Relevance of cortical thickness in migraine sufferers.

" What do cortical thickness increases mean and what are the potential implications? " Migraine is a very widespread and debili-tating disease and according to the WHO, one of the most common disorders of the nervous system. Prevalence studies estimate that migraine affects 15–25% of women and 6–8% of men [1–4], and over 2.5 million people in North America have migraine at least one day per week. Migraine has a huge economic impact [5,6], amounting to several billion dollars annually due to increased healthcare utilization and costs associated with absenteeism and reduced efficiency. Despite the public health significance of this problem, the pathophysiology of migraine is not yet fully understood, and the available treatments to prevent and to cure attacks are not optimal. Migraine attacks are characterized by unilateral and pulsating headache, lasting 4–72 h, often accompanied by nausea, phonophobia and photophobia [7]. In 30% of migraine sufferers, the headache is preceded by transient (<60 min) neuro-logical symptoms known as 'aura'. Auras include visual symptoms in 94% of cases [8], but symptoms may involve sensory and speech deficits and can be very subtle [9]. According to its phenotype, migraine is classified as either migraine without aura, or migraine with aura. Recently, our group has published two articles reporting cortical thickness differences in migraine sufferers [10,11]. In the first paper [10], we examined the visual cortex of migraineurs and found that areas involved in motion processing were thickened in migraineurs with or without aura. Additionally, we found that one area of thickening corresponded to the region where we had previously found the source of cortical spreading depression (CSD) during migraine aura [12]. The second article reported increased thickness in the somatosensory cortex of migraineurs, specifically in the area of head and face representation. What do these cortical thickness increases mean and what are the potential implications? We are at this point, facing a chicken and egg dilemma, not knowing whether our observations are the cause or the consequence of migraine. Our findings could indeed be explained in several ways, which are discussed below. The first possible explanation is that migraineurs have brain structural differences compared with healthy people, due to their genetic background [13–15]. Anatomical changes underlying increases in cortical thickness may include an increased number and/or density of neu-ronal and/or glial cells in certain parts of the cortex. These focal dysplasias may render the cortex more excitable; one of the …