BMJ neurology open · 2025
Cardiac involvement in anti-GABA-B receptor encephalitis: a case report.
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Tarrés Rosa Ferrer, García Sarreón Alexis, Pozo Ariza Francisco, Gutiérrez Naranjo Jorge, Gifreu-Fraixinó Ariadna, Boix-Lago Almudena, Álvarez-Bravo Gary
Аннотация
BACKGROUND: Anti-gamma-aminobutyric acid B receptor (GABA-B R) encephalitis is an uncommon autoimmune disorder typically presenting with seizures, memory impairment and a frequent paraneoplastic association with small cell lung carcinoma. Although GABA-B Rs are expressed in cardiac tissue, extracerebral manifestations have rarely been described.
CASE PRESENTATION: A 65-year-old man presented with status epilepticus. Cerebrospinal fluid (CSF) analysis revealed mild lymphocytic pleocytosis and type 3 oligoclonal bands. Anti-GABA-B R antibodies were detected in serum and CSF, confirming the diagnosis of autoimmune encephalitis. The patient improved after high-dose intravenous corticosteroids but died unexpectedly during recovery. Autopsy revealed perivascular CD3-positive lymphocytic infiltration in the brain and meninges, consistent with autoimmune encephalitis, and metastatic neuroendocrine carcinoma compatible with a pulmonary primary. Notably, CD3-positive lymphocytic infiltration was also found within myocardial fibres, consistent with lymphocytic myocarditis.
CONCLUSIONS: This case broadens the recognised spectrum of anti-GABA-B R encephalitis and raises the possibility of cardiac involvement in this disorder. The presence of GABA-B Rs in cardiomyocytes offers a potential link between receptor autoimmunity and myocardial inflammation. Although causality cannot be established, these findings suggest that cardiac monitoring may be advisable in patients with anti-GABA-B R encephalitis, particularly in paraneoplastic contexts.
CASE PRESENTATION: A 65-year-old man presented with status epilepticus. Cerebrospinal fluid (CSF) analysis revealed mild lymphocytic pleocytosis and type 3 oligoclonal bands. Anti-GABA-B R antibodies were detected in serum and CSF, confirming the diagnosis of autoimmune encephalitis. The patient improved after high-dose intravenous corticosteroids but died unexpectedly during recovery. Autopsy revealed perivascular CD3-positive lymphocytic infiltration in the brain and meninges, consistent with autoimmune encephalitis, and metastatic neuroendocrine carcinoma compatible with a pulmonary primary. Notably, CD3-positive lymphocytic infiltration was also found within myocardial fibres, consistent with lymphocytic myocarditis.
CONCLUSIONS: This case broadens the recognised spectrum of anti-GABA-B R encephalitis and raises the possibility of cardiac involvement in this disorder. The presence of GABA-B Rs in cardiomyocytes offers a potential link between receptor autoimmunity and myocardial inflammation. Although causality cannot be established, these findings suggest that cardiac monitoring may be advisable in patients with anti-GABA-B R encephalitis, particularly in paraneoplastic contexts.