A thity years old college graduate woman experienced the first episode of tonic clonic convulsion at the age of eighteen. Since then, the convulsion recurred every two or three years and sometimes developed into convulsive status epilepticus. Laboratory examination revealed an elevated level of resting lactate and pyruvate and computerized tomography exhibited low density area in the left middle and inferior temporal gyri. The clinical constellation of symptoms was suggestive of MELAS syndrome, but the results of muscle biopsy were not contributory to the diagnosis. The language examinations were performed at a secondarily generalized tonic clonic sezure twice : atfirst, ten minutes after the convulsion had stopped and, subsequently, one hour after the convulsion had stopped. The most striking difference beween the earlier misnamings and the later misnamings consisted in the nature of the produced verbal paraphasias and the sources of verbal perseverations. The intralist perseveration, that is, perseveration of one of the seven target words given in the examination, occurred three times more frequently in the later trial than in the earlier trial. On the other hand, the production of extralist paraphasia was four times more frequent in the earlier trial than in the later trial. In addition, in the earlier examination, almost all the extralist verbal paraphasias were semantically irrelevant to the taget words and some extralist verbal paraphasias were phonologically associated with each other. Circumlocution was a characteristic error type of the later misnamings. Phonemic paraphasias were found to the same extent in the later as well as in the earlier misnamings. From these results, we suggested that extralist and intralist perseverations (Helkala et al.,1989) were not a sign of different anatomical lesions but a manifestation of different levels of verbal breakdown, and that extralist perseverations were produced on deeper level of verbal breakdown than intralist perseverations.

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    Twenty cases of optic ataxia were reported together with progression in their symptoms Optic ataxia is a disorder of hand movement in which the patient is unable to grasp objects located in the central visual field (the so-called “optische Ataxie” ) and/or the peripheral visual field (the so-called “ataxie optique” ). Studies were carried out in relation to neuropsychological and neuroradiological findings.
    Cases were divided into four stages according to severity of symptoms. STAGE I : In the most severe cases, a disorder was noted in grasping objects in the central visual field ( “optische Ataxie” ), with “ataxie optique” in the peripheral visual field. STAGE II : In the next most severe cases, difficulties were observed in grasping objects in the peripheral visual field—both the peripheral visual field for the hand opposite to the lesion and the unilateral peripheral visual field for the other hand. STAGE III : In milder cases, a disorder was seen in grasping objects in the unilateral peripheral visual field by both hands. STAGE IV : In the mildest cases, a disorder existed in grasping objects in the unilateral peripheral visual field by unilateral hand. The lesion responsible for optic ataxia is indicated in the parieto-occipital junction area by CT. From these studies, it can be said that grasping of an object in the unilateral peripheral visual field by the hand on the contralateral side indicates a lesion of the major forceps.

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    The case of a 74-year-old right-handed man with alexia and agraphia of Kanji resulting from a car accident is described. CT scan revealed that the main lesion was in the left inferior temporal gyrus. The patient's chief complaint was his inability to read and write Kanji characters. Detailed examination showed that his alexia combined with agraphia was much more predominant for Kanji than for Kana syllabarias. The characteristics of his reading errors were as follows. A test of reading aloud 105 popular Kanji revealed that errors were made more frequently for graphically complicated characters than for simple ones. The greater the number of strokes in the Kanji the more frequently errors were made. The patient showed occasional graphical and confusion errors. After 18 months following onset, reading and writing of Kanji remained grossly disturbed.
    We analyzed 13 follow-up studies in addition to our previous case that had already confirmed alexia combined with agraphia in similar lesions. In the acute stage of these studies, alexia combined with agrahia was divided into four types. Moreover, these types of alexia combined with agraphia showed different clinical profiles in the chronic stage. Generally, reading and writing of Kanji remained grossly disturbed. At the same time, howerer, those of Kana showed good recovery.
    We indicated two types of alexia of Kanji in the same lesion. One had difficulty recognizing the whole Gestalt of Kanji (simultaneous agnosia type). The other had difficulty analyzing Kanji in detail (pure alexia type).

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