For understanding aphasia, I proposed a simple procedures and the point of view. First, we should divide brain function related language into two systems : one is the phonetic & phonemic system and the other is the content & context system. These systems also correspond to definite anatomical localization. Second, in terms of estimating speech output, I pointed out that it is simpler and more rational to adopt anarthria as a standard than using traditional fluent/non-fluent dichotomy because anarthria is an established focal sign of an impairment of the left precentral gyrus. Regarding estimating repetition ability, there is no clear standard to delineate between good and poor of repetition ability. Then it is helpful to estimate phonemic paraphasia and verbal short term memory, both of which are implicated in the anatomical localization. In addition I referred localization of four elementary impairments of language and implications in the classical aphasic terminology. With respect to aphasic terminology, there still remains many problems to be solved. I referred some of them, for example ; where to place transcortical motor aphasia, characteristics of subcortical aphasia, and sentence processing impairment. I also elucidated the influence of non linguistic background upon language ability : repetition ability which shows automatico-voluntary dissociation in Wernicke's apahsics, first order effect of naming ability in the aphasic patients with temporal lobe damages, how to improve naming ability in an aphasic patient using alternative tasks.

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Based on the assumption that an integration of sensory inputs through various modalities determines brain processings for praxis, I and my colleages have observed clinical symptoms for praxis for years. Then, we revealed that there can be three parallel processings for praxis : one is what to select as a target movement, another is how to determine a role of a limb, and the other is how to maintain the metrical accuracy. Each of these processings ingeniously utilizes somatosensation respectively. That is, there is a possibility that somatosensation may play an important role in learning movements to be selected (what to select as a target movement). There is a possibility that somatosensation can be used for determining roles of each limb for movements. In addition, impairments of somatosensation directly reduce a metrical accuracy of reaching and grasping (how to maintain the metrical accuracy).

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  Clinical skills in neuropsychology are closely related to hypothesis testing based on careful observation of symptoms and signs. Systematic observation is necessary to differentiate agnosia from other similar symptoms. Agnosia is defined as modality-specific disturbance of object recognition in the absence of elementary sensory dysfunction or beyond an elementary sensory failure when it exists. Anomia and impaired semantic knowledge of objects should be distinguished from agnosia.
  There are two types of agnosia. Accordingly, apperceptive agnosia results from a faulty synthesis of object features, whereas associative agnosia arises when intact perceptual extraction of object features cannot associate with semantic knowledge. Furthermore, integrative agnosia has been taken into consideration for visual agnosia. Systematic investigation could reveal an impaired stage of information processing in each type of agnosia. Category-specific agnosia has been reported in visual and auditory agnosia. Prosopagnosia, i. e. agnosia for faces, and landmark agnosia are different from the other visual agnosia in that recognition of an individual face or landmark is disturbed. Patients with prosopagnosia can recognize human face, but cannot tell who he/she is.
  Not only neuroimaging and neurophysiological findings in neuroscience but also careful and detailed clinical investigation with hypothesis and test cycle are essential to reveal neuronal bases of object recognition.

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In recent years, there has been considerable progress in expanding the differential diagnosis of Alzheimer's disease (AD) with clinical characterization of vascular dementia (VaD) , dementia with Lewy bodies (DLB) , and frontotemporal lobar degeneration (FTLD) . Each dementia has its own characteristic clinical course, cognitive profile, behavioral profile, and neurologic features. Both the onset and course of the disease are important in assessing its etiology. Neurodegenerative diseases such as AD, DLB, and FTLD have insidious onset with a slowly progressive and chronic course, whereas a stair-step progression suggests VaD. The first symptom of AD is usually progressive difficulty with recent memory. In DLB, visual hallucinations are prominent, whereas in FTLD stereotypic behavior and inappropriate eating behavior are more pronounced. Such cognitive and behavioral symptomatology is essential to early diagnosis and care of dementia.

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Descriptions on writing errors in patients with amyotrophic lateral sclerosis (ALS) were reviewed. A Japanese patient with ALS who showed writing errors with paragraphia was reported as early as 1893. This is now considered to be the first report on not only ALS with dementia (ALS-D) but also aphasia in Japan. Most of other literatures describing writing errors were reported in late 1990s, after the concept of frontotemporal lobe dementia (FTD) became recognized in association with ALS. In the literatures, we can find the descriptions on writing errors, including various types of paragraphia, syntactic errors and omission of letters. Although most of writing errors were observed in context with aphasia and/or dementia, we reported two case of ALS with isolated agraphia. This experience suggests that isolated agraphia could appear independently of existence of aphasia and/or dementia, and that isolated agraphia could be an early manifestation of ALS-D. We consider that isolated agrapahia might be associated dysfunction of the posterior part in the middle or inferior frontal lobes of the dominant hemisphere. In patients with ALS especially bulbar-onset, assessment of writing should be very important to assess language function masked under impaired speech.

