MRI plays an important role in the identification of migraine cerebral networks. Several fMRI studies revealed abnormalities of resting state functional connectivity in pain network involved in the migraine pathophysiology [6, 9, 10]. Migraine patients showed significant GM abnormalities of several brain regions involved in central pain processing [11–12]. In particular, VBM data established that the GMV was decreased in the anterior cingulate cortex, insula, amygdala, parietal operculum, middle and inferior frontal gyrus [13]. In addition, regions with reduced grey matter density are located in bilateral insula, motor premotor, prefrontal, cingulate cortex, right posterior parietal cortex and orbitofrontal cortex [14].
In this study, we applied the VBM approach to MA and MO patients and HS. We observed that MA and MO subjects had a significant reduction of GMV compared to HS in cerebellum, and frontal and temporal lobe. Our previous study [6] analyzed the resting state findings in the same patient simple and we found an increased hyperactivity in bilateral fusiform and cingulate gyrus of MO subjects compared with controls. In this study, the VBM approach showed a decrease in the volumes of same cerebral areas. Although the volume of bilateral fusiform and cingulate gyrus is descreased, the increase of their hyperactivity could be ascribed to the fact that the fusiform gyrus seems to be hyperactive in migraineurs, in ligh of its involvment in the treatment of cognitive pain, while the cingulate gyrus is involved in the process of transformation of migraine from “an episodic” to “a chronic brain disorder” [26].
In addition, the cerebellum of migraineurs and controls differs structurally. In a study of Mehnert [15] the GMV and the neuronal activity in response to trigeminal pain were increased in posterior part of the cerebellum (crus). Migraine patients had also a decreased connectivity in the thalamus and higher cortical areas, suggesting a decreased inhibitory involvement of migraine cerebellum on trigeminal nociception. The frontal cortex is an area associated with cerebral abnormalities in migraine patients [16–17]. Previous studies have suggested that the medial prefrontal cortex could be involved in mediating the attenuation of pain perception by a cognitive control mechanisms [18–19], which is associated with pain modulation [20–21]. Schmitz et al. [22] reported that migraine patients had decreased gray matter density in the medial prefrontal cortex which correlated significantly with a slower response time to the set-shifting task.
In coherence with previous VBM findings, in migraine patients [11–12, 17], our results corroborate with the study of Kim et al. [4], that found a decrease of volume of insula bilaterally, motor/premotor, prefrontal and cingulate cortex, right posterior parietal cortex, and orbitofrontal cortex. Moreover, Jin et al. [9] showed a decreased GMV in several brain regions involved in pain processing, such as left medial prefrontal cortex, cingulate, right occipital lobe, cerebellum, and brainstem. From the results obtained we can affirm that patients with migraine have a decreased GMV in the precentral gyrus as well as in the post-central gyrus and temporal lobe.
The possible mechanisms underlying the reduction of grey matter in migraine are currently unknown. The observed decrease in grey matter may reflect tissue shrinkage (changes in extracellular space and microvascular volume) as well as more complex processes such as neurodegeneration. Therefore, there are several possible explanations for the observed abnormalities in our patients. Variations in gray matter may result from repeated ischaemia caused by blood flow to the brain abnormalities observed both during migraine attacks and in the interictal phase. In contrast, the reduction of gray matter may be a consequence of migraine specific neurotoxic mechanisms. It has been hypothesized that migraine is associated with a state of neuronal hyperexcitability, involving over-activity of the amino acid exciters glutamate and aspartate. VBM analysis has shown that migraineurs present a significant reduction in the gray matter of different brain areas belonging to the pain activation network [6].