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Pathophysiology of Stroke

Cell Biology

  1. Andreas Meisel,
  2. Konstantin Prass,
  3. Tilo Wolf,
  4. Ulrich Dirnagl

Published Online: 15 SEP 2006

DOI: 10.1002/3527600906.mcb.200400145

Reviews in Cell Biology and Molecular Medicine

Reviews in Cell Biology and Molecular Medicine

How to Cite

Meisel, A., Prass, K., Wolf, T. and Dirnagl, U. 2006. Pathophysiology of Stroke. Reviews in Cell Biology and Molecular Medicine. .

Author Information

  1. Department of Experimental Neurology (Charitá) Humboldt University, in, Germany

Publication History

  1. Published Online: 15 SEP 2006


The current understanding of stroke pathophysiology is basically founded on experimental models. Among these, in vitro models with primary cultures of cerebral cells permit stroke pathophysiology to be examined on a molecular level, while animal models (mainly mouse and rat) are used to evaluate medical intervention. There is a highly complex sequence of events leading to the eventual ischemic cerebral damage that follows a well-defined spatiotemporal pattern. Overwhelming excitotoxicity leads to early necrotic cell death in what is to become the core of the infarction, while the tissue damage in the surrounding zone called penumbra happens on a longer timescale. The excitotoxic or inflammatory mechanisms are milder, bearing the biochemical hallmarks of apoptosis. The brain cells, challenged by such a large-scale assault, activate endogenous protective programs. These have been studied by experimentally inducing ischemic tolerance (i.e. ischemic preconditioning). Importantly, cerebral ischemia not only affects the brain but also impacts other systems. For example, stroke induces dramatic immunodepression through overactivation of the sympathetic nervous system. As a result, severe bacterial infections such as pneumonia occur. The complex signaling cascades not only decide over cell survival in the brain and the neurological deficit but also over mortality after stroke from extracerebral complications. Their ability to govern not only the maturation of the eventual infarction but also the immune system make them a promising target for intervention and the development of neuroprotective drugs.


  • Agnosia;
  • Amaurosis;
  • Apraxia;
  • Ataxia;
  • Dyslexia;
  • Dysphasia;
  • Excitotoxicity;
  • Hemianopia;
  • Hemiparesis;
  • Ischemic Tolerance;
  • Penumbra;
  • SAGE