Possible Autoimmune Encephalitis Associated with the Severe Acute Respiratory Syndrome Coronavirus 2 Omicron Variant Successfully Treated with Steroids: A Case Report.

We encountered a 55-year-old woman with possible autoimmune encephalitis associated with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. She was not vaccinated against coronavirus disease 2019 (COVID-19). Consciousness disturbance, myoclonic-like movements and gait disturbance occurred 10 days after the COVID-19 symptom onset. Her neurological symptoms improved two days after methylprednisolone pulse therapy. Cerebrospinal fluid (CSF) was negative for SARS-CoV-2 reverse transcription-polymerase chain reaction, the CSF-to-serum albumin quotient was mildly elevated, and interleukin 6 and 8 levels were normal in serum but mildly elevated in CSF. Omicron variant infection may increase blood-brain barrier permeability and intrathecal inflammation, causing autoimmune encephalitis.

Persistent intrathecal interleukin-8 production in a patient with SARS-CoV-2-related encephalopathy presenting aphasia: a case report.

BACKGROUND: Neurological manifestations of coronavirus disease 2019 (COVID-19) are increasingly recognized and include encephalopathy, although direct infection of the brain by SARS-CoV-2 remains controversial. We herein report the clinical course and cytokine profiles of a patient with severe SARS-CoV-2-related encephalopathy presenting aphasia. CASE PRESENTATION: An 81-year-old man developed acute consciousness disturbance and status epileptics several days after SARS-CoV-2 infection. Following treatment with remdesivir and dexamethasone, his consciousness and epileptic seizures improved; however, amnestic aphasia and agraphia remained. Two months after methylprednisolone pulse and intravenous immunoglobulin, his neurological deficits improved. We found increased levels of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1), but not IL-2 and IL-10 in the serum and cerebrospinal fluid (CSF), and the levels of serum IL-6 and MCP-1 were much higher than those in the CSF. The level of IL-8 in the CSF after immunotherapy was four times higher than that before immunotherapy. CONCLUSION: The cytokine profile of our patient was similar to that seen in severe SARS-CoV-2-related encephalopathy. We demonstrated (i) that the characteristic aphasia can occur as a focal neurological deficit associated with SARS-CoV-2-related encephalopathy, and (ii) that IL8-mediated central nervous system inflammation follows systemic inflammation in SARS-CoV-2-related encephalopathy and can persist and worsen even after immunotherapy. Monitoring IL-8 in CSF, and long-term corticosteroids may be required for treating SARS-CoV-2-related encephalopathy.