Cytokine release syndrome‐associated encephalopathy in patients with COVID‐19

• DOI: 10.1111/ene.14491
• Publication Date: 2020-08-28T04:27:56Z
• Authors: P. Perrin; N. Collongues; S. Baloglu; D. Bedo; X. Bassand; T. Lavaux; G. Gautier‐Vargas; N. Keller; S. Kremer; S. Fafi‐Kremer; B. Moulin; I. Benotmane; S. Caillard
• Keywords: Cytokine Release Syndrome; Dysautonomia

Background and purpose Neurological manifestations in coronavirus disease (COVID)‐2019 may adversely affect clinical outcomes. Severe COVID‐19 uremia are risk factors for neurological complications. However, the lack of insight into their pathogenesis, particularly with respect to role cytokine release syndrome (CRS), is currently hampering effective therapeutic interventions. The aims this study were describe patients gain pathophysiological insights CRS. Methods In longitudinal study, we performed extensive clinical, laboratory imaging phenotyping five admitted our renal unit. Results presentation included confusion, tremor, cerebellar ataxia, behavioral alterations, aphasia, pyramidal syndrome, coma, cranial nerve palsy, dysautonomia, central hypothyroidism. Notably, disturbances accompanied by evidence acute respiratory coronavirus‐2 (SARS‐CoV‐2) was undetectable cerebrospinal fluid (CSF). Hyperalbuminorrachia increased levels astroglial protein S100B suggestive blood−brain barrier (BBB) dysfunction. Brain magnetic resonance findings comprised leukoencephalitis ( n = 3, one whom had a hemorrhagic form), cytotoxic edema mimicking ischaemic stroke 1), or normal results 2). Treatment corticosteroids and/or intravenous immunoglobulins attempted, resulting rapid recovery from two cases. SARS‐CoV2 88 90 who underwent Reverse Transcription‐PCR testing CSF. Conclusions Patients can develop that share similarities those chimeric antigen receptor T‐cell‐related encephalopathy. underpinnings appear involve CRS, endothelial activation, BBB dysfunction, immune‐mediated mechanisms.