Remote Effects of Focal Lesions on Cerebral Flow and Metabolism

Abstract

Impairment of regional energy metabolism and hemodynamics in morphologically unaltered areas of the brain beyond the bounds of ischemic tissue damage is a common finding in positron emission tomography (PET) of stroke patients. This transneural depression of function resulting from an actual brain lesion was first described by von Monakow [38]. He used the term “diaschisis” to denote the phenomenon of transient dysfunction, e.g., in the cerebral hemisphere contralateral to a cortical infarct, which may initially be widespread, but finally and gradually through unknown repair processes returns to whatever level it will naturally attain. Physiological evidence in support of this concept was presented by Kempinsky [17], who demonstrated that for up to 1 h following unilateral cortical ablation there is depressed electrical activity at homotopic points in the opposite hemisphere, and by Hoedt-Rasmussen and Skinhoj [14], who found a bilateral decrease in cerebral blood flow (CBF) after ischemic stroke. The latter observation was confirmed in several other two-dimensional CBF studies [25, 27, 36], but a more precise demonstration of such regional effects occurring far from the site of infarction was feasible only after the development of PET and appropriate tracer kinetic methods for noninvasive studies of local cerebral metabolism and blood flow [9,16,30,31, 33,37].