Clinical aspects and neuropsychological mechanisms of anosognosias in the broad sense were mentioned : anosognosia in (1) Anton syndrome, (2) Wernicke aphasia, (3) anterograde amnesia and (4) denial of left hemiplegia (Anosognosia of type Babinski). We considered anosognosia of Babinski as the result of impaiment of “body consciousness”. Body Schema and Body Consciousness were distinguished along Edelman's hypothesis. The former might belong to Higher Order Consciousness and have symbolic nature. The latter belonging to Primary Consciousness might have immediate, non-symbolic nature. The author stressed the idea that if body consciousness would be represented predominantly by right hemisphere, namely bilateral body would be represented by right hemisphere and right side body by left hemisphere, we could explain ingeniously the phenomena of “denial of left hemiplegia” (anosognosia of type Babinski) and somatoparaphrenia described by Gerstmann.

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We summarized how to assess memory in amnesia patients. First, we have to exclude apparent amnesia due to attentional disturbance in assessing memory impairment in patients who seem to have poor memory. After excluding apparent amnesia patients, we evaluate memory impairment in real amnesia patients from various perspectives, such as modalities of stimuli the patients learn and remember (verbal memory/visual memory), types of remembering (recall/recognition), and types of amnesia (anterograde amnesia/retrograde amnesia). In Japan, we can use the Wechsler Memory Scale-Revised and the Rivermead Behavioral Memory Test for evaluating recent memory. However, there are no standardized remote memory tests but some tests were available in Japan. We should refer to the neuroimaging findings, such as those on magnetic resonance and single photon emission computed tomographic imaging studies of the patients, and information concerning causative diseases. Although many brain regions are associated with memory, the medial temporal lobe, thalamus, and basal forebrain play important roles in memory function. Patients with damage to these regions show characteristic amnesia corresponding to the respective regions. Patients with dissociative disorder also show retrograde amnesia and/or anterograde amnesia, although we cannot clarify any abnormalities in their brains using the neuroimaging techniques currently available. Patients with subcortical dementia, such as idiopathic normal pressure hydrocephalus, also show amnesia, but amnesia is milder in those patients than in patients with Alzheimer's disease (AD). In addition, recognition and cued recall are more preserved in patients with subcortical dementia than in those with AD. This finding is useful for discriminating patients with subcortical dementia and AD.

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  The psychopathological aspects of various behavioral disturbances commonly observed in people with dementia are discussed. Patients with Alzheimer's disease frequently keep up appearances under difficult conditions such as when they cannot answer the examiner's questions. This sort of behavior may be understood as coping skills of people with dementia who are unwilling for their disabilities to be exposed. Psychological aloneness and anxiety should play a major role in developing delusions of theft which are the most common type of delusions in dementia. Delusional misidentifications may be associated with denial of the unpleasant relationship between patients and their close relatives.
  To elucidate the pathogenesis of behavioral disturbances in dementia, and to offer appropriate therapeutic suggestions, we should approach the individual mind of people with dementia considering individual personality, biography, and the environments, in addition to neuropsychological evaluation.

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  As the frontal lobe is the largest association cortex in the brain, having fiber connections with all other cortical areas, frontal dysfunctions, especially prefrontal dysfunctions, are trans-modal in nature and would certainly be described as pattern of dysfunction. We have distinguished five patterns of frontal dysfunctions.
1. Difficulty of the change of category or set (perseveration of higher level)
2. Difficulty of the inhibition of stereotype
3. Difficulty of organizing information
4. Disturbance of fluency
5. Impaired verbal regulation on behavior
  Mild obsessive-compulsive disorder-like symptoms of a 61 year old male with a history of left prefrontal infarction are discussed neuropsychologically. These symptoms are thought to be closely related to the difficulty of the change of category and difficulty of organizing information.

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Imura (1943) described an unique aphasic syndrome shown by Japanese patients and designated it as Gogi (word-meaning) aphasia. Salient features are deficits in both recall and recognition of a nominal word with circumlocated repetitive phrases without any deficits in articulation or syntactic aspect of speech. It also shows selective impairments in processing kanji character words, besides kana or arithmetic processing are preserved. The core feature of this syndrome was introduced by Sasanuma & Monoi (1975) as a selective impairment of semantic processing of word meaning which is typically observed in processing kanji rather than kana. In 1992 Tanabe and his colleagues reported seven Gogi aphasic patients associated with lobar atrophy of the temporal lobes. The syndrome of progressive Gogi aphasia observed in those patients showed loss of semantic memory for words. This clinico-anatomical symptomatology is quite similar to the language symptom of semantic dementia. He also pointed out that it originated in descriptions of Pick's works on dementia. Progressive Gogi aphasia can screen with constant deficit patterns in nominal words assessed by word to picture naming and matching, loss of proverb completion and reading errors on idiomatic kun-reading kanji character words. Surface dyslexia is the most common error type of reading among English-speaking semantic dementia patients. We confirmed that surface dyslexia can also observed in Japanese patients with progressive Gogi aphasia by using controlled character-sound correspondence and frequency of kanji character words lists (Fushimi, et al.2009). Progressive Gogi aphasia is a key symptom to understanding semantic dementia.

