anti-GQ1b antibodies, serologic tests on Borrelia burgdorferi, syphilis, Campylobacter jejuni, CMV, hepatitis E, Mycoplasma pneumoniae and CMV
td	Normal cell count, normal proteins
td	Predominantly demyelinating AIDP
p	Predominantly demyelinating
p	AIDP
td	Brain: no pathological findings
td	IVIG 2 g/kg (5 days)
td	None
td	Persistence of mild symptoms at the discharge (after 14 days)
tr	Lampe et al. [29] RT-PCR (negative chest X-ray) Slightly increased CRP (1.92 mg/dL) Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus Increased total protein (56 mg/dL), normal cell count (2 cells/μL) Demyelinating AIDP NA IVIG 400 mg/kg (5 days) None Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days
td	Lampe et al. [29]
td	RT-PCR (negative chest X-ray)
td	Slightly increased CRP (1.92 mg/dL)
td	Negative anti-ganglioside antibodies; negative influenza and respiratory syncytial virus
td	Increased total protein (56 mg/dL), normal cell count (2 cells/μL)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	None
td	Improvement of GBS symptoms with persistence of generalized areflexia except for left biceps reflex, discharge after 12 days
tr	Lantos et al. [30] RT-PCR NA GM1 antibodies in the equivocal range NA NA Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III IVIG Hydroxychloroquine Improvement, discharge after 4 days
td	Lantos et al. [30]
td	RT-PCR
td	NA
td	GM1 antibodies in the equivocal range
td	NA
td	NA
td	Brain: enlargement, prominent enhancement with gadolinium, and T2 hyperintense signal of the left cranial nerve III
td	IVIG
td	Hydroxychloroquine
td	Improvement, discharge after 4 days
tr	Lascano et al. [31] RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later) WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3 Negative anti-ganglioside antibodies Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR Demyelinating AIDP Spinal: no nerve root gadolinium enhancement IVIG 400 mg/kg (5 days) + mechanical invasive ventilation Azithromycin Improvement of tetraparesis. Able to stand up with assistance.
td	Lascano et al. [31]
td	RT-PCR + chest X-ray + positive IgM (IgG positivity 2 weeks later)
td	WBC 8900 cells/mm3; lymphocytes 1200 cells/mm3; PC 45,500 cells/mm3
td	Negative anti-ganglioside antibodies
td	Increased total protein (60 mg/dL), leucocytes: 3 cells/μL, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Spinal: no nerve root gadolinium enhancement
td	IVIG 400 mg/kg (5 days) + mechanical invasive ventilation
p	IVIG 400 mg/kg (5 days) + mechanical
p	invasive ventilation
td	Azithromycin
td	Improvement of tetraparesis. Able to stand up with assistance.
p	Improvement of tetraparesis.
p	Able to stand up with assistance.
tr	Lascano et al. [31] RT-PCR + chest X-ray WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3 NA Normal total protein (40 mg/dl), cell count: 2 cells/μL Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP NA IVIG 400 mg/kg (5 days) Amoxicillin, clarithromycin Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia
td	Lascano et al. [31]
td	RT-PCR + chest X-ray
td	WBC 3300 cells/mm3; lymphocytes 800 cells/mm3; PC 119,000 cells/mm3
td	NA
td	Normal total protein (40 mg/dl), cell count: 2 cells/μL
td	Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern Predominantly AIDP
p	Mixed demyelinating (conduction blocks) and axonal with sural sparing pattern
p	Predominantly AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	Amoxicillin, clarithromycin
td	Dismissal with full motor recovery. Persistence of LL areflexia and distal paraesthesia
tr	Lascano et al. [31] RT-PCR + chest X-ray WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3 NA Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR Demyelinating with sural sparing pattern AIDP Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement IVIG 400 mg/kg (5 days) Amoxicillin Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia
td	Lascano et al. [31]
td	RT-PCR + chest X-ray
td	WBC 4000 cells/mm3; lymphocytes 600 cells/mm3; PC 322,000 cells/mm3
td	NA
td	Increased total protein (140 mg/dL), cell count: 4 cells/μL, negative SARS-CoV-2 PCR
td	Demyelinating with sural sparing pattern AIDP
p	Demyelinating with sural sparing pattern
p	AIDP
td	Brain: no pathological findings Spinal cord: lumbosacral nerve root enhancement
p	Brain: no pathological findings
p	Spinal cord: lumbosacral nerve root enhancement
td	IVIG 400 mg/kg (5 days)
td	Amoxicillin
td	Improvement of tetraparesis and ability to walk with assistance. Persistence of neuropathic pain and distal paraesthesia
tr	Manganotti et al. [32] RT-PCR + chest CT NA Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses NA Brain: no pathological findings IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%) Resolution of all symptoms except for minor hyporeflexia at the LL
td	Manganotti et al. [32]
td	RT-PCR + chest CT
td	NA
td	Negative anti-ganglioside antibodies negative serum anti-HIV, anti-HBV, anti-HCV antibodies
td	Increased total protein (74.9 mg/dL), negative CSF PCR for bacteria, fungi, Mycobacterium tuberculosis, Herpes viruses, Enteroviruses, Japanese B virus and Dengue viruses
td	NA
td	Brain: no pathological findings
td	IVIG 400 mg/kg (5 days)
td	Lopinavir/ritonavir, hydroxychloroquine, antibiotic therapy, oxygen support (35%)
td	Resolution of all symptoms except for minor hyporeflexia at the LL
tr	Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation Improvement of motor symptoms
td	Manganotti et al. [33]
td	RT-PCR
td	IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 113.0 pg/ml (0.8–6.4 pg/ml), IL-8: 20.0 pg/ml (6.7–16.2 pg/ml), TNF-α: 16.0 pg/ml (7.8–12.2 pg/ml)
td	Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders
td	Increased total protein (52 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine, oseltamivir, darunavir, methylprednisolone and tocilizumab + mechanical invasive ventilation
td	Improvement of motor symptoms
tr	Manganotti et al. [33] RT-PCR IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation Improvement of motor symptoms
td	Manganotti et al. [33]
td	RT-PCR
td	IL-1: 0.5 pg/ml (< 0.001 pg/ml), IL-6: 9.8 pg/ml (0.8–6.4 pg/ml), IL-8: 55.0 pg/ml (6.7–16.2 pg/ml), TNF- α: 16.0 pg/ml (7.8–12.2 pg/ml)
td	Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disorders
td	Normal total protein (40 mg/dl), leucocytes: 1 cell/mm3, negative SARS-CoV-2 PCR
td	Mixed demyelinating and axonal EMG subtype unknown
td	Brain: no pathological findings
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone + mechanical invasive ventilation
td	Improvement of motor symptoms
tr	Manganotti et al. [33] RT-PCR NA Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR Mainly demyelinating Predominantly AIDP Brain: no pathological findings IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone Improvement
td	Manganotti et al. [33]
td	RT-PCR
td	NA
td	Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes
td	Increased total protein (72 mg/dL), leucocytes: 5 cell/mm3, negative SARS-CoV-2 PCR
td	Mainly demyelinating Predominantly AIDP
p	Mainly demyelinating
p	Predominantly AIDP
td	Brain: no pathological findings
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone
td	Improvement
tr	Manganotti et al. [33] RT-PCR NA NA NA Mixed demyelinating and axonal EMG subtype unknown NA Methylprednisolone 60 mg for 5 days Methylprednisolone Stationary
td	Manganotti et al. [33]
td	RT-PCR
td	NA
td	NA
td	NA
td	Mixed demyelinating and axonal EMG subtype unknown
td	NA
td	Methylprednisolone 60 mg for 5 days
