Regeneration of synapses and restore of higher brain functions in CNS are reviewed including at molecular and cellular level. Two processes seems to be necessary to recover original functions after degeneration of CNS ; one is resynaptogenesis to make new neuronal networks which make it possible to get functional recovery ; another is, of course, learning by repetitive stimulation to repair original functions. The former process also may need long time and developments of new drugs which shorten this process are expected to facilitate rehabilitation of CNS.

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    An assessment of long-term recovery capacity was undertaken for 90 right-handed aphasics who have all suffered this condition for longer than two years and six months.
    The study was based on results on the Standard Language Test for Aphasia (SLTA).
    The study in aphasics with lesions present almost entirely throughout the middle cerebral artery (MCA) revealed these results as follows. The significant spread in SLTA results depended on the age of onset for all language modalities. Specifically, recovery tended to be notably better in these aphasics with an age of onset under 40 years compared against those with an age of onset of 40 years and olders. In the younger group, recovery typically started with renewed word comprehension since early periods from onset, followed by gradual improvement in comprehension of short sentences word recall, and processing of Kana letters. Severe disturbances generally remained, however, in terms of sentence repetition, and comprehension of complex sentences. In the aphasics suffered from lesions MCA territory with a later age of onset, serious difficulties persisted in all language modalities, with recovery especially tenuous in the area of Kana processing.
    Otherwise, aphasics sufferd from word deafness and apraxia of speech showed poor improvement in these disturbances.
    From these findings, it can be concluded that age of onset affects aphasic's ability to recover language functions, and that redundancy of functional recovery varies accoding to specific language modalities.

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    Patients with left unilateral spatial neglect were examined twice or more in the chronic stage to investigate recovery and compensation of neglect. They often recovered the ability to search leftward in the exploratory tasks such as the line cancellation test. Neglect for a single object, however, tended to persist even in the stage of recovery, as the patients continued to show rightward attentional bias. In the line bisection test, leftward searches were usually absent or insufficient. Bisection for individual lines was inaccurate, although mean rightward errors were decreased. Neglect also became obvious when the number of visual stimuli was increased. Appearance of awareness for neglect errors was an important recovery, even if such awareness was incomplete. Although normal visuospatial process was hardly regained, compensation for neglect became possible when some awareness for their errors appeared. Compensation based on verbally coded knowledge occurred before acquisition of awareness for neglect errors. Improvement of neglect seems to result from recovery and compensation, both of which may occur even in the late chronic stage of illness. As for neglect patients, rehabilitation for six months or more may contribute to improvement of neglect and adaptation to activity of daily living.

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    Recently, prosopagnosia, inability to recognize visually familiar faces, has been discussed on its heterogeneity based upon some differences in clinical symptoms, mechanisms, and lesions among reported cases. De Renzi et al (1991), Damasio et al (1990), and Benton and Tranel (1993) classified prosopagnosia into apperceptive, associative, and amnesic-associative types. The course of prosopagnosia should be considered to be related closely to these differences.
    We presented three prosopagnosia patients. The case I showed associative prosopagnosia following bilateral occipito-temporal infarctions. The two other cases showed apperceptive prosopagnosia. Prosopagnosia in the case II was caused by bilateral occipital hemorrhagic infarctions, and the case III had prosopagnosia due to infarction confined to the territory of the right posterior cerebral artery.
    We investigated the course of prosopagnosia in our patients and cases reported in the literature.
    The data suggested as follows :
    1 ) Prosopagnosia associated with bilateral damage of inferior mesial occipito-temporal regions supplied by the PCA is generally severe and persistent.
    2 ) Unilateral damage confined to the right hemisphere also may produce prosopagnosia. In cases with lasting prosopagnosia after unilateral damage it was found that the lesion was extended mesially in the right inferior mesial occipital region (area 18 and 19) and invaded inferior longitudinal fasciculus and the splenium of the corpus callosum. Alternatively, prosopagnosia resulted from the smaller lesion of the above regions, e. g. the damage located more laterally in inferior component of area 18 and 19, should be mild and recover within a year.