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A case of slight but persistent articulatory disturbance similar to apraxia of speech caused by infarction of the left putamen and corona radiata is reported. Generally, apraxia of speech and anarthria result from left central gyrus lesions, but some cases have presented symptoms similar to apraxia of speech with left basal ganglia or deep white matter lesions. Therefore we compared symptomatical differences due to a left putaminal lesion with those of a left central gyrus lesion producing apraxia of speech or anarthria, based on previous studies and our case. Two findings were revealed. (1) The main symptom is dysprosody relative to articulatory disturbance if the lesion is confined to the left central gyrus, while the main persistent symptom is articulatory disturbance relative to dysprosody in cases due to deep subcortical lesions including the putamen. (2) No significant basic dissociation of spontaneous-tasked speech impairment could be found between the two lesions. If dissociation exists, spontaneous speech is more impaired than tasked speech such as reading and repetition induced by deep subcortical lesions. We discussed the mechanism of these two findings from neuro-physiological viewpoints including probable lesions and neural compensation pathways. Our study suggests that articulatory disturbance resulting from a lesion of the left central gyrus and that from a subcortical lesion is essentially the same symptom.

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  We described a patient who exhibited action disorganization syndrome(ADS)with callosal disconnection syndrome. We studied the mechanism and the region concerned with ADS. ADS's characteristic action errors are object substitution, sequential errors, omissions, quality errors and place substitutions. These errors appear in activities of daily living which involve many steps. The concepts of the target action are preserved in ADS patients, but the action schema in the contention scheduling system is incorrectly represented. For example, an action schema is omitted or an inappropriate schema is represented. Moreover, the function of the supervisory attention system gets out of order. As a result, the disordered action schema in CSS is accepted and output in the state prescribed, and action disorders are exhibited.
  An MRI scan of our patient revealed damages in the left superior, middle frontal gyri and genu of the corpus callosum. The records of other ADS patients showed they were all damaged in the lateral or bilateral superior, middle frontal gyri. One was damaged in the corpus callosum as well. Due to the damage to the wide frontal lobe area which contains commissural fibers connected to the bilateral frontal lobes, especially the superior, middle frontal gyri, neural information is not integrated. Disorders of attention and inhibition are thought to relate to this disorder.

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  An ambidextrous female patient with callosal infarction showed agraphia that exhibited different features in the left and right hands. Several reports of previous cases of unilateral left agraphia following callosal damage in a right-handed patient have been described. In this case, agraphia was peculiar as it was observed in both hands. The agraphia of her left hand was characterized mainly by paragraphia including mirror paragraphia, while her right-handed writing showed prominent scrawl and distortion of characters.
  Two days after her stroke, a brain MRI revealed an abnormal signal intensity area in the left cingulate gyrus and the corpus callosum except for part of the splenium. Because left unilateral tactile anomia and right constructional disorder was observed in the patient, we hypothesize that in this case language function is predominantly lateralized in the left hemisphere, and that constructional ability of letter shaping is predominantly lateralized in the right hemisphere. The paragraphia including mirror paragraphia observed in the left hand suggests that incomplete character information and motor engram for writing also exist in the right hemisphere. The agraphia of her right hand can be interpreted as the effect of disconnecting the motor information for writing of characters and the constructional ability of letter shaping in the right hemisphere using the information in the left hemisphere. Furthermore, we suspect that the motor engram for writing of characters is stored more strongly in the right hemisphere. The interhemispheric transfer and integration of information between the right and left hemispheres was incomplete probably due to a callosal disconnection, resulting in the agraphia that affected both hands. This report discusses the apparent mechanisms of her agraphia and the hemispheric lateralization of her writing function.

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  Patients with Alzheimer's disease (AD) often produce false recall or intrusion errors in memory tests. We conducted two experiments to investigate three types of responses (correct recall, false recall, and non-recall) in 59 AD patients who participated in verbal paired association tasks (PAL), and whether the presence of false recall was related to memory (experiment one) or other neurocognitive functions such as attention and executive control (experiment two).
  The Spearman's correlation analysis was conducted in the first experiment, and it was found that false recall produced in PAL tasks did not correlate with poor performance on memory test such as WMS-R and ADAS. In experiment two, we investigated the relationship between the tendency for false recall and both attention and executive functions. We selected the poor PAL learners, i. e. those whose correct recall rate was less than 75%, and divided them into three groups : false recall (FR) group who exhibited false recall in more than 75% of the responses ; non-recall (NR) group, who exhibited non-recall in more than 75% of the responses ; and mixed (MIX) group, in which both types of errors were present. Performance of three groups on attention and category fluency (CF) tasks was then compared. Results of the Jonckheere-Terpstra test indicated that the more the subjects' false recall increased, the worse their performance on the attention and CF tasks. From these results, we concluded that false recall in AD patients is related to inattention, ineffective use of semantic knowledge, and executive dysfunction.

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