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Id Subject Object Predicate Lexical cue
T1 0-24 Sentence denotes Guillain-Barré syndrome:
T2 25-94 Sentence denotes The first documented COVID-19–triggered autoimmune neurologic disease
T3 95-135 Sentence denotes More to come with myositis in the offing
T4 137-145 Sentence denotes Abstract
T5 146-155 Sentence denotes Objective
T6 156-380 Sentence denotes To present the COVID-19–associated GBS, the prototypic viral-triggered autoimmune disease, in the context of other emerging COVID-19–triggered autoimmunities, and discuss potential concerns with ongoing neuroimmunotherapies.
T7 382-389 Sentence denotes Methods
T8 390-572 Sentence denotes Eleven GBS cases in four key COVID-19 hotspots are discussed regarding presenting symptoms, response to therapies and cross-reactivity of COVID spike proteins with nerve glycolipids.
T9 573-762 Sentence denotes Emerging cases of COVID-19–triggered autoimmune necrotizing myositis (NAM) and encephalopathies are also reviewed in the context of viral invasion, autoimmunity and ongoing immunotherapies.
T10 764-771 Sentence denotes Results
T11 772-996 Sentence denotes Collective data indicate that in this pandemic any patient presenting with an acute paralytic disease-like GBS, encephalomyelitis or myositis-even without systemic symptoms, may represent the first manifestation of COVID-19.
T12 997-1113 Sentence denotes Anosmia, ageusia, other cranial neuropathies and lymphocytopenia are red flags enhancing early diagnostic suspicion.
T13 1114-1470 Sentence denotes In Miller-Fisher Syndrome, ganglioside antibodies against GD1b, instead of QG1b, were found; because the COVID-19 spike protein also binds to sialic acid-containing glycoproteins for cell-entry and anti-GD1b antibodies typically cause ataxic neuropathy, cross-reactivity between COVID-19–bearing gangliosides and peripheral nerve glycolipids was addressed.
T14 1471-1695 Sentence denotes Elevated Creatine Kinase (>10,000) is reported in 10% of COVID-19–infected patients; two such patients presented with painful muscle weakness responding to IVIg indicating that COVID-19–triggered NAM is an overlooked entity.
T15 1696-1936 Sentence denotes Cases of acute necrotizing brainstem encephalitis, cranial neuropathies with leptomeningeal enhancement, and tumefactive postgadolinium-enhanced demyelinating lesions are now emerging with the need to explore neuroinvasion and autoimmunity.
T16 1937-2213 Sentence denotes Concerns for modifications-if any-of chronic immunotherapies with steroids, mycophenolate, azathioprine, IVIg, and anti-B-cell agents were addressed; the role of complement in innate immunity to viral responses and anti-complement therapeutics (i.e. eculizumab) were reviewed.
T17 2215-2226 Sentence denotes Conclusions
T18 2227-2399 Sentence denotes Emerging data indicate that COVID-19 can trigger not only GBS but other autoimmune neurological diseases necessitating vigilance for early diagnosis and therapy initiation.
T19 2400-2664 Sentence denotes Although COVID-19 infection, like most other viruses, can potentially worsen patients with pre-existing autoimmunity, there is no evidence that patients with autoimmune neurological diseases stable on common immunotherapies are facing increased risks of infection.
T20 2666-2913 Sentence denotes Guillain-Barré syndromes (GBSs) comprise a spectrum of polyneuropathies characterized by acute (within 1–4 weeks) ascending motor weakness, mild or moderate sensory abnormalities, occasional cranial nerve involvement, and muscle or radicular pain.
