## 4 Discussion
For this reason, we expected to find an association between morphologic changes and cutaneous allodynia, in addition to the evidence that patients with migraine often develop cutaneous allodynia over the years and once the pain frequency is increased [9]. Migraineurs can indeed exhibit maladaptive alterations in the somatosensory cortex, which can be compensatory or dysfunctional [13]. The cutaneous allodynia can be understood as a dysfunctional analgesic mechanism related to the abnormal representation of pain perception [11] and lowered pain thresholds during migraine attacks [26]. The increased pain perception can be explained by a hypofunction of the pain descendent inhibitory system, which modulates the nociceptive transmission, or by a facilitation of the ascendent pain system [27]. [PERSON] et al., (2017) verified that migraineurs with severe allodynia had reduced midbrain volumes and concluded that the brainstem is related to altered sensory processing in migraine, reflecting the severity of allodynia and pain hypersensitivity [18]. It was also evidenced that migraineurs without allodynia have decreased activation of the somatosensory cortices in contrast to migraineurs without allodynia and controls, which was correlated with allodynia severity [11]. The presence of allodynia was also associated with greater brain activation of the anterior cingulate cortex and the middle frontal gyrus [11]. Future studies should further explore this association between the morphology of other brain regions and cutaneous allodynia, considering different subgroups of migraine and different types of aura. We failed to demonstrate differences on cutaneous allodynia levels among the migraine subgroups. These results do not agree with previous studies that found a greater prevalence of cutaneous allodynia in patients with migraine with aura in contrast to the ones without aura [28; 29]. The authors hypothesize that the brain hyperexcitability triggered by the aura would be related to the augmented perception of tactile, visual, and auditory stimuli. However, to the best of our knowledge, there is no evidence of greater levels of photophobia or phonophobia among the subtype of patients who experience aura [28; 29]. Previous imaging studies also found morphological differences among patients with aura in contrast to the ones without aura. The presence of aura was related to reduced volume in the inferior and superior temporal gyrus, frontal and pre-central gyrus, and these changes do not correlate with clinical features [30; 31; 32]. We also did not find correlation with clinical features, and possibly due to sample homogeneity and absence of a control group, our imaging results do not corroborate with these findings. According to [PERSON] et al., imaging differences may reflect general bias between patients and healthy controls [30]. Furthermore, negative findings are not often published, introducing bias into meta-analysis and research misinformation [33]. One strength of our study is the inclusion of different migraine subtypes and thus a migraine representative sample. Furthermore, all patients belong to a tertiary headache clinic and therefore were diagnosed by headache specialists. For the first time, a reliable and valid questionnaire to assess self-reported cutaneous allodynia was used [19]. However, since the ASC-12/Brazil assesses allodynia retrospectively, a recall-bias could have influenced our results. Future studies associating the use of questionnaires with thermic and mechanic quantitative measurements are recommended. In addition, psychosocial aspects such as depression, catastrophism and self-reported disability were not considered in this study, and the lack of a control group limited further comparisons. Despite these limitations, our study suggests that the presence of cutaneous allodynia is not related to morphological changes of the somatosensory cortex, headache features, or different migraine subtypes.