Kyoko Kanazawa1, Riki Matsumoto2, Akihiro Shimotake1, Masako Kinoshita3, Akiko Otsuka4, Osamu Watanabe5, Keiko Tanaka6, Ryosuke Takahashi1, Akio Ikeda2. 1. Department of Neurology. 2. Department of Epilepsy, Movement Disorders and Physiology, Kyoto University Graduate School of Medicine, Kyoto. 3. Department of Neurology, Utano National Hospital, Utano. 4. Department of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto. 5. Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima. 6. Department of Neurology, Kanazawa Medical University, Kanazawa, Japan.
Abstract
AIM: To delineate a possible correlation between clinical course and EEG abnormalities in non-infectious "smoldering" limbic encephalitis. METHODS: Long-term clinical data, including video-EEG monitoring records, were analysed in two patients. RESULTS: The two patients were positive for anti-voltage-gated potassium channel complex antibody and unspecified antineuronal antibody, respectively. The latter patient had small cell lung carcinoma. Both patients had memory impairment and clinical seizures. EEG showed frequent subclinical seizure patterns in the bilateral temporal regions. Subclinical seizure patterns and memory impairment persisted over one to two years after clinical seizure remission. Therapy (prednisolone and chemoradiation in the two patients, respectively) resulted in decreased occurrence of subclinical seizure patterns and memory improvement. CONCLUSIONS: EEG seizure patterns may persist years after clinical seizure remission in "smoldering" limbic encephalitis and lead to memory impairment.
AIM: To delineate a possible correlation between clinical course and EEG abnormalities in non-infectious "smoldering" limbic encephalitis. METHODS: Long-term clinical data, including video-EEG monitoring records, were analysed in two patients. RESULTS: The two patients were positive for anti-voltage-gated potassium channel complex antibody and unspecified antineuronal antibody, respectively. The latter patient had small cell lung carcinoma. Both patients had memory impairment and clinical seizures. EEG showed frequent subclinical seizure patterns in the bilateral temporal regions. Subclinical seizure patterns and memory impairment persisted over one to two years after clinical seizure remission. Therapy (prednisolone and chemoradiation in the two patients, respectively) resulted in decreased occurrence of subclinical seizure patterns and memory improvement. CONCLUSIONS: EEG seizure patterns may persist years after clinical seizure remission in "smoldering" limbic encephalitis and lead to memory impairment.