PMC:7445716 / 11925-14096 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7445716","sourcedb":"PMC","sourceid":"7445716","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7445716","text":"Results of electrophysiological, CSF, biochemical, and neuroimaging investigations\nDetailed 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 \u003c 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).\nDetailed 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).\nFurthermore, 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.\nCranial 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 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