The excitatory neurotransmitters glutamate and aspartate are an important factor in the causation of ischemic brain damage. The concentration of glutamate and aspartate was serially measured in extracellular fluid using in vivo microdialysis after induction of a subdural hematoma or after a sham operation in the rat. Measurements were made in the cortex underlying the hematoma and in the ipsilateral hippocampus, and these findings were correlated with regional cerebral blood flow (CBF), measured autoradiographically 2 hours after hematoma induction. In the severely ischemic cortex underlying the hematoma (mean CBF less than 25 ml/100 gm/min), glutamate and aspartate content increased more than 750% over basal levels. In individual animals the magnitude of glutamate release correlated with the extent of the focal ischemic zone under the hematoma (r = 0.907). Hippocampal glutamate levels rose 339%, yet regional CBF was preserved (114 ml/100 gm/min). This accords with focal hypermetabolism in this model, and may imply a glutamate-mediated "excitotoxic" process after subdural hematoma.

The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 microliters homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 +/- 8 cu mm (mean +/- standard error of the mean) in vehicle-treated control rats to 29 +/- 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.

Hemangiopericytoma (HPC) is a rare tumor of the central nervous system and is usually found intracranially. Intraspinal HPCs are very rare and mostly involve the extradural bony structures. Primary intradural HPC has only been reported in 10 cases, all of which occurred in the extramedullary region. Intramedullary invasion has never been reported. Here, we describe a case of primary intradural HPC of the thoracic spine that presented initially with paresthesia and paraplegia of both legs. Magnetic resonance imaging of the thoracic spine showed an intradural dumbbell-shaped tumor at the T10 level. The initial impression was neurogenic tumor, meningioma, or metastasis. During operation, the tumor was found to have obvious intramedullary invasion. Gross-total removal was done, and the patient's neurological function improved; there was no recurrence at the 3-year follow-up. There is no consensus as to what constitutes the optimal treatment of HPC, but most neurosurgeons will advocate gross-total resection. A comparative analysis between intradural and extradural HPCs showed a higher chance of gross-total resection for intradural HPCs, while the recurrence rates showed no difference. The role of adjuvant radiotherapy remains uncertain. Due to the high risk of recurrence and metastasis of HPCs, close follow-up for a long period is mandatory.

A 32-year-old man had seizure attack since April 2008 and radiographic examination revealed a heterogeneous enhancing mass at the left subfrontal region. He underwent craniotomy for tumor removal on October 1, 2008. The tumor, which was grayish white with glistening appearance and rubbery consistency, was traced to the proximal part of left olfactory tract. Histopathological examination revealed a hypocellular tumor with dense hyalinization in most areas. The tumor cells had ovoid to elongate and often comma-shaped nucleus. Myxoid change of the stroma was apparent in places. Most of the tumor cells were immuno-reactive for S-100 protein. Staining for Leu 7 (CD57 or HNK-1) was negative. Bodian method illustrated many axons within the tumor. Ultrastructural study of the tumor cells showed features compatible with those of olfactory ensheathing cell. The tumor was designated as olfactory ensheathing cell tumor with neurofibroma-like features. There have been 14 nerve sheath tumors arising from the olfactory nerve reported in the literature; all of them had the morphology of schwannoma. Our case, which had the morphology simulating neurofibroma was the first of its kind to be recorded.