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Biomedical subjects

T Mimaki

Publications and source records attributed to T Mimaki.

At least 73 records · Page 4Linked to original sources
PubMed1983

Cerebral blood flow measured by Doppler flow meter during petit mal seizure.

We measured the cerebral blood flow velocity percutaneously using the Doppler ultrasound method while concurrently recording the EEG during seizures in two patients with petit mal epilepsy. The average maximal blood flow velocity (A/L) and end-diastolic blood flow velocity (d) of the internal carotid artery were measured. Somewhat increased A/L and d values were found at the onset of 3 Hz spike and wave bursts on EEG in one case. However, no increase or even reductions in A/L and d values were found during spontaneous petit mal seizures compared with interictal ones in the other case. These results are opposite to the previous other report.

Cerebrovascular Circulation↗
PubMed1983

Internal carotid velocity measurements in children with cerebrovascular disease.

Internal carotid artery flow velocity was evaluated by the Doppler ultrasound method in 32 children with cerebrovascular disease. The average maximal blood velocity (A/L) and end-diastolic blood velocity (d) were compared with each other as indices of blood flow velocity. The right and left mean A/L and d of moyamoya disease were significantly lower than those observed in normal children. The A/L and d of the affected side both in internal carotid artery occlusion and in middle cerebral artery occlusion were also significantly low. In the subarachnoid hemorrhage after rupture, these values were significantly low. In basilar artery occlusion, these values were similar to those in normal children. The results of this study indicate that Doppler ultrasound assessment of internal carotid flow velocity provides noninvasive reliable information for the diagnosis of cerebrovascular disease in childhood.

Basilar Artery↗
PubMed1983

Bilateral intracranial granulomas as a complication of infected subdural peritoneal shunt.

Intracranial granuloma in childhood is considered to be a very rare disorder. A three-year-old child is described who had bilateral intracranial granulomas originating from the ends of bilateral subdural-peritoneal shunts. Serial computerized tomographic examinations revealed variable and peculiar findings. Since subdural-peritoneal shunt is used in neonate, intracranial granuloma must be considered as a potential complication of unremoved subdural-peritoneal shunt.

Brain Diseases↗
PubMed1982

[3H]CL 218,872, a novel triazolopyridazine which labels the benzodiazepine receptors in rat brain.

We examined the specific binding of [3H]CL 218,872, a novel triazolopyridazine to benzodiazepine receptors in the rat cerebral cortex. Two binding sites with KD values of about 10-30 nM and 200-600 nM were demonstrated. A number of benzodiazepine anxiolytics inhibited [3H]CL 218,872 binding in a manner which correlates with the potency of these drugs for inhibiting [3H]benzodiazepine binding. Our initial studies show that [3H]CL 218,872 can label the benzodiazepine receptors and may prove to be a useful probe for studying benzodiazepine heterogeneity and regulation.

Animals↗
PubMed1982

Cerebral blood flow changes in orthostatic dysregulation fainters.

The changes in blood flow of both the internal carotid and the vertebral artery during orthostatic test with or without fainting attack were studied in 25 healthy children and 30 patients with orthostatic dysregulation (OD). In healthy children and non-fainted OD patients, no change in blood flow occurred in either the internal carotid artery or the vertebral artery during orthostatic test. On the other hand, a significant decrease in blood flow of the internal carotid artery and/or the vertebral artery occurred during fainting of OD patients. These data suggest that three mechanisms might be involved in fainting of OD patients; a decrease in blood flow of the internal carotid artery, the vertebral artery and a decrease in blood flow of both these arteries.

Adolescent↗
PubMed1982

Internal carotid blood flow velocity in children with cerebral palsy by Doppler Ultrasound method.

