As information moves up in the visual system’s hierarchy, area V2 is organized to respond to contours, textures and location, and thereafter it is distributed into different attributes such as color, face perception, etc. The LGN sends its projections to the primary visual cortex-or V1-where the information is arranged in columns of specific orientation, as described by Hubel and Wiesel at the end of the 1950s. Visual processing starts in the retina, where axons of the ganglion cells form the optic nerve and project to the thalamus (lateral geniculate nucleus (LGN) and pulvinar) and the superior colliculus. They reported that both MWA and MWoA had statistically lower phosphene thresholds compared to healthy control participants using a circular coil for the stimulation, further supporting the hypothesis of a hyperexcitable visual cortex in migraine. performed a meta-analysis of the TMS literature in migraine that included ten trials. They found that both migraine types had hyperexcitability over this region, compared to healthy control participants. applied their stimulations more anteriorly and laterally, and examined visual cortical excitability by stimulating over area MT/V5 (an area involved with motion processing) in their MWA and migraine without aura (MWoA) patients. found that their patients who had migraine with aura (MWA) showed a lower threshold excitability over the occipital cortex compared to healthy control participants, a finding that was replicated by Mullener and colleagues. TMS, a non-invasive technique that uses magnetic fields to stimulate the brain, has been used to probe brain excitability. We list below a series of findings revealed by these different methods. They tend to suggest a hyperexcitable brain and habituation deficits. Different studies have, on the other hand, provoked activation or deactivation of the cortex using transcranial magnetic stimulation (TMS) and compared brain excitability between groups. For example, N270 is a negative signal peaking at 270 milliseconds that is typically seen in the occipito-temporal region in response to the perception of faces. The electrical signal, recorded at the scalp, is expressed as positive (P) or negative (N) inflections at a certain time. ĭifferences in visual processing outside of migraine attacks have been studied for many years, using different techniques such as the recording of electrical/magnetic activity (electro-encephalography, EEG with visual evoked potential (VEP) also known as event-related potential (ERP), and magneto-encephalography, MEG). It has been shown in an animal model that increased susceptibility to CSD is reduced after ovariectomy, casting light on the much higher prevalence of migraine in females compared to males. Finally, (3) sex hormones play a complex role in cortical excitability. Because both these thalamic nuclei are highly connected with visual striate and extrastriate cortices, these differences could be associated with an altered modulation of excitability in the visual cortex, facilitating the occurrence of cortical spreading depression (CSD) and visual aura. Several hypotheses, however, can be put forward: (1) Abnormal function of ion channels-genes that have been associated with certain types of migraine, including the familial hemiplegic migraine CACNA1A, ATP1A2, and SCN1A genes, alter this balance in favor of increased excitability (2) Abnormalities in the thalamus, which plays a major role in cortical excitability control -in a study where we examined thalamus microstructure using a multiparametric approach, we showed microstructural differences in the lateroposterior and the pulvinar nuclei of patients with migraine compared with healthy control participants. The origins of this imbalance have not been totally elucidated. It appears that susceptibility to migraine is related to an imbalance between excitatory and inhibitory systems. The Excitable Migraine Brain: With Aura or without Aura, That Is the Question
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