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Astroblastoma is extremely rare brain tumor which mostly arise in cerebral hemisphere of children and young adult. Limited data exists on its clinical feature and molecular analysis. We recently experienced two female patients with astroblastoma in the cerebrum. Case 1 is three-year-old girl. She developed left hemiparesis. CT and MRI revealed large supratentorial mass with cystic component and calcification. Gross total removal was achieved. She is well without recurrence on MRI one year after surgery. Case 2 is 42-year-old lady. She developed partial seizure. CT and MRI revealed a mass with ring-enhancement in the left temporal lobe. Gross total removal was achieved under awake craniotomy. She is well without recurrence on MRI six months after surgery. Pathologic examination of both patients showed pseudorosette formation of tumor cells around vasculature. Molecular analysis revealed rearrangement of MN-1 in case 1 but not in case 2. Case 2 showed BRAF V600E mutation and loss of CDKN2A/2B. Both patients received no adjuvant therapy. Prognosis of astroblastoma varies and standard of treatment is not established. Gross total resection is associated with increased survival, but the role of adjuvant chemotherapy and radiation therapy are controversial. Advances in molecular analysis will lead to establish molecular classification and risk-adapted treatment strategy.

We examined the effects of mild to moderate hypothermia and the influence of rewarming on electrophysiological function using somatosensory evoked potentials (SEPs) in transient focal ischemia in the brain. Nineteen cats underwent 60 min of left middle cerebral artery occlusion under normothermic (36 degrees-37 degrees C, n = 6) or hypothermic (30 degrees -31 degrees C, n = 13) conditions followed by 300 min of reperfusion with slow (120 min, n = 6) or rapid (30 min, n = 7) rewarming. Whole-body hypothermia was induced during ischemia and the first 180 min of reperfusion. SEPs and regional cerebral blood flow were measured before and during ischemia and during reperfusion. The specific gravity of gray and white matter was examined as the indicator of edema. During rewarming, SEP amplitudes recovered gradually. After rewarming, SEPs in the normothermic and rapid rewarming groups remained depressed (20%-40% of pre-occlusion values); however, recovery of SEPs was significantly enhanced in the slow rewarming group (p0.05). Hypothermia followed by slow rewarming reduced edema in gray and white matter. Rapid rewarming did not reduce edema in the white matter. The recovery of SEPs correlated with the extent of brain edema in transient focal ischemia. Rapid rewarming reduced the protective effect of hypothermia.

Only small amounts of superoxide dismutase (SOD) are present in the extracellular space to scavenge excess amounts of superoxide anions (02-) released after traumatic brain injury (TBI). Experiments were performed in rats with cerebral contusion produced by weight-drop technique. We investigated the effects of exogenous lecithinized SOD (PC-SOD) on accumulation of 02- produced in our model, by measuring the level of SOD activity (using the NBT-reducing method) and the expression of copper, zinc-SOD (Cu, Zn-SOD) mRNA (by Northern blot analysis). As determined by tissue-specific gravity, administration of PC-SOD reduced brain edema in the periphery of the lesion 6 h after contusion. SOD activity increased in the peripheral region at 30 min after contusion, but returned to normal levels at 6 h after TBI. Administration of PC-SOD increased SOD activity up to 6 h after TBI. The expression of Cu, Zn-SOD mRNA increased in the core region, peripheral portion, and contralateral hemisphere up to 6 h after TBI, then was suppressed in all three regions by PC-SOD. Our results confirm the important role of 02- in the development of brain edema after TBI and indicate that PC-SOD diminishes brain edema through a protective effect against 02-.

