Age at migration of epileptic foci in children with partial epilepsy.
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Age Factors↗
Biomedical subjects
K Hongo
Publications and source records attributed to K Hongo.
Development of EEG background activity in children with benign partial epilepsy.
We investigated the developmental features of the EEG-background activity of the 30 patients with benign childhood epilepsy. We found significant spectral differences between the benign childhood epilepsy group (BECCT; 25 cases, CEOP; 5 cases) and the normal control group. Compared with the normal group, the epilepsy group showed a shift of the spectrum to slower frequencies, with an increase in Delta and Theta, and a decrease in Alpha 2. The decrease in the mean frequency (O1) was significant from 8 years old to 10 years old. But in both the following periods; before 8 years old and after 10 years old, the difference was not significant. In the patients with benign childhood epilepsy, the development of the EEG-background activity came to be stagnant from 6 years old or so, and after 10 years old it developed again and approached to that of the normal children. It is suspected that the EEG background activity of children with benign partial epilepsy shows a special development.
Brain Mapping↗
[Intracellular Ca ion movement in cardiac muscles].
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Aequorin↗
[Clinical evaluation of the patients with epilepsy following febrile convulsions].
We studied clinical, EEG and developmental features of 46 epileptic children following febrile convulsions. Incidence of developing epilepsy was 9.9 percent. Eleven patients (group G) out of 46 had generalized epileptic seizures, and 34 patients (group P) had partial seizures. Febrile convulsions of early onset, partial seizures and postictal neurological symptoms were more striking in group P (p less than 0.05), whereas febrile convulsions of late onset and prolonged seizures were slightly dominant in group G. And EEG abnormalities were more frequent in group P (p less than 0.05). Group P patients had significant number of risk factors (complex features of febrile convulsions) than group G patients (p less than 0.01). The interval between the last febrile convulsion and subsequent epileptic seizures was shorter in group G (p less than 0.01). Although subsequent epileptic seizures were well controlled in the both groups (91% in group G and 82% in group P), intractable seizures were recognized in 9% of group P patients. The patients who had risk factors of prolonged seizures, postictal neurological symptoms and early onset manifested poor controlled epileptic seizures (p less than 0.01). Motor or mental deficits were more frequently associated with group P: in some patients they had been observed before the onset of febrile convulsions. These results suggest that pathogenesis of epilepsy following febrile convulsions may be different among various seizure types of subsequent epilepsy. And the risk factors during febrile convulsions may be related to the prognosis of subsequent epileptic seizures as well as the incidence of developing epilepsy.
Child, Preschool↗
[Adult moyamoya disease with a transcranial internal carotid-external carotid (EC-IC) anastomosis through burr holes].
A case of adult Moyamoya disease, with formation of a transcranial external carotid-internal carotid (EC-IC) anastomosis through burr holes which had been made previously. A 43-year-old male suffered sudden headache and vomiting. Neurological examination revealed mild consciousness disturbance and dysarthria. The computed tomography (CT) scans showed intraventricular hemorrhage, which was drained through burr holes bifrontally. The diagnosis of Moyamoya disease was subsequently made by cerebral angiography. A month later he was discharged with mild gait disturbance and mental retardation. Seven years later he suddenly complained of gait disturbance, dysarthria and sensory disturbance involving the right upper extremity. A CT scan revealed a small hemorrhage in the left putamen. Carotid angiograms disclosed transcranial EC-IC anastomosis through the burr holes which had been made previously. It is suggested that revascularization can be expected after opening burr holes and incising the dura matter for Moyamoya disease in adults as well as, possibly, in children.
Anastomosis, Surgical↗
Rapid increase of prostaglandin F2-alpha in neurons after subarachnoid hemorrhage in rats: an immunohistochemical study.
The effects of subarachnoid hemorrhage (SAH) with various degrees of increase in intracranial pressure (ICP) on the staining of prostaglandin F2-alpha (PG F2alpha) were studied in rat brains. SAH was produced in 18 rats by injection of 0.18-0.20 ml of autologous arterial blood/100 g body weight into the cisterna magna. By changing the speed of injection, the ICP was transiently increased by 346 +/- 68 (mean +/- S.D.) mm Hg in eight rats (including three pretreated with indomethacin), by 200 +/- 42 mm Hg in five rats, and by 6 +/- 4 mm Hg in the other five. Three rats injected with the same volume of mock cerebrospinal fluid (CSF) with ICP increased by 217 +/- 67 mm Hg and five normal rats without injection served as controls. All animals were decapitated 15 min after injection. The cryosections were stained for PG F2 alpha using an indirect immunofluorescence method. Positive staining for PG F2 alpha was noted only in pial vessels in all normal and mock-CSF-injected rats. In SAH rats with ICP increased by 6 +/- 4 mm Hg, there was a positive reaction in hippocampal neurons and Purkinje cells as well as blood vessels. SAH rats with higher ICP showed stronger PG F2 alpha staining in the above areas, as well as in cerebellar granule cells. All rats pretreated with indomethacin showed a smaller increase in staining. The above results indicate that subarachnoid blood clots per se produce a rapid increase of PG F2 alpha in neurons and blood vessels of both cerebrum and cerebellum, and that this increase is augmented by intracranial hypertension.
