We induced experimental delayed cerebral vasospasm by the intracisternal injection of >0.5 ml blood in 30 rats. Seventy-two hours later the basilar artery was exposed via the transclival approach and photographed at high-power magnification through an operating microscope. We then evaluated the effect of topical (n=30) and intravenous («=20) magnesium sulfate on the spastic artery by computerized image analysis. A >50% reduction in baseline diameter of the basilar artery was observed in the rats subjected to subarachnoid hemorrhage compared with the 10 controls (p<0.0001). Intravenous magnesium sulfate dilated the spastic artery to approximately 75% of the baseline diameter in control rats (p<0.0001). Topical magnesium sulfate caused dramatic dilation of the basilar artery in both the control and the subarachnoid hemorrhage groups to near 150% of the baseline diameter in the controls (/?<0.001). All rats receiving intravenous magnesium sulfate reached therapeutic plasma levels of the ion. Hemodynamic effects were mild and immediately reversible upon cessation of magnesium sulfate administration. We suggest that magnesium has a role in the treatment of subarachnoid hemorrhage-induced vasospasm in humans. (Stroke 1991;22:922-927) C erebral vasospasm is a major complication of aneurysmal subarachnoid hemorrhage (SAH) that contributes to the high incidence of morbidity and mortality from this disease.1 Different physiological perturbations, such as the activation of lipid peroxidation and the liberation of free radicals, changes in the activity of scavenger enzymes, and the enhancement of arachidonic acid metabolism, have been implicated in the development of SAH-induced vasospasm.2 -5 Regardless of the many possible etiologies for SAH-induced vasospasm, it seems that impaired homeostasis of Ca 2+ is the final common pathway responsible for this complication.6 Numerous reports investigating the potential of calcium channel blockers and calmodulin inhibitors to prevent or reverse ischemic damage related to vasospasm have been published in recent years with contrasting results. 7 -13 Recently, cerebral vasospasm has been implicated in the pathogenesis of another disease - Received October 29, 1990; accepted March 8, 1991. toxemia of pregnancy. 14 Computed tomograms of eclamptic women have shown hypodense lesions in the basal ganglia and cortex suggestive of ischemia. "17 Cerebral angiography performed in such patients reveals widespread diffuse narrowing of all intracranial arteries.18 " 20Since 1925 21 eclampsia has been successfully treated with magnesium sulfate, which is considered to be the drug of choice for preeclampsia-eclampsia in toxemic women. 22 It has been suggested that magnesium prevents eclamptic vasospasm via Ca 2+ antagonism.23 Accordingly, we evaluated the effect of magnesium on SAH-induced vasospasm. Materials and MethodsWe divided 40 male Sprague-Dawley rats weighing 375-400 g into three groups. Twenty rats were subjected to SAH and were treated with intravenous magnesium followed by topical...

Delayed nonhemorrhagic encephalopathy following mild head trauma is a rare condition with an unknown etiology. The few cases reported in the literature are in young adults, all of them in the era before computerized tomography (CT) became available, and all had a devastating clinical course with multifocal ischemia or necrotic lesions found at autopsy. A case is presented of a young man with this syndrome who survived the acute encephalopathic phase with severe residual neurological deficits. Repeat CT scans during and following the acute phase as well as magnetic resonance imaging showed diffuse multifocal lesions compatible with ischemic changes and demyelination in the "watershed" areas of the brain.