The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.

The vasa vasorum have not been previously reported to contribute to the revascularization of occluded arteries. The four cases presented in this report suggest that the vasa vasorum can be a source of collateral circulation after carotid artery occlusion secondary to atherosclerotic disease.

There was a tendency toward left VA dominance in the hypertensive group compared with the control group, although a significant difference was shown by only one of the four reviewers. There were no differences in brainstem compression or rotation between the hypertensive and nonhypertensive groups. These results are contrary to those of recently published studies in which MR imaging and/or MR angiography revealed lateral brainstem vascular compression in hypertensive patients but not in nonhypertensive (control) patients. Reasons for this discrepancy are discussed. On the basis of their own experience and that of others, the authors believe that neurogenic hypertension does exist. However, thin-slice MR imaging may not be a reliable method for detecting neurovascularly induced essential hypertension and the prevalence of neurovascular compression as the source of hypertension may be overestimated when using current imaging techniques.

A hyperossified meningioma with significant calvarial thickening is fairly common. Craniectomy of the involved region followed by cranioplasty is usually required to resect the bone overgrowth. However, in some cases, the hyperossified calvaria is too thick to allow safe penetration with a craniotome or trephine. In this report, the authors present a technique for preserving the outer calvaria while still resecting the majority of the underlying tumor mass. The key is to perform a craniotomy in a region adjacent to the hyperossified bone and to remove the tumorous, ossified inner table through this "window" by means of a high-speed drill. A second craniotomy can then be performed over the undermined area; this maneuver can be advanced and repeated until the tumor is resected. Frameless stereotactic guidance and microplates are useful in performing this procedure.