Vertebral hydatid cysts are rare and found in less than 1% of all the cases of hydatidosis. Neural compression is common in vertebral hydatidosis. The prognosis is generally regarded as very poor. This paper examines the natural history and complications which may arise during the treatment of vertebral hydatid cyst, and discusses their treatment. Thirteen cases of hydatid disease a ecting the vertebrae are presented. The patients were admitted with symptoms of spinal cord compression. Twelve were treated by laminectomy and one by costotransversectomy. Low back pain radiating to the legs and lower extremity weakness were the predominant symptoms. Di erent degrees of pareses were present in 12 patients. Nine patients had impaired sensation in lower extremities. In 13 patients, 27 operations were performed. The major complication of surgery was the death of one patient due to the formaline irrigation. The surgical goal should be an extensive removal of the cysts and a ected bone. The surgical area needs to be irrigated with hypertonic saline. Mebendazole or albendazole therapy seems to retard the recurrences and control the disease.

Four rare cases of intracranial intravascular papillary endothelial hyperplasia (IPEH) manifesting as cranial nerve disturbances occurred in 16-, 18-, 24-, and 28-year-old females. Magnetic resonance imaging showed all lesions as isointense with strong enhancement on T 1 -weighted images, and as hyperintense on T 2 -weighted images. All lesions were removed via craniotomies. Histological examination found vascular structures and papillary spaces lined with endothelial cells showing immunoreactivity for CD31. Complete removal was curative in two cases, whereas incomplete removal resulted in cure in one case and residual deficits in one case. Iatrogenic deficits should be avoided in IPEH treatment by surgery. Differentiation from neoplasm such as angiosarcoma depends on histological characteristics.

Free radicals are thought to be the most important cause of the reperfusion injury subsequent to ischemia. The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free radical induced injury. This investigation was performed to evaluate the antioxidant enzyme capacity of the brain tissue in the ischemia-reperfusion period using an experimental global moderate (penumbral) ischemia model on rat brains. Experiments were performed on 45 male Sprague Dawley rats. Ischemia was induced by bilateral vertebral arteries cauterization and temporary bilateral carotid arteries occlusion and sustained for 10 minutes. At the end of ischemia (0 min reperfusion) and various reperfusion periods (20 min, 60 min, 240 min), rats were decapitated and brains were frozen in liquid nitrogen. Changes in the intracellular antioxidant enzyme (superoxide dismutase, glutathione peroxidase and catalase) activities were assessed in the rat brain tissues, by spectrophotometric methods. In all moderate ischemia-reperfusion groups, superoxide dismutase activities were found to have decreased significantly compared to the sham operated controls (P < 0.05). During ischemia superoxide dismutase activity was lowered to 31% of that of the control group. The decreases were more significant in reperfusion groups, particularly in 60 min reperfusion (40%). Relatively smaller but still significant diminution was observed in glutathione peroxidase activities (P < 0.05). The ratio of diminution was striking in 20 min and 60 min reperfusion groups with 26% of the sham operated rats. Conversely, moderate ischemia-reperfusion caused significant increase in catalase activities (P < 0.05). The increment was 63% of the preischemic level with 10 min of moderate ischemia. In conclusion, activities of the major antioxidant enzymes were changed significantly in moderate brain ischemia-reperfusion. These results suggest that the disturbance in oxidant-antioxidant balance might play a part in rendering the tissue more vulnerable to free radical induced injuries.

Local application of controlled- or sustained-release papaverine can be safely used in preventing vasospasm.

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