Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during <i>N</i>-methyl-<scp>d</scp>-aspartate superfusion

Ayata, Cenk; Moskowitz, Michael A.

doi:10.1152/ajpheart.01102.2005

Cited by 30 publications

(38 citation statements)

References 48 publications

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“…When present, this transient vasoconstrictive tone usually decreases CBF by 5-30% for 5-30 s, and can either precede the hyperemia leading to an early dip in CBF, or be superimposed on the rising slope giving the response a notched or jittery upstroke. Corresponding changes in vessel diameter have been detected by intravital microscopy of pial arteries (16,46,54,59,359,419,420). Moreover, several surface reflectance and light transmission studies have detected reduced CBV preceding the hyperemia (FIGURE 5A; component I), or notched or jittery upstroke, in multiple species including rats and cats (98,163,227,299,303,305,306,359,407,442,444,474,479,481).…”

Section: B Prototypical Cerebral Hemodynamic Response To Sdmentioning

confidence: 81%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

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472

600

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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leão, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

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Section: B Prototypical Cerebral Hemodynamic Response To Sdmentioning

confidence: 81%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

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472

600

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“…It is nevertheless interesting that common migraine prophylactic drugs were shown to lower the susceptibility to spreading depolarization [94].…”

Section: A Brief History Of Spreading Depolarizationmentioning

confidence: 99%

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

et al. 2011

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Spreading depolarization is a mechanism of abrupt, massive ion translocation between intraneuronal and extracellular space that entails cytotoxic edema in the brain’s gray matter. It is observed in patients as a large change of the slow electrical potential. Dependent on the energy status of the tissue, spreading depolarization is either preceded by nonspreading silencing due to neuronal hyperpolarization or accompanied by spreading silencing of electrical brain activity due to a depolarization block. Nonspreading silencing seems to translate into the initial clinical symptoms of ischemic stroke and spreading silencing translates into migraine aura. Direct electrophysiological evidence exists that spreading depolarization occurs in abundance in aneurysmal subarachnoid hemorrhage, delayed ischemic stroke after subarachnoid hemorrhage, malignant hemispheric stroke, spontaneous intracerebral hemorrhage and traumatic brain injury. Indirect evidence suggests its occurrence during migraine aura. In animals, spreading depolarizations facilitate neuronal death when they invade metabolically compromised tissue, whereas they are relatively innocuous in healthy tissue. Therapies targeting spreading depolarization may potentially treat these neurological conditions.

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“…The physiologic substrate of aura is CSD, a self-propagating wave of neuronal and glial depolarization. 33,34 Cascading depolarization marching across the cortical mantle initiates a series of cellular and molecular events, resulting in transient loss of membrane ionic gradients, as well as massive surges of extracellular potassium, neurotransmitters, and intracellular calcium.…”

mentioning

confidence: 99%

Migraine and cardiovascular disease

Bigal¹,

Kurth

Hu³

et al. 2009

Neurology

170

135

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Migraine, especially migraine with aura (MA), is an established risk factor for ischemic lesions of the brain. Recent evidence has also linked migraine to a broader range of ischemic vascular disorders including angina, myocardial infarction, coronary revascularization, claudication, and cardiovascular mortality. The mechanisms which link migraine to ischemic vascular disease remain uncertain and are likely to be complex. Cortical spreading depression, the presumed substrate of aura, may directly predispose to brain lesions and that would explain why MA is consistently demonstrated as a risk factor for cerebral ischemia, while for migraine without aura (MO), the evidence is less consistent. Additionally, individuals with migraine have a higher prevalence of risk factors known to be associated with cardiovascular disease (CVD), including hypertension, diabetes, and hyperlipidemia. The increased prevalence of CVD risk factors is also higher for MA than for MO. Since the evidence linking migraine and CVD is getting robust, neurologists should be aware of this association. Individuals with MO seem to be at little increased risk of CVD. MA is associated with an increased risk of ischemic stroke and likely also for other ischemic CVD events. Accordingly, heightened vigilance is recommended for modifiable cardiovascular risk factors in migraineurs, especially with MA. Ultimately, it will be important to determine whether MA is a modifiable risk factor for CVD and if preventive medications for migraine or antiplatelet therapy might reduce the risk of CVD in patients with MA. Neurology ® 2009;72:1864-1871 GLOSSARY BMI ϭ body mass index; CDH ϭ chronic daily headache; CI ϭ confidence interval; CSD ϭ cortical spreading depression; CVD ϭ cardiovascular disease; EPC ϭ endothelial progenitor cells; HR ϭ hazard ratio; MA ϭ migraine with aura; MMP ϭ matrix metalloproteinase; MO ϭ migraine without aura; MTHFR ϭ methyltetrahydrofolate reductase; RR ϭ relative risk.

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Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during N-methyl-d-aspartate superfusion

Cited by 30 publications

References 48 publications

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

Migraine and cardiovascular disease

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