T21 2914-4044 Sentence denotes According to the degree of involvement of the motor or sensory nerves, myelin sheath, axon, or cranial nerve predominance, the most common subtypes are the acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and the Miller Fisher syndrome (MFS) characterized by acute ophthalmoplegia, gait ataxia, and areflexia.1 GBS is one of the prototypic viral-triggered autoimmune neurologic diseases as approximately 70% of the patients have a preceding by 1–3 weeks, flu-like, viral illness.1–3 Among the infectious agents associated with triggering sporadic GBS are viruses, including influenza, enteroviruses, cytomegalovirus, Epstein–Barr virus, herpes simplex virus, hepatitis, or HIV, and bacteria, such as Campylobacter jejuni, Mycoplasma pneumoniae, and Haemophilus influenzae.1 GBS outbreaks have been also associated with viral epidemics or pandemics, including H1N1, swine flu A/New Jersey influenza strain, arthropod-borne flaviviruses, such as the West Nile virus, chikungunya, or Zika, and with coronaviruses, including the Middle East respiratory syndrome (MERS)-CoV and SARS-CoV.1–3
T22 4045-4743 Sentence denotes We are now more than 4 months into the peak of the COVID-19 pandemic with >5,000,000 infections and >330,000 deaths steadily increasingly worldwide, and although various respiratory and cardiac complications have been reported, we have not yet seen COVID-19–related neuroinflammatory or neuroautoimmune diseases as with the other viral outbreaks, including with coronaviruses MERS-CoV and SARS-CoV, which have 75–80% identical viral genome sequence with COVID-19.4 Whether this is due to COVID-19–inducing severe respiratory compromise soon after the median 4-day incubation period5 and underrecognition of neurologic events owing to overwhelming urgency to focus on life-saving efforts is unclear.
T23 4744-5517 Sentence denotes In the most up-to-date large published series, apart from multifactorial acute cerebrovascular events in 5.7% of patients, the main COVID-19–related neurologic symptoms have been hypogeusia (in 5.6%), hyposmia (5.1%), and very high creatine kinase (CK) levels, with myalgia (in 19.3%) indicating potential CNS, peripheral nervous system, and myopathic manifestations.6 Things are however rapidly changing as just only the last 4 weeks the first COVID-19–triggered neurologic events are reported with at least 11 cases of GBS, the prototypic viral-triggered autoimmune neurologic disease, observed in the 4 main COVID-19 hotspots, Wuhan, Italy, Spain, and now France.7–11 The cases are of special neuroimmunologic and practical interest while highlight what is more to come.
T24 5518-5898 Sentence denotes The very first case—and the only one from Wuhan—refers to a woman who 4 days after returning to Shanghai from Wuhan presented with acute lower extremity weakness and areflexia that progressed over 3 days to the arms without any systemic symptoms.7 When first seen, GBS was suspected and confirmed by elevated CSF protein and electromyographic features of demyelinating neuropathy.
T25 5899-5987 Sentence denotes Her laboratory test results were normal, except of lymphocytopenia and thrombocytopenia.
T26 5988-6125 Sentence denotes She was started on intravenous immunoglobulin (IVIg) but 4 days later developed fever, cough, and pneumonia and tested COVID-19 positive.
T27 6126-6194 Sentence denotes After 3 weeks, her strength normalized and lymphocytopenia resolved.
T28 6195-6400 Sentence denotes While at the regular neurology ward, however, 2 of her relatives taking care of her tested COVID-19 positive with pneumonia, while 2 of her neurologists and 6 nurses treating her GBS were put on isolation.
T29 6401-6650 Sentence denotes Italy has just reported 6 patients with GBS,8 1 in this issue.9 All presented with subacute onset of upper and lower extremity weakness, distal paresthesias, and sensory deficits 3–10 days after experiencing cough, anosmia, ageusia, and sore throat.
T30 6651-6757 Sentence denotes On admission, all had lymphocytopenia and high C-reactive protein (CRP) that led to diagnosis of COVID-19.
T31 6758-6887 Sentence denotes One patient had facial diplegia and sensory ataxia.8 The CSF showed elevated protein concentration but was negative for COVID-19.
T32 6888-6954 Sentence denotes Electrophysiology was consistent with demyelinating or axonal GBS.
T33 6955-7020 Sentence denotes MRI showed enhancement of the caudal nerve roots or facial nerve.
T34 7021-7097 Sentence denotes Symptoms rapidly progressed to tetraplegia requiring mechanical ventilation.
T35 7098-7162 Sentence denotes Antiganglioside antibodies in 3/6 tested patients were negative.
T36 7163-7212 Sentence denotes All received IVIg with variable recovery; 1 died.
T37 7213-7607 Sentence denotes The third series refers to 2 men from Spain who, 3–5 days after experiencing low-grade fever, malaise, anosmia, and ageusia, developed MFS or polyneuritis cranialis.10 The patient with MFS presented with oculomotor nerve palsies, diplopia, perioral paresthesias, areflexia, ataxia, and elevated CSF protein concentration and the other with diplopia, bilateral abducens nerve palsy, and anosmia.
T38 7608-7695 Sentence denotes Both had lymphopenia and tested positive for COVID-19; their SCF was COVID-19 negative.