td	Methylprednisolone
td	Stationary
tr	Manganotti et al. [33] RT-PCR IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml) Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR Mixed demyelinating and axonal EMG subtype unknown NA IVIG 400 mg/kg/day (5 days) Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation Improvement
td	Manganotti et al. [33]
td	RT-PCR
td	IL-1: 0.2 pg/ml (< 0.001 pg/ml), IL-6: 32.7 pg/ml (0.8–6.4 pg/ml), IL-8: 17.8 pg/ml (6.7–16.2 pg/ml), TNF- α : 11.1 pg/ml (7.8–12.2 pg/ml), IL-2R: 1203.0 pg/ml (440.0–1435.0 pg/ml), IL-10: 4.6 (1.8–3.8 pg/ml)
td	Negative anti-ganglioside antibodies, negative HIV, HBV, HCV negative serological tests for autoimmune disordes
td	Increased total protein (53 mg/dL), leucocytes: 2 cell/mm3, negative SARS-CoV-2 PCR
td	Mixed demyelinating and axonal EMG subtype unknown
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir, methylprednisolone, meropenem, linezolid, clarithromycin, fluconazole, doxycycline + mechanical invasive ventilation
td	Improvement
tr	Marta-Enguita et al. [34] RT-PCR + chest CT Thrombocytopenia, d-Dimer elevation NA NA NA NA NA NA Death after 10 days
td	Marta-Enguita et al. [34]
td	RT-PCR + chest CT
td	Thrombocytopenia, d-Dimer elevation
td	NA
td	NA
td	NA
td	NA
td	NA
td	NA
td	Death after 10 days
tr	Mozhdehipanah et al. [35] RT-PCR (negative chest CT) Normal WBC, CRP and ESR NA Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture Demyelinating AIDP NA Plasma exchange (5 cycles) NA Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis
td	Mozhdehipanah et al. [35]
td	RT-PCR (negative chest CT)
td	Normal WBC, CRP and ESR
td	NA
td	Increased total protein (139 mg/dL), normal cell count, negative CSF HSV serology and gram stain and culture
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	Plasma exchange (5 cycles)
td	NA
td	Significant improvement of muscle weakness after 3 weeks, persistence of mild bifacial paresis
tr	Mozhdehipanah et al. [35] RT-PCR Normal WBC, CRP and ESR NA Albuminocytological dissociation NA NA IVIG 400 mg/kg/day (5 days) NA Complete recovery, except for the persistence of hyporeflexia
td	Mozhdehipanah et al. [35]
td	RT-PCR
td	Normal WBC, CRP and ESR
td	NA
td	Albuminocytological dissociation
td	NA
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	NA
td	Complete recovery, except for the persistence of hyporeflexia
tr	Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis lymphopenia, elevated ESR and CRP NA Increased total protein (57 mg/dL), normal cell count and glucose (not further specified) Axonal AMSAN NA IVIG 400 mg/kg/day (3 days) Hydroxy chloroquine, lopinavir/ ritonavir Death after 3 days from starting treatment with IVIG
td	Mozhdehipanah et al. [35]
td	RT-PCR + chest CT
td	Leucocytosis lymphopenia, elevated ESR and CRP
td	NA
td	Increased total protein (57 mg/dL), normal cell count and glucose (not further specified)
td	Axonal AMSAN
p	Axonal
p	AMSAN
td	NA
td	IVIG 400 mg/kg/day (3 days)
td	Hydroxy chloroquine, lopinavir/ ritonavir
td	Death after 3 days from starting treatment with IVIG
tr	Mozhdehipanah et al. [35] RT-PCR + chest CT Leucocytosis, lymphopenia, elevated ESR and CRP NA Increased total protein (89 mg/dL), normal cell count and glucose (not further specified) Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) Hydroxy chloroquine, lopinavir/ ritonavir No significant clinical improvement
td	Mozhdehipanah et al. [35]
td	RT-PCR + chest CT
td	Leucocytosis, lymphopenia, elevated ESR and CRP
td	NA
td	Increased total protein (89 mg/dL), normal cell count and glucose (not further specified)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	Hydroxy chloroquine, lopinavir/ ritonavir
td	No significant clinical improvement
tr	Naddaf et al. [36] Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR) Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L) Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index Demyelinating AIDP Spine: smooth enhancement of the cauda equine roots Plasma exchange (5 sessions) Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid
td	Naddaf et al. [36]
td	Positive SARS-CoV-2 IgG (index value: 8.2, normal < 0.8) and IgA + chest CT (negative RT-PCR)
td	Normal completed blood count, elevated d-dimer (690 ng/mL), ferritin (575 mcg/L), ESR (26 mm/h), alanine aminotransferase (73 U/L)
td	Negative anti-ganglioside antibodies negative HIV, syphilis, West Nile virus, Lyme disease testing, EBV and CMV serology consistent with remote infection, negative paraneoplastic evaluation
td	Increased total protein (273 mg/dL), total cells count: 2/mm3, negative CSF SARS-CoV-2 RT-PCR, negative meningitis/encephalitis panel, negative oligoclonal bands and IgG index
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Spine: smooth enhancement of the cauda equine roots
td	Plasma exchange (5 sessions)
td	Hydroxy chloroquine, zinc, methylprednisolone 40 mg bid for 5 days
td	Improvement of motor and gait examination. Persistence of slight ataxia without requiring gait aid
tr	Oguz-Akarsu et al. [37] RT-PCR + chest MRT + chest CT Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77) HIV test negative Normal total protein (32.6 mg/dL) with no leucocytes Demyelinating with sural sparing pattern AIDP Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences Plasma exchange (five sessions, one every other day) Hydroxychloroquine, azithromycin Marked neurological improvement after 2 weeks and she was able to walk without assistance
td	Oguz-Akarsu et al. [37]
td	RT-PCR + chest MRT + chest CT
td	Mild neutropenia (1.49 cells/µL) and a high monocyte percentage (19.77)
td	HIV test negative
td	Normal total protein (32.6 mg/dL) with no leucocytes
td	Demyelinating with sural sparing pattern AIDP
p	Demyelinating with sural sparing pattern
p	AIDP
td	Cervical and lumbar and spine: asymmetrical thickening and hyperintensity of post-ganglionic roots supplying the brachial and lumbar plexuses in STIR sequences
td	Plasma exchange (five sessions, one every other day)
td	Hydroxychloroquine, azithromycin
td	Marked neurological improvement after 2 weeks and she was able to walk without assistance
tr	Ottaviani et al. [38] RT-PCR + chest CT Lymphopenia, increased d-dimer, CRP and CK Negative anti-ganglioside antibodies Increased total protein (108 mg/dL), cell count: 0 cells/μL Mainly demyelinating Predominantly AIDP NA IVIG 400 mg/kg (5 days) Lopinavir/ritonavir, hydroxychloroquine Progressive worsening with multi-organ failure
td	Ottaviani et al. [38]
td	RT-PCR + chest CT
td	Lymphopenia, increased d-dimer, CRP and CK
td	Negative anti-ganglioside antibodies
td	Increased total protein (108 mg/dL), cell count: 0 cells/μL
td	Mainly demyelinating Predominantly AIDP
p	Mainly demyelinating
p	Predominantly AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	Lopinavir/ritonavir, hydroxychloroquine
td	Progressive worsening with multi-organ failure
tr	Padroni et al. [39] RT-PCR + chest CT WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed Increased total protein (48 mg/dl), cell count: 1 × 106/L Motor sensory axonal AMSAN NA IVIG 400 mg/kg (5 days) + mechanical invasive ventilation NA At day 6 from admission: ICU with mechanical invasive ventilation
td	Padroni et al. [39]
td	RT-PCR + chest CT
td	WBC 10.41 × 109/L (neutrophils 8.15 × 109/L), normal d-dimer
td	Negative screening for Mycoplasma pneumonia, CMV, Legionella pneumophila, Streptococcus pneumoniae, HSV, VZV, EBV, HIV-1, Borrelia burgdorferi; auto-antibodies not performed
td	Increased total protein (48 mg/dl), cell count: 1 × 106/L
