No abstract available.
Hematoma, Subdural, Spinal* ; Spinal Puncture*

Our study was designed to determine whether methylprednisolone exerts a beneficial effect after experimental moderate diffuse brain injury and whether this possible beneficial effect is affected by the dosage, the timing of administration, and the methods of treatment. A total of 200 anesthetized adult rats were injured utilizing a weight-drop device through a Plexiglas guide tube. These rats were divided into eight groups: Group 1 (n=35) was assigned to receive no methylprednisolone after impact (control group), Group 2 (n=25) received an initial intraperitoneal administration of methylprednisolone with a dose of 5 mg/kg at 1hour after cranial impact, followed by administration with a maintenance dose of 5 mg/kg/4 hours. Group 3 (n=25), group 5 (n=25), and group 7 (n=20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours, respectively without a maintenance dose. Group 4 (n=25), group 6 (n=25), and group 8 (n=20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours after impact, with a maintenance dose of 15 mg/kg/4 hours. Measured water content of brain tissue expressed the amount of water as the difference between fresh and dry weight. At 48 hours after impact, the water content in group 4 and 6 were significantly lower than group 1. Mean SD was 61.4 0.37% in group 4 (p<0.03), 61.5 0.34% in group 6 (p<0.001), and 63.6 0.48% in group 1. Compared to group 1, the difference was not statistically significant in group 2 (p>0.1), group 3 (p>0.5), group 5 (p>0.6), group 7 (p>0.1), and group 8 (p>0.5). Groups treated with mega dose before 4hours after head injury, including maintenance dose, showed beneficial effects. Our study suggests that the efficacy of methylprednisolone in head injury was related to the dosage, the timing of administration, and method of treatment.
Animal ; Brain Edema/prevention | control* ; Brain Injuries/drug therapy* ; Dose-Response Relationship, Drug ; Injections, Intraperitoneal ; Methylprednisolone/therapeutic use* ; Neuroprotective Agents/therapeutic use* ; Rats ; Rats, Sprague-Dawley

Alveolar Soft Part Sarcoma(ASPS) in an unusual tumor of soft tissue, it has invariably ended in death from disseminated disease, and the lung has been the most common site of metastasis, but the brain was the 3rd most common site of metastasis. That proportion seems 0.4% of all soft tissue sarcoma. Clinical, pathological, and radiological features of metastatic cerebral lesions resulting from ASPS are presented. Angioarchitecture, and radiotherapic finding and chemotherapy are discussed. The unusual juxtaposition of the tumor cells to the endothelium seems responsible for the highly vascular appearance of the lesion on angiography, the frequency of hematogenous spread, and the grave, although delayed, prognosis. The purpose of this paper is to be report ASPS which has never been reported in Korea yet, with some references.
Angiography ; Brain ; Drug Therapy ; Endothelium ; Korea ; Lung ; Neoplasm Metastasis* ; Prognosis ; Radiotherapy ; Sarcoma ; Sarcoma, Alveolar Soft Part* ; Viperidae

A rare and tremendous skull metastasis from the follicular thyroid carcinoma is reported with review of the articles. Follicular carcinoma of the thyroid with distant metastasis is considered a relatively progressive tumor associated with poor five-year survival rate. The insidious character of the primary growth of the thyroid carcinoma is the long latent period which supervenes between the recognition of the primary growth and its secondary metastasis. The clinicopathological features, plain X-ray and C-T findings are discussed.
Adenocarcinoma, Follicular* ; Neoplasm Metastasis* ; Skull* ; Survival Rate ; Thyroid Gland ; Thyroid Neoplasms ; Tomography, X-Ray Computed

No abstract available.
Aneurysm* ; Bone Cysts* ; Spine*

A consecutive series of 34 severe head-injured patients (DAI) were studied prospectively. Patients were categorized according to a new, simple classification system comprised of four lesion types according to the compression or obliteration of the ventricles or cisterns. Five patients belonged to type II and 19 patients to type IV. Each type was further subdivided into two GCS score ranges (5 to 8 and below 5). The distribution of the posttraumatic infarction was mainly in the frontal and temporal lobes (60% of all cases). Our data demonstrated that the ICP was significantly lower at a 30 degrees head elevation than at 0 degree (18.6 +/- 7.21 mmHg vs 23.0 +/- 10.60 mmHg. t = 4.22 p< 0.001), but head position did not statistically affect CPP (69.4 +/- 19.86 mmHg vs 68.2 +/- 19.87 mmHg. t = -0.54, p< 0.59). The effect of intensive therapy on ICP, CPP and AVDO2 was studied in all cases, employing steroids and diuretics in a modified intensive care scale. In cases where barbiturates were employed, there were statistically significant changes in ICP and AVDO2 (p< 0.001), but CPP was not affected (p< 0.59). Surviving patients were analyzed by using the GOS and the neurological grading score (NGS, Nihon University) of the persistent vegetative state. Our data suggests that head elevation of 30 degrees and barbiturate therapy are more effective on ICP and AVDO2, and NGS more exact than GOS in vegetative patients.
Adolescent ; Adult ; Aged ; Cerebrovascular Circulation ; Craniocerebral Trauma/*physiopathology/radiography ; *Glasgow Coma Scale ; Human ; Intracranial Pressure ; Middle Age ; Oxygen/blood ; Posture ; Prospective Studies ; Tomography, X-Ray Computed

No abstract available.
Animals* ; Brain* ; Hypothermia* ; In Situ Nick-End Labeling* ; Models, Animal*