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[in Japanese]

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We applied a factor analysis to results of the Behavioural Assessment of the Dysexecutive Syndrome (BADS) , Japanese version. The data were collected from 65 subjects with brain damage. From the results, we extracted two factors. One factor was interpreted as action planning ability, and the other factor as estimating ability. These factor scores were distributed in accordance with overall BADS classifications. Next, correlations between factor scores and neuropsychological assessment (intelligence, memory and attention tests) were examined. The factor scores of action planning ability (factor 1) correlated general cognitive function, and the factor scores of estimating ability (factor 2) correlated with tasks associated with working memory. We were unable to find any association between neurobehavioral disabilities and overall BADS classification results. We concluded that BADS is useful to evaluate action planning ability and estimating ability in dysexecutive syndrome, but that it is not applicable to neurobehavioral disorders.

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  We provided Computer-assisted Attention Training (CAT) , a cognitive rehabilitation method that uses an originally developed program for personal computers, to 10 patients with cerebrovascular disease accompanied by attentional disorder using a study design closely related to the A-B-A' study design. We conducted an evaluation comprising assessments for attention (AMM, TMT, PASAT) , a rating scale of attentional behavior (Ponsford scale) , and a test for ADL (FIM) a total of four times and compared the results.
  The results showed significant improvements (p<0.01 or 0.05) in test results for assessments for attention (AMM, TMT, PASAT) , the Ponsford scale, and FIM after four weeks of CAT compared to before CAT. However, some results in assessments for attention (AMM hit rate, TMT-B, PASAT-2.0 sec pacing) showed significant improvements (p<0.01 or 0.05) even in the A phase. Moreover, in the A'phase, results for assessments for attention (AMM, TMT, PASAT) were maintained, and significant improvements (p<0.01) were observed for results on the Ponsford scale and FIM.
  Although the subjects were in convalescence and spontaneous recovery may thus have been partially responsible for the results, the overall test results suggest that CAT was effective to some degree. Therefore, CAT may be a useful training method for attentional disorder.

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  We examined the relationship between action production and action recognition in patients with probable Pick's disease with temporal lobe atrophy (semantic dementia ). The patients were a 60-year-old right-handed woman and a 79-year-old right-handed man, who showed disturbances in verbal semantic memory.
  We tested their action-production ability by using 6 different standard tests for apraxia (intransitive gestures on verbal command, imitation of intransitive gestures, transitive pantomimes on verbal command, transitive pantomimes to visually presented objects without touching them, imitation of transitive pantomimes, and actual object use ). Additionally, we examined their action-recognition ability by using 6tests (object naming, identification of the examiner's intransitive gestures and transitive pantomimes, and explanation of the use of objects in response to visually presented objects or name of them ).
  Action production and action recognition were generally impaired in our patients, with the exception of the imitation of intransitive actions. Since the scores of action-production tasks were significantly correlated with those of recognition tasks, a common factor may impair both action production and action recognition. Patients of Pick's disease with temporal lobe atrophy experienced difficulty in explaining intransitive gestures and transitive pantomimes. The present results indicated that not only semantic memory for words and objects but also that for actions may be impaired in these patients.

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We reported a case of nonfluent aphasia after cerebral infarction. An 83-year-old, right-handed female exhibited mild anarthria and severely decreased spontaneous speech without impairment of word fluency or sentence composition on any examinations, and she was highly motivated to speak. Comprehension, reading aloud, object naming, and repetition of phonemes, words, and sentences were preserved. An MRI of the brain showed an infarcted lesion in the posterior part of the left middle frontal gyrus and the anterior part of the left precentral gyrus. Although anarthria disappeared soon and she showed some improvement in fluency, she still had difficulty in starting and continuing speech a year after onset. This symptom was more obvious in open questions than in closed questions. Most cases of nonfluent aphasia are known to be caused mainly by anarthria and loss of motivation for speaking. These did not appear to be the reasons for our patient's nonfluency. We discussed impairment of thought, verbalization of thought, and choice of words as possible causes of the nonfluency. Most patients who show Broca's aphasia have lesions in the middle frontal gyrus and in the precentral gyrus in the linguistically dominant hemisphere. Therefore, we believe that this suggests that the cause in this case is one of the causes of nonfluency in Broca's aphasia.

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