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(Stroke. 2009;40:1547.)
© 2009 American Heart Association, Inc.

Editorials

Metabolic Penumbra in Intracerebral Hemorrhage

Paul M. Vespa, MD, FCCM

From the Department of Neurosurgery and Neurology, David Geffen School of Medicine at UCLA.

Correspondence to Paul Vespa, MD, Associate Professor of Neurosurgery and Neurology, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Room 6236A Ronald Reagan UCLA Medical Center, 750 Westwood Blvd, Los Angeles, CA 90095. E-mail PVespa@mednet.ucla.edu

Key Words: intracerebral hemorrhage • seizures • glycolysis • positron emission tomography • spread depression • stroke • coma

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

See related article, pages 1638–1643.

In the past decade there has been considerable scientific discussion about the metabolic state of the tissue surrounding a brain hemorrhage. The scientific discussion has focused mostly on the question of whether brain ischemia is present in this "penumbral tissue," which has great clinical relevance because the presence of ischemia would drive clinical treatment considerations such as blood pressure management and surgery.¹ Ischemia has classically been considered to be the deprivation of oxygen to tissue caused by arterial occlusion, with a resulting increase in oxygen extraction fraction (OEF) followed by local tissue acidosis and eventually cell death. This model of ischemia has been used to define tissue at risk and is a core principal used for ischemic stroke. The exact PET thresholds that define ischemia² have been proposed and are presently being used in research settings. In an important study, Zazulia et al³ reported that the tissue immediately surrounding a brain hemorrhage did not exhibit classical ischemia as defined by PET OEF, and that small reductions in cerebral blood flow did not elicit much change in cerebral blood flow.⁴ This implies that ischemia is not present in the perihematomal tissue. PET OEF imaging in traumatic hemorrhage similarly shows no increase in OEF in the peritraumatic region.⁵ Nonetheless, the surrounding tissue displayed reductions in oxidative metabolism, with very low rates of oxygen use. This reduction in oxygen use is thought to be attributable to impaired mitochondrial function, which has preliminarily been confirmed in tissue samples . . . [Full Text of this Article]

Related Article:

Transient Focal Increase in Perihematomal Glucose Metabolism After Acute Human Intracerebral Hemorrhage

Allyson R. Zazulia, Tom O. Videen, and William J. Powers
Stroke 2009 40: 1638-1643. [Abstract] [Full Text] [PDF]