T39 7696-7785 Sentence denotes The patient with MFS was positive for GD1b ganglioside antibodies and improved with IVIg.
T40 7786-7880 Sentence denotes In both, the neurologic features completely resolved, except for residual anosmia and ageusia.
T41 7881-8352 Sentence denotes Last, 2 cases from France, a 43-year-old man and a 70-year-old woman, also presented with acute anosmia, followed by rapidly progressive weakness, paresthesias, ataxia, areflexia, and multiple cranial palsies (including III, V, VI, VII, and VIII), MRI enhancement of cranial nerves, roots, and plexus, high CSF protein concentration but negative for COVID-19, typical features of acute demyelinating neuropathy by electrophysiology, and clinical improvement after IVIg.11
T42 8354-8382 Sentence denotes GBS in the COVID-19 pandemic
T43 8383-8821 Sentence denotes These early GBS cases, despite incomplete immunologic workup considering the enormous difficulties in highly stressed in-hospital settings, provide early clues on what to expect in the months ahead regarding the common acute autoimmune neurologic conditions, such as GBS, polyneuritis cranialis, encephalitis, encephalomyelitis, or myositis, which for years we have been casually referring to as postviral if seen after febrile illnesses.
T44 8822-9113 Sentence denotes First and foremost, the practicing neurologists in this pandemic should now be aware that a patient who presents with an acute paralytic disease—like GBS, encephalomyelitis, or myositis—even without fever, dyspnea, or any systemic symptoms, may represent the first manifestation of COVID-19.
T45 9114-9311 Sentence denotes This is compelling, considering that only 43% of COVID-19–positive patients on admission have fever,4–6 and many of the present patients with GBS did not have any COVID-19 symptoms at presentation.
T46 9312-9542 Sentence denotes These early GBS cases also highlight that 2 clinical and laboratory signs, anosmia/ageusia and lymphocytopenia/thrombocytopenia, are red flags in suspecting COVID-19 in otherwise asymptomatic patients with acute neurologic events.
T47 9543-10168 Sentence denotes They further confirm what we had feared from other viral pandemics that COVID-19 can trigger neurologic autoimmunity; in contrast to the other postviral neurologic diseases, however, COVID-19 requires high degree of suspicion as a potential hidden trigger to prevent inadvertent viral transmission to health care personnel and patient relatives, as in the Wuhan case.7 The series also highlights that GBS peaks 5–10 days after the first COVID-19 symptoms, which in intensive care unit (ICU) settings helps to distinguish GBS from critical illness neuropathy that usually appears later in the course of very sick ICU patients.
T48 10170-10233 Sentence denotes Significance of anosmia/ageusia and other cranial nerve palsies
T49 10234-10619 Sentence denotes The early manifestation of anosmia and ageusia not only in the present GBS series that often occurred in conjunction with other cranial neuropathies but also in large worldwide cohorts reporting sudden loss of smell and taste early in the infection in up to 60% of COVID-19 carriers5,6,12 is highly informative about COVID-19 neurovirulence or even possible viral entry into the brain.
T50 10620-10834 Sentence denotes In contrast to commonly reversible anosmia when the non-neural olfactory epithelial cells are virally infected, the often persistent anosmia/ageusia after COVID-19 suggests neurotropism targeting olfactory neurons.
T51 10835-11623 Sentence denotes SARS-CoV and MERS-CoV, the 2 coronaviruses similar to COVID-19, are neurovirulent and can enter the brain via olfactory nerves.13 In mice, after oronasal infection with SARS-CoV, the virus not only infects epithelial cells of the respiratory tract but also the olfactory receptor neurons in the neuroepithelium gaining access to the olfactory bulb and brainstem.13 These viruses can also enter the CNS via retrograde axonal transport through other cranial nerves, such as trigeminal, which possesses nociceptive neuronal receptors in the nasal cavity, the sensory fibers of the glossopharyngeal, and via peripheral nerves.13 The present GBS series, where oculomotor, trigeminal, and MRI-enhanced facial and nerves roots were concurrently affected, strengthens (but not prove) this notion.
T52 11624-11868 Sentence denotes Accordingly, it will not be unexpected in the weeks and months ahead to see other COVID-19–infected patients with neurologic signs related to multiple cranial nerves, brainstem, and peripheral nerves with MRI enhancement in nerves and meninges.
