ACUTE CEREBRAL INFARCTION - PATHOPHYSIOLO GY AND MODERN TREATMENT CONCEPTS

This review focuses on the pathophysiological changes in acute cerebra l ischemia, with special emphasis on disturbances of the cerebral bloo d flow (CBF) and the associated penumbra concept. Alternatively, the m odel of peri-infarct depolarization is demonstrated. Metabolic and mol ecular changes caused by cerebral ischemia and reperfusion are discuss ed, namely energy failure, release of glutamate with an excitatoric bu rst, calcium influx in neurons, generation of free radicals, activatio n of different proteases, disturbances of protein synthesis, induction of gene expression and apoptosis, loss of membrane integrity edema fo rmation and microvascular disturbances. In summary, the pathophysiolog ical changes after focal cerebral ischemia and reperfusion are most ad equately described by a network of interacting different mechanisms of tissue alterations. The simple concept of a cascade of ischemic effec ts which would be easy to block seems to be less applicable. A time wi ndow of approximately 6 h for the acute stroke therapy is postulated o n the base of the above mentioned pathophysiological changes. The rece ntly introduced treatment regimen with optimized basic treatment, reca nalization using thrombolysis and neuroprotection by different agents is presented. Different modes of a possible intervention are discussed . Modern concepts of stroke therapy including stroke-unit care and thr ombolysis with add-on neuroprotection seem to have potential for impro ving the outcome of acute stroke patients.