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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...

SUMMARY Eighty-nine cases of brain abscess, diagnosed over a period of 30 years, are reviewed. The incidence of this disease did not decline throughout the period. Abscesses of ear and nose origin constituted the largest group (38%). Postoperative abscesses seem to have increased in incidence, presumably due to routine postoperative antibiotic treatment. Antibiotics were possibly responsible for the suppression of signs of infection in 4500 of the patients, who presented as suffering from a space-occupying lesion. The most accurate diagnostic tool was angiography, which localized the lesion in 9000 and suggested its nature in 61%. Brain scan may prove as satisfactory.Staphylococcus was cultured in about two-thirds of the cases. Mortality seemed to decrease concomitantly with the advent of more potent antibiotics. The treatment of choice in terms of both mortality and morbidity seemed to be enucleation after previous sterilization. The hazards of radical surgery should be taken into consideration.

Seven children with rapid enlargement of the head and other clinical features resembling hydrocephalus are described. All children remained with relatively large heads, developed slowly and all but one had various degrees of mental and motor handicaps. The EEG was disturbed in all cases; two children developed seizures. Increased intracranial pressure was present. In all patients the subarachnoid space was markedly widened while the ventricular system was normal or minimally dilated. The characteristics of this syndrome, the features distinguishing it from similar conditions as well as its possible mechanism are discussed.