Rinsho Shinkeigaku (Clinical Neurology)

Brief Clinical Note

Subacute encephalitis with anti-glutamate receptor antibodies presented with epilepsia partialis continua

Motomi Arai, M.D., Ph.D.1) and Yukitoshi Takahashi, M.D.2)

1)Department of Neurology, Seirei Mikatahara General Hospital
2)National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders

A previously healthy 32-year-old man visited out clinic with a 5-week history of involuntary movement. Examination demonstrated continuous myoclonic jerks in the left elbow. Two days later, he developed generalized convulsion. Electroencephalography demonstrated small spikes over the right central region. Thus, we made a diagnosis of epilepsia partialis continua (EPC) with a secondary generalization. On admission, serum electrolytes, glucose and ceruloplasmin levels, and amino acid analysis were unremarkable. HIV serology was negative. Anti-cardiolipin, anti-MPO ANCA, and anti-Hu antibodies were negative. The cerebrospinal fluid (CSF) showed 151/μl lymphocytes and 23/μl polymorphs, 70 mg/dl of glucose, and 61 mg/dl of protein. Autoantibodies against the glutamate receptor subunits epsilon-2 and delta-2 were detected in the serum and CSF. Cranial MRI was unremarkable.
Treatment with acyclovir and high-dose methylprednisolone failed to halt the jerks. Two weeks after admission, he developed status epilepticus, which necessitated general anesthesia. Intravenous immunoglobulin infusion gave no beneficial effects. Two months after the onset of the status epilepticus, his convulsions were controlled with zonisamide, clobazam, and carbamazepine. While he had no motor dysfunctions, he had loss of spontaneity and memory impairment.
This report suggests that EPC might be the initial symptom of subacute encephalitis with a possible autoimmune mechanism.

(CLINICA NEUROL, 45: 610－612, 2005)
key words: epilepsia partialis continua, subacute encephalitis, anti-glutamate receptor antibodies

(Received: 22-Dec-04)