Spreading depression: a review of the clinical relevance

Gorji, Ali

doi:10.1016/s0165-0173(01)00081-9

Cited by 272 publications

(167 citation statements)

References 396 publications

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“…1 Clinically, CSD is postulated to play a role in the pathogenesis of stroke, 2 traumatic cortical injury, 3 cerebral ischemia, 4,5 migraine, 6 and transient global amnesia. 7 CSD can be induced by a variety of stimuli including pinprick or needle stab, 8,9 elevated potassium, 5,10 electrical stimulation, 1,11 or glutamate application. On a cellular level, electrophysiological changes are accompanied by significant shifts in intra-and extracellular ion concentrations, 12 cellular swelling, 13 dendritic beading, 14 and changes in gene expression.…”

Section: Introductionmentioning

confidence: 99%

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

et al. 2005

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Abstract. Cortical spreading depression (CSD) is a pronounced depolarization of neurons and glia that spreads slowly across the cortex followed by a period of depressed electrophysiological activity. The vascular changes associated with CSD are a large transient increase in blood flow followed by a prolonged decrease lasting greater than 1 h. Currently, the profile of functional vascular activity during this hypovolemic period has not been well characterized. Perfusion-based imaging techniques such as functional magnetic resonance imaging (fMRI) assume a tight coupling between changes in neuronal and vascular activity. Under normal conditions, these variables are well correlated. Characterizing the effect of CSD on this relationship is an important step to understand the impact acute pathophysiological events may have on neurovascular coupling. We examine the effect of CSD on functional changes in cerebral blood volume (CBV) evoked by cortical electrophysiological activity for 1 h following CSD induction. CBV signal amplitude, duration, and time to peak show little recovery at 60 min post-induction. Analysis of spontaneous vasomotor activity suggests a decrease in vascular reactivity may play a significant role in the disruption of normal functional CBV responses. Electrophysiological activity is also attenuated but to a lesser degree. CBV and evoked potentials are not well correlated following CSD, suggesting a breakdown of the neurovascular coupling relationship.

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Section: Introductionmentioning

confidence: 99%

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

et al. 2005

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“…A considerable body of work has equated SD as the underlying mechanism of classical migraine (see review by Gorji). 26 Now a series of studies have demonstrated that multiple SD waves can occur in patients following SAH. 12,27 Following middle cerebral artery occlusion (MCAO) in the baboon, Branston et al 28 identified transient increases in extracellular potassium with voltage alterations similar to those seen with SD in the ischemic penumbra.…”

