Encephalitis of Unknown Etiology with Anti-GluR ε2 Autoantibody, Showing Divergent Neuroradiologic and Clinical Findings

or drug abuse. He had been diagnosed with diabetes 2 years previously, but was lost to follow-up before any treatment. He had had a headache which lasted for several days 5 months before admission to our hospital. A short time later he developed severe memory impairment and pathologically increased appetite; he repeatedly stole food, even eating pet foods. Table 1 presents laboratory, neuropsychologic, electroencephalographic, and neuroradiologic findings over time. Biochemical examinations were normal except for a serum glucose concentration of 320 mg/dl and a glycosylated hemoglobin (HbA1c) value of 15.7%. Antibodies in the serum for HIV and syphilis were negative. The Wechsler Adult Intelligence Scale-Revised (WAIS-R) showed a verbal intelligence quotient (VIQ) of 85, a performance IQ (PIQ) of 85, and a full scale IQ (FIQ) of 84. The Wechsler Memory Scale-Revised (WMS-R) showed very poor general memory, visual memory, verbal memory, and delayed-recall memory (scores of ! 50, 64, ! 50, and ! 50, respectively), while the score on the attention-concentration scale was within the normal range (a score of 106). Electroencephalography (EEG) showed normal background activity and no epileptic discharges. Routine CSF study Dear Sir, A patient with severe temporal lobe atrophy, memory disturbance, and personality deterioration caused by encephalitis of unknown etiology was admitted for evaluation. Cerebrospinal fluid (CSF) studies disclosed no virus, but autoantibodies were detected against the N-methylD -aspartate-type glutamate receptor epsilon 2 (GluR 2). GluR 2 channels have been implicated in synaptic plasticity and localization associated with neural development and learning [1] . Recently autoantibodies against GluR 2 were found in some patients with Rasmussen’s encephalitis [2] and nonherpetic limbic encephalitis [3] , suggesting an autoimmune pathogenesis for some encephalitis. Surprisingly in our case, neuropsychiatric symptoms did not worsen when progressively severe neuroradiologic alterations in the temporal lobes appeared after hospitalization.