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Biomedical subjects

H Naritomi

Publications and source records attributed to H Naritomi.

At least 37 records · Page 2Linked to original sources
PubMed1998

Presymptomatic brain lesions on MRI in a patient with intravascular malignant lymphomatosis.

A 58-year-old man with a intravascular malignant lymphomatosis initially developed myeloradiculopathy without cerebral symptoms. His MRI, however, demonstrated solid, wedge-shaped, and well-demarcated lesions in the deep white matter and a string-shaped lesion along with nerve fibers in the splenium of corpus callosum. A variety of cerebral symptoms manifested a month afterward. The possibility of this disease should be considered in cases of undiagnosed myeloradiculopathy with such silent brain lesions.

Brain↗
PubMed1997

Serial assessments of middle cerebral artery flow velocity with transcranial Doppler sonography in the recovery stage of eclampsia. A case report.

The pathophysiologic changes of eclampsia and/or hypertensive encephalopathy are unclear. Changes of middle cerebral artery flow velocity during the recovery stage in a case of eclampsia are reported. After the disappearance of signs and symptoms, the flow velocity began to increase, owing probably to delayed vasospasm, which was confirmed by magnetic resonance angiography. The vasospasm may be a consequence of eclampsia and may be of small significance in the pathogenesis.

Adult↗
PubMed1997

[A case of multiple cerebral arterial thrombosis due to congenital protein C deficiency].

We report a 49-year-old man who had right hemiparesis and motor aphasia. A computed tomography revealed hypodense areas in the left frontal subcortex. A cerebral angiography demonstrated occlusion of the left distal internal carotid artery and both anterior cerebral arteries, as well as stenosis of the left internal carotid artery at the cervical portion. The second angiogram obtained a month later showed no changes. The diagnosis of atherothrombotic cerebral infarction was established on the basis of clinical profile and angiographic findings. Protein C activity and antigen levels were reduced to approximately one half of the normal level in the patient and his brother. The patient had no other risk factors for stroke. Protein C deficiency has been considered one of the risk factors for thrombotic diseases. Venous thrombosis is the most common clinical manifestation, whereas arterial thrombosis is relatively rare. It is generally believed that arterial ischemic stroke associated with protein C deficiency occurs with embolic mechanism, and atherothrombotic infarction is extremely rare. This is the first report suggesting the possibility that protein C deficiency can cause cerebral thrombosis.

Cerebral Angiography↗
PubMed1996

Role of insulin resistance associated with compensatory hyperinsulinemia in ischemic stroke.

BACKGROUND AND PURPOSE: Although insulin resistance and hyperinsulinemia play a crucial role in the pathogenesis of atherosclerosis, little is known about their roles in ischemic stroke. The purpose of this study was to clarify whether insulin resistance and hyperinsulinemia are causative factors in the pathogenesis of ischemic stroke. METHODS: Thirty-four consecutive patients with ischemic stroke, who were normotensive, nondiabetic, and not obese, were classified into three groups--atherothrombotic infarction (n = 16), lacunar infarction (n = 10), and cardioembolic infarction (n = 8)--based on clinical findings, brain imaging, and cerebral angiography. Both oral glucose tolerance tests and lipid analyses were performed. Insulin sensitivity was determined by the steady state plasma glucose method with the use of octreotide acetate. Data were compared with those of healthy control subjects (n = 15). RESULTS: Steady state plasma glucose levels were significantly higher in the atherothrombotic infarction group compared with control subjects and the other two stroke groups, indicating the presence of insulin resistance in patients with atherothrombotic infarction. In the atherothrombotic infarction group, the 2-hour insulin area (area under the plasma insulin concentration curve) during a 75-g oral glucose tolerance test was significantly increased and dyslipidemic changes (increased triglyceride and apolipoprotein B, decreased high-density lipoprotein) were observed, whereas these changes were not found in the lacunar infarction and cardioembolic stroke groups. CONCLUSIONS: Insulin resistance in association with compensatory hyperinsulinemia and dyslipidemia may be an important pathogenetic factor underlying the development of atherothrombotic infarction.

Aged↗
PubMed1996

Enlargement of spontaneous intracerebral hemorrhage. Incidence and time course.

