The Effects of Steroid and Calcium Channel Blocker on Single High Dose Irradiation-induced Apoptosis in Rat Brain

OBJECTIVE: Radiation injury includes radiation necrosis and apoptosis. The purpose of this study is whether steroids and calcium channel blockers are effective for the prevention of single high dose irradiation-induced apoptosis in the rat brain. METHODS: Eighty Sprague-Dawley rats were divided into four experimental groups: Control(nontreated, n=20), Dexamethasone-treated(0.1mg/kg, n=20), Prednisolone-treated(2mg/kg, n=20), Nimodipine-treated (0.5mg/kg, n=20). After drug was administered, the right hemisphere of rat's brain was exposed to a single 10Gy dose of gamma rays using Ir-192. All brains underwent histological examination at 1 week, 2 weeks, 4 weeks, and 8 weeks after irradiation to evaluate cortical thickness and number of apoptotic cells. Apoptotic cells were detected by TUNEL assay. RESULTS: In nimodipine-treated group, apoptotic cell count was reduced significantly, compared to that of control(non treated) group at 4 and 8 weeks after irradiation(p<0.05). The decrease of cortical thickness was reduced significantly in nimodipine-treated group, compared to that of control group(p<0.05). There was no significant changes in the number of apoptotic cells and cortical thickness in prednisolone and dexamethasone-treated groups compared with those of control. CONCLUSION: These results suggest that nimodipine treatment may have effects on the prevention of radiation-induced apoptosis. If it could be established that calcium channel blockers inhibit radiation injury, they might be useful in radiation therapy. Further investigation of calcium channel blockers including dosage effectiveness, intracellular calcium ion concentration and effects on tumor tissue are necessary to clarify the usefulness of nimodipine.

Emergency Trephination Site of Acute Subdural Hematoma

No abstract available.

Statistical Analysis of 631 Cases of Surgically Treated Brain Tumors in Korea University Hospital

The authors present a statistical survey of the general incidence, age distribution, and preferential site of 631 tumors of the brain which have been surgically treated at Korea university medical center, department of neurosurgery over the last period of 10 years from 1985 to 1994. Among them 269 cases were males and 362 were females. Of the 631 intracranial neoplasms verified histologically, tumors of neuroepithelial tissue comprised 34%(212 cases), tumors of meninges 23%(148 cases), pituitary adenoma 18%(114 cases), metastatic tumors 8%(50 cases), neurilemmomas 8%(49 cases), germ cell tumors 3%(13 cases), cyst and tumor like lesions 3%(16 cases), and lymphomas 1%(5 cases). Of the 178 gliomas, astrocytic tumors comprised 83%(148 cases), oligodendroglial tumors 11%(20 cases), ependymal tumors 3%(6 cases) and mixed gliomas 1.7%(3 cases). Brain tumors occurred most frequently in the age group of 45-50 years, as seen by an incidence of 63 cases(10%). The male to female ratio was 0.74: 1. Tumors that showed a definitive preponderance of females over males were meningiomas, neurilemmomas, and pituitary adenomas. Supratentoral and infratenorial cases were 73%(461 cases) and 26%(162 cases), respectively and the remaining cases involved both sites. Of the 114 cases of childhood and adolescent tumors, 60 were male and 54 were female. Supratentorial tumors were 56% and infratentorial were 44%. The tumors in order of frequency were astrocytomas(28%), primitive neuroectodermal tumors(21%), craniopharyngioma(10%) and so on. Meningiomas occurred most frequently in parasagittal/falx area(25%), followed by cerebral convexity 23%, sphenoid 14%, posterior fossa 13%. Among pituitary adenomas, prolactinomas(32%) were the most common and followed by null cell adenomas 31%, growth hormone cell adenomas 15%, mixed GH-PRL cell adenomas 11%.

