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Biomedical subjects

H Fukuyama

Publications and source records attributed to H Fukuyama.

At least 163 records · Page 9Linked to original sources
PubMed1994

Dissociation between contingent negative variation and Bereitschaftspotential in a patient with cerebellar efferent lesion.

Contingent negative variation (CNV) and Bereitschaftspotential (BP) were from the scalp in a patient with a discrete infarct in the mesial tegmentum of the midbrain involving the decussation of the superior cerebellar peduncle. Bereitschaftspotential in association with hand movements was completely absent while CNV was normally present at the frontocentral midline. This indicates that CNV is, as opposed to BP, generated without cerebro-cerebellar interactivation, suggesting different generating mechanisms.

Cerebellar Diseases↗
PubMed1994

Olivopontocerebellar atrophy studied by positron emission tomography and magnetic resonance imaging.

We examined 9 patients with olivopontocerebellar atrophy (OPCA) using positron emission tomography and magnetic resonance imaging (MRI). Regional cerebral blood flow and oxygen metabolism were compared with the findings in 10 normal age-matched volunteers. The volumes of the basis pontis and the cerebellar hemispheres were quantitated by MRI to assess the relationship between morphological changes of the pons or cerebellum and the cerebellar circulation and metabolism. In the patients with OPCA, cerebellar hemispheric blood flow and oxygen metabolism were significantly lower than in the normal volunteers. Pontine volume showed a significant correlation with the cerebellar blood flow and the metabolic rate of oxygen. In contrast, the cerebellar hemispheric volume showed no correlation with either of these parameters. Our results suggest that the disruption of pontocerebellar pathway may contribute to the reduction of both blood flow and oxygen metabolism in the cerebellum of OPCA and that detection of cerebellar circulatory impairment without marked cerebellar atrophy by neuroimaging may be suggestive of OPCA.

Adult↗
PubMed1994

Impaired stereoacuity due to a lesion in the left pulvinar.

A right-handed patient with a haematoma in the left pulvinar showed impaired stereoacuity. In contrast with previous reports, he did not show peripheral visual extinction or prolonged reaction times for targets on the side contralateral to the lesion.

Cerebral Hemorrhage↗
PubMed1994

Crossed cerebellar hypoperfusion indicates the degree of uncoupling between blood flow and metabolism in major cerebral arterial occlusion.

BACKGROUND AND PURPOSE: In patients who have major cerebral arterial occlusive disease with low perfusion, a decrease in cerebral metabolism may be reflected by a reduction in contralateral cerebellar blood flow (crossed cerebellar hypoperfusion). This study was done to investigate whether comparison of the extent of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion could be used to estimate the degree of uncoupling of cerebral blood flow and metabolism on the basis of a single blood flow study. METHODS: We used positron emission tomography before and after reconstructive vascular surgery to evaluate regional blood flow and oxygen metabolism in the cerebral and cerebellar cortexes of 11 patients with major cerebral arterial occlusive disease. RESULTS: Preoperatively these patients had cortical blood flow asymmetry in the middle cerebral artery territory. The degree of crossed cerebellar hypoperfusion had no relation to the extent of cerebral blood flow asymmetry but was significantly correlated with the extent of asymmetry in cerebral oxygen metabolism. The preoperative extent of asymmetry in the cerebral oxygen extraction fraction and the postoperative improvement of asymmetry in cerebral blood flow were correlated with the preoperative difference between the severity of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion. CONCLUSIONS: The difference between the extent of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion can be used to estimate the degree of uncoupling between blood flow and metabolism, which can in turn predict the postoperative improvement of cerebral blood flow asymmetry. We suggest that this approach may be a simple means of estimating the relative uncoupling between blood flow and metabolism from a single blood flow study in patients who have major cerebral arterial occlusive disease with low perfusion.

Aged↗
PubMed1994

Callosal atrophy in patients with lacunar infarction and extensive leukoaraiosis. An indicator of cognitive impairment.