BACKGROUND AND PURPOSE: Standard radiographic criteria for hematoma enlargement have not been established. We undertook this investigation to assess the incidence and time course of hematoma growth using objective cutoff values. METHODS: We reviewed the clinical records of 204 patients with spontaneous intracerebral hemorrhage treated nonsurgically who underwent initial computed tomography (CT) within 48 hours and repeat CT within 120 hours of the onset of symptoms. The consensus of five observers reading the CT films was considered the "gold standard" for hematoma enlargement. The discriminant values of the difference (V2-V1) or the ratio (V2/V1) of the hematoma volume on the initial (V1) and second (V2) CT scans were determined by use of receiver operating characteristic curves. We chose the cutpoint that had the highest sensitivity and specificity for identifying hematoma expansion. RESULTS: The cutpoint for hematoma enlargement was determined as V2-V1 = 12.5 cm3 or V2/V1 = 1.4 (sensitivity = 94.4%, specificity = 95.8%). Forty-one patients (20%) had changes that exceeded these criteria. Frequency of hematoma expansion was greatest among those who underwent the initial CT scan early (27 [36%] of 74 patients at < or = 3 hours) and progressively declined as the time to initial scan was prolonged (7 [16%] of 45 patients at 3 to 6 hours; 5 [15%] of 33 patients at 6 to 12 hours; 2 [6%] of 34 patients at 12 to 24 hours; and 0 [0%] of 18 patients at 24 to 48 hours). CONCLUSIONS: The enlargement of hematoma was defined radiographically as the increase of its volume by > or = 12.5 cm3 or by > or = 1.4 times. Although expansion of intracerebral hemorrhage on CT scan was common in the hyperacute stage, 17% of hematoma expansion occurred even after 6 hours of onset. Enlargement after 24 hours of onset seems extremely rare. Early CT scanning appears to increase the rate of detection of enlarging hematomas.

Aged↗
PubMed1996

In vivo evaluation of antiplatelet agents in gerbil model of carotid artery thrombosis.

BACKGROUND AND PURPOSE: Antiplatelet agents are widely used for the prevention of ischemic stroke. However, their effects on thrombus formation have rarely been evaluated in experimental animals in vivo. We introduce methods for evaluating antithrombotic action in gerbils and the effects of several antiplatelet agents on thrombus formation. METHODS: In gerbils 8 to 10 weeks of age, we tightly compressed the unilateral common carotid artery for 2 minutes using the device prepared for this purpose to damage the endothelium. Thrombus formation in the damaged artery was observed directly through the microscope for 30 minutes. In six animals, the damaged artery was examined immediately after the experiments by electron microscopy. We studied the effects of antiplatelets by injecting the drugs intravenously 10 minutes before endothelial damage. RESULTS: In control studies, 70% to 90% of animals developed thrombi after arterial compression. The electron microscopic examination displayed endothelial damage in association with platelet thrombus at the damaged site. Administration of 2 mg/kg aspirin, 3 and 10 mg/kg ticlopidine, and 0.3 and 1.0 mg/kg ibudilast, a novel prostacyclin accelerator, decreased the frequency of thrombus formation significantly, whereas 20 mg/kg aspirin and 20 mg/kg dipyridamole failed to decrease thrombus formation. CONCLUSIONS: This model is considered useful for evaluating the antithrombotic effects of drugs because of its feasibility and high reproducibility. The present results support the view that a lower dose of aspirin may prevent cerebral vascular accidents as efficiently as a higher dose of aspirin.

Animals↗
PubMed1996

[A case of progressive continuous muscular rigidity and painless and rhythmic muscle spasm associated with autoantibody against glutamic acid decarboxylase].

We described a 60-year-old man with 5-year history of insulin dependent diabetes mellitus who developed continuous rigidity of truncal muscle and painless, rhythmic muscular spasm of trunk and proximal lower and upper extremities. The rigidity continued even in sleep. The painless muscle spasm was often precipitated by volitional movement and emotional stimuli. Intravenous administration of diazepam strongly attenuated the muscle spasm as well as truncal rigidity. Surface electromyography showed the continuous contraction of abdominal and paraspinal muscles. The rhythmic, clonic spasm of shoulder, triceps brachii, intercostal, abdominal, paraspinal and quadriceps femoris muscle induced by voluntary neck flexion was not compatible with typical stiff-man syndrome. Antibody against glutamic acid decarboxylase (GAD) was detected in the serum and cerebrospinal fluid of this patient. His condition was getting well with oral intake of sodium valproate. While painless, rhythmic spasm and persistent rigidity during sleep ruled out the patient from typical stiff-man syndrome, he was supposed to have the same pathophysiological mechanism as the anti-GAD autoantibody positive stiff-man syndrome.