We developed an in vivo model of cerebral ischemia-reperfusion wherein on-line videoimages of fluorescently-labelled leukocytes following within pial venules of anesthetized newborn pigs can be obtained. A closed cranial window was implanted over the parietal cortex, and venules were imaged with an fluorescence microscope(Olympus BHMJ) outfitted with a 100 watt mercury lamp, rhodamine filter cube. 10 x immersion lens(Olympus; 0.4NA), and newvicon tube camera. Final image magnification captured to Super VHS videotape was 470x. Rhodamine 6G was administered as a 0.5mg/kg i.v. loading dose and a 0.5mg/kg/h i.v. maintenance dose in saline to selectively label circulating leukocytes. We made an ideal model with 6 piglets and under basaline conditions in piglets, few labelled leukocytes were observed adhering to the endothelium of 50-60 microm diameter venules. However, following 10min, of global cerebral ischemia induced by reversible subclavian and brachiocephalic occlusion, a dramatic increase in rolling and adherent leukocytes was observed at 30, 60, and go on, of reperfusion. At these times, cortical blood flow, measured by both laser doppler flowmetry and hydrogen clearance, was decreased by 25-40%(p<0.05). There findings demonstrate the feasibility of continuous in vivo monitoring of leukocyte adherence in cerebral venules, and suggest that reperfusion-induced adherence to venular endothelium may contribute to hypoperfusion following global cerebral ischemia.
Brain Ischemia* ; Endothelium ; Fluorescence* ; Humans ; Hydrogen ; Immersion ; Infant, Newborn ; Laser-Doppler Flowmetry ; Leukocytes* ; Microscopy, Video* ; Rabeprazole ; Reperfusion* ; Rhodamines ; Swine ; Venules* ; Videotape Recording

The biochemical factors related to moderation of secondary or delayed damage to the central nervous system (CNS) remain undefined. We have recently demonstrated that the weight- drop induced moderate diffuse axonal injury (mDAI) in rats causes a rapid decline in serum ionized magnesium (Mg2+) and a significant increase in the amount of serum ionized calcium (Ca2+) relative to Mg2+ (Ca2+/ Mg2+). For three hours, serum Mg2+ levels remained significantly depressed at 76% of preinjury values (p< 0.05), but total serum magnesium remained unchanged (tMg, p > 0.05). Head trauma resulted in a small decrease of Ca2+ (about 10%), but a significant increase in the amount of Ca2+/Mg2+ (mean value in control group: in injured group for 3 hours after trauma =4.65 +/-0.012 : 5.69 +/-0.015, p< 0.05) was observed. In order to further investigate the relationship between Mg2+ and brain injury, the effect of Mg2+ treatment on posttraumatic histological changes (apoptotic changes) was examined following the weight-drop induced brain injury. At 30 min postinjury, animals treated with MgSO4 (750micro Ml/kg) showed significant improvements of apoptotic changes when compared to the control group (54.8 +/- 1.7, 51.5 +/- 3.2 at 12, 24 h in control group, 24.8 +/- 2.6, 20.5 +/- 1.4 at 12, 24 h in treated group, p< 0.05). The early decline in serum Mg2+ and the increase in the amount of Ca2+/Mg2+ immediately following brain trauma uncovered by these findings suggest that they may be a critical factor in the development of irreversible tissue injury. If this proves to be the case, treatment with MgSO4 may be effective in improving histological findings following experimental traumatic brain injury in rats.
Animals ; Apoptosis/*drug effects ; Axons/*pathology ; Brain Injuries/blood/*drug therapy/pathology ; Calcium/blood ; Magnesium/blood/*therapeutic use ; Rats ; Rats, Sprague-Dawley

Although nitric oxide (NO) plays an important role in the pathophysiological process of cerebral ischemia or severe traumatic brain injury, its contribution to the pathogenesis of moderate diffuse axonal injury (mDAI) remains to be clarified. The alterations in nitric oxide synthase (NOS) activity and the histopathological response after mDAI was investigated. Forty anesthetized Sprague-Dawley adult rats were injured with a Marmarou's weight-drop device through a Plexiglas guide tube. These rats were divided into 8 groups (control, 1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 48 hr after trauma). The temporal pattern of apoptosis in the adult rat brain after mDAI was characterized using TUNEL histochemistry. In addition, the cDNA for NOS activity was amplified using RT-PCR. The PCR products were electrophoresed on a 2% agarose gel. eNOS activity was not detected, but nNOS activity was expressed after 3 hr and continuously 48 hr after impact, which was approximately double that of the control group at 12 and 24 hr. Subsequently, there was a decrease in activity after 48 hr. The iNOS activity increased dramatically after 12 hr and was constant for a further 12 hr followed by a dramatic decrease below the level of the control group. Significant apoptotic changes occurred 12 and 24 hr. after insult. nNOS and iNOS activity were affected after moderate diffuse axonal injury in a time-dependent manner and there was a close relation between the apoptotic changes and NOS activity. Although the nNOS activity was expressed early, its activity was not stronger th an iNOS, which was expressed later.
Animal ; *Apoptosis ; Craniocerebral Trauma/enzymology/*physiopathology ; Diffuse Axonal Injury/enzymology/*physiopathology ; Nitric-Oxide Synthase/*metabolism ; Rats ; Rats, Sprague-Dawley ; Wounds, Nonpenetrating/enzymology/*physiopathology