The Influence of Hyperglycemia on the Extent of Focal Cerebral Ischemia

The present study was undertaken to investigate the influence of hyperglycemia on focal cerebral ischemia in view of morphometric assay and neuropathological examination. Forty Sprague-Dawley rats were divided into two groups of 20 each. Rat MCA occlusion model was used for induction of focal ischemia. Hyperglycemia(20 rats, mean(SEM plasma glucose concentration 378(97.6 mg/dl) was established 30 minutes before MCA occlusion by intraperitoneal injection of 50% dextrose in water;the control group(20 rats, mean(SEM plasma glucose concentration 121(24.9 mg/dl) received normal saline only. Twenty-four hours after MCA occlusion neutral red staining and perfusion fixation was performed and ischemic area were measured using computerized image analysis on cortical surface and coronal cut surface. There was no significant difference on coronal cut surface, but on cortical surface showed increase of non-stained area(infarct core) and decrease of lightly stained area(transitional zone) in hyperglycemic rats(p<0.05) and the sum of two area was not different between two groups. Pathological findings were evaluated under light microscopy, in which the field scanning was carried out from the midline by 0.5 mm interval at cortical and basal ganglia level. There showed no significant difference at basal ganglia level, but at cortical level ischemic transitional zone was decreased in hyperglycemic rats(p<0.05). We conclude that hyperglycemia may worsen the brain from severe, focal ischemic neuronal damage.

The Effect of Allopurinol and Deferoxamine on Postischemic Lipid Peroxidation

It has been hypothesized that ischemia, followed by reperfusion, facilitates peroxidative free radical chain process in brain. This study was undertaken to investigate the effect of allopurinol and deferoxamine on cerebral lipid peroxidation, estimated by a thiobarbituric acid test, following transient bilateral forebrain ischemia in the rat model of four vessel occlusion. Sprague-Dawley rats fed ad libitum were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 48 hours later temporarily occluding the common carotid arteries for 20 minutes. Carotid artery blood flow was restored and rats were decapitated after 48 hours. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from hippocampus, basal ganglia, cortex and thalamus. The homogenates were subjected to 30 minutes of aerobic incubation. The production of lipid peroxides were decreased in all sampled area in the treated groups compared with the control group. Allopurinol and deferoxamine-treated groups showed decreased lipid peroxide levels in all the sampled area, but especially more in the hippocampus(p=0.02), (p0.05). The results suggest that allopurionl and deferoxamine play a role in protecting ischemic cellular damages by scavenging free radicals and subsequently lipid peroxides formed by oxygen supply through blood reperfusion.

Intradural Extramedullary Capillary Hemangioma in Thoracic Area

Spinal hemangioma is the uncommon, slowly growing benign tumor that arises from the blood vessels and commonly located in thoracic spine. We have recently experienced a caseof capillary Hemangioma in intradural extramedullary space of thoracic spine level. The patient presented with a slowly progressive weakness of both lower extremities and hypesthesia below T6 dermatome. The plain X-ray films, thoracic spine myelography and CT scan disclosed an intradural mass at T5 level. The mass was surgically removed and conformed by histological examination.

Reduction of Postischemic Cerebral Infarction and Cerebral Edema by Superoxide Dismutase and Allopurinol

The authors have inverstigated the hypothesis that ischemic injury could be attenuated by xanthine oxidase inhibitor(Allopurinol) and superoxide dismutase(SOD). This study used rat MAC model. Each animal was assigned to four groups which was composed with control group, allopurinol pretreated group(50mg/kg. I.P single). SOD pretreated group(16,000 I.U/kg I.V q 15min for 4hours) and combined pretreatment group. Oxygen derived free radicals have been implicated in various pathological conditions including ischemia. Xanthine oxidase serve as a source of oxidizing agents such as superoxide radical and hydrogen peroxide. The superoxide flux in normal cells appears to have necessitated the development of SOD, which scavenges the superoxide by dismutation. Infarcted area was measured by computerized morphometric analysis after triphenyl tetrazolium chloride staining, infarcted area was reduced in SOD treated group(p=0.005) and SOD, allopurinol combined group(P=0.035). Brain edema was measured by gravimetric method. And it was reduced in Allopurinol treated group(P=0.001) and SOD allopurinol combined group (P<0.001). Thus it was revealed that ischemic injury might be reduced by either decrease of production or increase of scavenger and the combination of two should be more efficious.