td	Motor sensory axonal AMSAN
p	Motor sensory axonal
p	AMSAN
td	NA
td	IVIG 400 mg/kg (5 days) + mechanical invasive ventilation
td	NA
td	At day 6 from admission: ICU with mechanical invasive ventilation
tr	Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased neutrophils and CRP NA Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5), Demyelinating AIDP NA IVIG + mechanical invasive ventilation None 17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running
td	Paterson et al. [40]
td	Definite diagnosis (not specified) (normal chest CT)
td	Increased neutrophils and CRP
td	NA
td	Increased total protein (0.5 g/L), leucocytes: 3 cells/μL (0–5),
p	Increased total protein (0.5 g/L),
p	leucocytes: 3 cells/μL (0–5),
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG + mechanical invasive ventilation
td	None
td	17 days of hospitalisation, at discharge able to walk 5 m (across an open space) but incapable of manual work/running
tr	Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Increased CRP and fibrinogen NA Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG Mechanical invasive ventilation 46 days (ongoing) of hospitalisation, still critical and requiring ventilation
td	Paterson et al. [40]
td	Definite diagnosis (not specified) (normal chest CT)
td	Increased CRP and fibrinogen
td	NA
td	Increased total protein (0.6 g/L) leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2)
p	Increased total protein (0.6 g/L)
p	leucocytes: 2 cells/μL (0-5), Glucose 3.4 (mmol/L; 2.2-4.2)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings
td	IVIG
td	Mechanical invasive ventilation
td	46 days (ongoing) of hospitalisation, still critical and requiring ventilation
tr	Paterson et al. [40] Definite diagnosis (not specified) (normal chest CT) Not significant findings NA Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2) Demyelinating AIDP Brain: no pathological findings IVIG NA 7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running
td	Paterson et al. [40]
td	Definite diagnosis (not specified) (normal chest CT)
td	Not significant findings
td	NA
td	Increased total protein (0.9 g/L) leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2)
p	Increased total protein (0.9 g/L)
p	leucocytes: < 1 cells/μL (0-5), Glucose 3.7 (mmol/L; 2.2-4.2)
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings
td	IVIG
td	NA
td	7 days (ongoing) of hospitalisation, able to walk 5 m (across an open space) but incapable of manual work/running
tr	Paybast et al. [41] RT-PCR NA NA Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture Mixed demyelinating and axonal EMG subtype unknown NA 5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol,
td	Paybast et al. [41]
td	RT-PCR
td	NA
td	NA
td	Increased total protein (139 mg/dL), normal glucose and cell count, normal CSF viral serology, negative gram stain and culture
td	Mixed demyelinating and axonal EMG subtype unknown
td	NA
td	5 sessions of therapeutic plasma exchange, intravenous bolus of labetalol to control sympathetic nervous system over-reactivity
td	Hydroxychloroquine sulphate 200 mg two times per day for a week
td	Persistence of generalized hyporeflexia, decreased light touch sensation in distal limbs, mild bilateral facial paresis, sympathetic over-reactivity successfully controlled with labetalol,
tr	Paybast et al. [41] RT-PCR NA NA Albuminocytological dissociation NA NA IVIG 20 g (5 days) Hydroxychloroquine sulphate 200 mg two times per day for a week Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs
td	Paybast et al. [41]
td	RT-PCR
td	NA
td	NA
td	Albuminocytological dissociation
td	NA
td	NA
td	IVIG 20 g (5 days)
td	Hydroxychloroquine sulphate 200 mg two times per day for a week
td	Persistence of generalized hyporeflexia and decreased light touch sensation in distal limbs
tr	Pfefferkorn et al. [42] RT-PCR + chest CT NA Negative anti-gangliosides antibodies At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count Demyelinating AIDP Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange NA At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation
td	Pfefferkorn et al. [42]
td	RT-PCR + chest CT
td	NA
td	Negative anti-gangliosides antibodies
td	At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR At day 13th: increased total protein (10.231 mg/L), normal cell count
p	At admission: Normal total protein, cell count: 9/µL, negative SARS-CoV-2 PCR
p	At day 13th: increased total protein (10.231 mg/L), normal cell count
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Spinal: massive symmetrical contrast enhancement of the spinal nerve roots at all levels of the spine including the cauda equina. Anterior and posterior nerve roots were equally affected
td	IVIG 30 g (5 days) + mechanical invasive ventilation + plasma exchange
td	NA
td	At day 31 from admission: motor improvement with regression of facial and hypoglossal paresis but still needed mechanical ventilation
tr	Rana et al. [43] RT-PCR NA NA NA Demyelinating with sural sparing AIDP Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy IVIG 400 mg/kg (5 days) Hydroxychloroquine and azithromycin On day 4 respiratory improvement, on day 7 rehabilitation
td	Rana et al. [43]
td	RT-PCR
td	NA
td	NA
td	NA
td	Demyelinating with sural sparing AIDP
p	Demyelinating with sural sparing
p	AIDP
td	Thoracic and lumbar spine: no evidence of myelopathy or radiculopathy
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine and azithromycin
td	On day 4 respiratory improvement, on day 7 rehabilitation
tr	Reyes-Bueno et al. [44] Serology (negative RT-PCR) NA Negative anti-ganglioside antibodies Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP NA IVIG 400 mg/kg (5 days) + Gabapentin NA After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation
td	Reyes-Bueno et al. [44]
td	Serology (negative RT-PCR)
td	NA
td	Negative anti-ganglioside antibodies
td	Increased total protein (70 mg/dl), cell count: 5 cells/µl, albuminocytological dissociation
td	Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement AIDP
p	Demyelinating with alteration of the Blink-Reflex. Further EMG: polyradiculoneuropathy with proximal and brainstem involvement
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days) + Gabapentin
td	NA
td	After the 18th day progressive improvement of facial and limb paresis, diplopia and pain. Consequent neurological rehabilitation
tr	Riva et al. [45] Chest CT + serology (negative RT-PCR) No pathological findings Negative anti-ganglioside antibodies Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV Demyelinating with sural sparing AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) None Slowly improvement after the 10th day
td	Riva et al. [45]
td	Chest CT + serology (negative RT-PCR)
td	No pathological findings
td	Negative anti-ganglioside antibodies
td	Normal total protein and cells; negative PCR for SARS-CoV2, EBV, CMV, VZV, HSV 1–2, HIV
td	Demyelinating with sural sparing AIDP
p	Demyelinating with sural sparing
p	AIDP
td	Brain: NA Spinal: no pathological findings
p	Brain: NA
p	Spinal: no pathological findings
td	IVIG 400 mg/kg (5 days)
td	None
td	Slowly improvement after the 10th day
tr	Sancho-Saldaña et al. [46] RT-PCR + chest X-Ray NA Negative anti-ganglioside antibodies Increased total protein (0.86 g/L), cell count: 3 leucocytes Demyelinating AIDP Whole spine: brainstem and cervical meningeal enhancement IVIG 400 mg/kg (5 days) Hydroxychloroquine, azithromycin Recovering by day 7 after the onset of weakness.
