ArticleNeurology(R) neuroimmunology & neuroinflammation2023
Anti-GABA-A Receptor Antibody-Mediated Epilepsia Partialis Continua After Treatment With Alemtuzumab: A Case Report.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Autoimmune Encephalitis in Acute Care-Pathology, Diagnosis, and Management.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Are "GABAergic" Agents Really So Selective for GABA? Implications for Single- versus Multi-Site Hypotheses From Promiscuous Behavior of Anesthetics and Their Molecular Targets In Vitro.Anesthesia and analgesia · 2026Review
- Recent advances in autoimmune encephalitis.Arquivos de neuro-psiquiatria · 2024Review
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Authors and funding
10 authors at 1 institution in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesPatients with anti-GABA-A receptor encephalitis characteristically experience therapy-refractory epileptic seizures. General anesthesia is often required to terminate refractory status epilepticus. The immunologic mechanisms leading to antibody formation remain to be elucidated. Described triggers of anti-GABA-A autoimmunity are tumors, mainly thymomas, and herpes simplex encephalitis.
methodsWe present a young woman with prediagnosis of relapse remitting multiple sclerosis (MS), treated with interferons, natalizumab, and alemtuzumab. Six months after one and only cycle of alemtuzumab, speech arrest and behavioral changes with aggressive and anxious traits appeared. She showed increasing motor convulsions resulting in focal status epilepticus.
resultsAnti-GABA-A receptor antibodies in CSF and serum were confirmed in different external laboratories, in a more extensive analysis after antibodies against NMDAR, CASPR2, LGI1, GABABR, and AMPAR were ruled out during in-house examination. Clinical condition improved temporarily with cortisone therapy, plasmapheresis, and IVIG but deteriorated rapidly after steroid discontinuation, resulting in brain biopsy. On histopathologic confirmation consistent with anti-GABA-A receptor antibody-associated CNS inflammation, completing the first rituximab cycle, continuing oral corticosteroids and supplementing immunosuppression with cyclosporine A led to quick recovery. DISCUSSION: Our case describes a severe autoantibody-induced encephalitis in a young patient with MS, with alemtuzumab as a potential trigger for anti-GABA-A receptor encephalitis.
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