Kudo T, Funakoshi A, Tanaka M, Matsuda K, Inoue Y, Yagi K, Seino M
National Epilepsy Center, Shizuoka Higashi Hospital.
Seishin Shinkeigaku Zasshi. 1993;95(2):125-50.
Semiology of postictal aphasia as well as its generating mechanism involving both the epileptogenic zone and language area has not yet been sufficiently elucidated. Therefore, postictal aphasias were studied in 3 patients with localization-related epilepsy. Postictal motor aphasia was observed in a patient (patient 1) with frontal lobe epilepsy whose recovery of language function progressed from loss of language function, to Broca's aphasia, and eventually to poor spontaneous speech. Postictal sensory aphasia was observed in 2 patients (patient 2 and 3) with temporal lobe epilepsy whose recovery of language function progressed from loss of language function, to jargon, and eventually to circumlocutory anomic speech. Both patient 2 and 3 did not show fluent speech. Seizure manifestations, EEG, IMP-SPECT and MRI indicated that epileptogenic zones were in the left frontal lobe including Broca's area in patient 1, the mesial part of the left temporal lobe in patient 2, and the middle and posterior part of the left temporal lobe including Wernicke's area in patient 3. A postictal verbal dichotic listening test showed the reduction of correct responses by right ear in the patient 3. Postictal auditory verbal learning tests showed the impairment of verbal memorization in patient 2 and 3. The impairment of verbal memorization was particularly marked in patient 2. These results suggest that 1) the characteristics of postictal motor and sensory aphasia are clearly elucidated by analyzing the sequence of recovery from postictal language dysfunction, 2) postictal aphasia is generated by the epileptogenic zone involving the language area or the ictal discharges propagating to the language area, and 3) not only the disturbance of language function, but also the impairment of verbal memorization seems to participate in the disturbance of repeating and understanding sentences in the patient with postictal sensory aphasia.
发作后失语症的症状学及其涉及致痫区和语言区的产生机制尚未得到充分阐明。因此,对3例定位相关癫痫患者的发作后失语症进行了研究。在1例额叶癫痫患者(患者1)中观察到发作后运动性失语,其语言功能的恢复从语言功能丧失进展为布罗卡失语,最终发展为自发言语贫乏。在2例颞叶癫痫患者(患者2和3)中观察到发作后感觉性失语,其语言功能的恢复从语言功能丧失进展为乱语,最终发展为迂回性命名性失语。患者2和3均未表现出流利的言语。癫痫发作表现、脑电图、单光子发射计算机断层扫描(SPECT)和磁共振成像(MRI)表明,致痫区在患者1的左侧额叶包括布罗卡区,患者2的左侧颞叶内侧部分,患者3的左侧颞叶中后部包括韦尼克区。发作后言语双耳分听测试显示患者3右耳正确反应减少。发作后听觉言语学习测试显示患者2和3存在言语记忆障碍。言语记忆障碍在患者2中尤为明显。这些结果表明:1)通过分析发作后语言功能障碍的恢复顺序,可以清楚地阐明发作后运动性和感觉性失语的特征;2)发作后失语症是由涉及语言区的致痫区或传播至语言区的发作期放电所产生;3)在发作后感觉性失语患者中,不仅语言功能障碍,而且言语记忆障碍似乎也参与了句子复述和理解的障碍。