td	Sancho-Saldaña et al. [46]
td	RT-PCR + chest X-Ray
td	NA
td	Negative anti-ganglioside antibodies
td	Increased total protein (0.86 g/L), cell count: 3 leucocytes
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Whole spine: brainstem and cervical meningeal enhancement
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, azithromycin
td	Recovering by day 7 after the onset of weakness.
tr	Scheidl et al. [47] RT-PCR No pathological findings Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA Increased total protein (140 g/L), albuminocytological dissociation Demyelinating AIDP Brain: NA Cervical spine: no pathological findings IVIG 400 mg/kg (5 days) None Complete recovery
td	Scheidl et al. [47]
td	RT-PCR
td	No pathological findings
td	Negative Campylobacter Jejuni and Borrelia serology, negative ANA, anti-DNA, c-ANCA,p-ANCA
td	Increased total protein (140 g/L), albuminocytological dissociation
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: NA Cervical spine: no pathological findings
p	Brain: NA
p	Cervical spine: no pathological findings
td	IVIG 400 mg/kg (5 days)
td	None
td	Complete recovery
tr	Sedaghat et al. [48] RT-PCR + chest CT Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP NA NA Motor sensory Axonal AMSAN Brain: no pathological findings Spinal: two cervical intervertebral disc herniations IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, azithromycin Not reported
td	Sedaghat et al. [48]
td	RT-PCR + chest CT
td	Increased WBC 14.6 × 103 (neutrophils 82.7%, lymphocytes 10.4%) and CRP
td	NA
td	NA
td	Motor sensory Axonal AMSAN
p	Motor sensory Axonal
p	AMSAN
td	Brain: no pathological findings Spinal: two cervical intervertebral disc herniations
p	Brain: no pathological findings
p	Spinal: two cervical intervertebral disc herniations
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir, azithromycin
td	Not reported
tr	Sidig et al. [49] RT-PCR + chest CT NA NA None Demyelinating AIDP Brain: no pathological findings NA NA Death after 7 days; because of progressive respiratory failure
td	Sidig et al. [49]
td	RT-PCR + chest CT
td	NA
td	NA
td	None
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings
td	NA
td	NA
td	Death after 7 days; because of progressive respiratory failure
tr	Su et al. [50] RT-PCR + chest X-ray WBC 12,000 cells/µl Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA Increased total protein (313 mg/dL), WBC: 1 cell Demyelinating AIDP NA IVIG 2gm/kg (for 4 days) None On day 28 persistence of severe weakness
td	Su et al. [50]
td	RT-PCR + chest X-ray
td	WBC 12,000 cells/µl
td	Negative anti- ganglioside GM1, GD1b and GQ1b antibodies, acetylcholine receptor binding, voltage-gated calcium channel, antinuclear and ANCA
td	Increased total protein (313 mg/dL), WBC: 1 cell
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 2gm/kg (for 4 days)
td	None
td	On day 28 persistence of severe weakness
tr	Tiet et al. [51] RT-PCR Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function. NA Increased total protein (> 1.25 g/L), cell count 1x106/L Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) None Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation
td	Tiet et al. [51]
td	RT-PCR
td	Elevated lactate on venous blood gas (3.3 mmo/L), mildly elevated CRP (20 mg/L). Normal WBC, sodium, potassium and renal function.
