A 61-year-old, left-handed male was admitted with a complaint of transient speech disturbance repeatedly occurring during three months prior to admission. During attacks, verbal expression was non-fluent and slow, and prosody was also disturbed. Substitution of phonemes/syllables sometimes occurred when he tried to speak fast. His abilities in language comprehension and writing were preserved normally. He showed no buccofacial apraxia, and articulatory muscles were intact.
    In Magnetic Resonance Imaging (MRI) performed on November 15, 1990, multiple lesions in the left frontal and parietal lobe subcortices, the deep layer of insular white matter and the caudate nucleus were demonstrated, which were intensified by Gadolinium-DTPA. Continual EEC monitoring during a given attack showed no abnormalities. Based on these findings, the patient was diagnosed as suffering from pure anarthria; as its cause, transient cerebral ischemia was suspected. During admission, the frequency of attacks gradually decreased after administration of ticlopidine. He was discharged on November 21, 1990, after the attacks ceased.
    On January 22, 1991, the patient was admitted again with complaint of the same speech disturbance, which had lasted more than ten days. On admission his speech disturbance was found to be milder than that which occurred earlier. At this time the main features were tardiness of speech and awkwardness in speech sound sequencing.
    Speech disturbance in this patient is compatible with the criteria of pure anarthria. The pattern of speech disturbance, however, is somewhat different from the classic pure anarthria, in that tardiness of speech and awkwardness in speech sound sequencing were the main features. This fact may be attributable to a different location of lesions ; i. e. simultaneous involvement of the commissure fibers communicating between both cerebral hemispheres as well as the left cortico-medullary tract.
    This case suggests the importance of the commissure fibers as one of the responsible lesions of pure anarthria.

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    Using CT, the brain lesion sites of 8 patients with Broca's aphasia were investigated. Also studied was their comprehension capability. All patients were right-handed and non-fluent aphasics as a result of a left hemisphere cerebrovascular accident. Cases that showed CT evidence of diffuse or multiple lesions, and/or putaminal hemorrhage were exclued from this study.
    The patients were clasified into two groups according to the CT findings. Group 1 consisted of patients with small lesions in the pars opercularis whereas Group 2 patients had larger lesions extending throughout the Broca's area. Comprehension deficits were evaluated by using the standard language test for aphasia (SLTA). Auditory comprehension of single words was found to be normal in the Group 1 patients, but those in Group 2 showed mild deficits.
    It is suggested that auditory comprehension of single words remains normal in patients with Broca's aphasia if the pars triangularis is spared.

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    Patients with aphasic fits were examined clinically. They were selected from five hundreds and sixty-three ambulatory patients with simple partial seizures. The aphasic fits consisted of twenty-four impairments of verbal comprehension, twenty-five impairments of verbal expression, five difficulties of finding words, four paraphasias, and two alexias.
    In order to elucidate clinical features of patients with aphasic fits, we compared cases of dreamy states without aphasic fits (DR group) with cases of aphasic fits without dreamy states (AP group). As a result, the following points were statistically confirmed : AP group had a higher rate of frontal EEG foci : lower rate of complex partial seizure ; higher rate of partial motor seizure ; lower rate of complex visual auras and anxiety auras. From these findings, we proposed that aphasic fits are more closely related to neocortex, although patients with aphasic fits as well as dreamy states showed temporal EEG foci in most cases.

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    The effects of stimulating three modalities in the treatment of picture naming problems are compared. Comparisons focused on a 60-year-old male patient with chronic Wernicke aphasia whose abilities in oral reading of kana words are preserved better than those in repetition and oral reading of kanji words. The three stimulated modalities were oral reading of kana words, oral reading of kanji words and repetition. Selecting two modalities out of three, we compared the efficiency of the three modalities as a facilitator for picture naming, i. e., oral reading of kana words vs. repetition, and oral reading of kana words vs. oral reading of kanji words.
    Results demonstrated that oral reading of kana words was generally efficient, while oral reading of kanji words was also efficient for certain words. By contrast, repetition was not efficient.
    We considered the underlying mechanism of the facilitation of word retrieval in this case, and discussed the importance of modality selection for stimulation in aphasia therapy according to patient type.