Animals↗
Time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage.
The time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage (SAH) was studied in 24 rabbits. Animals with SAH received two successive blood injections through the cisterna magna. Horseradish peroxidase (HRP) was given intravenously 30 minutes before sacrifice to assess the integrity of the barrier. In the basilar arteries taken from animals that were sacrificed 4 days after the first SAH, HRP-reaction products were diffusely observed in the subendothelial space. Three weeks following the first SAH, permeation of HRP was still observed in half of the animals. However, in animals sacrificed 7 weeks after the first SAH, no permeation of HRP into the subendothelial space was noted. Opening of the interendothelial space seemed to be the major mechanism for HRP permeation into the subendothelial space rather than transendothelial vesicular transport. Disruption of the blood-arterial wall barrier in the major cerebral arteries following SAH may play a role in the pathogenesis of vasospasm.
Animals↗
Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries.
An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteries in vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in the in vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0 U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10(-6)M prostaglandin F2 alpha. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.
Animals↗
Effect of the nonglucocorticoid 21-aminosteroid U74006F experimental cerebral vasospasm.
The present work was performed to establish whether the nonglucocorticoid, 21-aminosteroid, U74006F, could prevent the development of delayed cerebral vasospasm after experimental subarachnoid hemorrhage. The subarachnoid hemorrhage was produced by percutaneous injection of 4.5 mL of nonheparinized autologous blood into the cisterna magna of rabbits. U74006F (1 mg/kg) or placebo was injected intraperitoneally every 12 hours starting 12 hours prior to induction of hemorrhage for a total of six doses. The animals were sacrificed by perfusion fixation. The basilar artery was removed on day 2 and processed for morphometric analysis. Control/placebo and subarachnoid hemorrhage/placebo basilar artery diameters were 651.2 +/- 25.4 and 366.3 +/- 34.2 mu, respectively. Control/U74006F basilar artery diameters (669.8 +/- 21.8 mu) were not significantly different from that of the control/placebo group. U74006F treatment greatly minimized subarachnoid hemorrhage-induced reduction in mean luminal diameter (563.7 +/- 48.2 mu) (p less than 0.001). These results demonstrate considerable therapeutic promise for U74006F in the prevention of cerebral vasospasm.
Animals↗
Muscarinic cholinergic receptors on the endothelium of human cerebral arteries.
To characterize the muscarinic cholinergic receptors on the endothelium of human cerebral arteries, isometric tension measurement and receptor autoradiographic studies were performed. Acetylcholine (ACh) induced dose-dependent relaxation of human cerebral arteries precontracted by 10(-5) M serotonin, with an EC50 of 1.9 +/- 0.6 X 10(-6) M (n = 7). The relaxation was abolished by 10(-5) M hemoglobin. Autoradiography, using the muscarinic antagonist [3H]propylbenzilycholine mustard, demonstrated the high density of muscarinic cholinergic receptors on the endothelial cells of human cerebral arteries, especially on the luminal surface of the endothelium. These findings suggest that ACh-induced relaxation mediated by muscarinic cholinergic receptors on the endothelium has a physiological function in human cerebral arteries.
Acetylcholine↗
Characterization of muscarinic cholinergic receptors on the endothelium and the smooth muscle of the rabbit thoracic aorta.
Pharmacodynamic and quantitative autoradiographic studies were performed to characterize the muscarinic receptors on the endothelium and smooth muscle of the rabbit thoracic aorta. The antagonistic effect of atropine and pirenzepine on the relaxation induced by acetylcholine showed that the relaxation was mediated by muscarinic receptors with pA2 values of 9.4 and 6.6, respectively, suggesting the presence of muscarinic receptors on the endothelium with low affinity for pirenzepine. The quantitative autoradiographic study using [3H]-propylbenzilylcholine mustard (3H-PrBCM) showed that the specific 3H-PrBCM binding was time dependent and saturable. Saturation times of the bindings were not significantly different between the receptors on the endothelium and those on the smooth muscle layer. The density of the receptors was higher in the smooth muscle layer than in the endothelium. The specific [3H]-quinuclidinyl benzilate (3H-QNB) binding was displaced by atropine or pirenzepine dose dependently. IC50 of pirenzepine for the receptors on the endothelium was not significantly different from that for the receptors on the smooth muscle layer. These findings suggest that there is a smaller density of muscarinic receptors on the endothelium than on the smooth muscle layer of the rabbit thoracic aorta. The muscarinic receptors on the endothelium can be subclassified into the same subtype as the receptors on the smooth muscle layer, which have low affinity for pirenzepine.