td	NA
td	Increased total protein (> 1.25 g/L), cell count 1x106/L
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg/day (5 days)
td	None
td	Resolution of facial diplegia, improved upper and lower limbs weakness; able to mobilize unassisted 11 weaks after neurorehabilitation
tr	Toscano et al. [52] RT-PCR + Chest CT + serology Lymphocytopenia, increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR Axonal with sural sparing AMSAN Brain: no pathological findings Spinal: Enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation Paracetamol At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia
td	Toscano et al. [52]
td	RT-PCR + Chest CT + serology
td	Lymphocytopenia, increased CRP, LDH, ketonuria
td	Negative anti-ganglioside antibodies
td	Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR
p	Day 2: normal total protein, no cells, negative SARS-CoV-2 PCR
p	Day 10: increased total protein (101) mg/dl, cell count: 4/mm3, negative SARS-CoV-2 PCR
td	Axonal with sural sparing AMSAN
p	Axonal with sural sparing
p	AMSAN
td	Brain: no pathological findings Spinal: Enhancement of caudal nerve roots
p	Brain: no pathological findings
p	Spinal: Enhancement of caudal nerve roots
td	IVIG 400 mg/kg (2 cycles) + temporary mechanical non-invasive ventilation
td	Paracetamol
td	At week 4 persistence of severe UL weakness, dysphagia, and LL paraplegia
tr	Toscano et al. [52] RT-PCR (negative chest CT) Lymphocytopenia; increased ferritin, CRP, LDH NA Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR Motor sensory axonal with sural sparing AMSAN Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings IVIG 400 mg/kg Amoxycillin At week 4 improvement of ataxia and mild improvement of facial weakness
td	Toscano et al. [52]
td	RT-PCR (negative chest CT)
td	Lymphocytopenia; increased ferritin, CRP, LDH
td	NA
td	Increased total protein (123 mg/dl), no cells, negative SARS-CoV-2 PCR
td	Motor sensory axonal with sural sparing AMSAN
p	Motor sensory axonal with sural sparing
p	AMSAN
td	Brain: enhancement of facial nerve bilaterally Spinal: no pathological findings
p	Brain: enhancement of facial nerve bilaterally
p	Spinal: no pathological findings
td	IVIG 400 mg/kg
td	Amoxycillin
td	At week 4 improvement of ataxia and mild improvement of facial weakness
tr	Toscano et al. [52] RT-PCR + chest CT Lymphocytopenia; increased CRP, LDH, ketonuria Negative anti-ganglioside antibodies Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR Motor axonal AMAN Brain: no pathological findings Spinal: enhancement of caudal nerve roots IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation Azythromicin ICU admission due to respiratory failure and tetraplegia. At week 4 still critical
td	Toscano et al. [52]
td	RT-PCR + chest CT
td	Lymphocytopenia; increased CRP, LDH, ketonuria
td	Negative anti-ganglioside antibodies
td	Increased total protein (193 mg/dl), no cells, negative SARS-CoV-2 PCR
td	Motor axonal AMAN
p	Motor axonal
p	AMAN
td	Brain: no pathological findings Spinal: enhancement of caudal nerve roots
p	Brain: no pathological findings
p	Spinal: enhancement of caudal nerve roots
td	IVIG 400 mg/kg (2 cycles) + mechanical invasive ventilation
td	Azythromicin
td	ICU admission due to respiratory failure and tetraplegia. At week 4 still critical
tr	Toscano et al. [52] RT-PCR + serology (negative chest CT) Lymphocytopenia; increased CRP, ketonuria NA Normal protein, no cells, negative SARS-CoV-2 PCR Demyelinating AIDP Brain: no pathological findings Spinal: no pathological findings IVIG 400 mg/kg None At week 4 mild improvement in UL but unable to stand
td	Toscano et al. [52]
td	RT-PCR + serology (negative chest CT)
td	Lymphocytopenia; increased CRP, ketonuria
td	NA
td	Normal protein, no cells, negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: no pathological findings Spinal: no pathological findings
p	Brain: no pathological findings
p	Spinal: no pathological findings
td	IVIG 400 mg/kg
td	None
td	At week 4 mild improvement in UL but unable to stand
tr	Toscano et al. [52] Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL) Lymphocytopenia; increased CRP, LDH Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR Demyelinating AIDP Brain: NA Spinal: no pathological findings IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition None At week 4 flaccid tetraplegia, dysphagia, ventilation dependent
td	Toscano et al. [52]
td	Chest CT + serology (negative RT-PCR in nasopharyngeal swab and BAL)
td	Lymphocytopenia; increased CRP, LDH
td	Negative anti-ganglioside antibodies; negative screening for Campylobacter jejuni, EBV, CMV, HSV, VZV, influenza, HIV
td	Normal total protein (40 mg/dL), white cell count 3/mm3; negative SARS-CoV-2 PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	Brain: NA Spinal: no pathological findings
p	Brain: NA
p	Spinal: no pathological findings
td	IVIG 400 mg/kg + plasma exchange + mechanical invasive ventilation + enteral nutrition
td	None
td	At week 4 flaccid tetraplegia, dysphagia, ventilation dependent
tr	Velayos Galán et al. [53] RT-PCR + chest X-ray NA NA NA Demyelinating AIDP NA IVIG 400 mg/kg (5 days) Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy NA
td	Velayos Galán et al. [53]
td	RT-PCR + chest X-ray
td	NA
td	NA
td	NA
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg (5 days)
td	Hydroxychloroquine, lopinavir/ritonavir, amoxicillin, corticosteroids + low-flow oxygen therapy
td	NA
tr	Virani et al. [54] rt-pcr + chest mrt WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml NA NA NA Brain: NA Spinal: no pathological findings IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days) Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility
td	Virani et al. [54]
td	rt-pcr + chest mrt
td	WBC 8.6 × 103; Hb 15.4 g/dl; PC 211 × 103; procalcitonin: 0.15 ng/ml
td	NA
td	NA
td	NA
td	Brain: NA Spinal: no pathological findings
p	Brain: NA
p	Spinal: no pathological findings
td	IVIG 400 mg/kg (5 days) + mechanical invasive ventilation (4 days)
td	Hydroxychloroquine 400 mg bid for first 2 doses, then 200 mg bid for 8 doses
td	At day 4 of IVIG: liberation from mechanical ventilation, resolution of UL symptoms, persistence of LL weakness. Sent to a rehabilitation facility
tr	Webb et al. [55] RT-PCR + chest X-ray + chest CT Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L) Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR Demyelinating AIDP NA IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation Co-amoxiclav After 1 week in ICU: no oxygen requirement and ventilation
td	Webb et al. [55]
td	RT-PCR + chest X-ray + chest CT
td	Lymphopenia (0.9 × 109/L), thrombocytosis (490 × 109/L) raised CRP (25 mg/L)
td	Negative ANA, ANCA, anti-ganglioside antibodies, syphilis serology HIV, hepatitis B and hepatitis C
td	Increased total protein (0.51 g/L), normal glucose and cell count, negative SARS-CoV-2 PCR, negative viral PCR
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG 400 mg/kg/day (5 days) + Mechanical invasive ventilation
p	IVIG 400 mg/kg/day (5 days) + Mechanical invasive
p	ventilation
td	Co-amoxiclav
td	After 1 week in ICU: no oxygen requirement and ventilation
tr	Zhao et al. [56] RT-PCR + chest CT WBC 0.52 × 109; PC 113 × 109/L NA Increased total protein (124 mg/dL), cell count 5 × 106/L Demyelinating AIDP NA IVIG (dosing not reported) Arbidol, lopinavir/ ritonavir At day 30 resolution of neurological and respiratory symptoms
td	Zhao et al. [56]
td	RT-PCR + chest CT
td	WBC 0.52 × 109; PC 113 × 109/L
td	NA
td	Increased total protein (124 mg/dL), cell count 5 × 106/L
td	Demyelinating AIDP
p	Demyelinating
p	AIDP
td	NA
td	IVIG (dosing not reported)
td	Arbidol, lopinavir/ ritonavir
td	At day 30 resolution of neurological and respiratory symptoms
table-wrap-foot	AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset bAccording to Brighton diagnostic criteria [66]
p	AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor sensory axonal neuropathy; ANA, antinuclear antibodies; ANCA, anti-neutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; CK, creatine kinase; CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease, COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CSF, cerebrospinal fluid; CT, computed tomography; DM, diabetes mellitus; EBV, Epstein–Barr virus; ESR, erythrocyte sedimentation rate; F, female; GBS, Guillain–Barré syndrome; GGT, gamma-glutamyl transferase; GOT, glutamic oxaloacetic transaminase; GPT, glutamate pyruvate transaminase; Hb, haemoglobin; HIV, human immunodeficiency virus; HSV, herpex simplex virus; ICU, intensive-care unit; IL, interleukin; IVIG, intravenous immunoglobulins; IL, interleukin; LDH, lactate dehydrogenase; LL, lower limbs; M, male; MRI, magnetic resonance imaging; NA, not available; PC, platelet count; PCR, Polymerase Chain Reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TNF, tumor necrosis factor; UL, upper limbs; VDRL, Veneral Disease Research Laboratory; VZV, varicella-zoster virus; WBC, white blood cells; X-ray: radiography
p	aTime to Nadir refers to days elapsed between the onset of neurological symptoms and the development of the worst clinical picture when no progression was reported nadir was considered concomitant with GBS symptoms onset
p	bAccording to Brighton diagnostic criteria [66]
p	Interestingly, patients with no improvement or poor outcome (n = 19) showed a slightly higher (but not significant) frequency of clinical history and/or a radiological picture of COVID-19 pneumonia (14/19, 73.7%) compared to those with a favorable prognosis (29/48, 60.4%, p = 0.541). Moreover, the former group of patients was significantly older (mean 62.7 ± 17.8 years, p = 0.011), but with comparable distribution of sex (p = 0.622) and electrophysiological subtypes (p = 0.144) and similar latency between COVID-19 and GBS (p = 0.588) and nadir (p = 0.825), compared to the latter (mean age 51.8 ± 16.6 years). The same findings were confirmed even after excluding cases with no improvement from the analysis (to prevent a possible bias related to the short follow-up time).
