The purpose of this paper is to describe analytic data regarding cognitive errors observed in aphasic patients and normal adults subjected to a cognition test of environmental sounds.
    Twenty familiar environmental sounds were selected for the present study, including calling or singing of birds, chirping of insects, the sound of footsteps, vehicular noises, noises produced in a kitchen, barking, mewing, clucking, etc. These sounds and noises were recorded on magnetic tape and played back on a tape recorder. The subjects were 40 aphasic patients ranging from 30 to 60 years of age and 50 normal adults ranging from 20 to 60 years of age.
    Two experiments were designed to explore factors influencing cognitive function in both groups :
    1) The subjects were asked to answer orally or manually the name of the test materials presented through a loud-speaker at a comfortable level.
    2) The subjects were asked to point to the picture corresponding to the test sound, from four pictures on a sheet.
    Cognitive errors collected from the two groups were analyzed in terms of acoustics, distinctive feature theory and semantics. Latencies from beginning of stimulation to response were measured and compared between the two groups. The results obtained suggested :
    1) Misunderstanding or cognitive errors in the normal group may be caused by poverty of distinctive sound features, lack of knowledge of relevant signals or difference in familiarity among generations.
    2) In addition, in the aphasic groups some errors, including failure to respond, may be attributed to disturbance at the semantic level.
    3) Comparison of latencies may provide information on disturbances of auditory cognitive processing.

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     The sentence production deficits and their recovery characteristics were studied in Broca's, Wernicke's and global aphasia. Eleven Broca's aphasics, nine Wernicke's aphasics and seven global aphasics recieved syntactic therapy and a syntactic test. The syntactic therapy method and the syntactic test presented in this paper were designed based on the hierarchy of syntactic processing that we had already detected.
    The results showed that (1) sentence production abilities of each aphasic group had been disrupted and improved according to the hierarchy of syntactic processing. (2) Most Broca's aphasics and most Wernicke's aphasics improved the levels of sentence production, but most global aphasics did not improve the levels of sentence production. (3) The levels of sentence production were different among aphasic groups. Broca's aphasics had difficulty in producing the reversible sentences of which subject is not an actor. Wernicke's aphasics had difficulty in producing the reversible sentences with complement sentences. Wernicke's aphasics produced more simple sentences when they could not produce the reversible sentences with complete sentences. (4) The abilities of constructing canonical word order improved earlier than the abilities of producing particles in Broca's and Wernicke's aphasia. Broca's aphasics had particular difficulty in constructing canonical word order according to syntactic categories. Wernicke's aphasics had particular difficulty in selecting particles according to the already correctly assigned syntactic categories.
    The sentence production deficits and their prognosis were different among aphasic groups.

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     While complex stimuli, for examining auditory and visual extinction, are frequently used in the dichotic listening and tachistoscopic tests, they have not been generally employed in the tactile modality. Therefore the anatomical substratum of tactile extinction to complex stimuli has not been systematically studied. In the present study, CT scan analyses of the site of lesions producing so-called tactile extinction to complex stimuli in relation to the mechanisms underlying this phenomenon were examined in eight patients with cerebral infarction.
    The so-called tactile extinction was detected by using a modified Quality Extinction Test (QET). The test consists in simultaneously brushing the fingers of both hands with stimuli either identical or differing in tactile quality.
    Extinction observed in the modified QET resulted from interstimulus rivalry in two different levels of tactile processing, i. e. perception process and recognition process.
    Among eight patients with extinction to complex stimuli in the modified QET, three with extinction due to interstimulus rivalry in the process of perception had lesions of the inferior parietal gyrus. The other five patients with extinction due to interstimulus rivalry in the process of recognition showed a variety of lesions, i. e. temporo-parietal lesion (one patient), multiple lesions including temporo-parietal lesion (one patient), frontal lesion (two patients), occipital lesion (one patient), but they had no lesions in common. All eight patients showed extinction contralateral to the main lesion.
    Consequently, the lesion responsible for the so-called tactile extinction can be considered to vary with the mechanisms underlying the extinction.
    Schwartz et al. (1977, 1979) reported that left frontal lesion produced ipsilateral extinction and they proposed a model which was similar to the disconnection hypothesis to explain it. According to our results, the extinction due to frontal lesion seems to result from interstimulus rivalry in the process of recognition. In addition, we challenged their hypothesis by presenting two frontal lobe damaged patients and two anterior callosotomized patients who showed no extinction at all in the present study.

