A case of crossed dextral aphasia characterized by agrammatism was reported. The patient,55-year-old purely right-handed man, a teacher of Japanese, developed left hemiparesis, slight left unilateral spatial neglect and aphasia because of cerebral infarction. CT scan displayed a large hypodense area in subcortical region of the right hemisphere. His speech showed slight dysarthria, literal paraphasias and agrammatism. The characteristics of the agrammatic speech were as follows : dropping out of grammatical morphemes (including joshi, auxiliary verbs and conjugation of verbs), good word-findings, lots of pauses in spite of long and well-constructed sentences. The writing had some literal paragraphias and agrammatism such as in speech. The way of writing was disorderly. Grammatical morphemes and verbs in part were regarded as representing speaker's thought and attitude essentially, and in case a speaker's tension to maintain his intention of speech was reduced, they would be apt to be dropped. We pointed out that the mechanism of writing disturbance of this case was different from non-crossed left hemisphere damaged aphasic's, and that such aphasic symptom as this case might represent a type peculiar to crossed dextral aphasia.

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    Recovery mechanism of naming task was investigated based on the view that recovery process are not uniform across different modalities of language therapy, and that therapy must be planned according to the mechanism of each disorder. Three kind of naming training, namely, the first with Kanji writing, the second with initial syllable cue and repetition, and the third with Kana writing, were administered to 2 aphasics suffering from severe naming disability for more than a year.
The rate of improvement and the stability of their performance was then compared. The better result was obtained in the order of training with Kanji writing, training with Kana writing and training with repetition, in both the improvement rate and the stability of performance. These results can be understood in terms of the dual code theory in which the phonological processes and the visual semantic processes run parallel to each other.
Thus the effectiveness of such training as Kanji writing which activates the visual semantic processes suggests the trouble in the phono-logical processes. Kana writing, normally processed phonologically, is also thought to be processed visuo-semantically in these cases. Repetative naming training was not succesful, that is, the phonological processes were not activated in spite of the stimulation, suggesting that the direct stimulation of the processes with severe disorders may not be so effective. The recovery mechanism in these 2 cases can be viewed in the framework of functional reorganization theory.

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    A 62-year-old, right-handed woman complained of prosopagnosia and many other hemispheric symptoms due to recurrent cerebral hemorrhage involving bilateral cerebral hemispheres. Although “aphasia” or “optic aphasia” were not clearly differentiated, “aphasic factor” in a wider sense might be responsible for producing word finding difficulty recognized after the left hemisphere damage. But impaired categorization demonstrated in the present case might have been partially caused by agnosic factor (i. e. associative visual agnosia). Although prosopagnosia due to right hemisphere damage existed only for a short time (less than five months), impairment of recognission of unfamiliar faces has remained persistantly. A localization of bilateral lesions demonstrated by the brain CT scan did not occupy the medial portion of the occipital lobe but deviated more laterally. Furthermore, an incogruent right-sided homonymous hemianopsia was also detected. These findings were different from the classical ones reported hitherto. The facts that disturbed discrimination of unfamiliar faces and impairment of other visuo-spatial perceptions persisted without improvement might suggest an interference from the damage in the contralateral left hemisphere.

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    A case of acoustic-mnestic aphasia (by Luria) following a left hemisphere vascular stroke was reported. The patient was 32-year-old man whose symptoms were Wernicke's aphasia at the first examination. CT scan revealed the middle temporal to the superior temporal lobes, and supra marginal gyrus. After 12 months from the onset of the disease, his clinical pictures became that of acousticmnestic aphasia. His spontaneous speech was fluent with mild verbal paraphasia. The dominant symptom of his illness was the severe disturbance of auditory verbal memory. The features of his repetition difficulties were as follows : He easily retained and repeated one syllable. The longer the letter of nonsense syllables, the more the disturbances appeared. A series of two-words was relatively easy. No sooner did he attempt to repeat a series of three words, however, than he found it impossible to retain and recall them. He could not retain even two-word sentences. In constrast, the reading comprehension, oral reading, and writing was relatively preserved. After 42 months after the onset, further tests were carried out, but the recover of auditory verbal memory was poor.

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    A patient, 54 year-old right-handed man, showed intra-cerebral hematoms in bilateral occipito-temporal areas after a fall to the ground. Besides a left upper quadrantic homonymous hemianopsia, he had associative visual agnosia, prosopagnosia, central achromatopsia, pure alexia and slight agraphia and acalculia. He matched and copied well pictures and letters which he could not recognize. After three years, object recognition and reading improved greatly, prosopagnosia and achromatopsia remained almost unchanged. He could not identify human faces, nor discriminate the kind or the individual of animals, birds, flowers and vegetables. The visual recognition process was compared between in the case of human faces, animals etc. and in that of common objects.

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    A typical case of cerebral achromatopsia was reported. A patient, right handed 65-year-old male, has been complaining “everything looks only black or white” after his second stroke in 1982. Computed tomography demonstrated cerebral infarct in the medio-basal part of the left occipital lobe, having widespread lesion of the old infarction in the inferior part of the right temporal and occipital lobe due to the first stroke in 1977. He had no obvious aphasia, alexia, constructual apraxia. Impairment of color perception, prosopagnosia, topographical disorientation and dressing apraxia were observed. Ophthalmological examinations showed a superior altitudinal visual field defect, normal fundi and VEP.
    Detailed tests on color were succeeded. Color naming was severely disturbed except red. Hue tests and coloring showed poor resuits. Ordering according to the brightness was markedly well. On the Ishihara test (14 sheets) he answered 7 sheets correctly but showed minor errors in 2 sheets. Examinations with the Munsell color system revealed that he can discriminate many colored plates correctly (especially red-green system) in spite of his complaints.
    Tests on color perception with a red filter among normal controls showed similar results with the patient. These findings suggest that “cerebral achromatopsia” is caused by partial defect of color perception i. e. the patient with cerebral achromatopsia can discriminate colors according to a new “brightness-darkness axis” .

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