Background Evidence of immune-mediated neurological syndromes associated with the severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection is limited. We therefore investigated clinical, serological and CSF features of coronavirus disease 2019 (COVID-19) patients with neurological manifestations. Methods Consecutive COVID-19 patients with neurological manifestations other than isolated anosmia and/or non-severe headache, and with no previous neurological or psychiatric disorders were prospectively included. Neurological examination was performed in all patients and lumbar puncture with CSF examination was performed when not contraindicated. Serum anti-gangliosides antibodies were tested when clinically indicated. Results Of the 349 COVID-19 admitted to our center between March 23rd and April 24th 2020, 15 patients (4.3%) had neurological manifestations and fulfilled the study inclusion/exclusion criteria. CSF examination was available in 13 patients and showed lymphocytic pleocytosis in 2 patients: 1 with anti-contactin-associated protein 2 (anti-Caspr2) antibody encephalitis and 1 with meningo-polyradiculitis. Increased serum titer of anti-GD1b antibodies was found in three patients and was associated with variable clinical presentations, including cranial neuropathy with meningo-polyradiculitis, brainstem encephalitis and delirium. CSF PCR for SARS-CoV-2 was negative in all patients. Conclusions In SARS-Cov-2 infected patients with neurological manifestations, CSF pleocytosis is associated with para- or post-infectious encephalitis and polyradiculitis. Anti-GD1b and anti-Caspr2 autoantibodies can be identified in certain cases, raising the question of SARS-CoV-2-induced secondary autoimmunity.

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Transient cortical blindness (TCB) is a rare but striking complication following contrast agent injection. TCB might be secondary to a direct toxicity of the contrast agent, leading to an osmotic disruption of the blood-brain barrier (BBB), with a preferential involvement of the posterior circulation and occipital cortex. We report a series of three patients with contrast medium-associated TCB (intra-arterial injection of non-ionic contrast agent during diagnostic cerebral angiography for two of them and coronary angioplasty for the other one). In two patients, the magnetic resonance imaging (MRI) was unremarkable; in the other patient, typical MRI findings were observed, with FLAIR hyperintensities in the right occipital cortex and decreased apparent diffusions coefficient (ADC). Interestingly, this patient also presented posterior rhythmic epileptiform activities on electroencephalogram during the first 36 h. Visual evoked potentials (VEPs) showed normal retinal potential, but a massive destructuration of the later potentials of the cortical origin. To our knowledge, this is the first time that VEPs acquired during TCB are reported. We discuss these findings with respect to the pathophysiology of TCB.