Cerebral blood flow assessed noninvasively by Doppler ultrasound technique in 30 children with cerebral palsy. The average maximal blood velocity (A/L) and end-diastolic blood velocity (d) of internal carotid artery were measured before and during brief digital compression of contralateral common carotid artery. Both A/L and d values in children with cerebral palsy were significantly lower than those observed in normal healthy children. In 13 children with spastic hemiplegia, no significant difference in either A/L or d was seen between the non-affected side and affected side both before and during brief digital compression. This data suggests that mean cerebral blood flow decreases in our children with cerebral palsy, and that no lateralization of the decrease in hemispheric cerebral circulation in hemiplegic children may explain by supposing the existence of generalized bilateral brain damage in those subjects.

Adolescent↗
PubMed1982

Antiepileptic effects of clobazam in children.

Many benzodiazepines used as anticonvulsants have nitrogen radicals in positions 1 and 4. Clobazam has nitrogen radicals in positions 1 and 5. We studied the antiepileptic effect of clobazam in 36 patients with intractable epilepsies in childhood. Their ages were 1 year 1 month to 16 years 5 months (mean 8 years). The mean initial dose was 0.33 mg/kg of daily doses and increased up to 0.71 mg/kg. Nine cases (primary generalized epilepsy 2/2, secondary generalized epilepsy 7/29) were completely free from seizures, and another 9 (secondary generalized epilepsy 8/29, partial epilepsy 1/5) experienced a decrease of 50% or more in seizure frequency. Seizure frequency did not change in 16, and increased in the other 2 (secondary generalized epilepsy 2/29). The antiepileptic effects were observed on the first day to 10th day after clobazam treatment. There were recurrences of seizures in 4 out of 9 patients with complete control of seizures, 1 month alter in 3 and 10 months later in one. Mean serum clobazam level of 7 improved cases was 73 ng/ml and that of 3 cases with no response was 94 ng/ml. Although mild clinical side effects such as drowsiness were observed transiently in 17 cases, no abnormality was found in laboratory investigations performed.

Adolescent↗
PubMed1981

Neuronal localization of benzodiazepine receptors in the murine cerebellum.

Selective genetic and chemical lesions which affect specific neuronal populations in the cerebellum were studied for changes in benzodiazepine receptors. Destruction of cerebellar climbing fibers with 3-acetylpyridine, did not affect cerebellar benzodiazepine receptors. Destruction of Purkinje, basket and stellate cells with intracerebellar kainic acid, caused moderate decreases in benzodiazepine receptor density. Destruction of Purkinje cells with chronic high doses of phenytoin also caused a significant decrease in benzodiazepine receptor density. In "weaver" mice, which have a severe loss of granule cells, benzodiazepine receptor density was unchanged, while the absolute number of benzodiazepine receptors decreased by 57%. In "staggerer" mice which have diminished Purkinje cells dendritic thickenings at their synapses with parallel fibers and subsequent granule cell loss, there was a 45% decrease in benzodiazepine receptor density and a 90% decrease in the absolute number of benzodiazepine receptors. These results suggest that benzodiazepine receptors exist on cerebellar Purkinje cells, that they probably also occur on cerebellar granule cells, and that they do not appear to be present on cerebellar glial cells or on climbing fibers.

Animals↗
PubMed1980

Decreased benzodiazepine receptor density in rat cerebellum following neurotoxic doses of phenytoin.

The effect of acute and chronic administration of phenytoin on [3H]flunitrazepam binding was examined in the rat cerebellum. There was no significant effect of phenytoin on [3H]flunitrazepam binding in the rat cerebellum 1 and 6 h after a single i.p. injection of 200 mg/kg of phenytoin. However, after 14 days and 28 days of chronic phenytoin administration, significant decreases in [3H]flunitrazepam receptor density were observed, with no changes in apparent affinity constants in the rat cerebellum. This effect of phenytoin was dose-dependent, as lower doses of phenytoin (100 mg/kg/day) for 14 or 28 days produced no alterations in [3H]flunitrazepam binding the the rat cerebellum. Light-microscopic examination of the rat cerebellum treated with 200 mg/kg/day of phenytoin for 14 days showed degeneration of the Purkinje cells, with edematous Bergmann astrocytes. These data provide evidence for the neuronal localization of benzodiazepine receptors on cerebellar Purkinje cells.

