Abstract
In patients with atherothrombotic internal carotid artery (ICA) or middle cerebral artery (MCA) occlusive disease, the chronic reduction in cerebral perfusion pressure (chronic hemodynamic compromise) increases the risk for cerebral ischemic damage. We have shown that severe hemodynamic compromise, demonstrated as an increased oxygen extraction fraction (misery perfusion) with positron enmission tomography (PET), is a risk factor for subsequent ischemic stroke. Because a recent Japanease EC/IC bypass trial for patients with severe hemodynamic compromise demonstrated a benefit of bypass surgery for preventing ischemic stroke, detection of the patients with severe hemodynamic compromise is crucial for improving the prognosis of patients with atherothrombotic ICA or MCA occlusive disease. Hemodynamic cerebral ischemia due to ICA or MCA occlusive disease may not only cause cerebral infarction but also minor tissue damage in the cerebral cortex that is not detectable as an infarction on CT or MRI. Recently, imaging of the central type benzodiazepine receptors, which are expressed by most cortical neurons, has made it possible to visualize the neuronal alterations induced by ischemia in vivo in humans. Using PET, we have shown that selective neuronal damage demonstrated as a decrease in central benzodiazepine receptors in the normal-appearing cerebral cortex is associated with increased oxygen extraction fraction (misery perfusion). Misery perfusion is important for the development of selective neuronal damage as well as infarction in atherothrombotic ICA or MCA occlusive disease, and vascular reconstruction surgery may also lead to the prevention of selective neuronal damage. Benzodiazepine receptor imaging may become a useful tool for evaluating the success of future therapeutic interventions for protecting neurons from ischemic damage. Understanding the pathophysiology of hemodynamic cerebral ischemia is essential for the management of patients with atherothrombotic ICA or MCA occlusive disease.
