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SummaryNeurotoxic effects of endogenous tissue plasminogen activator (tPA) have recently been reported. Employing a rat model of thromboembolic stroke, we evaluated the extent and degree of extravasation of exogenous tPA administered for the purpose of fibrinolysis. In a thromboembolic model using Sprague-Dawley rats, focal cerebral ischemia was induced at the territory of the middle cerebral artery (MCA). Early reperfusion was induced by administering tPA (10 mg/kg) intravenously at 30 minutes after the onset of ischemia. Extravasated tPA was evaluated by immunohistochemistry, and the concentration of tPA in the brain tissue was quantified by enzyme-linked immunosorbent assay methods. The integrity of the blood-brain barrier (BBB) was examined electronmicroscopically. In a thread model of transient ischemia, reperfusion was induced without tPA adminis-tration at 30 minutes or 2 hours after the onset of ischemia, and the tPA content of the brain was quantified. In the rats with thromboembolic stroke, extravasation of tPA was observed at the territory of the MCA. Both the endogenous and exogenous tPA contents were 3.5±1.6 ng/ml of homogenized brain in saline. Electronmicroscopically, mild ischemic changes were observed, although the integrity of the BBB was preserved. In the thread model rats, the endogenous tPA contents of the ischemic hemisphere were 0.9±0.1 and 1.0±0.2 ng/ml in the 30-minute and 2-hour ischemia groups, respectively, and were significantly lower than the tPA contents in the thromboembolic stroke rats (p < 0.01). The present findings indicate that significant extravasation of exogenous tPA occurs through the cerebral vessels even though early reperfusion is induced.

Homonymous hemianopia due to lateral geniculate body (LGB) lesion has rarely been reported. It is difficult to detect the LGB lesion by neuroimaging. We report two patients with characteristic homonymous hemianopia due to cerebral infarction of the LGB. In both patients, Goldmann perimetry showed incongruous and wedge-shaped homonymous hemianopia, and magnetic resonance imaging demonstrated infarction of the LGB. In addition, occlusion of the lateral posterior choroidal artery was confirmed by magnetic resonance angiography in one of these patients. To diagnose of a LGB lesion, we should carefully observe characteristic visual field defects, accompanying neurologic symptoms, and neuroimaging findings, including magnetic resonance angiography.

✓ The authors report the case of a peripheral primitive neuroectodermal tumor (PNET) arising in the tentorium in a 5-year-old boy who presented with frequent vomiting and mild palsy of the left abducent nerve. Following complete surgical excision of the tumor via a transpetrosal approach, the patient has thus far been disease free for 7 years. The tumor tissue was composed of small cells with uniform round nuclei and minimal identifiable cytoplasm. Homer—Wright rosettes were frequently observed. Immunohistochemical studies demonstrated a positive reaction to HBA-71, which recognizes the cell surface glycoprotein p30/32, a product of the MIC2 gene. Both the clinical and immunohistochemical characteristics of this tumor are consistent with a diagnosis of peripheral PNET, which is genetically distinct from the more common intracranial PNET.

Both microglia and astrocytes respond immediately to traumatic brain injury (TBI). The present study was undertaken to examine whether or not excitatory amino acid (EAA) antagonists could attenuate such glial responses.EAA antagonists, including the broad spectrum EAA antagonist, kynurenic acid (KYN), specific N-methyl-D-aspartate (NMDA) receptor blocker, 2-amino-5-phosphonovalerate (AP-5), and AMPA-KA receptor blocker, 6,7-dinitroquinoxaline-2,3-dione (DNQX), as well as the voltage-dependent ion channel blocker, tetrodotoxin (TTX), were administered into the unilateral hippocampus of rats through a dialysis probe for 30 minutes before the induction of unilateral controlled cortical impact injury. The rats were killed 10 minutes after injury and their brains were processed immunohistochemically for OX42 (marker for microglia) and glial fibrillary acidic protein (GFAP; marker for astrocytes).Ten minutes after injury, microglial activation with increased OX42 immuno-reactivity was evident in the entire hemisphere including the hippocampus ipsilateral to the injury side. Similarly, swollen astrocytes with increased GFAP expression could be detected exclusively on the injury side. When KYN was administered in situ before injury, both the rapid microglial and astroglial responses in the hippocampus were significantly attenuated. However, AP-5, DNQX and TTX, the voltage-dependent ion channel blocker, at doses which can inhibit each channel activation, failed to attenuate these glial reactions.These findings indicate that massive ionic fluxes and/or concomitantly occurring EAA release may be closely related to the initiation of microglial and astroglial responses following TBI.

Background We present here the first report of a jugular bulb venous thrombosis after mild head injury, which lacked either a skull fracture or abnormal findings on CT scan. Case Description An 8-year-old boy was hit on the back of the head and experienced headache and vomiting beginning the next morning. A CT scan and cranial x-ray examination failed to reveal any abnormal findings. The patient was treated conservatively; however, his headache and vomiting persisted. At 13 days after the injury, he began to show double vision due to left VIth nerve palsy and bilateral papilloedemas, suggesting an increased ICP. Although repeated CT scan failed to detect abnormal findings in both the supra- and infra-tentorial regions, MRI clearly visualized a thrombus which was situated within the right jugular bulb. Furthermore, MRV demonstrated disruption of venous flow at the jugular bulb. The patient was administered heparin continuously. His symptoms improved and the CSF pressure on lumbar puncture returned to a normal level at 20 days after admission. Magnetic resonance imaging showed resolution of the clot, and MRV appeared to demonstrate partial recanalization simultaneously. The patient was discharged without any neurologic deficits. The clot in the jugular bulb disappeared completely after 4 months, and he could be followed up for 1 year. Conclusion This case underscores the fact that MRI may represent the exclusive screening examination in cases of sinus thrombosis when it occurs within the jugular bulb, as CT scan fails to reveal any findings suggestive of venous thrombosis.

