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H Chigasaki

Publications and source records attributed to H Chigasaki.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Calvarial metastasis of cervical carcinoma showing the dural tail sign on magnetic resonance imaging].

A 42-year-old female was admitted to our department on 3 August, 1993 with a 3-month history of steadily enlarging subgaleal mass (3.2 x 3.0 cm) in the parietal region. She had been doing well following radiotherapy for cervical carcinoma of the uterus one year previously. Neurological examination on admission was negative. Axial T1-weighted MR images showed a low-intensity mass with marked homogeneous enhancement in the area of bone destruction, and a dural tail adjacent to the tumor (flare sign) after Gd-DTPA administration. The tumor was totally resected, and was pathologically diagnosed as a calvarial metastasis of the cervical carcinoma. However, 5 months later the tumor recurred anterior to the site of the resection. Since the dura mater adjacent to the tumor exhibited collagen fiber proliferation, the dural tail sign was appeared to represent a reaction to the tumor. Other calvarial metastatic lesions appeared adjacent to the initial lesion 5 months after the initial lesion was resected, however, suggesting that tumor cell nests were present in the dura mater which exhibited the dural tail sign. Extensive pathological examination of the dura mater appears necessary whenever a dural tail sign is detected by magnetic resonance imaging.

Adult↗
PubMed1995

Selective vulnerability of hippocampal CA3 neurons to hypoxia after mild concussion in the rat.

Immunohistochemical staining for microtubule-associated protein 2 (MAP2) and synaptophysin was used to investigate the effect of hypoxia on hippocampal neurons after mild concussion in the rat. Male Sprague-Dawley rats were divided into four groups: Group 1 (n = 3) was subjected to a mild impact-acceleration closed head injury, group 2 (n = 3) was subjected to 30 min of moderate hypoxia, group 3 (n = 5) was subjected to head trauma followed by 30 min of moderate hypoxia, and group 4 (n = 3) comprised sham-operated controls. All rats were fixed by transcardial perfusion 24 h after insult. No damage was observed in CA1 or CA2 neurons in any of the rats. However, rats in group 3 showed selective damage of hippocampal CA3 neurons manifested by a pycnosis and a marked decrease in MAP2 immunoreactivity. Presynaptic terminals visualized by synaptophysin immunostaining showed no differences among groups. The loss of immunoreactivity for the post-synaptic somal and dendritic protein marker MAP2 from the CA3 subfield 24 h after combined insults indicates an increased vulnerability of pyramidal cells in this brain area.

Animals↗
PubMed1994

Resolution of peritumoral brain edema following excision of meningioma.

We studied the resolution of peritumoral brain edema after meningioma excision. In twenty-nine patients with meningioma, the total volume of tumor and the peritumoral edema were measured planimetrically by serial CT scans and MRI with or without contrast enhancement. Four different patterns of postoperative resolution of hypodense volume on CT were observed: Group A: a large hypodensity rapidly decreased and disappeared, which may be related to the clearance of the real peritumoral edema in meningioma. Group B: a small hypodensity gradually disappeared. Group C: the hypodensity remained unchanged, which may result from the damaged brain tissue. Group D: the hypodensity progressively decreased but persisted, which may represent both the peritumoral edema and damaged brain tissue. We have calculated the resolution rate of edema fluid using the clearance curve of Groups A and D. The average resolution rate of edema fluid during the passage through 1 cm3 of the peritumoral white matter was 0.0493 ml/day. We speculate that 50% of edematous white matter, which presented as hypodensity on a CT scan, may be resolved in 4 days after total removal, and that 90% may be resolved in 14 days.

Blood-Brain Barrier↗
PubMed1994

Blood-brain barrier, cerebral blood flow, and cerebral plasma volume immediately after head injury in the rat.

The purpose of the present study was to determine blood-brain barrier (BBB) permeability, regional cerebral blood flow (rCBF) and regional cerebral plasma volume (rCPV) in the period immediately after head injury, and thereby to evaluate the effects of vascular factors in the pathophysiology of traumatic brain injury. Male Sprague-Dawley rats (350-450 g) anesthetized with 1.0-1.5% halothane were subjected to an impact acceleration closed head injury at the moderate level. BBB permeability (n = 5), rCBF (n = 8) and rCPV (n = 9) were measured by quantitative autoradiographic techniques using 14C-alpha-aminoisobutyric acid (AIB), 14C-iodoantipyrine and 14C-sucrose, respectively. Intravenous administration of each radiotracer was simultaneous with the traumatic impact. At 10 min after injury, BBB permeability, the transfer constant for AIB, was less than 0.1 ml/kg/min for all regions except for those with a relatively leaky BBB. At 30 s after injury, a significant and heterogeneous increase in rCBF was observed at 9 subcortical regions (p < 0.05). RCPV increased significantly in the frontal cortex, parietal cortex, thalamus, and hypothalamus (p < 0.05). In our closed head injury model without severe hypertension, BBB disruption did not occur immediately after trauma. Vascular responses in the period immediately after trauma may result from the derangement of cerebral autoregulation.

