Immunohistochemical properties of human optic nerve glioma. Evidence of type 1 astrocyte origin.

The peroxidase-antiperoxidase method was used to study ten surgically obtained human optic nerve gliomas (pilocytic astrocytomas). All tissues were formalin fixed and paraffin embedded. Primary antisera included glial fibrillary acidic protein (GFAP), HNK-1 (type 1 astrocyte precursor marker), A2B5 (type 2 astrocyte precursor marker), S-100, vimentin, myelin basic protein (MBP), laminin, keratin, cytokeratin, epithelial membrane antigen (EMA), and neuron-specific enolase (NSE). Neoplastic astrocytes in optic nerve gliomas stained with GFAP, HNK-1, S-100, and vimentin. Oligodendrocytes and myelin sheaths stained for MBP, and NSE stained surviving axons in the tumors. Neoplastic astrocytes did not stain for A2B5, keratin, cytokeratin, EMA, or laminin. These results suggest that human optic nerve gliomas (pilocytic astrocytomas) arise from type 1 astrocytes.

Naloxone therapy during focal cerebral ischemia evaluation in a primate model.

Conflicting reports have appeared in the literature regarding the effect of the opiate antagonist naloxone on ischemic neurologic deficits. We report the results of a study using naloxone in our model of focal cerebral ischemia in the awake primate. A total of 14 adult baboons were subjected to six-hour occlusion of the left middle cerebral artery (MCA). Seven animals served as controls and seven received treatment with naloxone (5 mg/kg) beginning 30 min after MCA occlusion and continuing until two hours after reperfusion. All animals developed profound hemiparesis and homonymous hemianopsia within seconds of inflating the MCA occluder. Acutely, therapy with naloxone partially reversed ischemic neurologic deficits in five of the seven treatment animals. Within minutes of receiving the loading dose of naloxone, responding animals were more alert and demonstrated improvements in motor function. Naloxone did not affect mortality: Three animals in the treatment group and two in the naloxone group died secondary to malignant intracranial pressure within 48 hours of the ischemic episode. In animals surviving the ischemic insult however, treatment with naloxone significantly improved neurologic outcome at 10 days (p less than 0.05). Neuropathologic examinations in these animals revealed amelioration of ischemic tissue damage, with three of the five suffering only small focal areas of infarction. (All control animals suffered large infarcts of the MCA territory.) Our results verify that naloxone can reverse ischemic deficits, and more importantly may improve the outcome from focal ischemic insults.

Barbiturate-induced coma therapy for focal cerebral ischemia. Effect after temporary and permanent MCA occlusion.

The authors have studied the therapeutic effect of barbiturate coma following middle cerebral artery (MCA) occlusion in primates. The relationship of the efficacy of barbiturate protection to the presence or absence of recirculation was examined. Barbiturate therapy was begun 30 minutes after MCA occlusion. The findings were as follows: 1) barbiturate-induced coma, with its attendant monitoring, was safely tolerated by primates for 96 hours; 2) 6 hours of MCA occlusion followed by recirculation resulted in a neurological deficit that was worse than the neurological deficit produced by permanent MCA occlusion; 3) barbiturate-induced coma for 96 hours, initiated 30 minutes after the onset of MCA occlusion, in the absence of reperfusion, was in fact detrimental; 4) barbiturate-induced coma for 96 hours, initiated 30 minutes after MCA occlusion, with the establishment of reperfusion at 6 hours, provided nearly complete protection from ischemic damage.