Cortical spreading depression and meningeal nociception

Carneiro-Nascimento, Simone; Levy, Dan

doi:10.1016/j.ynpai.2022.100091

Cited by 26 publications

(14 citation statements)

References 121 publications

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“…Melo-Carrillo and colleagues further demonstrated that CSD leads to sensitization of central trigeminal nociceptive neurons. That study also found that systemic administration of an anti- CGRP antibody, used in migraine prophylaxis, inhibited the development of both the activation and sensitization of high threshold trigeminal neurons following CSD, further substantiating the link between CSD, meningeal nociception, and migraine headache ( Figure 5 ) ( Carneiro-Nascimento and Levy, 2022 ).…”

Section: Relationship Between Cgrp and Energy Metabolism Of Migrainesupporting

confidence: 56%

Energy metabolism disturbance in migraine: From a mitochondrial point of view

Wang

Yue

et al. 2023

Front. Physiol.

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Migraine is a serious central nervous system disease with a high incidence rate. Its pathogenesis is very complex, which brings great difficulties for clinical treatment. Recently, many studies have revealed that mitochondrial dysfunction may play a key role in migraine, which affects the hyperosmotic of Ca2+, the excessive production of free radicals, the decrease of mitochondrial membrane potential, the imbalance of mPTP opening and closing, and the decrease of oxidative phosphorylation level, which leads to neuronal energy exhaustion and apoptosis, and finally lessens the pain threshold and migraine attack. This article mainly introduces cortical spreading depression, a pathogenesis of migraine, and then damages the related function of mitochondria, which leads to migraine. Oxidative phosphorylation and the tricarboxylic acid cycle are the main ways to provide energy for the body. 95 percent of the energy needed for cell survival is provided by the mitochondrial respiratory chain. At the same time, hypoxia can lead to cell death and migraine. The pathological opening of the mitochondrial permeability transition pore can promote the interaction between pro-apoptotic protein and mitochondrial, destroy the structure of mPTP, and further lead to cell death. The increase of mPTP permeability can promote the accumulation of reactive oxygen species, which leads to a series of changes in the expression of proteins related to energy metabolism. Both Nitric oxide and Calcitonin gene-related peptide are closely related to the attack of migraine. Recent studies have shown that changes in their contents can also affect the energy metabolism of the body, so this paper reviews the above mechanisms and discusses the mechanism of brain energy metabolism of migraine, to provide new strategies for the prevention and treatment of migraine and promote the development of individualized and accurate treatment of migraine.

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Section: Relationship Between Cgrp and Energy Metabolism Of Migrainesupporting

confidence: 56%

Energy metabolism disturbance in migraine: From a mitochondrial point of view

Wang

Yue

et al. 2023

Front. Physiol.

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“…This pathophysiological mechanism underpinning the VEP habituation is not permanently impacted by ictal events, regardless of the link between the ictal CSD and the inter-ictal VEP. These MWA groups are more pronounced pathophysiological dysfunctions as a result of genetic abnormalities that produce cortical spreading depression, which fuels meningeal nociception in migraine with aura, and are particularly affected by the lack of habituation between inter-ictal [ 16 , 65 , 66 ]. This shows that when the interval between migraine attacks lengthens, inhibitory performances and the habituations with the stimulus recurrence decline.…”

Section: Discussionmentioning

confidence: 99%

Lack of Habituation in Migraine Patients Based on High-Density EEG Analysis Using the Steady State of Visual Evoked Potential

