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(Stroke. 2003;34:2533.)
© 2003 American Heart Association, Inc.

Controversies in Stroke

Measurement of the Ischemic Penumbra With MRI: It’s About Time

From the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

Correspondence to Steven Warach, MD, PhD, National Institute of Neurological Disorders and Stroke, 10 Center Dr, MSC 1063, Bldg 10, Rm B1D733, Bethesda, MD 20892-1063. E-mail warachs@ninds.nih.gov

Key Words: cerebral blood flow • magnetic resonance imaging • penumbra • randomized controlled trials

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The idea that there exist 2 ischemic thresholds in the pathogenesis of cerebral infarction came from seminal microelectrode studies of the baboon cortex the late 1970s^1,2 that measured the effects of progressive reductions in cerebral blood flow (CBF). These studies described a level of CBF reduction that led to cessation of cortical evoked responses in the absence of terminal increases in extracellular potassium or reductions in pH and a yet lower level of CBF reduction, at which occurred large increases in extracellular potassium and reductions in pH indicative of failure of membrane ion homeostasis and cell death.

Derived from animals too few and results too variable to specify a precise threshold, the insight nonetheless emerged that there were 2 levels of ischemia, one for tissue dysfunction without destruction and a lower one for irreversible cell injury. The metaphor of the ischemic penumbra was coined to describe this intermediate zone of ischemia between functionally normal and dead brain tissue. Restoration of normal CBF to the penumbral zone may reverse the functional disturbance.

Over the past 25 years, many investigators and clinicians have taken poetic liberties with the ischemic penumbra to suit their technologies and purposes. To some it is any variable that is intermediate in value between normal and that measured within the infarct. To others it is simply any noninfarcted brain with reduced CBF. To still others it is that region that is the optimal target of stroke therapy, destined for infarction if untreated but potentially salvageable if effectively treated. . . . [Full Text of this Article]

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