Analgesia↗
PubMed1995

Ultrastructural localization and translocation of nitric oxide synthase in the endothelium of the human cerebral artery.

An electron microscopic immunocytochemical study was undertaken to clarify ultrastructural localization and translocation of nitric oxide synthase (NOS) in endothelial cells (EC) of the human cerebral and superficial temporal arteries (STA) employing antibody against endothelial NOS (EC-NOS). NOS immunoreactivity was found in all EC examined, in association with the plasma membrane and cytoplasmic organelles such as endoplasmic reticulum, Weibel-Palade body and subplasmalemmal vesicles, and in the cytoplasm devoid of organelles and extracellular regions, irrespective of arteries. The immunoreactivity in subplasmalemmal vesicles was, however, demonstrated only in human cerebral arteries. In the human STA exposed to bradykinin which induces EC-NOS phosphorylation, the gold particles significantly increased in the cytosol and decreased in the areas associated with cytoplasmic organelles; however, the number of particles did not change significantly in the plasma membrane. The results implicate that NOS may be translocated from the area associated with cytoplasmic organelles to cytosol following EC exposure to bradykinin.

Adult↗
PubMed1994

Induction of ischaemic tolerance in gerbil hippocampus by pretreatment with focal ischaemia.

We investigated the induction of ischaemic tolerance in the hippocampal CA1 neurones to transient forebrain ischaemia following pretreatment with unilateral middle cerebral artery occlusion (MCAO) in gerbils. Histological evaluation was carried out after 5 min bilateral carotid artery occlusion (5BCO) in the gerbils with no MCAO pretreatment, MCAO pretreatment 3 days prior to 5BCO (MCAO-3d-5BCO), MCAO pretreatment 7 days prior to 5BCO and sham MCAO pretreatment 3 days prior to 5BCO. CA1 neurones were preserved at > 40% of normal controls only in the left hippocampus in the MCAO-3d-5BCO gerbils. CA1 neurones in the right side of MCAO-3d-5BCO gerbils as well as in both sides of animals in the other pretreatment groups almost completely disappeared after 5BCO. While the exact mechanism remains to be resolved, pretreatment with focal ischaemia seems to induce ischaemic tolerance in neurones outside of the primary ischaemic lesion.

Adaptation, Physiological↗
PubMed1994

Glutamate release in the gerbil hippocampus after middle cerebral artery occlusion.

In a modified version of the unilateral middle cerebral artery occlusion (MCAO) model in gerbils, both sides of hippocampus are spared from direct ischaemic insult. Using this newly employed left MCAO model in gerbils, we investigated the concentrations of extracellular amino acids in the left hippocampus by microdialysis and histological changes in both sides of hippocampus one month after ischaemia. The concentrations of glutamate and aspartate were significantly increased by more than 3.5 times basal levels after MCAO. Glutamate maintained this peak level for 40 to 120 min after the onset of ischaemia. However, hippocampal neurones were well preserved one month after MCAO. While the exact mechanism of the survival of hippocampal neurones remains to be elucidated, we suggest it may be crucial that the hippocampus be protected from ischaemic insult.

Amino Acids↗
PubMed1994

MRI in subacute combined degeneration.

We describe a patient with clear lesions in the spinal cord on MRI due to subacute combined degeneration. T2-weighted images clearly showed abnormal high signals in the posterior columns, which disappeared on recovery from the disease.

Aged↗
PubMed1994

Musical auditory hallucinations caused by a brainstem lesion.

A man with left-sided deafness developed right-sided hearing loss after hypertensive hemorrhage at the right pontine tegmentum and began to experience ipsilateral musical hallucinations. Two weeks later, the right hearing returned, and the hallucinations disappeared. Auditory hallucinations due to brainstem lesions may be musical in nature and associated with hearing loss.

Brain Stem↗
PubMed1994

Effects of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1- benzopyran-6yl-hydrogen phosphate] potassium salt on cerebral energy state and consciousness recovery following transient forebrain ischemia in gerbils.