A Clinical Analysis of 81 Cases of Arseriovenous Malformations

The authors present a consecutive series of 81 patients admitted to the Department of Neurosurgery of Korea University and Ewha Woman's University with an intracranial arteriovenous malformation(AVM). Of these, 56 received surgical treatment, and 23 were treated conservatively. We have reviewed the modes of clinical presentations, result of diagnostic evaluation, and surgical consideration. Partial of total removal of the AVM was performed in all but 7 of the patients treated surgically. Operative mortality in this surgical series was 9%, with significant morbidity in 20%.

The Effect of Systemic Nicardipine and Intracisternal Nicardipine on the Experimental Cerebral Vasospasm

This study reports the protective of systemic nicardipine and intracisternal nicardipine administration in the three-hemorrhage canine model of chronic cerebral vasospasm. Twenty-one dogs were assigned to one of three groups : control, intravenous nicardipine, and intracisternal nicardipine. All animals received a total of 12ml of fresh unheparinized autologous blood via three cisternal injection. Selective vertebral angiograms were obtained before intravenous nicardipine for 7 days continuously, the other seven were treated by intracisternal nicardipine for 7 days, and the remaining were not treated. Animals were sacrificed at day 9. Comparisons were based on the percentage of reduction in basilar artery diameter(% RBAD). The ultrastructural changes were studied by transmission electron microscopy(TEM). There was a mean reduction(+/- standard deviation) of 54+/-6% in control dogs, 35+/-4% in dogs with intravenous nicardipine, 32+/-6% in dogs with intracisternal dicardipine(difference significant, t-test, P<0.05). The preventive effects of intracisternal nicardipine was superior to those of intravenous nicardipine. There was a strong trend toward reduction of medial necrosis in the basilar artery in dogs with intravenous and intracisternal group compared to control dogs. All basilar arteries showed structural changes with celectron microscopic examination ; these included medial necrosis, lysosome, initial changes, endothelial cell vacuoles, and adventitial erythrocytes, leukocytes. Intimal proliferation was unusual in all three groups, but reduction of intimal proliferation was found in dogs with treatment, and it was believed that vasospasm in this stage is due to long-standing smooth muscle contraction and not to arterial wall thickening. There was significant reduction of blood clot in intracisternal nicardipine group, which may be due to inhibitory action on platelet aggregation of nicardipine. These investigations support the hypothesis that the presence of clotted blood around the intracranial arteries is the cause of vasospasm.

The Effect of Nimodipine on Experimental Spinal Cord Injury

Nimodipine the potent, centrally active, clacium channel blocker, is known to increase cerebral and spinal blood flow. In the present study, the authors investigated the effect on Nimodipine on injured spinal cord. The experiment was a randomized blind study in which four groups of five cats received Nimodipine(0.05mg/kg) intravenously, and control groups of five cats received only Diluent. As a step in the investigation of the possible effect of spinal cord trauma on biochemical and ultrastructural changes in the injured cord, activities of lipid peroxidation were measured in the frozened-dried sample of the spinal cord and fine structure of the mylinated nerve fiber in the white matter were observed. An increase of lipid peroxidation level was found as early as 1 hour after the injury and the highest concentration was reached at 5 hours after the injury(P<0.01). Fine structures of the myelinated nerve fibers were changed progressively with the lapse of time after the injury. The effect of Nimodipine on lipid peroxidation and fine ultrastructural changes of myelinated nerve fibers were studied, and the result of this study revealed that Nimodipine groups showed a lower level of lipid peroxidation with statistical significance(P<0.05) and preservation of ultrastructural myelinated nerve fiber was prominent.