BACKGROUND AND PURPOSE: It is unclear why only some patients with lacunar infarction and radiological evidence of diffuse white matter abnormalities have dementia. The purpose of this study is to investigate the value of callosal atrophy as an indicator of cognitive impairment. METHODS: We used magnetic resonance imaging to evaluate 11 right-handed male patients with lacunar infarction and extensive white matter hypodensities on computed tomography (8 with dementia and 3 without dementia). The midsagittal corpus callosum area on T1-weighted images was compared with the IQ determined by the Wechsler Adult Intelligence Scale. The relation between these parameters and cerebral oxygen metabolism measured with positron emission tomography was also evaluated in the 8 patients with dementia. RESULTS: All patients showed diffuse high-intensity areas in the bilateral hemispheric white matter on T2-weighted images. Compared with 19 age- and sex-matched right-handed normal control subjects, the patients had a significantly smaller callosal area. The severity of callosal atrophy, which varied from mild to severe, was significantly related to the total IQ. In the 8 demented patients, the total callosal area was significantly correlated with the mean level of oxygen metabolism in the cerebral white matter. CONCLUSIONS: In patients with lacunar infarction and diffuse white matter abnormalities, the presence of callosal atrophy may indicate cognitive impairment. Callosal atrophy may reflect the severity and extent of white matter damage associated with a decrease in oxygen metabolism, which may determine the severity of intellectual decline.

Adult↗
PubMed1994

[Altered energy metabolism in Alzheimer's disease].

To evaluate the energy metabolic status of Alzheimer's disease, we examined the cerebral arteriovenous differences of glucose, oxygen, lactate, pyruvate, ketone bodies, and free fatty acids and N-isopropyl-p-(123I) iodoamphetamine (IMP) single-photon emission computed tomography in 5 patients with Alzheimer's disease (4 male and 1 female patients; mean age of 64.80 +/- 8.47 years). Compared with 5 age matched normal control subjects (4 males and 1 female; mean age of 63.20 +/- 10.76 years), the patients showed significantly decreased regional cerebral blood flow only in the parietotemporal region. The global cerebral glucose metabolic rate (CMRGlu) had significantly low value, whereas the global cerebral oxygen metabolic rate (CMRO2) was not changed. The metabolic ratio (CMRO2/CMRGlu) was significantly elevated to 9.73 in the patients with Alzheimer's disease, compared with 5.50 in the normal controls. The cerebral metabolic rates of ketone bodies and free fatty acids were unchanged. The cerebral pyruvate output was significantly decreased. The cerebral lactate output became negative, but the decrease did not reach statistical significance. We concluded that the markedly elevated metabolic ratio suggests an altered energy metabolism in Alzheimer's disease.

Aged↗
PubMed1994

Altered cerebral energy metabolism in Alzheimer's disease: a PET study.

UNLABELLED: In an effort to better understand the metabolic basis for the reported decreases in regional cerebral cortex glucose metabolism in patients with Alzheimer's disease, glucose utilization oxygen consumption and regional cerebral blood flow were examined. METHODS: Nine patients with Alzheimer's disease and nine age-matched normal controls were imaged using 18F-labeled deoxyglucose and 15O-labeled gases. RESULTS: Regional analysis of the cerebral metabolic rate of glucose (CMRglu), cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF) revealed that these values were significantly low in the frontal, parietal and temporal regions. The parietotemporal region had an abnormally high metabolic ratio (CMRO2/CMRglu), while the frontal, sensorimotor and occipital visual cortices had a metabolic ratio similar to that of the normal controls. CONCLUSIONS: These findings suggest that the abnormal parietotemporal metabolism in Alzheimer's disease involves a metabolic shift from glycolytic to oxidative metabolism. This impairment of glucose degradation may be the basis for synoptic dysfunction underlying the impairment observed in Alzheimer's disease.

Aged↗
PubMed1993

Callosal atrophy parallels decreased cortical oxygen metabolism and neuropsychological impairment in Alzheimer's disease.

