Cortical spreading depression

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Metrics details. Spreading depression SD is a slowly propagating wave of near-complete depolarization of neurons and glial cells across the cortex. SD is thought to contribute to the underlying pathophysiology of migraine aura, and possibly also an intrinsic brain activity causing migraine headache. Experimental models of SD have recapitulated multiple migraine-related phenomena and are considered highly translational. In this review, we summarize conventional and novel methods to trigger SD, with specific focus on optogenetic methods. We outline physiological triggers that might affect SD susceptibility, review a multitude of physiological, biochemical, and behavioral consequences of SD, and elaborate their relevance to migraine pathophysiology.

Cortical spreading depression

Federal government websites often end in. The site is secure. Cortical spreading depression CSD and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow CBF. There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves. In normal brain tissue studied experimentally, CSD usually has to be induced by a deliberate perturbation of the brain such as electrical or mechanical stimulation Leao, In hypoxic, ischemic, or hypoglycemic brain tissue, CSDs will usually occur spontaneously, and recovery occurs with a prolonged time course Kraig and Nicholson, In this review, we use the abbreviation CSD as a generic term for all brain waves characterized by near-complete sustained depolarization of neurons Leao, Peri-infarct depolarizations PIDs; spontaneous and other spreading depolarization waves accompanying brain injury may not be accompanied by depression of the electroencephalography EEG , as the EEG is already silent in the compromised brain tissue.

Traces 3 and 4: band-pass filtered ECoG 0.

Federal government websites often end in. The site is secure. Migraine is a very common disorder of the nervous system. It shares similar physiological processes with stroke. Migrainous infarction is a rare complication of migraine with aura. The neuro-logical symptoms of migraine aura correspond to the cortical spreading depression and this depression can lead to a migrainous infarction.

Metrics details. Spreading depression SD is a slowly propagating wave of neuronal and glial depolarization lasting a few minutes, that can develop within the cerebral cortex or other brain areas after electrical, mechanical or chemical depolarizing stimulations. These ionic shifts produce slow direct current DC potential shifts that can be recorded extracellularly. Moreover, CSD is associated with changes in cortical parenchymal blood flow. CSD has been shown to be a common therapeutic target for currently prescribed migraine prophylactic drugs. Yet, no effects have been observed for the antiepileptic drugs carbamazepine and oxcarbazepine, consistent with their lack of efficacy on migraine.

Cortical spreading depression

Metrics details. Spreading depression SD is a slowly propagating wave of near-complete depolarization of neurons and glial cells across the cortex. SD is thought to contribute to the underlying pathophysiology of migraine aura, and possibly also an intrinsic brain activity causing migraine headache. Experimental models of SD have recapitulated multiple migraine-related phenomena and are considered highly translational.

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The prodromal phase can be followed by the aura phase in which the patient usually suffers from visual disturbances and numbness or tingling on one side of the body, symptoms that can last for minutes. Clin Exp Pharmacol Physiol 23 10—11 — Secondary ICH is caused by bleeding in tumors or congenital malformations or is due to coagulopathy or anticoagulant treatment. The same migraine-causing mechanisms may induce an infarction, potentially through a vasospasm. Platelet-activating factor PAF in internal jugular venous blood of migraine without aura patients assessed during migraine attacks. To determine whether CSD contributes to the maturation of cortical contusions in normally perfused and oxygenated animals, Baumgarten et al applied an approach used earlier by others in experimental stroke: they elicited additional CSDs, remote and independent from the primary injury, which then invaded the evolving contusion. USA , — Curr Pain Headache Rep 20 7 Accepted : 31 July It is pertinent to state that some derangements in the vascular function accompany migraine which may also serve as targets for research and treatment. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. Articles from Discoveries are provided here courtesy of Applied Systems. Table 3 Migraine and stroke related disorders and their associated genes and clinical presentations

Wannan Tang and Gry Fluge Vindedal contributed equally to this work. Looger, Erlend A.

Migraine with aura; Abnormal circadian rhythms. Download citation. Ebersberger A, Schaible HG, Averbeck B, Richter F Is there a correlation between spreading depression, neurogenic inflammation, and nociception that might cause migraine headache? Harriott View author publications. The link between migrainous infarction and cortical spreading depression. Pathology and etiology of cortical spreading depression. In normal rats, -arginine pretreatment prevents the development of low CBF after CSD, and increases the rate of recovery of the cerebrovascular responsiveness after CSD Gault et al , ; Fabricius et al , We outline physiological triggers that might affect SD susceptibility, review a multitude of physiological, biochemical, and behavioral consequences of SD, and elaborate their relevance to migraine pathophysiology. Changes in energy metabolites, cGMP and intracellular pH during cortical spreading depression. We hypothesize that this delay might reflect the time necessary to reach threshold levels of extracellular glutamate-glutamatergic plumes consequent to impairment of glutamate clearance. JAMA 4 — Extracellular Ph changes during spreading depression and cerebral-ischemia—mechanisms of brain Ph regulation. Dreier Neurocritical Care Found in children; Migraine with abdominal disturbances; Seizures; Hearing loss. This depression spreads across the cortical surface at the rate of 2 mm to 5 mm.