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Background Case Presentation Conclusions Bickerstaff brainstem encephalitis (BBE) is an autoimmune disease affecting the brainstem, typically caused by a prior infection. However, BBE after coronavirus disease 2019 (COVID‐19) infection is rare. Here, we present a severe case of BBE after COVID‐19 infection, highlighted by increased levels of CXCL‐10.A 28‐year‐old woman presented with symptoms of cold and fever lasting 5 days, accompanied by numbness, weakness and unsteadiness in the distal parts of her limbs before being admitted. Upon admission, her condition was classified with a Glasgow Coma Scale score of E1V1M4, absence of bilateral ocular cephalic reflexes, eyes fixed in the midline position and pathological reflex in lower limbs. COVID‐19 antigen tests were positive, and cerebrospinal fluid CXCL‐10 levels were elevated. Positive serum anti‐GQ1b antibodies, along with other clinical findings, confirmed the diagnosis of BBE. Initial treatment with high‐dose intravenous immunoglobulin was ineffective, leading to mechanical ventilation on day 2 from admission. Additional steroid pulse therapy and plasmapheresis were initiated on day 7. Communication abilities were restored by day 19, and the patient was extubated on day 21. Continuous alleviation of symptoms was observed, with no sequelae at discharge on day 42.BBE related to COVID‐19 with high CXCL‐10 levels can become severe. However, early intensive immunotherapy, including plasmapheresis, might result in favorable prognosis. [ABSTRACT FROM AUTHOR]

Objectives: To examine the chemokine profile in the cerebrospinal fluid (CSF) of patients with glial fibrillary acidic protein astrocytopathy (GFAP‐A), central nervous system immune‐related adverse event (CNS‐irAE), neurosarcoidosis (NS), neuromyelitis optica spectrum disorders (NMOSD), multiple sclerosis (MS), and human T‐cell leukemia virus‐1 (HTLV‐1)‐associated myelopathy (HAM). Methods: The study included 38 patients presenting to St. Marianna University Hospital between May 2013 and November 2021 with GFAP‐A, CNS‐irAE, NMOSD, MS, NS, HAM and noninflammatory neurological diseases (NIND). We recorded the age, sex, duration of disease, brain/spinal lesions on magnetic resonance imaging (MRI), blood data, and measured chemokines (CXCL9, −10, −13, CCL3, −4, −17, −20, −22) in CSF. In patients with GFAP‐A, clinical symptoms, and CSF CXCL10 levels were compared before and after steroid treatment. Results: Patients with GFAP‐A had higher CSF levels of CXCL10, CXCL13, and CCL22 (10736.1 [8786.7–149079.0] pg/ml (p <.05), 378.4 [239.9–412.2] pg/ml (p <.01) and 159.9 [130.5–413.9] pg/ml (p <.01), respectively). The CSF levels of CXCL10 improved from 10736.1 [8786.7–149079.0] pg/ml to 1879.0 [783.9–4360.0] pg/ml in patients with GFAP‐A by steroid therapy. Conclusion: CSF CXCL10 levels were particularly high in GFAP‐A, and changes in levels after treatment correlated with clinical improvements, suggesting CXCL10 involvement in GFAP‐A pathogenesis. [ABSTRACT FROM AUTHOR]