OBJECTIVE: To evaluate the relationship of corpus callosum atrophy to cerebral cortical oxygen metabolism and cognitive function in patients with Alzheimer's disease. DESIGN: Prospective clinicoradiologic correlation with magnetic resonance imaging and positron emission tomography. SETTING: A university hospital. PATIENTS, PARTICIPANTS: Ten right-handed male patients with Alzheimer's disease, aged 46 to 70 years (mean +/- SD 57 +/- 6 years), and 14 age- and sex-matched right-handed control subjects. MAIN OUTCOME MEASURES: The midsagittal corpus callosum areas (on T1-weighted magnetic resonance images), cerebral metabolic rate of oxygen (measured with positron emission tomography using the oxygen-15 steady-state technique), and the IQs of the Wechsler Adult Intelligence Scale. RESULTS: Compared with control subjects, the patients had significantly decreased callosal areas with a posterior predominance of the degree of atrophy. The area of anterior and posterior halves of the corpus callosum had a significant correlation with the value of oxygen metabolism in the frontal and parietotemporo-occipital association cortices, respectively. The total area of the corpus callosum was significantly related to the total and verbal IQs of the Wechsler Adult Intelligence Scale. CONCLUSION: Atrophy of corpus callosum reflects the severity and pattern of cortical damage associated with hypometabolism and cognitive impairment in Alzheimer's disease.

Aged↗
PubMed1993

Lack of prolonged cerebral blood flow change after transcranial magnetic stimulation.

To study the physiological changes in the human brain induced by transcranial magnetic stimulation (TMS), we measured cerebral blood flow (CBF) before and after TMS in 3 healthy volunteers with positron emission tomography (PET). The intersecting point of the figure-of-eight coil was positioned at C3. TMS was delivered 20-32 times at maximum intensity. CBF measured at 50 sec after the termination of TMS showed no significant change in the cerebral cortex corresponding to C3 or any other area. This finding indicates that the hemodynamic change in the brain induced by TMS, if any, lasts only for a short period.

Adult↗
PubMed1993

Regional cerebral blood flow in catatonic schizophrenia.

Single photon emission computed tomography (SPECT) with 123I-iodoamphetamine (IMP) as tracer was used to study regional cerebral blood flow (rCBF) distribution in six patients with the catatonic subtype of schizophrenia (DSM-III-R). IMP-SPECT imaging revealed a significant reduction of rCBF in the parietal lobes of both hemispheres. Three-dimensional reconstruction of the SPECT images identified the superior region of the frontoparietal lobe as the most severely affected region. The pattern of rCBF deficits observed in catatonic schizophrenia differs markedly from that seen in 13 patients with other subtypes of schizophrenia and 7 normal control subjects. These observations indicate that parietal lobe dysfunction may be an important component in the pathology of the catatonic subtype of schizophrenia.

Adolescent↗
PubMed1993

Pharmacological effects of ibudilast on cerebral circulation: a PET study.

To evaluate the pharmacological effects of ibudilast on cerebral circulation, we examined 5 ischaemic stroke patients, using positron emission tomography, and we measured cerebral blood flow (CBF). Ibudilast loading per os led to a remarkable increase in CBF after 30 min. This CBF elevation was observed in the lesion side as well as in the nonlesion hemisphere. Therefore, we can confirm that ibudilast ameliorates the chronic low perfusion state of CBF in the ischaemic stroke patient.

Aged↗
PubMed1993

Functional brain imaging of a catatonic type of schizophrenia: PET and SPECT studies.

A brain imaging study was conducted in the case of a catatonic type of schizophrenia (DSM-IIIR) by applying (i) positron emission tomography (PET) and (ii) single photon emission computed tomography (SPECT). A PET study using [18F]-2-fluoro-2-deoxy-D-glucose revealed a lower glucose utilization in the dorsal frontal and parietal lobes of both cerebral hemispheres. Correlative SPECT studies using [123I]-iodoamphetamine showed a diminished regional cerebral blood flow in similar regions of the cerebral hemisphere. A three-dimensional volume rendering method of the SPECT images (TITAN) identified the dorsal region of the fronto-parietal lobe as the most severely affected region. These patterns of deficits implicated the role of the dorsal frontal and parietal lobes in the pathogenesis of catatonic syndromes.

Activities of Daily Living↗
PubMed1993

Callosal atrophy with reduced cortical oxygen metabolism in carotid artery disease.

