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The purpose of this study is to clarify the relationship between hereditary predisposition and social-psychological factors in terms of drinking behavior of Japanese male students. The subjects were 123 male students who belonged to athletic clubs of K university in 1993. Regular drinking was evaluated as "drinking at home or with intimate friends" and party drinking as "drinking at club parties". On the two drinking occasions, the frequency and amount of drinking, and social drinking behavior were evaluated. Problem drinking behavior was investigated by a modified version of Aoyama's questionnaire (1984). Low Km aldehyde dehydrogenase (ALDH2) activity was evaluated by the facial flushing response to alcohol and the ethanol patch test. Evaluable results of the ethanol test as well as replies of the questionnaire were obtained from 109 students. Twenty-three students positive for both the facial flushing response to alcohol and the ethanol patch test were considered to be flushers, and 42 negative for both to be non-flushers. The non-flushers consumed a higher amount of alcohol than the flushers did on drinking occasions at home or with intimate friends. The number of problem drinking behavior items in the non-flushers was significantly higher than that in the flushers and increased with the amount and frequency of drinking. The ratio of students who had inappropriate drinking motivations, began to drink by themselves, or continued to offer alcohol to drinkers showing flushing even when they declined it, was significantly higher in the non-flushers than in the flushers. In addition, non-flushers showing such social drinking behavior drank more than those not showing such behavior. The frequency of positive or inappropriate drinking behavior was significantly lower in the flushers than in the non-flushers. However, the amount and frequency of drinking and problem drinking behavior were similar in the flushers and non-flushers. These results indicate that social drinking behavior of non-flushers influences not only themselves but also other drinkers, and that drinking of flushers is strongly influenced by social factors.

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Over 60% of men and women with terminal illness wish for providing hospice care at home. The goal of hospice is to enhance the quality of life through relief of physical, emotional, social and spiritual pain. Hospice must be accepted by patients and family when their illness is without cure and hospice medicine is palliative. Providing patients with truthful information about their illness is essential for patients to control in determining how best to spend the remaining lives. Above described conditions allow patients choice, "informed choice". However as for Japanese concern, it is not yet sufficient enough about providing the patients and family what hospice medicine means with truthful information about illness. Therefore, the urgent needs enforce us to ask the questionnaire to let them understanding what is hospice medicine about and providing the patient and family with maximum self-determination. The results indicated that the most of men and women are expecting to exercise self-determination rights (over 80%) with their appropriate information to choice the specialized program of hospice medicine.

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The purpose of this study was to assess possible correlations between paraplegia in flexion and dementia in elderly patients in our special nursing home and geriatric hospital. At the time of our study, 10.5% of all our patients were suffering from paraplegia in flexion, with the ratio increasing with advancing age. Disorders of the nervous system, and in particular disorders caused by cerebrovascular disease were found at a high rate of frequency among the paraplegia in flexion patients, in whom the incidence of dementia was 97.8%. In most cases, the degree of dementia was severe, the types and respective percentages being as follows: vascular type 37.8%, Alzheimer's type 24.4%, mixed type 22.2% and others 15.6%. Many of these patients demonstrated pseudobulbar palsy, frontal sign, Babinski's sign, and typical reflexes of spinal automatism. We think that paraplegia in flexion is probably caused by reflexes of spinal automatism and extensive cerebral lesions.

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Central conduction was studied in 12 patients with X-linked recessive bulbospinal neuronopathy (XBSN) using percutaneous electrical cortical, cervical and lumbar stimulation and somatosensory evoked potentials (SEPs). The central motor conduction time from the motor cortex to the cervical and lumbar segments of the spinal cord was normal in XBSN. SEPs, however, were abnormal or central sensory conduction time was prolonged in patients with XBSN. These results are consistent with the clinicopathological findings of XBSN in which the primary sensory neurons are involved as well as the lower motor neurons in the CNS, whereas the upper motor neurons are well preserved.

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The corticomotoneuronal pathway in the aged was studied using the technique of percutaneous electrical stimulation of the brain and the spinal cord. Central motor conduction time (CMCT) from the cerebral motor cortex to the cervical segment of the spinal cord (C-CMCT) was measured in 26 intact volunteers (20-85 years old) by substracting the latency to onset of EMG activity of the thenar muscle after cervical stimulation from the latency to onset of EMG activity of the same muscle after cortical stimulation. The latencies to onset of action potential of the anterior tibial muscle after cortical stimulation and the onset of action potential of the same muscle after lumbar stimulation were also measured in 11 volunteers (aged 46-67 years), and the difference between the two latencies was evaluated as the central motor conduction time from the cortex to the lumbar segment of the spinal cord (L-CMCT). Mean C-CMCT was 5.1 ms. and mean L-CMCT was 12.8 ms. Neither was related to the patient's height or age. There was no difference in either C-CMCT or L-CMCT between males and females. The results suggested that the conduction of the pyramidal tract is not affected by age, and this must be recognised when motor functions in the aged are studied.