Section: A New Mechanismmentioning

confidence: 99%

New concepts regarding cerebral vasospasm: glial-centric mechanisms

Mutch

2010

Can J Anesth/J Can Anesth

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Purpose Poor outcome in patients with cerebral vasospasm following subarachnoid hemorrhage remains a serious clinical problem. The current management with focus on the cerebrovascular constriction accounts for the use of ''triple-H'' therapy (hypertension, hypervolemia, and hemodilution) to enhance cerebral blood flow through constricted vessels. Recent work suggests that spreading depression (a stereotypical response of cerebral cortical tissue to noxious stimuli with subsequent oligemic blood flow) occurs in patients with cerebral vasospasm. A narrative review was conducted to examine the relationship between spreading depression and subarachnoid hemorrhage and to identify the anesthetic effects on the propagation of spreading depression. Principal findings Following review of the literature, an underlying mechanism is advanced that cerebral vasospasm is not primarily a problem of the cerebral vasculature but a consequence of glial cell dysfunction following spreading depression -a glial-centric cause for vasospasm. Such a mechanism for vasospasm becomes manifest when spreading depression waves transition to peri-infarct depolarization waves -with protracted ischemic blood flow in compromised tissue. The extracellular microenvironment with high potassium and low nitric oxide tension can account for conducting vessel narrowing. Conclusions The implication for clinical management is discussed supposing glial cell dysfunction is an underlying mechanism responsible for the vascular spasm. RésuméObjectif Les mauvais pronostics chez les patients manifestant un vasospasme ce´re´bral a`la suite d'une he´morragie sous-arachnoı¨dienne demeurent un proble`me clinique majeur. La prise en charge actuelle se concentre sur la constriction vasculaire ce´re´brale, ce qui explique le recours au traitement dit des « trois H » (hypertension, hypervole´mie et he´modilution) dans le but d'ame´liorer le de´bit sanguin ce´re´bral dans les vaisseaux contracte´s. Des recherches re´centes sugge`rent qu'une de´pression propage´e (une re´action typique du tissu cortical ce´re´bral aux stimuli nociceptifs, laquelle est suivie d'un de´bit sanguin re´duit) survient chez les patients manifestant un vasospasme ce´re´bral. Un compte-rendu narratif a e´te´entrepris afin d'examiner la relation entre la de´pression propage´e et l'he´morragie sous-arachnoı¨dienne ainsi que d'identifier les effets des anesthe´siques sur la propagation de la de´pression propage´e. Constatations principales Apre`s avoir passe´en revue la litte´rature sur le sujet, l'hypothe`se d'un me´canisme sous-jacent est avance´e, selon laquelle le vasospasme ce´re´bral n'est pas un proble`me principalement lie´a`la vasculature ce´re´brale mais plutôt la conse´quence d'un dysfonctionnement des cellules gliales apre`s une de´pression propage´e -en d'autres mots, le vasospasme est cause´principalement au niveau glial. Ce me´canisme qui provoque le vasospasme est manifeste lorsque les vagues de de´pression propage´e se changent en vagues de de´polarisation autour de l'infarct...

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“…[1][2][3] CSD is an important disease model for migraine 4 and is related to other neurological disorders, such as neurotrauma, 5 seizure, 6 and ischemia. 7,8 CSD initiated in vivo has been discussed in terms of the changes in tissue optical properties related to hemodynamics originating from neurovascular coupling in brain tissue.…”

Section: Introductionmentioning

confidence: 99%

In vivoestimation of light scattering and absorption properties of rat brain using a single-reflectance fiber probe during cortical spreading depression

et al. 2015

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Abstract. Diffuse reflectance spectroscopy using a fiber optic probe is a promising technique for evaluating the optical properties of biological tissue. We herein present a method for determining the reduced scattering coefficient, μ 0 s , the absorption coefficient, μ a , and the tissue oxygen saturation, StO 2 , of in vivo brain tissue using a single-reflectance fiber probe with two source-collector geometries. We performed in vivo recordings of diffuse reflectance spectra and of the electrophysiological signals for exposed rat brain during the cortical spreading depression evoked by the topical application of KCl. The time courses of μ a at 500, 570, and 584 nm indicated the hemodynamic change in the cerebral cortex as well as StO 2 . At 570 nm, the time course of μ 0 s was well correlated with that of μ a , which also reflects the scattering by RBCs. On the other hand, increases in μ 0 s at 500 and 584 nm and a decrease in μ 0 s at 800 nm were observed before the profound increase in μ a , and these occurrences were synchronized with the negative dc shift of the local field potential. The resultant change in the slope of μ 0 s ðλÞ is indicative of the morphological changes in the cellular and subcellular structures induced by the depolarization due to the temporal depression of the neuronal bioelectrical activity. The results of the present study indicate the potential application of the proposed method in evaluating the pathophysiological conditions of in vivo brain. © The Authors. Published by SPIE under a Creative Commons Attribution 3.0 Unported License. Distribution or reproduction of this work in whole or in part requires full attribution of the original publication, including its DOI.

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Spreading depression: a review of the clinical relevance

Cited by 272 publications

References 396 publications

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

New concepts regarding cerebral vasospasm: glial-centric mechanisms

In vivoestimation of light scattering and absorption properties of rat brain using a single-reflectance fiber probe during cortical spreading depression

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