Central neurogenic hyperventilation with pontine tumor. Case report and a review of the literature.
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Biomedical subjects
Publications and source records attributed to J Handa.
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Effects of a new Ca2+ antagonist, 1-[bis(4-fluorophenyl) methyl]-4-(2,3,4-trimethoxybenzyl) piperazine dihydrochloride (KB-2796), on the regional cerebral blood flow (rCBF) and somatosensory evoked potentials (SEPs) were investigated using a model of focal cerebral ischemia in cats. In experiment 1, an occlusion of the middle cerebral artery for 4 hours persistently reduced the ipsilateral rCBF in both the control and the KB-2796-treated groups. However, the flow reduction was much milder in the treatment group than in the control group. Amplitudes of the SEPs diminished in both groups but the rate of deterioration was much slower in the treatment group than in the control group. In experiment 2, an occlusion of the middle cerebral artery for 1 hour was followed by reperfusion for 3 hours. The ipsilateral rCBF decreased during occlusion in both the control and the treatment groups. In the control group, postischemic hyperperfusion was seen in the ectosylvian gyrus after reperfusion, whereas the ipsilateral rCBF recovered rapidly to the control values without showing a phase of hyperperfusion in the treatment group. The rate of recovery of the SEPs was also much more rapid in the treatment group.
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A case of dural arteriovenous malformation (AVM) in the base of the anterior cranial fossa associated with a ruptured anterior communicating aneurysm was reported in a 67-year-old man. The dural AVM was fed by the left anterior ethmoidal artery and drained by the left frontal ascending vein with a varicose dilatation. The aneurysm was clipped and the dural AVM was removed in two stages. Dural AVM in the base of the anterior cranial fossa is rare, and we could find only 17 previous reports. Two of them presented with exophthalmos, whereas the remaining 15 cases presented with an intracranial hemorrhage from rupture of the dural AVM. An association of an aneurysm with the dural AVM in this location has not been reported previously.
This study concerns 16 cases with spontaneous subarachnoid hemorrhage (SAH) of unknown etiology experienced in our department during a period from September 1979 through August 1986. SAH was confirmed by computed tomographic scanning (CT) or lumbar puncture. All cases were studied by four or three-vessel study. In the case of three-vessel study, adequate opacification of the posterior inferior cerebellar artery contralateral to the injected vertebral artery was considered as a necessary condition. Panangiography was repeated in all patients one to two weeks after the initial study and was negative. The severity of SAH in these patients on admission was relatively mild (Hunt and Kosnik grade I + II = 75%), and the degree of subarachnoid bleeding on CT was also mild. Medium to long-term outcome was excellent or good in 81% of cases, and none of them experienced rebleeding. Only one patient died of severe vasospasm on the 20th hospital day, but no aneurysm was found at autopsy. Illustrative 3 patients in whom the cause of SAH had been finally found was briefly reported. In the first patient, SAH was secondary to a paraventricular cryptic angioma. In the second patient, a microaneurysm had been concealed at the initial angiography by the parent arteries or intra-aneurysmal clot. In the third case of a fusiform aneurysm of the vertebral artery, the aneurysm proximal to the posterior inferior cerebellar artery could not be found at the first three-vessel angiography. Importance of CT and the necessity of repeat panangiography including magnification or oblique views so as not to over-look the causative vascular abnormalities were emphasized.
Diagnosis of hydrocephalus after aneurysmal subarachnoid hemorrhage has been facilitated by CT, but the true incidence and pathogenesis of the condition remain to be clarified. Extent of ventricular dilatation does not necessarily correlate with clinical symptoms and the indication of shunting operation is by no means definite. Consecutive 117 patients with ruptured aneurysm were retrospectively studied for possible factor(s) for development of hydrocephalus in the chronic stage. The incidence of chronic hydrocephalus was found to be high in those patients with aneurysm of the anterior communicating artery, those harboring acute hydrocephalus, those admitted with higher clinical grades, those showing thick clots and gyral enhancement on initial CT, and those who received tranexamic acid in excess of 30 g.