Animals↗
PubMed1994

Blood-brain barrier, cerebral blood flow, and brain edema in spontaneously hypertensive rats with chronic focal ischemia.

This study was conducted to explore the participation of blood-brain barrier (BBB) permeability and cerebral blood flow (CBF) on the development of ischemic brain edema in rats with chronic arterial hypertension. Young spontaneously hypertensive rats were used, and focal ischemia was produced by occluding the distal middle cerebral artery (MCA). On day 7 after MCA occlusion, BBB permeability and CBF were measured by autoradiographic methods using 14C-alpha-amino-isobutyric acid (AIB) and 14C-iodoantipyrine. BBB permeability (transfer constant for AIB) was significantly higher in the ischemic center and periphery. The CBF of the ischemic cortex showed a graded reduction from the ischemic center to the surrounding area. The ischemic brain regions showed significantly decreased specific gravity. We conclude that SHRSP may be more vulnerable to BBB disruption after ischemia.

Animals↗
PubMed1994

Calcium accumulation following middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats.

Delayed neuronal damage in the ischemic region of the rat brain following middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats was studied. The distribution of neuronal damage was determined by 45Ca autoradiography. Accumulation of 45Ca was observed in the corpus callosum and ipsilateral cerebral cortex immediately following MCA occlusion. After 3 days of occlusion, 45Ca had accumulated in the ipsilateral pyramidal tract, the ventral posterior nucleus of the thalamus, and the lateral portion of the striatum. Significant accumulation of 45Ca was observed in the same areas after 7 and 14 days of occlusion. Next the effect of MK-801 on accumulation of 45Ca after MCA occlusion was examined using the same technique. MK-801 (0.5-10 mg/kg i.v.) or saline was administered 15 min before MCA occlusion, and volumes of accumulation of 45Ca were calculated 1 week after ischemic insults. MK-801 significantly reduced 45Ca uptake in the cortex, striatum, and thalamus. Furthermore, there was a strong statistical correlation between the volume of accumulation of 45Ca in the cortex and that in the thalamus (r = 0.8974; p < 0.001; n = 25). We speculate that delayed neuronal damage in the corpus callosum, ipsilateral pyramidal tract, and thalamus may be caused by secondary neuronal degeneration. However, neuronal damage in the striatum, a segment not supplied by the MCA, may be related to excessive release of glutamate.

Animals↗
PubMed1994

Local cerebral blood flow and glucose metabolism in chronic focal ischaemia of stroke-prone spontaneously hypertensive rats.

The relationship between local cerebral blood flow (ICBF) and local cerebral glucose metabolism (ICGU) at the chronic stage of focal cerebral ischaemia was assessed in young stroke-prone spontaneously hypertensive rats (SHRSP) following occlusion of the distal middle cerebral artery (MCA). On day 7 following this occlusion, ICBF and ICGU were measured by autoradiographic methods using 14C-iodoantipyrine and 14C-2-deoxyglucose (2DG), respectively. The infarct was limited to the ipsilateral cerebral cortex. A narrow band of increased uptake of 14C-2DG was observed in the border zone at the periphery of infarcted areas. The ICBF in the ischaemic cortex revealed a graded reduction from the ischaemic centre to the surrounding tissues. A significant reduction in ICGU coupled to CBF was also observed in 4 of 13 selected noninfarcted regions ipsilateral to the MCA occlusion. The ischaemic regions had a significant increase in water content. The region with ischaemic oedema was limited to a narrow area compared with the findings regarding ICBF and ICGU. The SHRSP strain has more severe cerebral ischaemia, oedema formation, and metabolic derangement at the chronic stage of focal ischaemia, compared to normo-tensive animals.

Animals↗
PubMed1994

Giant intracranial aneurysm with rapid thrombus formation and intramural hemorrhage--case report.

