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Alshamrani, F.J.; Alsheikh, M.H.; Almuslim, N.; Al Azman, H.; Alkhamis, F.; Nazish, S.; Alnajashi, H.; Alsulaiman, A. Migraine with Aura. Encyclopedia. Available online: https://encyclopedia.pub/entry/51644 (accessed on 30 June 2024).
Alshamrani FJ, Alsheikh MH, Almuslim N, Al Azman H, Alkhamis F, Nazish S, et al. Migraine with Aura. Encyclopedia. Available at: https://encyclopedia.pub/entry/51644. Accessed June 30, 2024.
Alshamrani, Foziah J., Mona Hmoud Alsheikh, Noora Almuslim, Hatem Al Azman, Fahad Alkhamis, Saima Nazish, Hind Alnajashi, Abdulla Alsulaiman. "Migraine with Aura" Encyclopedia, https://encyclopedia.pub/entry/51644 (accessed June 30, 2024).
Alshamrani, F.J., Alsheikh, M.H., Almuslim, N., Al Azman, H., Alkhamis, F., Nazish, S., Alnajashi, H., & Alsulaiman, A. (2023, November 16). Migraine with Aura. In Encyclopedia. https://encyclopedia.pub/entry/51644
Alshamrani, Foziah J., et al. "Migraine with Aura." Encyclopedia. Web. 16 November, 2023.
Migraine with Aura
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This entry is adapted from the peer-reviewed paper 10.3390/biomedicines11112979

A sizable portion of the world’s population suffers from migraines with aura. Estrogen is crucial in migraine pathophysiology, especially in women, which might be used to develop hormone-regulating medications. Migraine’s underlying mechanism or visual abnormalities may explain migraine sufferers’ variations in brain activity or visual system processing.

cortical excitability latency aura migraine visual-evoked potentials

1. Introduction

Twelve percent of the world’s population suffers from migraines. Patients generally suffer nausea, vomiting, and light and sound sensitivity, as well as moderate to severe headaches [1][2][3]. The neurological disorder migraine causes recurring headaches. Although the actual pathophysiological mechanisms that cause migraines are unknown, various theories have been proposed. Headaches are connected to variations in neurotransmitters like serotonin and dopamine, which constrict and expand brain blood vessels. Several research organizations believe that brain inflammation causes pain. Since migraines commonly run in families, genetic predisposition must be considered. One idea links migraines to neurotransmitters like serotonin, dopamine, and noradrenaline. These changes may activate brain pain circuits, causing migraineurs to experience headaches, nausea, and light and sound sensitivity. Migraines can impair a person and be costly personally and socially [4]. Migraines are linked to anatomical changes in pain-processing brain regions [5]. Despite the need for more research, there is mounting evidence that estrogen, particularly in women, contributes to migraines [5]. To draw significant results from these studies, a thorough statistical analysis must account for all confounding factors [5]. Changes in the functional connection patterns between the visual, auditory, olfactory, gustatory, and somatosensory cortices may explain some sensory processing changes [6]. Migraines cause repeated headaches, light and sound sensitivity, nausea, and vomiting. These symptoms are common migraine symptoms, according to research. Studies have linked neurogenic inflammation and neuropeptides to migraines, although their exact cause is unknown.
Sensory neurons in the trigeminal nerve system release neuropeptides such as CGRP and substance P, causing neurogenic inflammation. These neuropeptides cause neurogenic inflammation. These neuropeptides dilate and permeabilize blood vessels, causing inflammation and pain. Migraines are associated with greater brain concentrations of neuropeptides, including CGRP and PACAP. These neuropeptides may activate brain pain circuits, causing migraines [7][8][9][10]. Migraine sufferers may benefit from a new medication that inhibits the CGRP pathway. Monoclonal antibodies against CGRP or its receptor have been demonstrated to prevent migraines in clinical trials. Neurogenic inflammation and neuropeptides are thought to produce migraines, although further research is needed to confirm this and understand their roles. Electrophysiological testing may reveal migraine headache pathomechanisms. Because they monitor brain and nerve electrical activity, these diagnostic methods can detect minute physiological changes in patients. Research has shown that migraine sufferers have problems with their brains’ sensory absorption and cortex excitability [11][12][13]. These data support the idea that brain neurobiological changes may cause migraines. If researchers can comprehend these changes, they may build better migraine medications. Brain rhythmic irregularities are linked to several neurological and neuropsychiatric diseases. Parkinson’s disease patients had greater cortical gamma-band oscillations and fewer basal ganglia beta-band oscillations. Alzheimer’s disease causes theta and alpha brainwave irregularities in the hippocampus and cortex. Gamma-band oscillations in the prefrontal cortex are disrupted in schizophrenia. Abnormal brain rhythms may be a biomarker for detecting and tracking the development of several diseases and revealing their causes, according to several studies.

