Compromised metabolic recovery following spontaneous spreading depression in the penumbra

Selman, Warren R.; Lust, W. David; Pundik, Svetlana; Zhou, Yanguang; Ratcheson, Robert A.

doi:10.1016/j.brainres.2003.11.016

Cited by 77 publications

(64 citation statements)

References 51 publications

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“…Despite these changes, CSDs do not cause any longlasting structural damage to otherwise healthy brain tissue (Nedergaard and Hansen, 1988). In ischemic brain, however, repetitive waves of depolarization result in stepwise depletion of energy stores and functional as well as structural deterioration of the penumbra leading to an increase of infarcted tissue volume (Ohta et al, 2001;Selman et al, 2004;Hopwood et al, 2005;Umegaki et al, 2005). The deleterious effects of CSDs are believed to be mainly mediated by a lack of compensatory hyperperfusion usually occurring to match the metabolic strain caused by repolarization (Back et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

Baumgarten¹,

Trabold²,

Thal³

et al. 2008

J Cereb Blood Flow Metab

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In recent years, several studies have unequivocally shown the occurrence of cortical spreading depressions (CSDs) after stroke and traumatic brain injury (TBI) in humans. The fundamental question, however, is whether CSDs cause or result from secondary brain damage. The aim of the current study was, therefore, to investigate the role of CSDs for secondary brain damage in an experimental model of TBI. C57/BL6 mice were traumatized by controlled cortical impact. Immediately after trauma, each animal showed one heterogeneous direct current (DC) potential shift accompanied by a profound depression of electroencephalogram (EEG) amplitude, and a temporary decrease of ipsi-and contralateral regional cerebral blood flow (rCBF) suggesting bilateral CSDs. Within the next 3 h after TBI, CSDs occurred at a low frequency (0.38 CSD/h per animal, n = 7) and were accompanied by rCBF changes confined to the ipsilateral hemisphere. No significant relationship between the number of SDs and lesion size or intracranial pressure (ICP) could be detected. Even increasing the number of posttraumatic CSDs by application of KCl by more than six times did not increase ICP or contusion volume. We therefore conclude that CSDs may not contribute to posttraumatic secondary brain damage in the normally perfused and oxygenated brain.

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Section: Discussionmentioning

confidence: 99%

Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

Baumgarten¹,

Trabold²,

Thal³

et al. 2008

J Cereb Blood Flow Metab

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show abstract

“…3). Because it has been shown that peri-infarct depolarizations not only enhance energy depletion (Busch et al, 1996;Selman et al, 2004) but also impair penumbral microcirculation by reducing capillary red blood cell perfusion despite arteriolar dilatation (Pinard et al, 2002), we assume that, in a deleterious feedback cascade, cascadelike pathophysiological sequelae of electrophysiological, metabolic, and microcirculatory perturbations generate progressive infarction. The role of brain swelling and ICP rise should not be underestimated in this process.…”

Section: Biphasic Appearance Of Depolarizations and Malignant Course mentioning

confidence: 99%

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Umegaki¹,

Sanada²,

Waerzeggers³

et al. 2005

J. Neurosci.

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Spreading depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in cortical border zones of experimental focal ischemia. We intended to investigate the relevance of ischemic depolarization in subcortical regions of ischemic territories.Calomel We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in cortical but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra. The generation of these ischemic depolarizations is a multifocal process possibly linked to brain swelling and intracranial pressure rise in the later course of focal ischemia, and therefore a relevant correlate of progressively worsening conditions.

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“…necrotic), hypo-functional, but also normoand hyper-functional (i.e. regenerating) tissue compartments and the post-treatment metabolic changes may reflect the tissue reactivity in this functionally composite region [59,60].…”

Section: Glucose Metabolism Before and After Treatmentmentioning

confidence: 99%

Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study

Szilágyi¹,

Nagy²,

Balkay³

et al. 2005

Journal of the Neurological Sciences

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Compromised metabolic recovery following spontaneous spreading depression in the penumbra

Cited by 77 publications

References 51 publications

Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

Peri-Infarct Depolarizations Reveal Penumbra-Like Conditions in Striatum

Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study

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