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I.はじめに
近年ウィルス学の発展に伴い,血清学的診断,組織培養をもちいてのウィルス分離等中枢神経系感染症に対して従来不明の成因とされていた疾患に,漸次病因的解明の糸口を与えてきつつあるが,これら向神経性ウィルスが,その発症に大きな役割を演じていると考えられ,主に今までまつたく健康であつた小児において,特異的に小脳をtarget organとして急激に小脳炎症状,すなわち急性小脳失調症状を呈し,1905年のBattenの報告1)以来acute cerebellar ataxiaまたは,encephalitis cerebelli acutaと称せられている一疾患単位がある。われわれは,今回成人において,嗜眠を伴つた広範囲な脳の皮質障害を思わせる所見のうちに,特に小脳を中心とした病像が前景にでた小脳失調の著明であつた1例を経験したのでいささかの文献上の考察も加えて報告をおこないたい。
Authors believe that the most important diagnostic clue of encephalitis mainly depends on the basis of clinical symptom and signs, because causative agent of encephalitis is difficult to elucidate in some cases. We reported the case who developed diffuse cerebral dysfunction with acute onset and gradually localized in cerebellar signs which lasted for long period of time.
Case was 25 years old male patient who was admitted to our hospital with chief complaints of drowsiness, dizziness and ataxia. Patient was in good health until August 8, 1962 when he developed headache, dizziness and weakness in extremities. 5 days later he started to be drowsy and to have vomiting. There was no fever or seizure.
Neurological examination on admission revealed that patient was lethargy and responded to verbal stimuli very slowly with slurred speech and fluctuated state of consciousness. Cranial nerves and motor system seemed to be intact. No definite sensory impairment was found. Reflexes were hypoactive throughout without pathological reflex. Cerebrospinal fluid showed slight mononuclear pleocytosis with normal protein. Bacteriological study of cerebrospinal fluid failed to demonstrate any causative agent. Cerebral circulation study, carotid and vertebral arteriography, and electromyelography showed no abnormality. However EEG at onset showed diffuse cerebral dysfunction and marked improvement in following 2 records. Serum compliment fixation test of Japanese B encephalitis, polio I, II and III, Coxsackie B I, III, V., adeno V, influenza A, B, mumps and herpes simplex were all negative. After hospitalization confusional state of consciousness persisted for one month and gradually returned to normal condition. On the other hand, cerebellar signs such as ataxia, slurred speech, horizontal nystagmus, dysdiadochokinesis, Holmes-Stewart sign and cere-bellar titubation have developed. These lasted a few months and gradually improved, however, these signs are still remained in slight degree up to the present time. Pathogenesis of this disease was discussed and literatures were reviewed.
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