Cortical spreading depression

Metrics details. A Correction to this article was published on 20 December There is increasing evidence from human and animal studies that cortical spreading depression CSD is the neurophysiological correlate of migraine aura and a trigger of migraine pain mechanisms. Cortical spreading depression mechanisms of initiation of CSD in the brain of migraineurs remain unknown, and the mechanisms of initiation of experimentally induced CSD in normally metabolizing brain tissue remain incompletely understood and controversial, cortical spreading depression.

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 , a slowly propagated wave of depolarization followed by suppression of brain activity, is a remarkably complex event that involves dramatic changes in neural and vascular function. Since its original description in the s, CSD has been hypothesized to be the underlying mechanism of the migraine aura. Substantial evidence from animal models provides indirect support for this hypothesis, and studies showing that CSD is common in humans with brain injury clearly demonstrate that the phenomenon can occur in the human brain.

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. We shall, however, present the evidence that a clear distinction needs to be made between spreading depolarizations 1 that are accompanied by spontaneously reversible recovery of normal function and 2 PIDs—accompanied by prolonged recovery of cortical function, or no recovery at all.

What to Do? Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology.

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.

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. Despite the attention that CSD has received over more than six decades, however, many fundamental questions regarding its initiation, propagation, functional consequences, and relationship to migraine and other human disorders remain unanswered. Advances in genetics and cellular imaging have led to important insights into the basic mechanisms of CSD, with increasing attention focused on specific neuronal ion channels, neurotransmitters and neuromodulators. In addition, there is growing recognition that astrocytes and the vasculature may play an active, rather than simply a passive or reactive role in CSD. Several recent descriptions of CSD in humans in the setting of brain injury provide definitive evidence that this phenomenon can occur and have important functional consequences in the human brain. Although the exact role of CSD in migraine has yet to be conclusively established, there is strong evidence that the investigation of CSD in animal models can provide meaningful information about migraine that can be translated into the clinical setting. This review will briefly address the extensive work that has been done on CSD over more than half a century, but focus primarily on more recent studies with a particular emphasis on relevance to migraine. Spreading depression SD is a slowly propagated wave of depolarization of neurons and glial cells, followed by a subsequent sustained suppression of spontaneous neuronal activity, accompanied by complex and variable changes in vascular calibre, blood flow, and energy metabolism.

Cortical spreading depression

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. Some molecules of interest for migraine have been tested for their effect on CSD.

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Decreased visual field sensitivity measured 1 day, then 1 week, after migraine. You can also search for this author in PubMed Google Scholar. Received : 17 June J Neurophysiol 10 6 — Charles, A. Found in children; Migraine with abdominal disturbances; Seizures; Hearing loss. Effect of anoxia on ion distribution in the brain. Ann Neurol 87 6 — The artery first dilated during the passage of a CSD wave followed by a prolonged constriction. Hartings Jens P.

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.

Tfelt-Hansen, P. The spreading depression theory. Optical current source density analysis in hippocampal organotypic culture shows that spreading depression occurs with uniquely reversing currents. Cortical spreading depression and peri-infarct depolarization in acutely injured human cerebral cortex. Ann Neurol 49 1 :7— The marked depression of spontaneous EEG lasts for about 30 seconds to a minute, returning to the normal in 5 to 10 minutes. These ischemia-evoked SDs may be triggered by supply-demand mismatch transients [ 77 ], circle around and enlarge the ischemic lesions [ 77 , 78 ], and be suppressed by migraine preventive drugs [ 70 ]. It is unknown if BBB breakdown is only a consequence of inflammation or if it may play a contributory role in trigeminal pain or other associated features of migraine. In vivo models can be challenging and time consuming due to microsurgical preparation and maintenance of stable systemic physiological conditions under anesthesia. It is very difficult to differentiate between migraine with aura and a stroke, because symptoms of migraine with aura can mimic the symptoms of a stroke. Temporal relationship between neurotransmitter release and ion flux during spreading depression and anoxia. Download PDF.