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Spinocerebellar degeneration (SCD) is associated with other various degeneration of the nervous systems such as the optic tract, pyramidal pathway, extrapyramidal system, nuclei of the brain stem and autonomic nervous system as well as changes of heart. The clinical pattern, also have the great variability. We investigated the mode of progression of clinical symptoms and signs in 214 cases of SCD which were examined 2 times at intervals of about 10 years. 79 of 214 cases were reported to be died at the last examination. 135 alive cases included 3 with the Holmes type, 14 with late cortical cerebellar atrophy (LCCA) 10 with Menzel type, 18 with olive-ponto-cerebellar atrophy (OPCA), 33 with spinocerebellar form (SCF), 6 with Friedreich's ataxia, 18 with hereditary spastic paraparesis (HSP) and 33 with the other type. 79 dead cases included 0 with the Holmes type, 6 with LCCA, 5 with Menzel type, 32 with OPCA, 16 with SCF, 1 with Friedreich's ataxia, 4 with HSP and 15 with the other type. The disability of daily living in SCD revealed slower progression in the advanced stage than in the early stage. Every type of SCD had some different progression of disability each other. In the early stage, Friedreich's ataxia showed the highest progression of disability, but in the advanced stage, Holmes type and the OPCA did. Holmes type showed progression of ataxia without any remarkable change of other systems. LCCA showed increase of abnormality in the eye movements, pyramidal tract and autonomic nervous system in addition to the cerebellar system. OPCA involved multiple systems as ataxia worsening, but Menzel type had no remarkable changes of incidence in eye movement disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

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We observed changes in postganglionic efferent discharges of muscle sympathetic nerve (muscle sympathetic activity, MSA) microneurographically before and after the oral administration of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), a precursor of norepinephrine, in a patient with Shy-Drager syndrome and irregular fluctuations of blood pressure. Before drug administration, MSA was only rarely observed with the patient in the supine position. There was a slight increase in MSA during head-up tilting to 40 degrees, and orthostatic hypotension (OH) occurred just after the body was tilted head upward to 40 degrees. MSA became prominent 30 minutes after the oral administration of 200 mg of L-threo-DOPS while the patient was in a 40 degree head-up position, and the OH was improved. The MSA discharge rate decreased and OH reappeared 3 hours after oral administration, when the plasma concentration of norepinephrine was at its highest level. We suggest that the OH improved mainly because of the increase in MSA due to L-threo-DOPS, and that the drug may activate sympathetic outflow at a site proximal to the sympathetic ganglion.

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A 21-year-old woman in a family with a history of Fabry's disease showed orthostatic hypotension and whorl-like corneal opacity typical for Fabry's disease. Biochemical studies revealed that she was a heterozygote of the Fabry gene. A variety of autonomic function tests demonstrated both sympathetic and parasympathetic dysfunction. To our knowledge, the present case is the first report of a heterozygous female carrier of Fabry's disease presenting dysfunction of the autonomic nervous system.

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The distribution of neurotransmitter and neuromodulator receptors was studied in the brain of the rolling mouse Nagoya (RMN) and in controls, using in vitro receptor autoradiography. Quantitative autoradiography was used to map adenosine A1 (labeled with [3H]cyclohexyladenosine), GABAA [( 3H]muscimol), opiate [( 3H]naloxone), L-glutamate [( 3H]L-glutamate), benzodiazepine [( 3H]flunitrazepam), and muscarinic cholinergic [( 3H]quinuclidinyl benzilate) receptors. In the cerebellar cortex, GABAA and adenosine A1 binding sites were significantly reduced in the RMN, whereas other transmitter binding sites were not significantly altered. Adenosine A1 binding sites were also reduced in the cerebral cortex and caudate-putamen. Benzodiazepine binding was significantly decreased in the cerebral cortex and increased in the CA1 subfield of the hippocampus. These results suggest that neurochemical alterations in the caudate-putamen as well as in the cerebellar cortex play important roles in the ataxia and motor dysfunction of the RMN.

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We studied ocular movements in 130 patients with spinocerebellar degenerations. Patients had blurred vision (33.3%), diplopia (40.2%), oscillopsia (18.6%), ocular flutter (22.3%), rebound nystagmus (25.4%), square-wave jerks, (29.2%), macro square-wave jerks (6.2%), and macro saccadic oscillations (10.8%). Electro-oculographic abnormalities included reduction of saccadic velocity, dysmetria, and saccadic smooth pursuit. All the abnormal movements were improved by the injection of thyrotropin-releasing hormone.

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