T53 11870-11985 Sentence denotes Autoimmunity of COVID-19–GBS: significance of sialic acids present in the coronaviruses and peripheral nerve myelin
T54 11986-12135 Sentence denotes In 7/11 tested patients with COVID-19–GBS, the virus was not detected in the CSF, implying no direct root infection or intrathecal viral replication.
T55 12136-12529 Sentence denotes The improvement of several patients with IVIg and the presence of GD1b antibodies in 1 tested patient suggest a postviral-triggered immune response similar to other postviral-induced GBS cases1–3 or other postviral autoimmune neurologic disorders.14 The reported GD1b ganglioside antibodies, however, although in contrast to GQ1b antibodies typically seen in MFS, are of very special interest.
T56 12530-14322 Sentence denotes The SARS-CoV 3a protein contains oligosaccharides with direct evidence that sialic acids play a critical role in human coronavirus infection.15 It has been just shown that the attachment of coronaviruses to the surface of respiratory cells is mediated by the spike (S) viral protein, which binds not only to the angiotensin-converting enzyme 2 (ACE-2) receptor for entry16 but also to sialic acid–containing glycoproteins and gangliosides on cell surfaces.15 Such a dual receptor/attachment is proposed to be a reason for the increased transmissibility of COVID-19 compared with SARS-CoV that binds only to ACE-2 receptor.15,16 Of relevance to GBS is that various gangliosides, most commonly those containing either a disialosyl moiety, such as GD1b, GQ1b, and GT1b, or 2 gangliosides that share epitopes with GM2, or a combination of GM2 and GM1, GM1 and GD1b, can serve as antigens in patients with neuropathies.17 When IgM recognizes the Gal (pl-3) GalNAc moiety of GM1, which is found on the surface of motor neurons, there is clinically a motor neuropathy, but if recognizes epitopes containing disialosyl groups of GDlb, which is present on the dorsal root ganglionic neurons, there is sensory ataxic neuropathy.17 Immunization of rabbits with GDlb also causes sensory ataxic neuropathy mimicking the human disease.18 Of interest, the first described patient with sensory ataxic neuropathy and GDlb antibodies had also ophthalmoplegia,19 as seen in MFS and the present series.10 As COVID-19 spike interacts with the GalNAc residue of GM1 and ganglioside dimers for anchoring to cell surface gangliosides,15 cross-reactivity between epitopes within the COVID-19 spike-bearing gangliosides and signature sugar residues of surface peripheral nerve glycolipids is a very likely possibility.
T57 14323-14628 Sentence denotes Such typical molecular mimicry has been shown between peripheral nerve glycolipids and Campylobacter jejuni or Zika virus that also trigger GBS.1–3 Accordingly, all GBS subtypes (AIDP, AMAN, and MFS) can be expected with COVID-19, necessitating screening for ganglioside antibodies to assess autoimmunity.
T58 14629-15136 Sentence denotes An interesting therapeutic component in this association is the emerging data that chloroquine, an antimalarial drug under investigation for treating COVID-19, binds with high-affinity sialic acids and GM1 gangliosides and, in the presence of chloroquine, the SARS-CoV viral spike cannot bind gangliosides to infect the targeted cells.15 If benefit is confirmed and safety is established, chloroquine may be of added therapeutic value in future patients with COVID-19–triggered GBS in conjunction with IVIg.
T59 15138-15186 Sentence denotes What is more to come with myositis in the offing
T60 15187-15684 Sentence denotes Among the other potential COVID-19–associated autoimmune diseases, the first alarming concern is inflammatory myopathy, especially necrotizing autoimmune myositis (NAM) because very high CK levels >10,000 with myalgia and weakness are now reported in more than 10% of COVID-19–infected patients.6 Although COVID-19–associated myopathy has not yet been studied but only characterized as skeletal muscle injury or rhabdomyolysis,6 2 just published cases suggest an autoimmune COVID-19–triggered NAM.
T61 15685-16018 Sentence denotes One, an 88-year-old man from New York presented with acute bilateral thigh weakness and inability to get up from the toilet, without fever or other systemic symptoms, and very high CK level (13,581 U/L).20 He was found COVID-19 positive and given hydroxychloroquine, and a week later, his painful weakness improved with CK reduction.
T62 16019-16370 Sentence denotes The other, a 60-year-old man from Wuhan had a 6-day history of fever, cough, and COVID-19–positive pneumonia with normal strength and CK; 7 days later, although systemically had improved, his CRP doubled and developed painful muscle weakness with very high CK (11,842 U/L).21 He was given IVIg and his strength improved while became COVID-19 negative.