Acetylcholine↗
Clinical study of epileptic children with history of febrile convulsion.
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Child, Preschool↗
Effect of subarachnoid hemorrhage on calcitonin gene-related peptide-induced relaxation in rabbit basilar artery.
An isometric tension measurement of ring segments was performed in the rabbit basilar and common carotid arteries in vitro to investigate the regional differences in the calcitonin gene-related peptide (CGRP)-induced vasodilation and the effect of subarachnoid hemorrhage on CGRP-induced vasodilation. CGRP elicited vasodilation of the rabbit basilar artery in a dose-dependent fashion when the artery was precontracted by 10(-5) M 5-hydroxytryptamine, whereas almost no relaxation occurred in the rabbit common carotid artery. The relaxation of the basilar artery was 64.03 +/- 1.85% at 3 x 10(-8) M CGRP, with an EC50 of 8.46 +/- 0.08. Two days after experimental subarachnoid hemorrhage, CGRP-induced relaxation of the rabbit basilar artery was 53.96 +/- 8.08% of the 10(-5) M 5-hydroxytryptamine-induced contraction, not significantly different from that of the basilar artery of the control rabbit. Our findings suggest that CGRP induces potent vasodilation in the rabbit basilar artery and that no impairment of vasodilation occurred after experimental subarachnoid hemorrhage. We speculate that CGRP may have therapeutic potential in cerebrovascular disease such as vasospasm after subarachnoid hemorrhage.
Animals↗
The influence of experimental subarachnoid hemorrhage on the relaxation induced by vasoactive intestinal polypeptide in the cerebral arteries of the rabbit.
The influence of subarachnoid hemorrhage (SAH) on vasodilatation induced by vasoactive intestinal polypeptide (VIP) was investigated in rabbit basilar arteries. VIP-induced relaxation was measured in ring sections of the basilar arteries precontracted by 10(-5) M serotonin using an isometric tension recording method. The cyclic adenosine monophosphate (cAMP) content was measured using radioimmunoassay as an indicator of the intracellular mechanism in the arterial smooth muscle cells. VIP (10(-11)-10(-6) M) evoked dose-dependent relaxation of the basilar arteries. The relaxation achieved with 10(-6) M VIP was 85 +/- 4% (n = 7) of the initial contractile tone in control arteries and 47 +/- 5% (n = 8) in the arteries evaluated 2 days after SAH, suggesting that VIP-induced relaxation was suppressed significantly after SAH (P less than 0.01). The cAMP content was significantly higher in the basilar arteries 2 days after SAH (425 +/- 48 pmol/g of tissue, n = 7) than in the control basilar arteries (194 +/- 57 pmol/g of tissue, n = 7). In normal arteries, the cAMP content was increased to a significant degree by VIP (10(-6) M) (325 +/- 60% of control cAMP content, n = 5), whereas the increase was less in the arteries evaluated 2 days after SAH (112 +/- 16% of control cAMP content, n = 5). These results suggest that SAH has an influence on cAMP metabolism in the arteries and that SAH impairs the postsynaptic mechanism of VIP-induced dilatation of the arteries.
Animals↗
Effect of intracisternal antithrombin III on subarachnoid hemorrhage-induced arterial narrowing.
The ability of antithrombin III, an endogenous plasma glycoprotein, to reverse the arterial narrowing in a rabbit model of cerebral vasospasm was evaluated. The vasodilator activity of antithrombin III on rabbit arteries was first assessed in vitro using a myograph-arterial ring preparation. Antithrombin III (10 IU/ml) induced a 55.4% +/- 2.66% (mean +/- standard error of the mean) relaxation in basilar artery precontracted with serotonin (5-HT) in five specimens as compared with a 9.8% +/- 1.6% relaxation of common carotid artery in six specimens. For in vivo analysis, 21 New Zealand White male rabbits were separated into three groups: Group 1 served as normal controls; Group 2 received a subarachnoid blood injection (SAH) and were sacrificed on Day 3 thereafter; and Group 3 animals were subjected to SAH, then received a 2-hour intracisternal infusion of antithrombin III (100 IU) in saline prior to sacrifice on Day 3. Basilar artery caliber was determined using a morphometric method to analyze perfusion-fixed arterial segments. Control basilar artery diameter in Group 1 was 0.64 +/- 0.02 mm. In Group 2 a 27% reduction in arterial caliber to 0.47 +/- 0.03 mm was observed by Day 3 post SAH (p less than 0.0001). Group 3 animals had a mean basilar artery diameter of 0.68 +/- 0.02 mm. This was significantly larger than the untreated SAH rabbits in Group 2 (p less than 0.0001), but not different from control artery diameters in Group 1. The findings demonstrate that antithrombin III in saline has a significant ability to reverse delayed narrowing of the rabbit basilar artery after SAH.