Animals↗
PubMed1980

Anticonvulsant therapy and vitamin D metabolism: evidence for different mechanisms for phenytoin and phenobarbital.

Combined therapy of epileptic children with phenobarbital (PB) and phenytoin (DPH) significantly decreased serum 25-hydroxyvitamin D (25-OH-D) levels, whereas PB alone significantly increased serum 25-OH-D levels after one to two months of therapy [Sumi et al, 1978]. Studies were conducted in rats to test the hypothesis suggested by the human studies that DPH and PB had different effects on Vitamin D metabolism. Male Wistar rats treated for five days with PB (75 mg/kg/day) had significantly (P less than 0.05) decreased 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels (7.1 +/- 1.6 ng/dl, mean +/- SD) compared to controls (12.0 +/- 4.0 ng/dl) and significantly (P less than 0.005) increased conversion of [3H]-vitamin D into [3H]-25-OH-D and [3H]-24,25-(OH)2D, but no increased conversion into [3H]-25-(OH)2D. Age- and weight-matched rats treated for five days with DPH (75 mg/kg/day), however, had significantly (P less than 0.03) decreased 25-OH-D levels (41.9 +/- 5.7 ng/ml) compared to controls (52.4 +/- 4.4 ng/ml) and significantly (P less than 0.01) increased conversion into [3H]-1,25-(OH)2D. These results are consistent with clinical data, which suggest that different alterations in vitamin D metabolism occur after short-term DPH versus PB therapy.

25-Hydroxyvitamin D 2↗
PubMed1978

Effect of anticonvulsant therapy on serum 25-hydroxyvitamin D level.

Serum 25-hydroxyvitamin D levels in young patients receiving anticonvulsants were assayed. They had neither retardation of physical and psychomotor development nor malnutrition. The patients treated with phenobarbital alone revealed rather high levels of serum 25-hydroxyvitamin D during 2 months after institution of the therapy, then they gradually returned to the normal level by the end of 3 to 5 months and thereafter decreased further, while a marked decrease of serum 25-hydroxyvitamin D levels was observed in patients receiving combined anticonvulsant (phenobarbital, diphenylhydantoin and others) therapy even during 1 to 2 months after initiation of the treatment. Our results suggest that the patients who have combined anticonvulsant therapy will have more tendency to suffer from osteomalacia than those who have phenobarbital alone.

Adolescent↗
PubMedDate not supplied

Xeroderma pigmentosum with versive seizures.

A boy with group A xeroderma pigmentosum and a series of progressive neurologic complications developed versive seizures at 8 years of age. Electroencephalography at 6 years of age revealed no epileptic changes or focal abnormalities. He was seizure-free until versive seizures developed; electroencephalography revealed frequent spike discharges in the right central and temporal regions. Neurologic complications and electroencephalographic abnormalities of 34 patients with group A xeroderma pigmentosum also were assessed. Only 3 patients with xeroderma pigmentosum have been reported to have a seizure disorder. This patient is the fourth reported with group A xeroderma pigmentosum associated with a convulsive disorder. Although neurologic manifestations in group A xeroderma pigmentosum are progressive and severe, it is unknown why so few of these patients develop seizure disorders.

Brain↗
PubMedDate not supplied

Aicardi syndrome associated with an embryonal carcinoma.

A Japanese girl is reported who had the typical clinical features of Aicardi syndrome associated with embryonal carcinoma. She developed infantile spasms at approximately 4 weeks of age; her seizures were intractable in spite of treatment with numerous antiepileptic drugs and ACTH. At 22 months of age, her left cheek gradually became swollen. Laboratory findings were normal except for a marked increase in serum alpha-fetoprotein. A transoral biopsy of the tumor revealed an embryonal carcinoma. This patient is the first reported with Aicardi syndrome and embryonal carcinoma. The relationship between congenital malformations and neoplasms is discussed.

Agenesis of Corpus Callosum↗