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Forty-six patients with medically controlled open angle glaucoma were scheduled to undergo extracapsular cataract extraction with implantation of a posterior chamber intraocular lens. Surgery was performed in 43 eyes; three eyes had an intraoperative complication that prevented a posterior chamber lens implantation. The mean preoperative intraocular pressure was 17.6 mm Hg with the patients receiving a mean of 1.9 medications. The mean intraocular pressure (16.2 mm Hg) and the number of medications (1.4) administered to the 43 eyes having the planned surgery were significantly decreased an average of 23.4 months following cataract surgery. Seventy-two percent of the eyes had a postoperative visual acuity of 20/40 or better. Operative complications were similar to those reported for the same type of cataract surgery in nonglaucomatous eyes. However, there seemed to be an increased incidence of postoperative cystoid maculopathy (11.6%) in these glaucomatous eyes compared with previous reports in the literature and with the incidence in nonglaucomatous eyes that we treated. Our study shows that extracapsular cataract extraction with a posterior chamber lens can be effective in restoring vision without compromising intraocular pressure control in eyes with preexisting open angle glaucoma.
Somatosensory-evoked potentials were recorded during and after 31 operations for intracranial aneurysms, and the changes in the central conduction times, namely, the interpeak latencies between the N14 and N20 peaks in response to bipolar stimulation of the median nerve, were studied. Neuroleptanalgesia and routine intracranial operative procedures such as opening the dura mater, drainage of the cerebrospinal fluid, gentle retraction of the brain, and microsurgical dissection of the circle of Willis, were found to have no significant adverse effect on the evoked responses, whereas the temporary clipping of the major cerebral artery or premature rupture of the aneurysm associated with hypotension or both, often caused significant prolongation of the central conduction time. Prolongation of the central conduction time exceeding 1.2 ms or disappearance of the N20 peak adversely affected the postoperative conditions in 8 of 13 patients (62%).
Using an experimental model of global ischemia of the brain in rats, we have shown that a Ca2+ antagonist nicardipine attenuates, and a Ca2+ agonist YC-170 accelerates, the liberation of free fatty acids in the ischemic whole brain. The effects of YC-170 were negated by the previous administration of an adequate dose of nicardipine. This is the first report on the action of a Ca2+ agonist on the metabolism of the brain, and the results seem to provide supportive evidence for the role of Ca2+ in ischemic injury of the brain.
A 9-year-old boy with mild left hemiparesis and left abducens nerve palsy was found to have chordoma of the clivus. Magnetic resonance imaging (MRI) was most useful not only for diagnosis but also for selection of operative approaches. The tumor was subtotally resected by a transoral-transpharyngeal approach followed by a retroauricular retromastoid craniotomy, and postoperative radiation therapy was administered. Intracranial chordomas are rare in children; only 12 cases have previously been reported in detail. Eleven patients were male and one was female. Progressive cranial nerve involvement and long tract signs without increased intracranial pressure constitute the cardinal symptomatology of intracranial chordomas, but a separation of cranial sutures and enlargement of the head may be seen in children. The role of MRI in diagnosis and patient management cannot be overemphasized.
Using a model of global cerebral ischemia in rats, we examined the effects of a dihydropyridine Ca2+ antagonist, nicardipine, on the liberation of free fatty acids (FFAs). After decapitation of the animals, FFAs showed a rapid progressive increase for a whole experimental period of up to 60 minutes without reaching a plateau. Nicardipine in a dosage of 1 mg/kg effectively attenuated the liberation of FFAs, particularly that of arachidonic acid which is known as the precursor of prostaglandins, thromboxanes, and leukotrienes. The FFAs of the brain have been known as one of the biochemical markers that indicate ischemic damage of the brain cell membrane. The results of the present study support a possible protective effect of Ca2+ antagonist against cerebral ischemia.
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