てんかん精神病の1例における辺縁系発作後血清prolactin濃度の推移—病態生理としてのlimbic permeability

Serum Prolactin Levels Following Limbic Seizures in a Case of Epileptic Psychosis:limbic permeability as a possible explanation for pathophysiogenesis

　【抄録】てんかん精神病の1例において，辺縁系発作後の血清prolactin（PRL）濃度を測定し，間接的に脳内の発作発射拡延の様子を検討した。症例はてんかん発症から19年目より被害関係妄想を中心とする慢性の精神病状態を呈している現在39歳の男性の側頭葉てんかん患者である。その常習発作は，複雑部分発作，精神発作で，複雑部分発作については2回，精神発作については計3回について発作後血清PRL濃度を経時的に測定した。その結果，基準値10.0±4.0ng/mlに対して，発作15分後に得られた最高値は複雑部分発作の場合は94，95ng/ml，精神発作については84，43，28ng/mlであり，これらの上昇は過去の報告と比較して程度が高いと考えられた。そしてこれは側頭葉内側構造での発作発射の強度と拡がりやすさ（limbic permeability）を反映しているものと考え，これをBearの提唱した感覚－辺縁系過剰結合理論と併せて，てんかん精神病の病態生理基盤の一部をなしうるものと推定した。

　Postictal serum prolactin (PRL) elevation results from the spread of ictal discharge involving limbic structures to the hypothalamus. To indirectly explore the nature of the ictal discharge in a male psychotic temporal lobe epileptic aged 39 (seizure and psychosis onset at the ages of 6 and 25, respectively), serial PRL levels following limbic seizures (2 complex partial and3 psychic) were studied.

　The baseline samples were drawn a week after each event when the patient was seizure-free for at least 12 hours. The peak levels (15 minutes after the onset of events) following complex partial seizures revealed 94 and 95ng/ml, and those of psychic seizures, 84, 43 and 28ng/ml. These peak levels are about 9 times as high as the basal level (10.0±4.0ng/ml) in complex partial seizures and 3 to 8 times in psychic seizures. The degree of elevations in this case far exceeds those recorded in previous reports. If it is true that the higher the peak level, the more intensified and inclined to spread is the ictal discharge, limbic permeability may develop in this patient. As shown in this case, ictal fear sometimes heralds illusion of reference, a feeling of somebody being nearby and Ma vu, all of which are ascribed to sensory-limbic hyperconnection (Bear, D).

　In conclusion, limbic permeability in combination with sensory-limbic hyperconnection is partly the pathophysiogenesis of epileptic psychosis.