Cortical spreading depression

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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Cortical spreading depression CSD is a self-propagating wave of cellular depolarization that has been implicated in migraine and in progressive neuronal injury after stroke and head trauma. Using two-photon microscopic NADH imaging and oxygen sensor microelectrodes in live mouse cortex, we find that CSD is linked to severe hypoxia and marked neuronal swelling that can last up to several minutes. Changes in dendritic structures and loss of spines during CSD are comparable to those during anoxic depolarization.

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. 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. The possibility of constructing a recurrent episodic or chronic migraine model using SD is also discussed. SD is characterized by a profound change in transmembrane ion gradients and loss of all spontaneous or evoked synaptic activity and action potentials, resulting in depression of electrocortical signals [ 2 ]. Since the original publications of Leao [ 1 , 7 ], experimental SD has been recorded in the cortices of both lissencephalic e. A link between SD and migraine pathogenesis has been hypothesized for decades [ 12 ], in particular the visual aura [ 13 , 14 ] and more recently the migraine headache. The visual disturbance can be variable and include fortification spectra, sparkling or shimmering colored dots and blobs, and scotoma [ 15 , 16 , 17 ]. While visual symptoms are the most commonly described aura event of migraine, other auras including sensory and speech disturbance have been described. In those with more than one aura symptom, the onset of the second or third aura symptom seem to follow the first or second aura symptom in succession, i. There are several clinical studies supporting SD as the likely mechanism involved in the aura event of migraine which has been the topic of multiple well written review articles.

Article Google Scholar. Timing and topography of cerebral blood flow, aura, and headache during migraine attacks. Nat Rev Neurosci 15 6 —

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.

Cortical spreading depression or CSD is an electrophysiological phenomenon affecting various perspectives of brain physiology such as ionic balance, neurotransmitter level, and blood flow in the brain. This phenomenon has greater impact on the brain function and results in the pathological contribution of many diseases in humans such as migraine with aura, stroke, and traumatic brain injury. Various factors such as nutrition, stress, sleep, age, alcohol, inflammation and oxidative stress worsen the condition and affect CSD susceptibility. Thus, correction of these main culprits might ameliorate the cumbersome effect of CSD, thereby providing benefits in diseases associated with CSD. This review collates most of the triggering factors that makes one prone to the CSD condition along with its underlying mechanisms. This is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve. Institutional subscriptions. Alcohol Clin Exp —

Cortical spreading depression

Federal government websites often end in. The site is secure. Since its original extensive description by Leao in , thousands of publications have characterized the phenomenon of cortical spreading depression CSD.

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Cortical spreading depression CSD or spreading depolarization SD is a wave of electrophysiological hyperactivity followed by a wave of inhibition. Interplay between Cortical Spreading Depolarization and Seizures. Most of the literature reporting so-called spontaneous SD involve SDs in or around unhealthy cortical tissue. This is explained by the high impedance of dura and skull and the evidence that it is a narrow cortical zone, only a few centimeters across, that undergoes local electrical EEG silence. Heart Circ. Nitric oxide formation during cortical spreading depression is critical for rapid subsequent recovery of ionic homeostasis. SD has been found to alter the permeability of BBB by activating brain matrix metalloproteases [ ]. The endothelial damage caused by the cortical spreading depression can result in hypercoagulability, leading to an increased risk of stroke. Provided by the Springer Nature SharedIt content-sharing initiative. In vitro studies have shown similar results. And what is the mechanism underlying the ignition of CSD by a threshold stimulus and not by a just subthreshold stimulus which produces a rapid depolarization only slightly smaller than that at the threshold?

Wannan Tang and Gry Fluge Vindedal contributed equally to this work.

Dendritic spines lost during glutamate receptor activation reemerge at original sites of synaptic contact. CSD can activate perivascular trigeminal afferents and evoke a series of cortico-meningeal and brainstem events consistent with the development of headaches [ 32 , 33 , 34 , 35 , 36 ]. Glymphatic flow The glymphatic system, a glial-dependent perivascular network, is a newly characterized macroscopic extracellular compartment system that clears waste from the brain parenchyma into paravascular spaces, dural lymphatics, and then cervical lymph nodes [ , ]. An entirely different scenario may apply in the human brain acutely injured for example by ischemic stroke, brain trauma, or subarachnoid or intracerebral hemorrhage ICH Hansen and Lauritzen, ; Strong et al , ; Fabricius et al , ; Dreier et al , ; Dohmen et al , Microemboli may link spreading depression, migraine aura, and patent foramen ovale. Transient elevations of extracellular potassium resembling CSD were demonstrated as early as in a baboon focal ischemia model Branston et al , , and not much later, CSD-like depolarizations were described in stroke models in cats Strong et al , and rats Nedergaard and Astrup, E-mail: kd. Acta Physiol Scand 4 — It highlights the link between migrainous infarction and cortical spreading depression through hemo-dynamic implications, coagulation disorders and genetic implications. Introduction Migraine is a complex neurovascular disorder. Migrainous infarction is a rare complication of migraine with aura. Channels Austin 5 2 — The clinical deterioration of patients we have monitored is often accompanied by clusters of CSD, which show a gradual increase of recovery time. Cephalalgia 27 12 — Karatas, H.