sec	Discussion COVID-19 pandemic prompts all efforts for the early recognition and treatment of its manifestations. In analogy to other viruses, belonging or not to the coronavirus family [63, 67], neurologic complications in COVID-19 are emerging as one of the most significant clinical chapters of this pandemic. In this regard, peripheral and central nervous system damage in COVID-19 has been postulated to be the consequence of two different mechanisms: 1) hematogenous (infection of endothelial cells or leucocytes) or trans-neuronal (via olfactory tract or other cranial nerves) dissemination to central nervous system in relation with viral neurotropism, and 2) abnormal immune-mediated response causing secondary neurological involvement [62, 68, 69]. The first mechanism is supposed to be responsible for the most common neurological symptoms developed by patients with COVID-19 (e.g., hypogeusia, hyposmia, headache, vertigo, and dizziness). In contrast, the second can lead to severe complications during or after the course of the illness, either dysimmune (e.g., myelitis, encephalitis, GBS) or induced by cytokine overproduction (hypercoagulable state and cerebrovascular events) [68, 69]. In the present systematic review, we reviewed clinical features, results of diagnostic investigations, and outcome in 73 cases of COVID-19-associated GBS spectrum [5–56]. In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70, 71]. However, pediatric cases with GBS have been increasingly reported in the literature [21, 27, 35, 41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus–GBS [72]. This finding may also reflect the gender epidemiology of SARS-CoV-2. In this regard, males typically show a worse COVID-19 outcome compared to the females [70, 71], possibly due to a generally shorter life expectancy or to higher circulating Angiotensin-Converting-Enzyme 2 (ACE2) levels, the cellular receptor for SARS-CoV-2, in the former compared to the latter [71]. Moreover, given that GBS is a rare disease [57] the epidemiological distribution of the reported cases seems to reflect current worldwide outbreaks, with Europe being the “hottest” spot in March–May 2020 and USA together with Asia in the following period [73, 74]. On another issue, despite a few GBS cases seemed to have a para-infectious profile [10, 37, 38, 40, 55, 56] as described for Zika virus [75], all other reported patients developed neurological symptoms with a typical latency after COVID-19 (median time 14 days). This feature, together with the frequently reported negative nasopharyngeal swab at GBS onset [22, 24, 36, 44, 45, 52] and clinical improvement after IVIG therapy, seems to support the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [76, 77]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.) in GBS tested cases may reinforce the hypothesis of a systemic inflammatory storm in COVID-19 [76, 77]. However, given the limited data, we could not perform an accurate analysis of the distribution and, eventually, prognostic value of inflammatory markers in COVID-19-associated GBS. Moreover, we cannot exclude that in cases with GBS developing before or together with COVID-19 symptoms, the disease might have progressed sub-clinically in the early phase to manifest afterwards with its typical systemic clinical picture. Indeed, two cases [10, 12], who tested positive for SARS-CoV-2, never developed COVID-19 respiratory or systemic symptoms and one of them showed an asymptomatic pneumonia at chest-CT [12]. However, only more extensive epidemiological and translational studies, with the aim to compare the characteristics of GBS associated or not with COVID-19, could clarify these issues. In our population, most common clinical manifestations and distribution of clinical variants resemble those of classic GBS confirming the predominance of the sensorimotor syndrome compared to MFS and other rare variants [57–59, 66]. Similarly, the results of CSF analysis reflected typical neurochemical findings in non-COVID-19 GBS. In the latter, elevated CSF proteins and pleocytosis were described in about 50–80% [57, 78] and 11–15% cases, respectively [58, 79, 80], largely overlapping with the percentages in our cohort. In this regard, the mostly normal cell count, together with the absence of SARS-CoV-2 RNA in all tested CSF samples [6–9, 12–14, 16, 21–24, 31, 33, 36, 42, 44, 52, 55], makes the possibility of a direct invasion from SARS-CoV-2 into the nerve roots with intrathecal viral replication less probable. However, a possible bias might rely on the lack of systematic data concerning the latency between symptom onset and CSF sampling in COVID-19 GBS cases. On another issue, in a further case of MFS associated withCOVID-19, who came to our attention, we observed the absence of intrathecal synthesis of SARS-CoV-2 antibodies together with a massive increase of CSF phosphorylated neurofilament heavy chain (pNfH) and serum neurofilament light chain (NfL) proteins, supporting the role of neurochemical markers as easily implementable tools for the detection of nervous system affection in COVID-19-related diseases [81, 82]. At variance with CSF findings, we found a discrepancy concerning MRI findings between classic GBS and COVID-19-related GBS. Specifically, while most cases of the former group showed typically spinal root enhancement at MRI [83], in the latter group, in analogy with Zika-associated GBS, the same finding was less frequently reported [84]. However, caution should be warranted in the interpretation of these results, given that MRI findings might have been underestimated, due to lack of a sufficient number of exams in the context of pandemic-imposed restrictions in the routine clinical setting. Regarding the distribution of GBS electrophysiological variants, our analysis showed that COVID-19-associated GBS manifests prevalently with AIDP and, to a lesser extent, with AMSAN and AMAN, in line with classic GBS in Western countries [66, 85]. Conversely, the observation of positive anti-GD1b antibodies in one COVID-19-related MFS patient and negative anti-ganglioside antibodies in other five cases appear in discordance with the high prevalence (≈ 90%) of anti-GQ1b antibodies among non-COVID-19 MFS cases [86], and may suggest different immune-mediated mechanisms. However, these results could not be generalized until a wider population would be tested. In analogy to classic GBS, approximately one-fifth of COVID-19-associated GBS subjects required mechanical ventilation during hospitalisation [87]. In this regard, cases with no improvement or unfavorable outcome showed, in comparison to those with a good prognosis, an older age, confirming similar findings both in classic GBS [58, 88] and in COVID-19 [89], and a slightly higher frequency (without reaching a statistical significance) of past or concurrent COVID-19 pneumonia. However, given the short