In order to assess the role of circulating blood in early microglial activation after traumatic brain injury (TBI), controlled cortical impact injury was applied to adult rat brain slices (400 microm in thickness) and the microglial response was examined. The complement receptor (CR3) expression and morphological transformation of the microglia were evaluated by OX42 immunohistochemistry. At 5 min following injury, activated microglia with intense CR3 expression appeared throughout the hemisphere on the injured side. In contrast, the morphology and CR3 expression of the microglia on the contralateral side were indistinguishable from those of the resident ramified microglia seen in normal brains. At 30 min following injury, microglial activation was more pronounced on the injured side, while the microglia on the contralateral side still retained a ramified morphology. These results are consistent with our previous observations made in in vivo experiments, which indicate that, as the brain slice paradigm excludes variables arising from the circulating blood, the rapid and widespread microglial activation observed following TBI can not be attributed exclusively to the infiltration of blood-borne macrophages or molecules. Rather this activation is most likely caused by intrinsic mechanisms within the brain tissue, such as traumatic depolarization.

The jugular bulb oxygen saturation (SjO 2 ) and end-tidal carbon dioxide (ETCO 2 ) were monitored continuously during surgery in six cases of Moyamoya disease who had demonstrated multiple episodes of transient ischemic attacks (TIAs) and/or fluctuating neurological deficits preoperatively. The arterial carbon dioxide tension (PaCO 2 ) levels were also measured repeatedly at predetermined interval. In two cases (group H), the ETCO 2 was controlled at hypercapnic levels during surgery (45.5±1.5 mmHg) and the remaining four (group N) were operated on in a normocapnic state (39.0±2.0 mmHg). The group H patients demonstrated high levels of SjO 2 ranging from 72 to 85%, indicative of excessive hyperemia. One of the group H patients demonstrated mild and transient motor weakness postoperatively. The group N patients demonstrated normal levels of SjO 2 ranging from 66 to 78%. All the patients in both groups demonstrated fluctuations in SjO 2 levels in clear positive correlation with spontaneous changes in PaCO 2 levels. The present findings indicated that: (1) Global carbon dioxide reactivity of cerebral perfusion is well preserved in patients with Moyamoya disease; and (2) hypercapnia in these patients often causes excessive hyperemia. The occurrence of postoperative neurological deficits in association with such an excessive hyperemia suggests that hyperapnia during surgery is not always beneficial. Intraoperative monitoring of SjO 2 is useful for maintaining cerebral perfusion within the optimum range.

The role of microglia in the response to CNS injury is not fully understood. We characterized the temporal activation of microglia in the adult spinal cord following a lesion that severed the axons of the dorsal columns and corticospinal tract at T8. Two days after lesion, microglia in the severed T4-T5 fasciculus (f.) gracilis were ameboid and expressed intense OX42 and increased class I major histocompatibility complex (MHC) antigen (OX18) immunoreactivities. No activated microglia were seen in the intact f. cuneatus or the corticospinal tract. Five days postlesion, OX42 immunoreactivity was slightly decreased in the f. gracilis, and OX18 expression was slightly enhanced. By 12 days postlesion, OX42 and OX18 immunoreactivities were near control levels. At L1-L2, activated microglia with increased OX18 expression were restricted to the corticospinal tract and were maximal 5 days postlesion, returning to near control levels by 12 days postlesion. In the medulla, enhanced OX42 and OX18 immunoreactivities were seen in the nucleus (n.) gracilis, but not the n. cuneatus, at 2 days postlesion. At 5 days postlesion, OX42 immunoreactivity was markedly decreased, but class I MHC antigen expression was still enhanced. GFAP immunoreactivity increased only in the n. gracilis and remained elevated 2-12 days postlesion. Microglial activation is an early lesion-induced event in the CNS, and activated microglia may play a role in mediating the regenerative capacity of injured CNS axons.

A case of meningioma with extensive xanthomatous metaplasia occurring in the left frontal convexity of a 37-year-old woman is reported. The tumour was demonstrated as a hypodense mass with minimal enhancement on CT. Our findings suggest that magnetic resonance imaging may provide a clue to the diagnosis of meningiomas with extensive xanthomatous metaplasia when CT is less specific.

The influence of interstitial oedema on the survival of fetal raphe cells transplanted into serotonin (5-HT)-denervated rats and the fibre outgrowth from these cells was investigated. Fetal raphe cells were transplanted into the corpus callosum in which long-lasting interstitial oedema had been induced by intracisternal kaolin injection. The 5-HT and 5HIAA levels in the corpus callosum were restored to their maximum within 5–6 weeks post-transplantation regardless of whether interstitial oedema was induced or not. Furthermore, it was appeared that the presence of interstitial oedema even facilitated fibre growth as demonstrated by the 5-HT immunohistochemistry and the restoration of the 5-HT and 5-HIAA levels in brain areas distant from the transplantation sites. These results imply favourable effects of interstitial oedema on the survival of transplanted raphe cells and their fibre outgrowth.