We carried out a time course study of cerebral superoxide scavenging activity using a modified microdialysis technique. Twelve cats were divided into two groups; six were the reperfusion injury models, and six were cold injury models. In the reperfusion injury model, dialysates were collected during 60 minutes of middle cerebral artery occlusion and at 300 minutes during reperfusion. In the cold injury model, dialysates were collected 240 minutes after the injury. Regional cerebral blood flow on the injured side decreased during occlusion in the reperfusion injury model and 60 minutes after injury in the cold injury model. In the reperfusion model, superoxide scavenging activity, as determined with electron spin resonance, increased in the first 30 minutes and decreased 300 and 330 minutes after occlusion. In the dialysate, albumin increased 180 minutes after cold injury, which may show the progress of vasogenic edema. An increase in water content was observed on the injured side of both models, and a correlation between water content and superoxide scavenging activity was found in the reperfusion injury model. By this technique, a method of detecting the alteration of superoxide scavenging activity in the extracellular space of the brain was established.

To determine the effect of hypothermia on superoxide injury after cerebral contusion, the induction of Cu,Zn-superoxide dismutase was examined 6 h after contusion in rats using Northern blotting. Cu,Zn-superoxide dismutase gene expression increased at the periphery of the contusion, which may indicate the severity of the superoxide stimulus. This increase was preserved after contusion under hypothermia, which may show that superoxide injury is still severe although brain edema is decreased.

Brain surface elastance, defined as the pressure needed to compress the cortex 3 mm, was measured using the ophthalmodynamometer in six cats using three burr holes (frontal, parietal, and occipital) on each side. An intracranial mass was then used to compress the right side for 3 hours, and cardiac arrest was induced after the mass was removed. Elastance was measured four times: before insertion of the mass, 10 and 70 minutes after removal of the mass, and 60 minutes after cardiac arrest. The results showed that: brain surface elastance does not change between sides, but varies among regions with the parietal region having the highest elastance; elastance increases after compression by an intracranial mass, but not after cardiac arrest; and stiff brain tends to restore poorly. Elastance is apparently increased by the formation of edema. Measuring brain elastance may be useful in predicting brain restoration subsequent to removal of mass lesions.

To analyze the effect of lecithinized superoxide dismutase (SOD) on superoxide accumulation after traumatic brain injury (TBI) in rats, we studied the SOD activity by NBT-reducing method and the expression of Cu,Zn-SOD mRNA by Northern blot analysis. As determined by the specific gravity method, the administration of lecithinized SOD decreased brain edema in the periphery of the lesion at 6 hr after contusion. SOD activity, without lecithinized SOD administration, increased at the peripheral portion at 30 min after contusion, but decreased to the normal level at 6 hr after TBI. By administration of lecithinized SOD, the increase of SOD activity was preserved until 6 hr after TBI. The expression of Cu,Zn-SOD mRNA increased in the core lesion, peripheral portion, and contralateral hemisphere until 6 hr after TBI, then was suppressed in all three areas by lecithinized SOD. These results support the hypothesis that superoxide anions may play an important role in the development of brain edema after TBI, and that leciyhinized SOD appears to prevent brain edema through a protective effect against superoxide anions.

We analyzed the expression of Cu,Zn-superoxide dismutase (SOD) mRNA in both contusion and cold injury. Twenty-three rats were divided into 3 groups: a control group, a contusion group, and a cold injury group. Six hours after the injury, the rats were decapitated and the gray matter was resected from 3 portions: the core of the injured cortex, its periphery, and a distal portion on the non-lesion side. Based on the specific gravity of each sample, almost the same degree of edema developed in both injury groups. The mRNA expression in the cold injury group, however, significantly decreased in all portions. The extremely low temperature associated with cold injury is a possible cause of the decrease in Cu,Zn-SOD mRNA.

We used a microdialysis technique to establish a method to detect sequential changes in disruption of the blood parenchymal border. Twelve cats were divided into two groups; one group underwent occlusion of the middle cerebral artery for 60 minutes, the other a cold injury model. Microdialysis probes were implanted bilaterally into the white matter, and dialysates were collected successively at 30 minute intervals for 6 hours in the occlusion model and 4 hours in the cold injury model. Regional cerebral blood flow was measured simultaneously using the hydrogen clearance method. The water content of the white matter was measured using specific gravity. The proteins in the dialysate were analyzed using electrophoresis with silver stain, and, with densitometric analysis, the density of the 66.2 kDa band was quantified as albumin. The ratio of this density to the preoperative density was defined as the“albumin index.”On the side of the lesion in the cold injury model, this index significantly increased 3 hours after the cold injury compared with the contralateral side, and a correlation between the water content and this index was observed. The albumin index was believed to indicate the severity of disruption of the blood parenchymal border.