follow-up time in most cases, we could not reach a definite conclusion on the impact of past or concurrent COVID-19 restrictive syndrome due to pneumonia on the prognosis of GBS patients. Future prospective studies are needed to clarify this issue. Moreover, given that also preceding diarrhea (mostly caused by Campylobacter Jejuni infection) is a strong negative prognostic factor in classic GBS [57, 88], further prospective studies are needed to compare the severity of GBS related to COVID-19 to that associated with C. jejuni. Finally, in the context of respiratory failure and ventilation associated with COVID-19, the differential diagnosis should always take into consideration critical illness neuropathy and myopathy, which tend to develop later during the critical course [90]. Despite these findings, approximately one-third of COVID-19-related GBS patients showed no clinical and/or radiological evidence of pneumonia, providing evidence that GBS may also develop in the context of a paucisymptomatic or even asymptomatic COVID-19. However, given that among the GBS population only two asymptomatic COVID-19 patients were reported to date, we may speculate that, in most cases, a certain degree of lung injury (even minimal) or at least hematic dissemination (e.g., fever underlying significant viral load) is necessary to trigger the immuno-mediated process through lymphocytic recognition of self-antigens or molecular mimicry. Major strengths of our review are the inclusion of a high number of patients, together with an in-depth analysis of the clinical and diagnostic features of COVID-19-associated GBS. We are aware that selection bias might have occurred, given that most reported cases to date have been described mostly in Europe (47 out of 73) and during COVID-19 highest spreading. Therefore, future extensive epidemiological studies are necessary to ascertain the nature of the association between COVID-19 and GBS (causal or coincidental). Moreover, we cannot exclude the possibility that at least some of the cases represent instances of CIDP, given the frequent absence of a follow-up longer than 2 months. On another issue, the low but possible evidence of an epidemiological link between vaccines and GBS development [57, 58] should aware the clinicians of the possible occurrence of GBS after COVID-19 vaccination in the long-term future. In conclusion, based on the systematic review of 73 cases, we showed that the clinical picture of COVID-19-associated GBS seems to resemble that of classic GBS or Zika-associated GBS. Moreover, the chronological evolution, the response to IVIG, and the absence of SARS-CoV-2 RNA in CSF may suggest a prominent post-infectious immune-mediated mechanism rather than a para-infectious one. Although most cases were symptomatic for COVID-19, the preliminary report of a few patients without respiratory or systemic symptoms raises a significant healthcare issue, namely the importance of SARS-CoV-2 testing in all patients with suspected GBS during the pandemic, with the aim to provide an eventual rapid case isolation. Nevertheless, only further analyses on more comprehensive cohorts could help in clarifying better all these issues.
title	Discussion
p	COVID-19 pandemic prompts all efforts for the early recognition and treatment of its manifestations. In analogy to other viruses, belonging or not to the coronavirus family [63, 67], neurologic complications in COVID-19 are emerging as one of the most significant clinical chapters of this pandemic. In this regard, peripheral and central nervous system damage in COVID-19 has been postulated to be the consequence of two different mechanisms: 1) hematogenous (infection of endothelial cells or leucocytes) or trans-neuronal (via olfactory tract or other cranial nerves) dissemination to central nervous system in relation with viral neurotropism, and 2) abnormal immune-mediated response causing secondary neurological involvement [62, 68, 69]. The first mechanism is supposed to be responsible for the most common neurological symptoms developed by patients with COVID-19 (e.g., hypogeusia, hyposmia, headache, vertigo, and dizziness). In contrast, the second can lead to severe complications during or after the course of the illness, either dysimmune (e.g., myelitis, encephalitis, GBS) or induced by cytokine overproduction (hypercoagulable state and cerebrovascular events) [68, 69].
p	In the present systematic review, we reviewed clinical features, results of diagnostic investigations, and outcome in 73 cases of COVID-19-associated GBS spectrum [5–56].
p	In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70, 71]. However, pediatric cases with GBS have been increasingly reported in the literature [21, 27, 35, 41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus–GBS [72]. This finding may also reflect the gender epidemiology of SARS-CoV-2. In this regard, males typically show a worse COVID-19 outcome compared to the females [70, 71], possibly due to a generally shorter life expectancy or to higher circulating Angiotensin-Converting-Enzyme 2 (ACE2) levels, the cellular receptor for SARS-CoV-2, in the former compared to the latter [71]. Moreover, given that GBS is a rare disease [57] the epidemiological distribution of the reported cases seems to reflect current worldwide outbreaks, with Europe being the “hottest” spot in March–May 2020 and USA together with Asia in the following period [73, 74]. On another issue, despite a few GBS cases seemed to have a para-infectious profile [10, 37, 38, 40, 55, 56] as described for Zika virus [75], all other reported patients developed neurological symptoms with a typical latency after COVID-19 (median time 14 days). This feature, together with the frequently reported negative nasopharyngeal swab at GBS onset [22, 24, 36, 44, 45, 52] and clinical improvement after IVIG therapy, seems to support the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [76, 77]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.) in GBS tested cases may reinforce the hypothesis of a systemic inflammatory storm in COVID-19 [76, 77]. However, given the limited data, we could not perform an accurate analysis of the distribution and, eventually, prognostic value of inflammatory markers in COVID-19-associated GBS. Moreover, we cannot exclude that in cases with GBS developing before or together with COVID-19 symptoms, the disease might have progressed sub-clinically in the early phase to manifest afterwards with its typical systemic clinical picture. Indeed, two cases [10, 12], who tested positive for SARS-CoV-2, never developed COVID-19 respiratory or systemic symptoms and one of them showed an asymptomatic pneumonia at chest-CT [12]. However, only more extensive epidemiological and translational studies, with the aim to compare the characteristics of GBS associated or not with COVID-19, could clarify these issues.