Abdulhussein

Alyasseri

Mohammed

et al. 2022

Entropy

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Migraine is a periodic disorder in which a patient experiences changes in the morphological and functional brain, leading to the abnormal processing of repeated external stimuli in the inter-ictal phase, known as the habituation deficit. This is a significant feature clinically of migraine in both two types with aura or without aura and plays an essential role in studying pathophysiological differences between these two groups. Several studies indicated that the reason for migraine aura is cortical spreading depression (CSD) but did not clarify its impact on migraine without aura and lack of habituation. In this study, 22 migraine patients (MWA, N = 13), (MWoA, N = 9), and healthy controls (HC, N = 19) were the participants. Participants were exposed to the steady state of visual evoked potentials also known as (SSVEP), which are the signals for a natural response to the visual motivation at four Hz or six Hz for 2 s followed by the inter-stimulus interval that varies between 1 and 1.5 s. The order of the temporal frequencies was randomized, and each temporal frequency was shown 100 times. We recorded from 128 customized electrode locations using high-density electroencephalography (HD-EEG) and measured amplitude and habituation for the N1–P1 and P1–N2 from the first to the sixth blocks of 100 sweep features in patients and healthy controls. Using the entropy, a decrease in amplitude and SSVEP N1-P1 habituation between the first and the sixth block appeared in both MWA and MWoA (p = 0.0001, Slope = −0.4643), (p = 0.065, Slope = 0.1483), respectively, compared to HC. For SSVEP P1–N2 between the first and sixth block, it is varied in both MWA (p = 0.0029, Slope = −0.3597) and MWoA (p = 0.027, Slope = 0.2010) compared to HC. Therefore, migraine patients appear amplitude decrease and habituation deficit but with different rates between MWA, and MWoA compared to HCs. Our findings suggest this disparity between MWoA and MWA in the lack of habituation and amplitude decrease in the inter-ictal phase has a close relationship with CSD. In light of the fact that CSD manifests during the inter-ictal phase of migraine with aura, which is when migraine seizures are most likely to occur, multiple researchers have lately reached this conclusion. This investigation led us to the conclusion that CSD during the inter-ictal phase and migraine without aura are associated. In other words, even if previous research has not demonstrated it, CSD is the main contributor to both types of migraine (those with and without aura).

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“…Reports of spreading oliguria during the migraine attack, maybe optional to the spreading depression of Leb, feel somewhat skeptical on this speculation. In any case, this is also controversial 28 .…”

Section: Monogenic Migrainementioning

confidence: 99%

“…This was similarly insisted by Gross et al 13 Expanding proof from animals concentrates on upholding the possibility that CSD, the fundamental system of the atmosphere, can enact trigeminal nociception and hence trigger cerebral pain components. A direct nociceptive impact of CSD was shown by observing that a solitary CSD can prompt a dependable expansion in a continuous movement of dural nociceptors and focal trigeminovascular neurons in shallow and profound laminae of the TCC 14 . In many neurons initiation happened with a postponement reliable with that between the beginning of visual quality and the beginning of migraine, the deferral, as well as the greatness and term of neuronal 16 .…”

Section: Cortical Spreading Depressionmentioning

confidence: 99%

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2023

IJPSR

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The review briefs the information mainly about migraine disease. It tells about genes that are responsible for migraine. Alternating Hemiplegia in Childhood, Cortical spreading depression, Monogenic Migraine, Hemicrania Ophthalmoplegia, Hemicrania Alia Definite, Hemicrania, Complicated Migraine, Status Migrinous these are types of migraine, sign and symptoms also included. The history gives all the information of scientists researching the migraine disease. Ketone bodies like D-β-hydroxybutyrate, Acetoacetate, and Acetone treat migraine. Oxidative stress and Deoxyribonucleic acid damage in patients with migraine and different channel information are given. The researcher observed new mammalian TRP channels: Canonical, Vanilloid, Melastatin, Polycystic kidney illness, Mucolipin, and Ankyrin. 31P Spectroscopy is a theory in which the quality of exemplary headache is brought about by vasospasm-initiated cerebral ischemia and the migraine by the expanded cerebral bloodstream from the resulting cerebral acidosis. The important part is a dietary antioxidant, and plant antioxidants are used for migraine disease. INTRODUCTION:A headache is a typical migraine issue that influences around 15% of females and 6% of males. It is a neurobiological disorder that is primarily described by one-sided pulsating cerebral pain. Other significant side effects incorporate sickness, vomiting, and sensitivity to light. During the headache assault, veins of the cerebrum get expanded because of a decrease in the level of the vasoconstrictor known as 5-hydroxytryptamine (5-HT), which causes extraordinary migraines.

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Cortical spreading depression and meningeal nociception

Cited by 26 publications

References 121 publications

Energy metabolism disturbance in migraine: From a mitochondrial point of view

Energy metabolism disturbance in migraine: From a mitochondrial point of view

Lack of Habituation in Migraine Patients Based on High-Density EEG Analysis Using the Steady State of Visual Evoked Potential

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