Thickening in the somatosensory cortex of patients with migraine

Abstract

Objective-To examine morphologic changes in the somatosensory cortex (SSC) of patients with migraine.Methods-Cortical thickness of the SSC of patients with migraine was measured in vivo and compared with age-and sex-matched healthy subjects. The cohort was composed of 24 patients with migraine, subdivided into 12 patients who had migraine with aura, 12 patients who had migraine without aura, and 12 controls. Group and individual analyses were performed in the SSC and shown as average maps of significant changes in cortical thickness.Results-Migraineurs had on average thicker SSCs than the control group. The most significant thickness changes were noticed in the caudal SSC, where the trigeminal area, including head and face, is somatotopically represented.Conclusions-Our findings indicate the presence of interictal structural changes in the somatosensory cortex (SSC) of migraineurs. The SSC plays a crucial role in the noxious and nonnoxious somatosensory processing. Thickening in the SSC is in line with diffusional abnormalities observed in the subcortical trigeminal somatosensory pathway of the same migraine cohort in a previous study. Repetitive migraine attacks may lead to, or be the result of, neuroplastic changes in cortical and subcortical structures of the trigeminal somatosensory system. Migraine is a chronic painful disease in which frequent headache attacks affect a great part of the patient's life, from childhood to late adulthood. The consequences of such persistent suffering on the cortex of migraineurs are not known. Using diffusion tensor imaging (DTI), we have recently shown interictal alterations in trigeminal somatosensory pathway in patients who have migraine with aura (MWA) and migraine without aura (MWoA), confirming the involvement of the somatosensory system in the migraine pathophysiology. 1 Based on that evidence, and taking advantage of the large somatotopic representation of the head in the somatosensory cortex (SSC) that receives trigeminal noxious and innocuous sensory inputs, we examined for the presence of cortical thickness changes in the same group of patients.

Closing remarks: what future prospects can we expect in migraine management?

“…Probably neuroimaging will guide the way here as further exploration of the pain matrix within the central nervous system and their connectivities are elucidated [15]. Already important work has been done to show that there are obviously functional changes in the cortex, subcortical and brainstem structures and there are significant volumetric changes in the cortex of the migraine brain [16]. Functional changes are seen in the visual cortex in migraine [17], and in chronic migraine there appears to be some degree of reversibility particularly after overuse of medication is reversed [18].…”

Migraine and Reward System—Or Is It Aversive?

“…With the extensive direct and indirect connectivity of the numerous cortical regions with the mesolimbic pathway, it is not surprising that stress and illness can affect reward and motivational behavior [56,57]. Research has demonstrated altered cortical structure and function following migraine attacks [58][59][60][61], and thus represents one likely pathway by which migraine, stress, the accompanying negative affect, and altered motivational states are intimately linked.…”

Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective

“…New findings from extensive functional imaging studies on central pain networks allowed the identification of patterns of cortical and brainstem activation in some way ''specific'' for different primary headache subtypes [12][13][14]. In addition, structural alterations (either as hypertrophic or hypotrophic changes) of these areas have been consistently reported in headache series [15,16] as well as in other chronic pain syndromes [17][18][19] leading to the assumption that the repeated activation of the pain networks may promote neuroplastic cortical changes causing a permanent facilitation of pain signals, ultimately leading to the chronicisation of pain [20].…”