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A series of 15 patients who underwent neurosurgical procedures for recurrent spheno-orbital meningioma is reported. There were 11 women and four men, with a mean age of 46 years. The mean duration between the first and second operations was 46 months. Progressive proptosis without neurological deficit was the most common symptom. All tumors were large at the time of reoperation and involved the greater and lesser wings of the sphenoid bone and the orbit. Aggressive resection in all patients resulted in no deaths and only slight morbidity, with the exception of one patient who developed blindness 24 hours after surgery due to central retinal artery occlusion. Fourteen patients were improved cosmetically and one patient, treated early in the series, had persistent proptosis due to inadequate bone removal. No attempt was made to remove tumor within the cavernous sinus in patients who were neurologically normal. Although postoperative imaging demonstrated complete gross excision of tumor in nine patients, 10 underwent conventional radiation therapy for residual tumor visualized at the time of surgery in the dura of the superior orbital fissure, the cavernous sinus, or the basal optic canal. Although this study is inconclusive and requires further long-term documentation, no recurrences have been seen to date in the follow-up period, ranging from 16 to 95 months. The following important points are discussed: 1) the failure by experienced surgeons to radically excise bone, tumor, and involved dura at the first operation; 2) the importance of early aggressive therapy, depending upon the patient's age and medical condition; 3) the almost invariable intracranial dural involvement, which at times was seen only by gadolinium-enhanced magnetic resonance imaging and not visualized on computerized tomography; 4) an illustrated stepwise surgical technique for complete resection through a small craniotomy without the need for complicated reconstruction of the orbit or temporal fossa; 5) the role of radiation therapy when removal is incomplete or deemed hazardous because of cavernous sinus involvement; and 6) the excellent cosmetic results possible with minimal morbidity and no mortality.

We tested the efficacy of various putative neuroprotective agents in the gerbil model of delayed neuronal death. The selective loss of anterior CA1 neurons of the hippocampus 4 days after 5 minutes of bilateral ischemia was complete in >90% of the gerbils examined. We tested 11 agents for their ability to protect against neuronal loss. Only those agents that were associated with the GABAergic system exhibited protection and only when administered before the ischemic insult. The possibility that delayed neuronal death is the result of a primary defect in inhibitory neurotransmission is considered. (Stroke 1989;20:281-287) S elective vulnerability (SV) of hippocampal neurons was first reported more than 100 years ago, 1 and the mechanism for this phenomenon has yet to be elucidated. Many hypotheses have been proposed to explain the delayed neuronal death (DND) that occurs in the CA1 pyramidal cells following an ischemic event.2 -10 A more recent hypothesis proposes that certain excitatory amino acids (i.e., glutamate and aspartate) may act as endogenous neurotoxins following seizures, ischemia, and hypoglycemia." While extracellular glutamate in low concentrations is toxic to selected neuronal populations, 12 it is still unclear whether glutamate antagonists can prevent DND. 13MFurther support of the excitotoxic hypothesis was provided by Rothman, 15 who reported that hippocampal neuronal cultures could be protected from anoxic damage by blocking synaptic activity. These results, along with the demonstration that deafferentation of the Schaeffer collaterals blocked postischemic CA1 neuronal death, suggest that synaptic transduction is an important component of SV. 1617While glutamate may be the toxin, the primary insult that gives rise to glutamate toxicity does not necessarily have to be intrinsic to this system. We questioned whether the insult is an exaggerated excitation secondary to an inhibitory defect within the hippocampus. The major inhibitory pathway

In the Intraoperative Hypothermia for Aneurysm Surgery Trial, neither systemic hypothermia nor supplemental protective drug affected short- or long-term neurologic outcomes of patients undergoing temporary clipping.