Local cerebral glucose utilization (LCGU) was studied using the 14C-deoxyglucose method in rats with focal thermally induced lesions in the left parietal cortex. A depression of LCGU developed with time after production of the lesion, being most prominent throughout the cortical areas of the lesioned hemisphere: 42 +/- 2% (SE) of normal 3 days after the lesion was induced. Corresponding results in other regions were: contralateral cortical areas, 86 +/- 2%; ipsilateral and contralateral subcortical structures, 74 +/- 2% and 84 +/- 1%, respectively. Brainstem structures were not affected. In white matter, bilateral depression of LCGU reached its peak 24 hours after production of the lesion--the reduction ipsilateral to the lesion was 61 +/- 4% of normal and the contralateral reduction was 64 +/- 4%. LCGU returned to normal within 5 days in all affected areas. No corresponding changes in local cerebral blood flow were observed. These results suggest a widespread depression in the functional state of traumatized brain.

The capacity for biosynthesis of prostaglandin F2alpha (PGF2alpha) and prostaglandin E2 (PGE2) from endogenous precursors by brain tissue slices and homogenates was measured by a gas chromatography - mass fragmentography method using deuterated prostaglandins as internal standards. Mean biosynthesis in rat cerebral cortex slices incubated for 60 min was 60.2 ng PGF2alpha and 17.4 ng PGE2 per 100 mg of tissue. The corresponding values for homogenates were 78.1 ng and 28.9 ng. Synthetic capacity of cat cerebral cortex was considerably greater but that of human tissue was smaller than that found in rat brain. Cat cerebellum in contrast to other regions synthesized more PGE2 than PGF2alpha. The time-course of prostaglandin formation in slices was linear for the initial 60 min. Catabolism in cerebral tissues was found to be very small. Prostaglandins formed or added to the incubation media distributed between tissue and medium in a manner indicating some specific binding as well as nonspecific solubilization in tissue lipids. Norepinephrine, 3,4-L-dihydroxyphenylalanine, dopamine, adrenochrome and apomorphine greatly stimulated PGF2alpha formation probably through a nonenzymatic reduction of endoperoxides. Norepinephrine added to homogenates appeared to stabilize the fatty acid cyclo-oxygenase preventing it from inactivation. Indomethacin and Ketoprofen were potent inhibitors of biosynthesis. Paracetamol was found to be a less potent synthetase inhibitor than aspirin. The biosynthetic capacity of brain tissue in vitro appears to be orders of magnitude more than that of normal brain in situ.

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...

Following several days of partial status epilepticus, three patients developed striking focal cerebral edema as demonstrated by computed axial tomography (CT) scan. An angiogram done in one patient showed a capillary blush and early cortical draining veins in the corresponding area. All patients developed severe focal neurological deficit which resolved as the edema improved, and this was demonstrated on serial CT scans (at 6 months, 1 month, and 2 months, respectively). In the first patient, an underlying tumor, and in the second and third, vascular occlusions, were suspected because we were not aware that edema due to status epilepticus could produce changes of such intensity and duration. The neurological disability after the partial status was long-lasting but reversed completely in our patients. Maximal radiological changes occurred in the area of maximal epileptic discharge. Minimal atrophic changes persisted in two of the three patients. The clinical, CT scan, and angiographic findings suggest that partial status epilepticus can be associated with abnormal vascular permeability leading to prolonged focal cerebral edema. Similar pathophysiology of lesser intensity may be responsible for shorter postictal neurological deficits. Awareness of this clinical and radiological entity should avoid misdiagnosis of cerebral tumor or infarction.