Reconsideration of Hemodynamic Cerebral Ischemia Using Recent PET/SPECT Studies

Hemodynamic cerebral ischemia has been conceptually confirmed by positron emission tomography (PET) imaging, and misery perfusion could be compensated with both vascular and metabolic reserve; however, these compensatory reserve capacities do not always respond in the same manner from short-term to long-term compromise of hemodynamic cerebral ischemia.In patients with acute misery perfusion, CMRO2 is immediately compensated by a marked increase of OEF combined with a limited increase of CBV. In patients with chronic misery perfusion, a moderate increase of OEF is compatible with a moderate increase of CBV, which could correlate with a moderate decrease of vascular reserve (VR). In moyamoya disease with long-standing misery perfusion, hemodynamic cerebral ischemia is initially compensated with a great deal of vasodilation, and can then be followed with an increased OEF in response to the degree of progression.The stage of hemodynamic cerebral ischemia has been defined by an increase of OEF, but could be reconsidered from different patterns of the engagement of compensatory reserve capacities, and misery perfusion could be classified into three subtypes, such as acute, chronic, and long-standing misery perfusion.