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    The purpose of this study was to clarify differences in speech sound errors among Broca's aphasics, conduction aphasics and Wernicke's aphasics. While this issue has been analyzed in former researches within single modalities (confrontation naming and/or repetition) separately, the present study focused on similarity of error patterns observed across various speech modalities : confrontation naming, repetition, and reading aloud of Kanji and Kana words. The subjects were four Broca's aphasics, three conduction aphasics and five Wernicke's aphasics. 60 words ranging from three to five syllables were used. Consonant errors were analyzed and classified into five categories : substitution, transposition, omission, addition and distortion. The results indicated the following.
    1) In conduction aphasics and Wernicke's aphasics, substitution and transposition accounted for almost 90% of the errors observed. The rates of these two error patterns varied for each case. In the Broca's aphasics, error categories which took the largest rates varied from case to case.
    2) Relatively similar error patterns were observed across all four speech modalities in the Broca' s aphasics and conduction aphasics. On the other hand, in Wernicke's aphasics error patterns were varied over different speech modalities. These findings suggest that :
    1) In classifying speech sound errors according to types of aphasia, it is beneficial to focus on similarity of error patterns across four speech modalities rather than to compare error patterns within each modality respectively.
    2) With regard to Broca's aphasics and conduction aphsics, speech sound errors in the four speech modalities are caused by the same mechanism for each aphasic type, since common error patterns are observed throughout all speech modalities. On the other hand, speech sound errors in Wernicke's aphasics seemed to be caused by several factors.

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    We reported a peculiar speech symptom obsereved in a patient with transcortical sensory aphasia following head trauma. His speech was fluent but contaminated by a lot of irrelevant verbal paraphasias. Naming and word comprehension were severely impaired. His paraphasias, although irrelevant to the target words, were semantically associated with each other. This kind of speech symptom was considered to correspond to the iterative pattern of semantic variation, which was described by Hadano in his report of semantic jargon aphasia. We considered that word comprehension disorder and relative intactness of lexical items, in addition to heightened impulse to produce verbal output, play an important role in the pathogenesis of irrelevant paraphasias. Output of a series of irrelevant paraphasias belonging to the same semantic category would be explained in terms of semantic perseveration. Because of a severe lexical-semantic impairment, in out patient, once a semantic field was activated, another semantic field could not be activated properly. Therefore, he had to select only words within the semantic field under improperly persistent excitement, which would result in this unique speech symptom.

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    We analyzed the processes of writing to dictation and copying letters with the use of VTR recordings of performances in two agraphic patients ; a patient with alexia with agraphia and a patient with pure agraphia.
    The patient with alexia with agraphia due to an infarction that mainly involved the left angular gyrus wrote nothing when he could not make a correct response to dictation. However, his copying of letters was satisfactory and performed with normal sequences of strokes. The writing speed in copying was not different for the Kanji characters that the patient could or could not write to dictation. These findings suggest that the motor pattern for writing letters was preserved in this patient. Patients with alexia with agraphia may have difficulty in the recollection, selection, or both of letters to be written.
    The patient with pure agraphia following an infarction in the left superior parietal lobule wrote letters without spatial distortion. His erroneous writings were characterized by partial lacking and incorrectness of the letters. The patient showed abnormal sequences of strokes and completed a stroke by piecing out several fragments. This abnormal motor pattern for writing was observed more frequently in writing the letters that could not be written to dictation than in the correct responses. Copying letters was better than writing to dictation, but it was also performed with the abnormal motor pattern. The writing speed in copying was slower for the Kanji characters that could not be written to dictation than for those written correctly. Copying requires no recollection or selection of letters to be written. We thus considered that the disordered motor pattern for writing may play a role in the pathogenesis of pure agraphia.

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