Effect of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H -1- benzopyran-6yl-hydrogen phosphate] potassium salt (EPC-K1, CAS 127061-56-7), a diester of alpha-tocopherol and ascorbic acid, on transient cerebral ischemia was studied in Mongolian gerbils. Cerebral energy metabolism and intracellular pH (pHi) were estimated employing in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Intraperitoneal injection of EPC-K1 (5 or 10 mg/kg) prior to ischemia significantly ameliorated pHi reduction in a dose dependent manner during ischemia. After reperfusion, energy and pHi recoveries were significantly faster in the EPC-K1 groups than in the control group. EPC-K1 (10 mg/kg) significantly reduced the extent of cerebral edema. Moreover, administration of EPC-K1 immediately after reperfusion significantly shortened the consciousness recovery in a dose dependent manner. The results suggest that EPC-K1 may exert protective effects on ischemic brain and may have therapeutic value in ischemic stroke.

Animals↗
PubMed1993

Sequential changes on 23Na MRI after cerebral infarction.

23Na MRI changes from the acute to chronic phase were investigated in seven patients with cerebral infarcts. They showed no signal increase during the first 13 h after the stroke and revealed a definite signal increase thereafter. This reached a maximum 45-82 h after stroke and became slightly less marked in the subacute and chronic phases, probably as a result of disappearance of cerebral oedema. In the early acute phase of stroke, 23Na MRI appears to fail to demonstrate Na+ increases in the ischaemic area, due presumably to the invisibility on MRI of intracellular 23Na in the intact brain. The increase more than 13 h after stroke, during which ischaemic cells are likely to die, is presumably because of increased visibility of intracellular 23Na in the dead cells. 23Na MRI is apparently insensitive to early ischaemic changes, but may be useful for assessing the cell viability in the ischaemic brain.

Aged↗
PubMed1993

Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.

BACKGROUND AND PURPOSE: Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated. METHODS: Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient. RESULTS: Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 5), and occlusive changes of the carotid artery (n = 3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the A1 segment contralateral to the infarction was hypoplastic. CONCLUSIONS: In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction.

Adult↗
PubMed1993

[In vivo autoradiographic benzodiazepine receptor imaging with 125I-iomazenil (Ro 16-0154)].

The biodistribution of 125I-Iomazenil (Ro 16-0154), a benzodiazepine receptor antagonist, was examined using in vivo autoradiography of gerbil brain. 125I-Iomazenil was administrated i.v. into male gerbils, and autoradiography was prepared from coronary sections of the animals decapitated at 5, 60, 120 and 180 min after injection. Initial uptake images (5 min) of 125I-Iomazenil were thought to show blood flow distribution. On the images obtained 120-180 min after administration, high activity of 125I-Iomazenil was observed in the cerebral cortex, amygdala, hippocampus, globus pallidus, thalamus, hypothalamus, superior colliculus, substantia nigra and cerebellar cortex in the areas of which benzodiazepine receptor concentration was reported to be high. However, low activity was observed in the caudate-putamen. Accumulation of 125I-Iomazenil was blocked by pre-administration of flumazenil. 123I-Ro 16-0154 has a high potentiality for benzodiazepine receptor mapping by SPECT.

Animals↗
PubMed1992

Sequential changes of sodium magnetic resonance images after cerebral hemorrhage.

Four patients with cerebral hemorrhage were examined serially from the acute to chronic phase by 1H magnetic resonance imaging (MRI), 23Na MRI and computed tomography (CT). At 1-2 days after bleeding, the 23Na image revealed no visible signal change in the area of hemorrhage, although CT and 1H images clearly demonstrated the existence of a hematoma in the thalamus or putamen. At 4-7 days after the hemorrhage, the 23Na images began to exhibit a small increase in signal intensity at the hematoma site, while at 2-3 weeks, a marked increase in 23Na signal intensity was observed. These findings suggest that the hematoma consisted mainly of a corpuscular component, with a low Na+ concentration, with little serum component. Lack of signal from the corpuscular component on the 23Na image was confirmed by an in vitro study. In the late acute phase, Na+ accumulation may occur in the corpuscular component due to failure of the Na+ pump. The intracellular 23Na appears to be totally visible to MRI, resulting in an increase in signal intensity. In the subacute or chronic phase, the corpuscular component may be destroyed, leaving fluid in its place. A high Na+ concentration in this fluid may give markedly increased 23Na signal intensity on MRI. 23Na MRI appears to provide important information for understanding the evolution of cerebral hemorrhage and for estimating the viability of cells, although its value for diagnosis may not be great.

Aged↗