Atherosclerotic cerebral infarction: pathophysiologic aspects.
When the supply of substrate to the brain is threatened, homeostatic mechanisms induce cerebral vasodilatation to compensate for the insufficiency. When a region of the brain is rendered completely ischemic, local infarction occurs. The size of the infarct depends partly on the availability of collateral circulation and the adequacy of the homeostatic mechanisms controlling blood flow in stillpatent vessels. Several approaches to acute-phase treatment of stroke derive from clinical and experimental studies of cerebral blood flow and metabolism. We must conclude that both surgical and nonsurgical therapeutic measures have been of limited value in the treatment of cerebral infarction and that the basic therapy for completed stroke remains good medical management of complications and attentive nursing care.
D001783:Blood Flow Velocity; D001921:Brain / Q000378:metabolism*; D001929:Brain Edema / Q000209:etiology / Q000628:therapy; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy; D004734:Energy Metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000150:complications; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D013997:Time Factors