Leukoencephalopathy Associated with 5-Fluorouraeil and Cisplatin Therapy

Increasing vigorous chemotherapy for cancers including primary and matastatic tumors has resulted in prolonged survival. However, there has been an associated increase in neurotoxicity as a result of it. All classes of chemotherapeutic agents contain drugs that are potentially neurotoxic. The authors has studied three cases of leukoencephalopthies developed during adjunctive therapy with 5-flurouracil and cisplatin for adenocarcinoma of the stomach. None of the patients had evidence of metastasis or any previous neurologic diseases. The duration of chemotherapy before onset of neurological symptoms ranged from 8 to 12 weeks. Two of the 3 patients presented progressive decline in mental status and ataxia after 2~3 weeks, while the third one had two unexplained episodes of loss of consciousness. In all of these patients, magnetic resonance imagings demonstrated prominent periventricular white matter lesions. Cerebral biopsies were performed stereotaxically in 2 patients. The morphological features were active demyelinating disease and edema. All three patients had improved after the cessation of chemotherapy and a short course of corticosteroid therapy, suggesting that these alarming events such as nausea, vomiting dizziness, dysarthria, and mental change were a toxic reversible side effects from these chemotherapeutic agents. This syndrome may represent the pathological basis for 5-fluorouracil neurotoxicity, however we cannot completely exclude the role of cisplatin in the occurences of the above syndromes.

Metastatic Thoracic Intramedullary Small Cell Carcinoma: Case Report

The incidence of metastasis to the spinal cord in patients with systemic carcinoma has been extimated to be 0.9 to 8.5%. Attempts to aggressively remove intramedullary spinal cord tumor may cause increased neurologic deficits and a worsend outcome. The authors present the case of a multiple intramedullary meetastatic spinal cord tumor which had metastasized from the lung to the thoracic spinal level. Pathologic diagnosis of the small cell carcinoma was made from the tumor specimen obtained by stereotaxic-guided neddle biopsy after which the patient was treated with radiotherapy and chemotherapy.

Experimental Studies of Hydroxyl Radical Generation in Reperfusion Injury after Cerebral Ischemia

The time course of hydroxyl radical generation in the brain and the intensity of brain hydroxyl radical(OH) generation were examined in rat during the first four hours after postischemia reperfusion. Hydroxyl radical production was measured using the salicylate trapping method in which the production of 2, 3-dihydroxybenzoic acid(DHBA) in hippocampus(CA1) 5 minutes after salicylate administration was used as an index of OH formation. The interstitial concentration changes of salicylate and 2, 3-DHBA were detected by intracerebral microdialysis following the intraperitoneal administration of salicylate(150mg/kg) using high pressure liquid chromatography-electrochemical(HPLC-EC) and -ultraviolet(-UV). Adult Sprague-Dawley rats were subjected to 20 minutes of bilateral carotid artery occlusion(BCAO) in either normotensive or hypotensive state. Serial changes of cerebral blood flow(CBF) were monitored by H2 clearance method. CBF of normotensive BCAO group(n=6) was found to be decreased only to 52% of baseline value, and OH production after reperfusion did not develop in this group. Rats in the BCAO hypotensive group(n=10) showed remarkable reduction of CBF to 27% of baseline(p<0.05) and 2~4 folds increase of 2, 3-DHBA/salicylate during the first 40 minutes of recirculation . Hydroxyl radical production in rats died(n=5) after the insult was significantly higher and lasted longer than that in rats survived(n=5)(p<0.05). Concentration of salicylate in perfusate increased during 100 minutes after the peritoneal injection and before reaching to a plateau, which lasted for 3 hours. The changes of cerebral tissue concentration of 2, 3-DHBA differed from those of salicylate. In 2, 3-DHBA, the plateau was reached rather slowly than that of salicylate and lasted for 2 hours. These data indicate that lobal cerebral ischemia could be induced by temporary BCAO only if the systemic hypotenion is accompanied, it can not be induced in normotensive group. The hydroxyl radical produced brain damage is prone to develop early in the reperfusion period and is correlated with the severity of ischemic insult.