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     A case of conduction aphasia was analyzed and reported. The patient was a 67-year-old right handed male. He developed aphasia after having recovered from the first stroke involving the right hemisphere 18 months before. MRI study revealed old subcortical lesions in the right parietooccipital region and a new lesion confined in the left supramarginal gyrus.
    Neuropsychologically the patient presented with a typical profile of conduction aphasia, i. e. fluent speech contaminated with literal paraphasias, good comprehension of spoken language, and severe difficulty of repetition.
    Three features of the present case were thought to be worth reporting.
    First, unlike typical cases reported previously responses in repetition in the present case tended to disintegrate into jargon. Especially there was a tendency that irrelevant series of syllables were added toward the end of a response, making the response unnecessarily longer than a target word. From the phonological analysis of the nature of this type of responses we concluded that difficulty of selection of the number of necessary syllables as well as the correct syllable itself was at the base of this symptom.
    Second, the patient had the right hemisphere lesion in addition to the left supramarginal lesion. It was postulated that jargon production was probably enhanced by this right hemisphere lesion. Also the latter lesion was thought to be contributory to the poor recovery of repetition capacity.
    Finally the importance of the supramarginal cortical lesion in conduction aphasia was stressed.

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     The incidence and nature of intentional perseveration in buccofacial apraxia were investigated. Out of 30 left-hemisphere damaged patients perseverative errors in sequential oral movements were found in 10 cases of 17 buccofacial apraxia. The perseverative errors were classified into two types ; immediate and delayed type according to temporal relation of a response to the stimuli. In addition we divided buccofacial apraxia into two groups, that is, buccofacial apraxia with non-fluent aphasia and that with fluent aphasia. We could not find the differences of the nature of perseveration in two groups. And there were no correlations between verbal perseveration and oral perseveration. On CT findings the lesion of frontal lobe, temporal lobe, insula and parietal lobe were detected. Without frontal lobe lesions the oral perseveration were observed. Oral perseveration was supposed to be related with the disinhibition of the motor memory trace.

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     This report focuses on a case of articulation disorder caused by left putarminal hemorrhage. The patient showed slight aphasia at the onset of stroke, which gradually improved except for a disorder of articulated language. We investigated the influence of the articulation disorder by means of phonetic analysis and undertook comparison with a case of pseudobulbar palsy where no aphasia was present. For phonetic analysis, speech duration in each speech modality (Kana read aloud for phonograms, Kanji read aloud for ideograms and picture naming) was determined spectrographically and the coefficient of variation was computed. Results indicated that the patient showed disturbance of the phonemic coding process according to the difference of speech modality, whereas the pseudobulbar palsy displayed no corresponding disturbance, we suggested that the patient shifted from a slight subcortical aphasia to a condition nearly allied to pure word dumbness.

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     The subject was a 9-year-old girl with aphasia caused by occlusion of the left middle cerebral artery. Linguistic condition was near mutism soon after onset of disease at the age of 4 years 4 months. She recovered early from aphasia and entered primary school, but had difficulty in learning Kana letters.
    Reading tended to be inferior to writing. When she was 8 years 1 month, her verbal and performance IQ statistics were normal on the WISC. She also had no difficuety in speech or visual perception.
    Although we have continued therapy for three years, the subject's reading and writing difficulty are still observed at present. The lesion that extended to the regions of the left angular gyrus is belived to be affecting her learning ability in reading and writing.

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     We reported on a patient who developed alexia with agraphia associated with left posterior cerebral artery occlusion. The subject was a 53-year-old right handed male. Neuropsychologically, alexia with agraphia and color agnosia were observed. Reading disturbance was moderate, and motor facilitation had almost no effect. Writing disturbance was severe. Spontaneous writing, dictation and letter copying were disturbed, although letter copying was relatively unimpaired.
    One and a half months after onset, alexia and disturbance in letter copying improued but agraphia and color anomia did not. During the clinical course, cerebral angiography revealed occlusion in the left posterior cerebral artery, while CT scan showed only small infarctions in the left thalamus and bilateral corona radiata. 54 days after onset, hemorrhagic shock developed, and subsequently a new infarction appeared from the medial aspect of the occipital lobe to the temporal lobe. However, neuropsychologically no marked changes were observed. Agraphia and color anomia remained and have continued for 3 years.
    Findings indicate that the patient developed alexia with agraphia associated with damage to the basin of the left posterior cerebral artery, especially the left temporal lobe. However, evaluation of changes in the neuropsychological findings suggests that different mechanisms are involved in the development of alexia and agraphia.

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