p	In our population, most common clinical manifestations and distribution of clinical variants resemble those of classic GBS confirming the predominance of the sensorimotor syndrome compared to MFS and other rare variants [57–59, 66]. Similarly, the results of CSF analysis reflected typical neurochemical findings in non-COVID-19 GBS. In the latter, elevated CSF proteins and pleocytosis were described in about 50–80% [57, 78] and 11–15% cases, respectively [58, 79, 80], largely overlapping with the percentages in our cohort. In this regard, the mostly normal cell count, together with the absence of SARS-CoV-2 RNA in all tested CSF samples [6–9, 12–14, 16, 21–24, 31, 33, 36, 42, 44, 52, 55], makes the possibility of a direct invasion from SARS-CoV-2 into the nerve roots with intrathecal viral replication less probable. However, a possible bias might rely on the lack of systematic data concerning the latency between symptom onset and CSF sampling in COVID-19 GBS cases. On another issue, in a further case of MFS associated withCOVID-19, who came to our attention, we observed the absence of intrathecal synthesis of SARS-CoV-2 antibodies together with a massive increase of CSF phosphorylated neurofilament heavy chain (pNfH) and serum neurofilament light chain (NfL) proteins, supporting the role of neurochemical markers as easily implementable tools for the detection of nervous system affection in COVID-19-related diseases [81, 82].
p	At variance with CSF findings, we found a discrepancy concerning MRI findings between classic GBS and COVID-19-related GBS. Specifically, while most cases of the former group showed typically spinal root enhancement at MRI [83], in the latter group, in analogy with Zika-associated GBS, the same finding was less frequently reported [84]. However, caution should be warranted in the interpretation of these results, given that MRI findings might have been underestimated, due to lack of a sufficient number of exams in the context of pandemic-imposed restrictions in the routine clinical setting.
p	Regarding the distribution of GBS electrophysiological variants, our analysis showed that COVID-19-associated GBS manifests prevalently with AIDP and, to a lesser extent, with AMSAN and AMAN, in line with classic GBS in Western countries [66, 85]. Conversely, the observation of positive anti-GD1b antibodies in one COVID-19-related MFS patient and negative anti-ganglioside antibodies in other five cases appear in discordance with the high prevalence (≈ 90%) of anti-GQ1b antibodies among non-COVID-19 MFS cases [86], and may suggest different immune-mediated mechanisms. However, these results could not be generalized until a wider population would be tested.
p	In analogy to classic GBS, approximately one-fifth of COVID-19-associated GBS subjects required mechanical ventilation during hospitalisation [87]. In this regard, cases with no improvement or unfavorable outcome showed, in comparison to those with a good prognosis, an older age, confirming similar findings both in classic GBS [58, 88] and in COVID-19 [89], and a slightly higher frequency (without reaching a statistical significance) of past or concurrent COVID-19 pneumonia. However, given the short follow-up time in most cases, we could not reach a definite conclusion on the impact of past or concurrent COVID-19 restrictive syndrome due to pneumonia on the prognosis of GBS patients. Future prospective studies are needed to clarify this issue. Moreover, given that also preceding diarrhea (mostly caused by Campylobacter Jejuni infection) is a strong negative prognostic factor in classic GBS [57, 88], further prospective studies are needed to compare the severity of GBS related to COVID-19 to that associated with C. jejuni. Finally, in the context of respiratory failure and ventilation associated with COVID-19, the differential diagnosis should always take into consideration critical illness neuropathy and myopathy, which tend to develop later during the critical course [90]. Despite these findings, approximately one-third of COVID-19-related GBS patients showed no clinical and/or radiological evidence of pneumonia, providing evidence that GBS may also develop in the context of a paucisymptomatic or even asymptomatic COVID-19. However, given that among the GBS population only two asymptomatic COVID-19 patients were reported to date, we may speculate that, in most cases, a certain degree of lung injury (even minimal) or at least hematic dissemination (e.g., fever underlying significant viral load) is necessary to trigger the immuno-mediated process through lymphocytic recognition of self-antigens or molecular mimicry.
p	Major strengths of our review are the inclusion of a high number of patients, together with an in-depth analysis of the clinical and diagnostic features of COVID-19-associated GBS. We are aware that selection bias might have occurred, given that most reported cases to date have been described mostly in Europe (47 out of 73) and during COVID-19 highest spreading. Therefore, future extensive epidemiological studies are necessary to ascertain the nature of the association between COVID-19 and GBS (causal or coincidental). Moreover, we cannot exclude the possibility that at least some of the cases represent instances of CIDP, given the frequent absence of a follow-up longer than 2 months. On another issue, the low but possible evidence of an epidemiological link between vaccines and GBS development [57, 58] should aware the clinicians of the possible occurrence of GBS after COVID-19 vaccination in the long-term future.
p	In conclusion, based on the systematic review of 73 cases, we showed that the clinical picture of COVID-19-associated GBS seems to resemble that of classic GBS or Zika-associated GBS. Moreover, the chronological evolution, the response to IVIG, and the absence of SARS-CoV-2 RNA in CSF may suggest a prominent post-infectious immune-mediated mechanism rather than a para-infectious one. Although most cases were symptomatic for COVID-19, the preliminary report of a few patients without respiratory or systemic symptoms raises a significant healthcare issue, namely the importance of SARS-CoV-2 testing in all patients with suspected GBS during the pandemic, with the aim to provide an eventual rapid case isolation. Nevertheless, only further analyses on more comprehensive cohorts could help in clarifying better all these issues.
back	Acknowledgements Open Access funding provided by Projekt DEAL. This work was in part supported by a COVID-19 grant from the state Baden-Württemberg. Authors’ contributions Conceptualization: all authors; methodology, formal analysis, and investigation: Samir Abu-Rumeileh, Ahmed Abdelhak, and Matteo Foschi; writing—original draft preparation: all authors; figure preparation: Matteo Foschi; writing—review and editing: all authors; supervision: Markus Otto and Hayrettin Tumani. Compliance with ethical standards Conflicts of interest The authors declare that they have no conflict of interest related to the content of this article. Ethical standard For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.
ack	Acknowledgements Open Access funding provided by Projekt DEAL. This work was in part supported by a COVID-19 grant from the state Baden-Württemberg.
title	Acknowledgements
p	Open Access funding provided by Projekt DEAL. This work was in part supported by a COVID-19 grant from the state Baden-Württemberg.
notes	Authors’ contributions Conceptualization: all authors; methodology, formal analysis, and investigation: Samir Abu-Rumeileh, Ahmed Abdelhak, and Matteo Foschi; writing—original draft preparation: all authors; figure preparation: Matteo Foschi; writing—review and editing: all authors; supervision: Markus Otto and Hayrettin Tumani.
title	Authors’ contributions
p	Conceptualization: all authors; methodology, formal analysis, and investigation: Samir Abu-Rumeileh, Ahmed Abdelhak, and Matteo Foschi; writing—original draft preparation: all authors; figure preparation: Matteo Foschi; writing—review and editing: all authors; supervision: Markus Otto and Hayrettin Tumani.
notes	Compliance with ethical standards Conflicts of interest The authors declare that they have no conflict of interest related to the content of this article. Ethical standard For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.
title	Compliance with ethical standards
notes	Conflicts of interest The authors declare that they have no conflict of interest related to the content of this article.
title	Conflicts of interest
p	The authors declare that they have no conflict of interest related to the content of this article.
notes	Ethical standard For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.
title	Ethical standard
p	For the present study, no authorization to an Ethics Committee was asked, because the original reports, nor this work, provided any personal information of the patients.

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