Peri-Infarct perfusion in human ischemia: Its relation to tissue metabolism, morphology, and clinical outcome.

Although experimental cerebral ischemia is well studied, little is actually known about the pathophysiology of human peri-infarct tissue. In a follow-up study concentrating on human peri-infarct tissue, we assessed the relationship among different perfusion conditions, metabolism, morphological damage, and clinical outcome. Cerebral blood flow was examined in 22 patients within 6-48 h after the ictus using (15)O-H2O positron emission tomography. The outcome of peri-infarct tissue was judged functionally, by using (18)F-2-fluoro-2-deoxy-D-glucose positron emission tomography for repeated measurements of glucose metabolism, and morphologically, by obtaining computed tomography or magnetic resonance images that were three-dimensionally aligned to the positron emission tomography scans. The individual clinical outcome was estimated using the Barthel index. In nine patients, both hyper- and hypoperfused peri-infarct tissue was seen. The clinical outcome of the patients with or without hyperperfused peri-infarct tissue was found not to be different. None of the hyperperfused peri-infarct regions underwent complete cystic degeneration, yet magnetic resonance imaging showed definite signal intensity changes. Glucose metabolic rates of hypoperfused peri-infarct tissue, measured initially and at least 2 weeks after the ictus, were significantly lower (p < 0.01) than those of hyperperfused or normoperfused peri-infarct tissue. Early spontaneous peri-infarct hyperperfusion occurs frequently. The metabolic and morphological data are suggestive of partial ischemic damage in these areas. It was only for hypoperfused peri-infarct tissue that a significantly poorer tissue outcome was demonstrated. The metabolic and morphological fate of hyper- and normoperfused peri-infarct tissue did not differ.