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Related Experiment Videos

The ischemic penumbra

W D Heiss1, R Graf

  • 1Max-Planck-Institut für neurologische Forschung, Köln, Federal Republic of Germany.

Current Opinion in Neurology
|February 1, 1994
PubMed
Summary
This summary is machine-generated.

The ischemic penumbra, brain tissue at risk during stroke, is a dynamic process. Interventions targeting its molecular changes may offer a wider therapeutic window than reperfusion alone.

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Area of Science:

  • Neuroscience
  • Cerebrovascular Biology
  • Molecular Medicine

Background:

  • The ischemic penumbra is defined as brain tissue with impaired perfusion and metabolism, potentially salvageable after ischemic stroke.
  • This tissue is characterized by uncertain chances for infarction or recovery, with dynamic changes over time.
  • Understanding the penumbra's propagation is crucial for developing effective stroke therapies.

Purpose of the Study:

  • To review the concept of the ischemic penumbra as a dynamic process.
  • To discuss the electrophysiologic and biochemical mediators involved in ischemic penumbra propagation.
  • To highlight the therapeutic implications of the ischemic penumbra's time-dependent nature.

Main Methods:

  • Review of accumulated research on the ischemic penumbra.

Related Experiment Videos

  • Discussion of electrophysiologic events (e.g., depolarization waves).
  • Analysis of biochemical/molecular events (e.g., excitatory amino acids, gene expression).

    • Main Results:

    • The ischemic penumbra is a dynamic process, propagating from the center of ischemia over time.
    • Multiple mediators, including depolarization, excitatory amino acids, and gene induction, modulate this process.
    • Positron emission tomography demonstrates viable penumbra tissue for several hours post-stroke.

    Conclusions:

    • The ischemic penumbra represents a dynamic cascade of events following stroke.
    • Therapeutic interventions targeting molecular processes within the penumbra may extend beyond the short window for reperfusion.
    • Further research is needed to clarify the contribution of specific events to neuronal damage and to optimize therapeutic strategies.