In this longitudinal study, recently published in the European Journal of Neurology, the authors sought to describe the neurological manifestations of patients with COVID‐19 and gain pathophysiological insights especially with respect to the cytokine release syndrome (CRS). Extensive clinical, laboratory, and imaging phenotyping was performed in five patients. Neurological presentation included confusion, tremor, cerebellar ataxia, behavioural alterations, aphasia, pyramidal syndrome, coma, cranial nerve palsy, dysautonomia, and central hypothyroidism. Neurological disturbances were remarkably accompanied by laboratory evidence of CRS. SARS‐CoV‐2 was undetectable in the cerebrospinal fluid (CSF). Hyperalbuminorrachia and increased levels of the astroglial protein S100B were suggestive of blood‐brain barrier (BBB) dysfunction. Brain MRI findings comprised evidence of acute leukoencephalitis (n = 3, of whom one with a haemorrhagic form), cytotoxic oedema mimicking ischaemic stroke (n = 1), or normal results (n = 2). Treatment with corticosteroids and/or intravenous immunoglobulins was attempted, resulting in rapid recovery from neurological disturbances in two cases. SARS‐CoV2 was undetectable in 88 of the 90 patients with COVID‐19 who underwent RT‐PCR testing of CSF. The authors concluded that patients with COVID‐19 can develop neurological manifestations that share clinical, laboratory, and imaging similarities with those of chimeric antigen receptor‐T cell‐related encephalopathy. The pathophysiological underpinnings appear to involve CRS, endothelial activation, BBB dysfunction, and immune‐mediated mechanisms.
Cytokine release syndrome‐associated encephalopathy in patients with COVID‐19
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