An experimental model of cerebral ischemia and infarction can be produced by occluding a middle cerebral artery in animals. Most surgical approaches to the artery require removal of some portion of the cranium, which may modify or prevent the changes of intracranial pressure and the development of pressure gradients that are caused by ischemic cerebral edema or brain swelling. A transorbital approach for the exposure of a middle cerebral artery requires only enlargement of the optic foramen, which can be sealed immediately after occlusion of the artery. The lack of disturbance and manipulation of the brain and the maintenance of the integrity of the cranium result in a superior experimental model.

SUMMARY A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition.Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.THE IMPORTANCE of brain swelling in the pathogenesis of stroke assumes growing significance as physicians increase their understanding of cerebrovascular diseases and their attempts to provide treatment. For example, a recent report 1 shows that in 32 of 100 patients who died as the result of cerebral infarction, transtentorial herniation was considered to be the most serious factor contributing to death. In the experience of most clinicians, a "swollen brain" can be demonstrated as well in a substantial number of patients who come to autopsy as a result of cerebral hemorrhage.The study group members appreciate fully the difficulties involved in understanding and interpreting current knowledge of cerebral edema pathogenesis gained from animal experimentation. Nevertheless, the basic information derived from a variety of animal models and reported in detail in the first pages of this report is considered essential to understanding the cerebrovascular events occurring in man. The ultimate objectives are to prevent cerebral edema wherever possible and to treat the condition when it develops, with the expectation of reducing the morbidity and mortality resulting from this complication. Classification of Cerebral EdemaCerebral edema is defined as an increase in brain tissue volume resulting from an increase in its fluid content.2 It must at all times be differentiated from brain engorgement caused by an increase in the volume of blood within a region of the brain 3 and from brain swelling due to intracerebral hemorrhage.• A priori, one might suppose that edema associated with cerebrovascular lesions would be primarily of the vasogenic type, since both overt injury to blood vessels and often a discrete focal brain lesion are present. However, experimentally, the increase in tissue volume and water is found usually to reach a peak prior to the extravasation of protein or of BBB indicators. Clinically, swelling in and around an area of infarction may be present before the radionuclide (RN) scan used to monitor BBB leakage becomes positive. This evidence suggests that brain edema due to focal ischemia begins as a cytotoxic type and is followed by a vasogenic edema. But the pathophysiology of this edema and its pattern of development are sufficiently specific to warrant a separate classification as ischemic brain edema. Biochemical Measures of Exp...

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