Structural and Functional Reorganization of the Brain in Migraine Without Aura

Abstract

It remains unknown whether migraine headache has a progressive component in its pathophysiology. Quantitative MRI may provide valuable insight into abnormal changes in the migraine interictum and assist in identifying disrupted brain networks. We carried out a data-driven study of structural integrity and functional connectivity of the resting brain in migraine without aura. MRI scanning was performed in 36 patients suffering from episodic migraine without aura and 33 age-matched healthy subjects. Voxel-wise analysis of regional brain volume was performed by registration of the T1-weighted MRI scans into a common study brain template using the tensor-based morphometry (TBM) method. Changes in functional synchronicity of the brain networks were assessed using probabilistic independent component analysis (ICA). TBM revealed that migraine is associated with reduced volume of the medial prefrontal cortex (mPFC). Among 375 functional brain networks, resting-state connectivity was decreased between two components spanning the visual cortex, posterior insula, and parietal somatosensory cortex. Our study reveals structural and functional alterations of the brain in the migraine interictum that may stem from underlying disease risk factors and the “silent” aura phenomenon. Longitudinal studies will be needed to investigate whether interictal brain changes are progressive and associated with clinical disease trajectories.

Functional Alterations in the Posterior Insula and Cerebellum in Migraine Without Aura: A Resting-State MRI Study

“…Though the role of the cerebellum (including crus I) in migraine is not well defined, it is known to exert an inhibitory control on cerebral cortex (Brighina et al, 2009 ; Moulton et al, 2010 ; Mehnert and May, 2019 ). The DMN is involved in several cognitive processes, such as memory, problem solving, and planning (Buckner et al, 2008 ; Lo Buono et al, 2017 ), as well as perception and processing of painful stimuli (Soheili-Nezhad et al, 2019 ). Specifically, the hippocampus and PHG are associated with learning and memory formation, as well as pain-related attention and anxiety (Buckner et al, 2008 ; Liu and Chen, 2009 ).…”

“…However, findings across the resting-state MRI studies on migraine are complex and often inconsistent (Skorobogatykh et al, 2019 ). For example, while some researchers reported increased FC for the insula (Hadjikhani et al, 2013 ; Yuan et al, 2013 ) or the periaqueductal gray (Mainero et al, 2011 ) in patients with migraine, others reported decreased FC in these regions (Chen et al, 2017 ; Yu et al, 2017b ; Soheili-Nezhad et al, 2019 ). Furthermore, though reduced FC within the DMN and executive network has been repeatedly detected, negative or opposite results have also been observed in some migraine studies (Ellingson et al, 2019 ).…”

Effectiveness of cathodal tDCS of the primary motor or sensory cortex in migraine: A randomized controlled trial

“…Moreover, evidence suggests atypical sensory processing in the cortex of migraine patients, especially in the somatosensory, visual, and olfactory-related areas [18,19]. The results of a study based on whole-head magnetoencephalography (MEG) showed aberrant functional connectivity between the sensory cortex and the frontal cortex in a group of migraine patients compared to a healthy control group [20].…”

Genetic Screening of Plasticity Regulating Nogo-Type Signaling Genes in Migraine

“…It has repeatedly been demonstrated how the migraine brain differs morphologically from the healthy brain in several brain regions. Moreover, these alterations appear to progress over time and with attack frequency [25,28,[31][32][33][34][35]. However, there may well be alterations at the level of structural synaptic plasticity that cannot be detected in vivo in humans with available methods.…”

“…Results from these investigations have identified differences between control and migraine brains with regard to resting state activity and structure of gray and white matter. Differences have been detected in the frontal lobes, corpus callosum, the limbic system, cerebellum, the brainstem and nociceptive regions, although findings are not consistent across studies [22,24,25,[27][28][29][30][31][32][33][34][35][36]. In addition to regional differences, cortical thickness has been reported to differ between migraine patients and controls, and even correlate to attack frequency [37].…”