2. Migraine with Aura

In most cases, migraine symptoms can be divided into four stages: the prodrome, the aura, the headache, and the postdrome [14][15]. A comprehensive approach to diagnosing and treating migraine symptoms is essential at all stages of the condition [16][17][18][19]. This is because it is generally accepted that migraine symptoms negatively impact both a person’s day-to-day existence and their overall quality of life. There are no visual symptoms connected to a migraine without an aura. Aura-accompanied headaches have been linked to aberrant sensory processing in the brain, including thalamocortical dysrhythmia [20][21], according to some research. Inflammatory neuropeptides and neurotransmitters are released into the brain and bloodstream in response to a migraine episode, setting off a cascade of inflammatory reactions. Migraine sufferers may report worsening headaches as a result of this. Migraines and auras may have their origins in these changes [22][23]. They can either make it easier or more stimulating for the brain to process sensory data. Aberrant activity between the thalamus and the cortex, as might occur with thalamocortical dysrhythmia, is one mechanism underlying sensory hypersensitivity [24]. This is a mechanism underlying heightened sensitivities in the senses. When the suppression of incoming information that the cortex needs to process moves from primary to secondary cortices, visual features become perceptually available [25]. According to electrophysiological studies using instruments like the electroencephalograph (EEG) and the magnetoencephalogram (MEG), migraine attacks are associated with changes in brain activity patterns and excitability [26]. These alterations have been linked to decreased beta-wave activity and increased theta- and alpha-wave activity in some parts of the brain. Migraine-related changes in sensory pathways can be analyzed with noninvasive methods like visual evoked potentials (VEPs) and other types of sensory evoked potentials (SEPs) [27][28][29]. Patients suffering from migraines frequently exhibit these kinds of anomalies.
The cause of migraines has been the subject of numerous studies in recent years. According to studies done on animals, female hormones may be the cause of migraines, at least in part [30]. DNA methylation is just one example of the growing body of research suggesting an epigenetic role in migraine pathophysiology [31]. Although estrogen’s precise involvement in the onset of migraines is unclear [32], a careful evaluation of the data suggests that it plays a significant role. These studies highlight the need for thorough data analysis that accounts for the presence of biases and confounding variables in order to obtain an accurate depiction of migraine pathophysiology. Although they have been recorded during migraine attacks, the reliability of electroencephalograms (EEGs) and visual evoked potentials (VEPs) has not been demonstrated. A SCN1A carrier patient with a migraine in 2016 [33] demonstrated visual evoked potentials (VEPs), although this area still needs extensive investigation. The full range examined migraine can be diagnosed with the help of electroencephalography (EEG) and steady-state visual evoked potentials (VEPs). However, short-lived visual evoked potentials (VEPs) cannot be used for this purpose. However, a recent VEP experiment employing four different spatial frequencies looked into two visual circuits that overlap in migraine sufferers. More research into this area could help scientists figure out what sets off migraines, which would lead to more effective treatments. The S index was found to be correlated with allodynia severity (as judged by the Allodynia Symptoms Checklist, or ASC-12), both at the outset of the study and after three months of topiramate treatment. This was observed prior to and during the patient’s administration of topiramate for the study’s specified treatment period. According to the results of this investigation, the S index shows promise as a biomarker for both the migraine cycle and cortical sensitization. Migraines are thought to originate less from an issue with the blood vessels in the head and more from an issue with the brain’s ability to comprehend sensory information. This is a complex procedure that may require a great deal of effort and several years to perfect.

References

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Subjects: Medicine, Research & Experimental
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Foziah J. Alshamrani
,
Mona Hmoud AlSheikh
,
Noora Almuslim
,
Hatem Al Azman
,
Fahad Alkhamis
,
Saima Nazish
,
Hind Alnajashi
,
Abdulla Alsulaiman
View Times: 259
Entry Collection: Neurodegeneration
Revisions: 2 times (View History)
Update Date: 16 Nov 2023
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