A 50-year-old female presented with an unusual giant intracranial aneurysm that showed rapid, spontaneous thrombus formation and subsequent intramural hemorrhage. The thrombus appeared as a homogeneous area on magnetic resonance images, in contrast to the usual heterogeneous appearance. Two months after thrombus formation, the aneurysm had grown and developed intramural hemorrhage. The growth of giant intracranial aneurysms is related to neovascularization and recurrent intramural hemorrhage. The rapid formation of an intra-aneurysmal thrombus may stimulate neovascularization, resulting in intramural hemorrhage and aneurysmal growth.

Basilar Artery↗
PubMed1994

[Werner's syndrome associated with meningioma and a cerebrovascular disorder].

We present a case of Werner's syndrome associated with intracranial meningioma and a cerebrovascular disorder. A 49-year-old male was transferred to this hospital with a head injury as a result of a car accident, and a CT scan revealed a traumatic intracerebral hemorrhage. The patient displayed the characteristic clinical features of Werner's syndrome, including premature senility, juvenile cataract, atrophic skin, and a tendency to ward familial occurrence was present. MRI and cerebral angiography revealed multiple intracerebral hemorrhages, perhaps due to amyloid angiopathy, multiple lacunar infarctions and parasagittal meningioma. This is the first report on the MRI findings in the brain of a patient with Werner's syndrome. We suspect that of Werner's syndrome also shows evidence of premature aging on MR images.

Cerebral Angiography↗
PubMed1993

Successful treatment of increased intracranial pressure by barbiturate therapy in a patient with severe sinus thrombosis after failure of osmotic therapy. A case report.

A patient with sinus thrombosis and characteristic magnetic resonance imaging (MRI) findings, who was managed successfully by barbiturate therapy is reported. MRI showed massive high intensity lesions on T2-weighted image which indicated venous cerebral infarction and brain oedema. Intravenous infusion of thiopental decreased increased intracranial pressure (ICP). The effectiveness of barbiturate therapy is discussed in terms of the similarity between this case and experimental sinus thrombosis. Barbiturate therapy should be considered in cases of severe sinus thrombosis with elevated ICP.

Adult↗
PubMed1993

Local cerebral blood flow and glucose metabolism in hydrostatic brain edema.

This study investigated the effect of hydrostatic pressure gradient on the cerebrovascular dynamics and metabolism during the development of brain edema. Hydrostatic brain edema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, with craniectomy (Cr+ group) and without (Cr- group). Animals were sacrificed 0, 24, and 48 hours after hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow and local cerebral glucose utilization were measured by the quantitative autoradiographic method using [14C]iodoantipyrine and [14C]deoxyglucose, respectively. Hypertensive insult produced multifocal lesions stained by Evans blue. Brains from the Cr- group showed a transient increase in water content and no significant change in cerebrovascular dynamics and metabolism. Brains from the Cr+ group showed a pronounced increase in water content which persisted 48 hours later. Misery perfusion was also observed 24 hours after the insult and the cerebrovascular dynamics and metabolism were significantly decreased after 48 hours. These results indicate that an increased hydrostatic pressure gradient enhances tissue damage and causes reopening of the blood-brain barrier.

Animals↗
PubMed1992

The effect of hypoxia on brain edema--the promoting effect of superimposed hypercapnia or hypertension.

The effects of hypoxia and superimposed hypercapnia or hypertension during hypoxia on brain tissue water content, pH, and electric activity were studied in Sprague-Dawley and stroke-prone spontaneously hypertensive rats. Auditory brainstem responses and sensory evoked potentials were recorded during the experiment as the indices for cerebral oxygen metabolism. The brains were removed immediately, 1 day, and 2 days after hypoxic insult for gravimetric study. The brain water content increased in all groups on the 1st and 2nd days after hypoxia. The percentage change from the control water content increased only on the 1st day in hypoxic rats. In contrast, it increased on both the 1st and 2nd days after hypoxia in hypercapnic or hypertensive rats. The evoked potentials of hypoxic and hypercapnic-hypoxic rats showed that peak latencies were prolonged significantly during hypoxia and recovered 1 and 2 days after hypoxia. The brain tissue pH decreased during hypoxia and recovered after hypoxia. This study suggests that brain edema develops within 2 days of hypoxic insult and that superimposed hypercapnia or hypertension promotes the brain edema.

Animals↗
PubMed1992

[A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equina].

