title: Assessment of pathophysiology of stroke by positron emission tomography.
abstract: In stroke patients, multitracer positron emission tomography (PET) permits the assessment of acute changes in regional cerebral blood flow (rCBF), blood volume (rCBV), oxygen consumption (rCMRO2) and glucose metabolism (rCMRgl), which are the initial steps in the complex molecular and biochemical process leading to ischaemic cell damage. While early infarcts exhibit low flow and oxygen consumption, increased oxygen extraction fraction (OEF) due to preserved metabolism at reduced flow suggests viability of tissue. However, most initially "viable" tissue will be metabolically deranged and will become necrotic in the further course; only in a few instances do these tissue compartments recover to normal function. Increased glucose uptake at reduced oxygen supply induces non-oxidative glycolysis with noxious lactacidosis, whereas hyperperfusion beyond the metabolic demand is of controversial effect. In subacute or chronic states after ischaemia reduced flow can be compensated by increased blood volume; when perfusional reserve is exhausted, oxygen extraction increases. Such findings may guide therapeutic decisions and predict the severity of permanent deficits. Functional deactivation of tissue remote from the lesion is found regularly as a sign of damaged connecting pathways. Flow and metabolic studies during the performance of specific tasks help to detect alternative functional loops and may yield prognostic information. Repeat studies in the course of stroke are employed for the evaluation of therapeutic strategies targeted to improve reperfusion or to effect metabolic or biochemical alterations. In the future PET may gain additional clinical importance when patients are selected for elective treatment according to the prevailing pathophysiological pattern.
authors.affiliation: Max-Planck-Institut für neurologische Forschung and Neurologische Universitätsklinik, Köln, Germany.
authors.forename: W D
authors.initials: WD
authors.lastname: Heiss
authors.forename: K
authors.initials: K
authors.lastname: Herholz
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D010101:Oxygen Consumption; D014055:Tomography, Emission-Computed
chemical_list: D005947:Glucose