T63 16371-17048 Sentence denotes Myopathic symptoms in a severe systemic viral disease are multifactorial, but an acute onset of severe muscle weakness with increased inflammatory markers and very high CK levels in the thousands, as described above, is consistent with autoimmune inflammatory myopathy within the spectrum of NAM, similar to what was first reported with HIV early in that epidemic.22,23 The most common causes of NAM are not chronic statin use as overstated, but autoimmune, paraneoplastic, or postviral.22–25 Considering that very high CK level and painful muscle weakness were seen in 10% of COVID-19–positive patients,6 a potentially treatable autoimmune myopathy has been likely overlooked.
T64 17049-17511 Sentence denotes Studies with muscle biopsy and antibody screening are urgently needed in such patients because therapy with IVIg can improve strength, reduce morbidity, and facilitate recovery, as reported in the first 2 cases.20,21 COVID-19–associated myositis is also highly interesting because ACE-2, the SARS-CoV receptor, is reportedly expressed in skeletal muscle.26 If this is confirmed, COVID-19 may represent the first virus directly capable of infecting muscle fibers.
T65 17512-17803 Sentence denotes None of the viruses implicated in viral-triggered myositis has so far been shown to infect muscle27,28; instead, viruses induce an immune T cell with clonal expansion of viral-specific T cells or macrophage-mediated, muscle fiber autoinvasion with abundant proinflammatory cytokines.22,29,30
T66 17805-17866 Sentence denotes Other emerging postinfectious autoimmune neurologic disorders
T67 17867-18047 Sentence denotes Acute disseminated encephalomyelitis, as described for the other coronaviruses, or postinfectious brainstem encephalitis, myelitis, and radiculoneuropathies will not be unexpected.
T68 18048-19128 Sentence denotes An atypical case of acute necrotizing encephalopathy, attributed to immune-mediated process and proinflammatory cytokines, and another with meningoencephalitis and leptomeningeal enhancement have been already noted.31 This picture is now becoming more clear with 2 reports in this issue of the Journal, documented by impressive MRIs; one, a case of acute necrotizing brainstem encephalopathy, presented with epilepsy and changes in the right mesial temporal lobe and hippocampus32 and another with altered mental status and multiple white matter tumefactive lesions with postgadolinium enhancement in periventricular areas and corpus callosum suggestive of demyelination.33 Not underestimating the overwhelming burden of acute COVID-19 to medical staff, vigilance for these disorders is needed along with screening for autoimmune encephalitis autoantibodies14 because these cases can potentially respond to early initiation of immunotherapy, especially with IVIg, whenever indicated, which may additionally offer various potentially protective antibodies and anticytokine effects.
T69 19130-19218 Sentence denotes Residual neurologic deficits in COVID-19–recovered patients: need for a systematic study
T70 19219-19337 Sentence denotes No neurologic data are yet available about the discharged patients who survived the catastrophic effects of the virus.
T71 19338-19559 Sentence denotes We know that several people have permanently lost smell and taste, which is a form of disability affecting quality of life, depriving tasting pleasures, and the ability to detect danger signals, like smelling gas or fire.
T72 19560-20097 Sentence denotes Many discharged patients require assistance because of muscle weakness and gait unsteadiness, which is arguably multifactorial; some patients may have had critical illness neuropathy and deconditioning with significant muscle atrophy worsened by comorbidities; others may have neurotoxicity or myocytotoxicity from antiviral therapies, like first described with antiretrovirals or chloroquine34–36; still others may have the residual effects from an unrecognized primary myopathy, neuropathy, or myelopathy due to postviral autoimmunity.
T73 20098-20425 Sentence denotes A study exploring the patients' current causes of residual muscle weakness and sensory deficits is urgently needed using EMG, muscle or nerve biopsies, autoantibody screening, and CSF or imaging studies to determine immediate or long-term recovery prospects, identify potential reversibility, and accelerate return to normalcy.
T74 20427-20548 Sentence denotes Patients with autoimmune neurologic diseases: how is COVID-19 changing ongoing immunotherapies and the role of complement
T75 20549-20933 Sentence denotes Patients with autoimmune neuropathies, especially chronic inflammatory demyelinating polyneuropathy and multifocal motor neuropathy, but also with other autoimmunities like myasthenia gravis, MS, and inflammatory myopathies, have been justifiably concerned as to whether their disease status adds an additional risk placing them into an immunosuppressed or immunocompromised category.