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Neural processes involving recovery from pure alexia were considered on the basis of findings from three cases of our own with pure alexia. Case 1 presented pure alexia following left PCA occlusion which evolved to Kana-specific alexia with very good recovery in Kanji. Case 2 presented pure alexia following right PCA occlusion which evolved to Kanji-specific alexia with very good recovery in Kana. Case 3, though having presented pure alexia shortly after the onset, seemed non-alexic in daily life after eight years. These cases were examined on reading in their chronicities. Case 1, while showing marked word-length effect on latencies in reading aloud Kana, presented no effect of stroke-numbers in reading aloud Kanji. His performance in semantic decision for Kanji was excellent. Case 2 showed mild word-length effect in Kana and remarkable stroke-number effect in reading Kanji. In Case 3, who seemed "recovered" from pure alexia, latencies were tangibly longer than non-alexic control subjects in reading both Kana and Kanji. These findings suggest there should be two distinctive processes for recovery from pure alexia in the Japanese ; 1) compensatory kinesthetic route mediated by motor imagery for letters (kinesthetic reading), which might be more effective for Kana, and 2) another compensatory route mediated by semantics, which would probably be more effective for Kanji. Recovery from pure alexia seems not qualitative but quantitative, in that even if the compensatory strategies would decrease the quantity of reading inability, tangible abnormalities would remain to be revealed under detailed scrutinies.

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    A 30 year follow-up study of 24 cases of acute carbonmonoxide poisoning due to mining accidents which were caused by explosions at two coal mines (Miike and Yamano mines) are herein described.
    The paitients conditions ranged from relatively moderate to severe among these victims. The duration of conscious disturbance in the acute stage showed a significant correlation to the degree of aphasia, apraxia and agnosia at 4 months after the accident. The average age at the time of the explosions was about thirty-six years of age. Most cases tended to show an improvement in the degree of aphasia, apraxia and agnosia from 10 to 20 year after the accident.
    The symptoms of many cases, however, worsened over the next decade probably due to normal aging.
    At 30 years after the accidents, the average of age of the patients had become 66 years of age.
    The degree of exacerbation, however, did not differ substantially from the degree of aphasia, apraxia and agnosia observed four months after the accident.
    In some cases an exacerbation of symptoms was observed to be worse than the degree seen four month after the accident, however, such cases may have also demonstrated complications from CVD association with hypertension and or senile dementia. There was greater improvement in the degree of the higher cortical functions in the later stage than the degree of the lower cortical functions. The symptoms which patients could monitor and evaluate by themselves through such feed back mechanisms in daily life as taking meal tended to improve. Such symptoms included visual inattention, visual disorientaion, ideational apraxia, and agraphia without alexia.
    However some symptoms which the patients could not accurately judge by themselves regarding daily life activities demonstrated either an exacerbation or no improvement. Such symptoms included ideomotor apraxia, drawing impairment and agraphia with agnosia.
    Based on the above findings the victims of these two mining accidents will continue to require long-term rehabilitation.

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    We studied long-term recovery process of memory disturbance in 11 patients with severe or moderate head injury. Their cognitive functions were assessed for more than one year after head injury. They were tested by forward digit span, digit learning, five words memory and recall of five words after five minutes. Their lesions were localized by CT and/or MRI. Seven cases complaining of memory disturbance obtained zero score for the recall of five words after five minutes. Their lesions were included 3 left temporal lobe and 4 diffuse extended lesions. Four cases who did not complain of memory disturbance obtained normal score for the same test. Verbal memory disturbance related to the left temporal lobe. We found the recovery of verbal memory disturbance in patients with posterior or lateral left temporal lobe cortex lesion, and no recovery in anterior or mesial left temporal lobe lesions extending from cortex to subcortex.

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    The course and symptoms in 11 years of a patient with left prefrontal infarction are described. Early symptoms or complaints are thought to be a manifestations of the disorder of working memory. However, recent symptoms or complaints are not interpretable as the disorder of working memory, but may closely relate to a frontal symptom “adhesion to a single standard or set” including the difficulty of the change of set and the difficulty of the organization of multiple information.

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    A study was made on reading and writing disturbances in two cases which showed typical Wernicke aphasia due to lesion in the Wernicke's area (left-posterior superior temporal gyrus). Examinations of reading-aloud and dictation were carried out concerning single Kanji characters which are supposed to be learned in 1 st to 3 rd grades at primary school, multiple Kana letters corresponding to single Kanji, and single Kana. The results showed better reading-aloud than dictation for both Kanji and Kana examinations in each of the two cases. Many errors were observed as phonemes of erroneous characters or letters similar to those of the subject character or letter (correct character or letter) in both the reading-aloud and dictation examinations of Kanji and Kana. Results suggest that “selection disturbances of phonemes” and “hearing-sense processing disturbances of phonemes,” which are characteristics of spoken language seen in Wernicke aphasia, are also seen in the written language. In the dictation of single Kana, both cases showed a similar tendency, and responses were observed in many cases where the correct letter was written but with addition of extra letters (additional response). The additional response in dictation is considered to be influence of “fluent talkative tendency,” a characteristic of spoken language seen in Wernicke aphasia.

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