PET in Cerebrovascular Disease

Measurements of CBF and CMR in ischemia and infarction have provided valuable insight into the pathophysiology of cerebrovascular disease. Much has been learned about the compensatory responses of the brain to reductions in perfusion pressure and in the evolution of changes in blood flow and metabolism that occur when these mechanisms fail. Knowledge of these changes can help guide therapy when multiple factors such as ischemia, hypoxemia, hypocarbia, or hypotension may be affecting CBF. Understanding the hemodynamic effects of arterial stenosis or occlusion on the downstream perfusion pressure has been instrumental in designing new trials for treatment. 94 In acute ischemic stroke, measurements of CBF and metabolism have been used to define the ischemic penumbra'' and to predict both tissue and clinical outcome, although the clinical utility of these markers of ischemia in distinguishing viable from irreversibly damaged tissue in the acute period still requires further study. Blood flow and metabolic studies in ICH have documented the integrity of autoregulation, and have suggested that hematomas exert a primary depression of metabolism rather than inducing ischemia in the surrounding tissue. This finding has important implications for future consideration of therapeutic interventions in this disease. Studies in SAH have differentiated the primary effects of the hemorrhage on cerebral hemodynamics and metabolism from those of vasospasm and surgical retraction. In addition, vasospasminduced ischemia has been demonstrated to be reversible. In summary, defining the pathophysiological changes in CBF and metabolism in human cerebrovascular disease has provided and will continue to provide the basic foundation for development and testing of new treatment strategies.