Animals↗
Immunohistochemical demonstration of transient increase in prostaglandin F2-alpha after recirculation in global ischemic rat brains.
The changes in prostaglandin F2-alpha (PG F2 alpha) staining over 3 days of recirculation in both fore- and hindbrains were studied. Five minutes of global ischemia was produced in 24 rats by Pulsinelli's method with hypotension around 50 mm Hg of mean arterial blood pressure. Eight rats (including three pretreated with indomethacin) were recirculated for 5 min, three for 1 h, five for 2 h and five for 3 days. Five normal rats without occlusion of vessels served as controls. The brains were snap frozen. Ten-micrometer cryosections were stained for PG F2 alpha by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2 alpha was noted in pial vessels in all normal and ischemic rats. Recirculated rats revealed the strongest reaction at 5 min after recirculation in blood vessels and in neuronal cytoplasm (especially in hippocampi and in Purkinje cells). The intensity of staining was markedly reduced after 1 h. Rats pretreated with indomethacin showed less increase in staining. The above results indicate that recirculation after ischemia produces a transient increase in PG F2 alpha in blood vessels and neurons of both fore- and hindbrains.
Animals↗
Immunohistochemically demonstrated increase of prostaglandin F2-alpha in neurons after reoxygenation in anoxic rats.
Immunohistochemical staining for prostaglandin F2-alpha (PG F2 alpha) was conducted to identify PG F2 alpha synthesizing or binding sites in anoxic rat brains. Anoxia was produced in 22 rats to lower the arterial oxygen tension (PaO2) to 21 +/- 4 mmHg by ventilation with a 95% nitrogen and 5% carbon dioxide gas mixture. In 8 animals anoxia was continued for 30 sec, and in 14 rats for 3 min. Prior to decapitation, 5 animals in the 30-sec anoxia group and 8 rats in the 3-min anoxia group were reoxygenated for 5 min, while the remaining 9 were not. Five-min reoxygenation returned the PaO2 to 106 +/- 7. Three non-reoxygenated and 3 reoxygenated rats, all pretreated with indomethacin, and 5 normal rats served as controls. The brains were snap-frozen. The cryosections were stained by the indirect immunofluorescence method. PG F2 alpha was noted mainly in pial vessels in all normal rats. All reoxygenated rats showed a positive reaction not only in blood vessels, but also in neurons, particularly hippocampal neurons and Purkinje cells. The staining of the above neurons was noted to be less in non-reoxygenated rats. The stronger staining was observed in rats reoxygenated after 3-min anoxia than 30-sec anoxia. The indomethacin-pretreated rats showed almost no increase in staining intensity. The above results indicate that reoxygenation after anoxia results in an increase of PG F2 alpha in neurons of both cerebrum and cerebellum.
Animals↗
Comparison of intraluminal and extraluminal inhibitory effects of hemoglobin on endothelium-dependent relaxation of rabbit basilar artery.
To determine whether extraluminal or intraluminal hemoglobin inhibits endothelium-dependent relaxation, we measured the vascular responsiveness of rabbit basilar artery in an in vitro perfusion system and we performed immunohistochemical staining for hemoglobin. In the in vitro study, we applied agents from either the intraluminal or the extraluminal side of excised basilar arteries. KCl-induced contraction was the same with either application. Acetylcholine-induced maximal relaxations were 57.6 +/- 8.5% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 3.3 +/- 0.3% for intraluminal, and 34.9 +/- 8.6% for extraluminal applications. Adenosine triphosphate-induced maximal relaxations were 64.2 +/- 4.1% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 26.9 +/- 3.8% for intraluminal, and 42.2 +/- 6.0% for extraluminal applications. Hemoglobin's inhibition of acetylcholine- and adenosine triphosphate-induced relaxation was significantly greater with intraluminal than with extraluminal application (p less than 0.05). The immunohistochemical study revealed hemoglobin in the outer layer of the smooth muscle and in the adventitia when 10(-5) M hemoglobin was applied extraluminally for 5 minutes, whereas hemoglobin was observed on the surface of the endothelial cells after intraluminal application. Our findings suggest that hemoglobin inhibits acetylcholine- or adenosine triphosphate-induced relaxation by binding to endothelium-derived relaxing factor (EDRF) and by inhibiting production of EDRF. Hemoglobin's inhibitory effect on endothelium-dependent relaxation may be important in the pathogenesis of vasospasm after subarachnoid hemorrhage.
Acetylcholine↗