BACKGROUND AND PURPOSE: In cerebrovascular disease, brain atrophy may be a reflection of ischemic changes. Minor changes that are not detectable as infarction on computed tomography may result in atrophy with metabolic depression. We evaluated the relation between size of the corpus callosum and cerebral cortical oxygen metabolism in carotid artery disease. METHODS: We used magnetic resonance imaging and positron emission tomography to evaluate 13 right-handed male patients with transient ischemic attacks or minor strokes and unilateral internal carotid artery occlusive disease, two with stenosis and 11 with occlusion. Computed tomography showed only minor subcortical abnormalities in the affected hemisphere. Midsagittal corpus callosum areas on T1-weighted magnetic resonance images, white matter lesions on T2-weighted images, and the cerebral metabolic rate of oxygen measured by the oxygen-15 steady-state technique were analyzed. RESULTS: Compared with 13 age- and sex-matched control subjects showing the same degree of white matter areas of high intensity, the patients had significantly decreased callosal areas. The degree of corpus callosum atrophy was significantly correlated with the mean cortical oxygen metabolic rate. The same tendency was also found in five patients without infarcts on computed tomography. However, neither the callosal area nor the hemispheric metabolic rate was correlated with the extent of white matter lesions. CONCLUSIONS: These findings indicate that atrophy of the corpus callosum occurs in association with a decrease in cortical oxygen metabolism. Corpus callosum atrophy may be a useful morphological index that reflects the cerebral cortical metabolic state in carotid artery occlusive disease.

Aged↗
PubMed1993

Hemodilution improves cerebral hemodynamics in internal carotid artery occlusion.

BACKGROUND AND PURPOSE: Hemodilution may be a useful form of therapy for patients with carotid occlusive disease and hemodynamic ischemia. Accordingly, we evaluated the effects of hemodilution on cerebral hemodynamics and oxygen metabolism in patients with carotid artery occlusion. METHODS: Using positron emission tomography, we analyzed regional cerebral blood flow, oxygen extraction fraction, oxygen metabolic rate, and blood volume before and after isovolemic hemodilution in five patients with unilateral internal carotid artery occlusion and minor stroke. Hemodilution was accomplished by phlebotomy of 400 mL and infusion of 400 mL of hydroxyethyl starch. RESULTS: Before hemodilution, the patients had a significant decrease in blood flow and oxygen transport along with significantly elevated oxygen extraction fraction in the cerebral hemisphere with carotid artery occlusion compared with six control subjects. After hemodilution, the hematocrit and arterial oxygen content decreased from 41.2% and 18.6 mL/dL to 36.3% and 16.5 mL/dL, respectively. Both cerebral blood flow and oxygen transport were increased and oxygen extraction fraction was decreased without any change in oxygen consumption. The degree of increase in blood flow and oxygen transport was positively correlated with the ratio of oxygen extraction fraction to blood volume before hemodilution. CONCLUSIONS: These findings indicate that hemodilution improves oxygen transport as well as blood flow in patients with internal carotid occlusion and decreased perfusion and that this improvement may be more prominent in patients with a severely compromised hemodynamic state. Thus, hemodilution may be useful in patients with hemodynamic ischemia.

Aged↗
PubMed1993

Response of post-ischemic myocardium to sympathetic stimulation--relation to local norepinephrine release.

Myocardial ischemia interrupts neurotransmission and causes the depression of norepinephrine release. However, the effects of sympathetic nerve stimulation on neurotransmission and norepinephrine release in post-ischemic myocardium are not well defined. We measured regional myocardial length and norepinephrine (NE) release during sympathetic nerve stimulation in anesthetized dogs. Dogs were divided into 2 groups: Group 1 (n = 14); sympathetic nerve stimulation, Group 2 (n = 9); pre-treatment with alpha-blockade yohimbine hydrochloride (0.2 mg/kg) followed by sympathetic nerve stimulation. The left anterior descending artery was occluded for 15 min. Sympathetic nerve stimulation was performed before coronary occlusion and after reperfusion. In group 1, the decrease in systolic shortening in the ischemic region persisted for more than 60 min. Although sympathetic nerve stimulation caused an increase in systolic shortening, it was lower than the pre-ischemic value. NE release from the post-ischemic myocardium remained decreased for 60 min. The decrease in the post-ischemic myocardial response to sympathetic nerve stimulation was associated with diminished NE release. When the cardiac sympathetic nerve was denervated with an epicardial phenol application, NE release decreased even further. In group 2, NE release did not decrease following reperfusion. These results suggest that sympathetic nerve conduction is not completely impaired in post-ischemic myocardium and that pre-synaptic alpha -2 receptors might play an important role in diminished NE release.

Animals↗