The diagnosis of migraine with aura was based on the International Classification of Headache Disorders criteria (beta version) ( 4). Attention was focused on 1) comparing the cortical morphometric features between migraineurs and healthy controls, 2) comparing the cortical morphometric features between subgroups (MVA+ and MVA) in migraineurs, and 3) correlating cortical morphometric features in migraineurs with characteristics of the disease.Īll migraineurs with an aura who visited the Headache Center at the Neurology Clinic, from the beginning of 2013 to the end of 2015, were considered as participants of this study. The purpose of this study was to investigate the cortical gray matter in migraineurs with an aura with a surface-based morphometry approach. In the present study, a group of MA in the interictal phase of the disorder were investigated. Further research is required for more conclusive results. However, a small number of migraineurs were included in those studies, as well as the lack of differentiation between patients with migraine without aura and migraine with aura or different MA subtypes. A recent study found concomitant cortical thickness and functional MRI differences between patients with migraine and control subjects were correlated with the frequency of attacks ( 15). While certain studies found an increased cortical thickness of the primary sensorimotor cortex ( 8) or motion-processing visual areas (fifth and third visual cortex) ( 16), another study displayed no cortical thickness abnormalities ( 14). A few studies have assessed cortical thickness in migraineurs with conflicting results ( 8, 13, 14, 15, 16). Previous research found reduced cortical surface area in the inferior temporal gyrus and decreased gray matter volume in the superior temporal gyrus, inferior frontal gyrus, and precentral gyrus ( 11, 12, 13). Previous studies strongly suggested that MA is related to a dysfunctional cortex during ( 9), and also between migraine attacks ( 10). Magnetic resonance imaging (MRI) studies have suggested a relationship between migraines and an altered gray matter structure ( 7, 8). The differences between these two migraineurs with aura (MA) subtypes is supported by a higher prevalence and frequency of interictal microembolic signals in the visual, migraineurs who experienced only visual aura (MVA) compared to migraineurs who had visual, somatosensory and dysphasic symptoms (MVA+) ( 6). The reason that migraine aura is limited to visual symptoms (e.g., excitation of occipital cortex) in some patients yet in others is extended with somatosensory and/or dysphasic symptoms (e.g., spreading depolarization to other cortical regions) is not clear. Recently, language disturbances, memory problems and dyspraxia during an aura were recorded in 65% of patients ( 5). Typical symptoms of an aura are homonymous visual symptoms, less often followed by one-sided somatosensory symptoms (tingling or numbness pricking) and dysphasia ( 4). Migraine aura is thought to be caused by cortical spreading depolarization followed by cortical spreading depression, which results in a variety of symptoms that corresponds with an affected cortex ( 3). In about one-third of migraineurs, a headache is accompanied or preceded by an aura ( 2). Migraines are a common, disabling primary headache disorder, affecting approximately 15% of people worldwide ( 1).
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