T76 20934-21205 Sentence denotes There is no current evidence that any of the aforementioned autoimmune disorder itself makes them more susceptible to COVID-19, but some immunosuppressive or even immunomodulating therapies they are receiving may have this potential, although there are no validated data.
T77 21206-21386 Sentence denotes Most autoimmune neuromuscular patients are maintained on steroids, mycophenolate, or azathioprine while most chronic inflammatory demyelinating polyneuropathy receive monthly IVIg.
T78 21387-21517 Sentence denotes The same applies to patients with MS where it seems safe to start or continue treatment with the standard disease-modifying drugs.
T79 21518-21675 Sentence denotes If clinically stable and not lymphopenic, there are no compelling or data-driven reasons to change anything in these patients and disturb clinical stability.
T80 21676-22254 Sentence denotes For patients on monthly IVIg, there may be even a theoretical advantage that IVIg offers additional protection due to natural autoantibodies; if IVIg is not infused as home infusion, switching to self-administered subcutaneous IgG might be an option to diminish exposure, as has been proven effective.37 For patients on rituximab, the infusion intervals can be prolonged to more than 6 months because both B-cell reduction and clinical benefit can persist longer.38 New emerging data provide credence and reassurance regarding these issues, especially on immunomodulating drugs.
T81 22255-22540 Sentence denotes In a large number of patients from Wuhan, published in this issue of the Journal,39 it was shown that altered immunity induced by disease-modifying drugs in patients with MS or neuromyelitis optica spectrum disorder appears insufficient to enhance susceptibility to COVID-19 infection.
T82 22541-22785 Sentence denotes The results are important but not unexpected considering that most of these therapies target the adaptive immune response with little, if any, effect on suppressing the innate immunity that facilitates infection of macrophages and viral spread.
T83 22786-23994 Sentence denotes Similar data from New York City area show that the incidence of hospitalization among patients with immune-mediated inflammatory diseases on therapy with steroids and biologic agents was consistent with that among patients with COVID-19 in the general population, concluding that ongoing use of biologics is not associated with worse COVID-19 outcomes.40 There is also new evidence suggesting possible beneficial effect of anticomplement therapies.41 Complement is an integral component of the innate immune response to viruses and an instigator of proinflammatory responses with evidence that activation of C3 exacerbates SARS-CoV–associated acute respiratory distress syndrome and C3-C5 complement deposits are abundant in the lung biopsies from patients with COVID-19.41 It was proposed that complement inhibition may alleviate the inflammatory complications of COVID-19 infection leading to ongoing trials with anti-C3 and anti-C5 agents.41,42 On this basis, eculizumab, an anti-C5 monoclonal antibody approved for neuromyelitis optica spectrum disorder and myasthenia gravis with some benefits in patients with GBS, may not be withheld, if indicated, as, like IVIg, may theoretically have added benefit.
T84 23996-24009 Sentence denotes Study funding
T85 24010-24039 Sentence denotes No targeted funding reported.
T86 24041-24051 Sentence denotes Disclosure
T87 24052-24054 Sentence denotes M.
T88 24055-24100 Sentence denotes Dalakas is an associate editor for Neurology:
T89 24101-24137 Sentence denotes Neuroimmunology & Neuroinflammation.
T90 24138-24160 Sentence denotes Disclosures available:
T91 24161-24178 Sentence denotes Neurology.org/NN.
T92 24179-24187 Sentence denotes Glossary
T93 24188-24225 Sentence denotes ACE-2 angiotensin-converting enzyme 2
T94 24226-24278 Sentence denotes AIDP acute inflammatory demyelinating polyneuropathy
T95 24279-24313 Sentence denotes AMAN acute motor axonal neuropathy
T96 24314-24332 Sentence denotes CK creatine kinase
T97 24333-24355 Sentence denotes CRP C-reactive protein
T98 24356-24383 Sentence denotes GBS Guillain-Barré syndrome
T99 24384-24407 Sentence denotes ICU intensive care unit
T100 24408-24439 Sentence denotes IVIg intravenous immunoglobulin
T101 24440-24477 Sentence denotes MERS Middle East respiratory syndrome
T102 24478-24504 Sentence denotes MFS Miller Fisher syndrome
T103 24505-24540 Sentence denotes NAM necrotizing autoimmune myositis