A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equina is reported here. The patient, a 76 year-old woman, who had fallen down by accident 1 month before, was admitted to our hospital presenting lumbar pain radiating into her right thigh, monoplegia of the right leg and urinary incontinence. Myelography and metrizamide CT demonstrated a filling defect mimicking intradural extramedullary tumor at the level of L1 and L2. Magnetic resonance imagings (MRI) revealed a subacute or chronic hematoma compressing the conus medullaris and the cauda equina. Operation was performed and an old hematoma, which occupied most of the spinal subarachnoid space and compressed the conus and cauda equina from right to left, was removed. No definite bleeding point was detected and no traumatic change was seen on the cord. Neither tumor nor abnormal vessel was detected. After surgery, the symptoms improved partially. On a review of the literature, we found only 4 cases of traumatic spinal subarachnoid hematoma, all of which occupied the cervical or thoracic portion of the spine. Our case is the first report, except for the cases following lumbar spinal tap, of traumatic spinal subarachnoid hematoma causing compression of the cauda equina. Though usually blood in CSF diffuses immediately, a clot may be formed when a large amount of bleeding obstructs the spinal canal. In our case, furthermore, deformity and narrowing of the spinal canal had preceded for many years, following lumbar vertebral compressed fracture related with osteoporosis. This might have promoted the process of canal obstruction and clot formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Myelopathy due to thickened ligamenta flava and abnormal fibrous tissue of the cervicothoracic junction--case report.

A 49-year-old female with subacute myelopathic symptoms due to thickened cervicothoracic yellow ligament and abnormal epidural fibrous tissue is reported. Myelography showed a complete block at the Th3 level. Magnetic resonance imaging demonstrated an extra-axial mass lesion in the spinal canal at the cervicothoracic junction causing the spinal cord compression. Laminectomy with resection of the lesion resulted in good neurological recovery. Histological examination revealed a thickened ligamenta flava and abnormal epidural fibrous tissue without calcification foci.

Cervical Vertebrae↗
PubMed1990

Local cerebral blood flow and glucose metabolism in hydrostatic brain oedema.

Two hydrostatic factors such as acute hypertension and decompressive craniectomy were chosen and assessment was focused on how the hydrostatic pressure gradient altered the cerebrovascular dynamics and metabolism during the process of development of brain oedema. Hydrostatic oedema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, one with craniectomy (Cr+) and the other without craniectomy (Cr-). Animals were sacrificed immediately, 24 and 48 h after the hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow (rCBF) and glucose metabolism (1CGU) were measured by quantitative autoradiographic methods using 14C-iodoantipyrine and 14C-deoxyglucose, respectively. The hypertensive insult produced multifocal lesions stained by Evans blue. In the brains of the Cr- group, there was a transient increase in water content and no significant change of rCBF and 1CGU. In the Cr+ group, the increase in water content was pronounced and continued until 48 h later. In addition, misery perfusion was observed at 24 h after the insult and both rCBF and 1CGU were significantly decreased after 48 h. These results indicate that the increased hydrostatic pressure gradient enhances tissue damage and causes the reopening of blood-brain barrier.

Animals↗
PubMed1990

Post-ischaemic treatment with the prostacycline analogue TTC-909 reduces ischaemic brain injury.

The effects of stable PGI analogue TTC-909 on CBF and glucose metabolism was studied in the chronic stage of cerebral ischaemia produced by occluding the distal MCA in SHRSP. Administration of TTC-909 (100 ng/kg/day during 7 days) prevented the development of ischaemic oedema and improved secondary metabolic derangement coupled to flow in postischaemic tissues, particularly in the ischaemic rim.

Animals↗
PubMed1990

Effects of naloxone on prolactin-secreting pituitary adenomas.

The investigators assessed the effects of the opioid antagonist naloxone on anterior pituitary hormone release in hyperprolactinemic females with pituitary microadenoma (n = 6) and macroadenoma (n = 7). In those with microadenoma, intravenous bolus injection of naloxone significantly increased serum luteinizing hormone (LH) concentrations but had no significant effect on serum prolactin (PRL), follicle-stimulating hormone, and thyroid-stimulating hormone concentrations. In patients with macroadenoma, naloxone significantly decreased serum LH and serum PRL concentrations. The response of LH to naloxone differed considerably between the two groups of patients. The results suggest that LH and PRL secretion is influenced by changes in endogenous opiates and in gonadotropin-releasing hormone and PRL inhibitory factor due to hypothalamic dysfunction.

Adenoma↗