Using a new devised model of dural sinus occlusion, we investigated the pathophysiology including venous hemorrhage. Sixteen cats received, the occlusion of superior sagittal sinus(SSS) and diploic veins(DV). Intracranial pressure(ICP), cerebral blood volume(CB V) and regional cerebral blood flow(rCBF) were measured for 12 hours. At sacrifice, cerebral water content was determined. Other 8 cats received the additional occlusion of cortical veins(CV). In both groups, the blood-brain barrier(BBB) permeability was evaluated with Evans blue. The SSS and DV occlusion produced a significant increase in ICP and CBV and a significant decrease in rCBF. Cerebral water content also increased significantly. However, neither extravasated Evans blue nor venous hemorrhage could be observed, when thrombus was defined within SSS. Contrarily, the additional CV occlusion produced hemorrhagic infarctions in 6 cats, where Evans blue dye extravasated. These data suggest that durai sinus occlusion led to an increase in CBV and cerebral water content resulting in intracranial hypertension, and decreased rCBF. The brain edema in this model seemed to be hydrostatic edema. The obstruction of CV might be essential in the development of hemorrhage in this model, and the BBB was disrupted in these areas.

Fourteen patients with symptoms of vertebrobasilar insufficiency caused by vertebral artery stenosis in the distal first portion underwent surgical reconstruction. They ranged in age between 42 and 73 years, with a median age of 57 years. Their symptoms included vertigo, dysarthria, syncope, hemiparesis, and homonymous quadrant anopsia. The etiologies of the stenoses involved kinking in 12 cases and mechanical compression due to cervical sympathetic nerve, osteophyte, or fibrous bands in two cases. Digital subtraction angiography revealed that stenosis was maximal at systole and minimal at diastole in six of eight cases. In two of the 14 cases, stenosis was not demonstrated in the neutral position, but stenosis of the left vertebral artery appeared when the head was rotated to the right. Surgical procedures involved 13 decompressions of the vertebral artery and one subclavian artery-vertebral artery bypass using the saphenous vein. Postoperatively, 12 cases of miosis and one of asymptomatic phrenic nerve palsy were observed, but there were no serious complications. All but two patients had complete resolution of their symptoms. Stenosis due to kinking and/or mechanical compression disappeared in all cases after decompression of the vertebral artery. The effects of arterial pulse and neck rotation on vertebral artery stenosis in the distal first portion are discussed.

Fourteen patients with symptoms of vertebrobasilar insufficiency caused by vertebral artery stenosis in the distal first portion underwent surgical reconstruction. They ranged in age between 42 and 73 years, with a median age of 57 years. Their symptoms included vertigo, dysarthria, syncope, hemiparesis, and homonymous quadrant anopsia. The etiologies of the stenoses involved kinking in 12 cases and mechanical compression due to cervical sympathetic nerve, osteophyte, or fibrous bands in two cases. Digital subtraction angiography revealed that stenosis was maximal at systole and minimal at diastole in six of eight cases. In two of the 14 cases, stenosis was not demonstrated in the neutral position, but stenosis of the left vertebral artery appeared when the head was rotated to the right. Surgical procedures involved 13 decompressions of the vertebral artery and one subclavian artery-vertebral artery bypass using the saphenous vein. Postoperatively, 12 cases of miosis and one of asymptomatic phrenic nerve palsy were observed, but there were no serious complications. All but two patients had complete resolution of their symptoms. Stenosis due to kinking and/or mechanical compression disappeared in all cases after decompression of the vertebral artery. The effects of arterial pulse and neck rotation on vertebral artery stenosis in the distal first portion are discussed.

In severely head-injured patients with intracranial hypertension, irregular vital signs are frequently observed indicating medullary dysfunction. This study was carried out to investigate the effects of stimulating the medullary reticular formation on brain edema and ICP in a cerebral contusion model.