Pathogenic mechanisms in ischemic damage: A computational study

Eytan Ruppin*, Elad Ofer, James A. Reggia, Kenneth Revett, Goodall Sharon Goodall

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

The pathogenesis of penumbral tissue infarction during acute ischemic stroke is controversial. This peri-infarct tissue may subsequently die, or survive and recuperate, and its preservation has been a prime goal of recent therapeutic trials in acute stroke. Two major hypotheses currently under consideration are that penumbral tissue is recruited into an infarct by cortical spreading depression (CSD) waves, or by a non-wave self-propagating process such as glutamate excitotoxicity (GE). Careful experimental attempts to discriminate between these two hypotheses have so far been quite ambiguous. Using a computational metabolic model of acute focal stroke we show here that the spatial patterns of tissue damage arising from artificially induced loci of infarction having specific geometric shapes are inherently different. This is due to the distinct propagation characteristics underlying self-regenerating waves and non-wave diffusional processes. The experimental testing of these predicted spatial patterns of damage may help determine the relative contributions of the two pathological mechanisms hypothesized for ischemic tissue damage.

Original languageEnglish
Pages (from-to)39-59
Number of pages21
JournalComputers in Biology and Medicine
Volume29
Issue number1
DOIs
StatePublished - Jan 1999

Funding

FundersFunder number
National Institute of Neurological Disorders and StrokeR01NS029414
Bloom's Syndrome Foundation96-00238
Ministry of Health, State of Israel01350931

    Keywords

    • Computational modeling
    • Cortical spreading depression
    • Glutamate excitotoxicity
    • Penumbra
    • Stroke
    • Tissue damage

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