Takuya Kudo: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan.
Yuichi Hayashi: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan.
Kenjiro Kunieda: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan.
Nobuaki Yoshikura: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan.
Akio Kimura: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan.
Mika Otsuki: Faculty of Health Sciences, Graduate School of Sciences, Hokkaido University, Kita 15, Nishi 7, Kitaku, 060-8638, Sapporo, Japan.
Takayoshi Shimohata: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, 501-1194, Gifu, Japan. shimohata@gmail.com. ORCID
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.
