Functional connectivity changes in complex migraine aura: beyond the visual network

Abstract

Background and purpose Although the majority of migraine with aura (MwA) patients experience simple visual aura, a discrete percentage also report somatosensory, dysphasic or motor symptoms (the so‐called complex auras). The wide aura clinical spectrum led to an investigation of whether the heterogeneity of the aura phenomenon could be produced by different neural correlates, suggesting an increased visual cortical excitability in complex MwA. The aim was to explore whether complex MwA patients are characterized by more pronounced connectivity changes of the visual network and whether functional abnormalities may extend beyond the visual network encompassing also the sensorimotor network in complex MwA patients compared to simple visual MwA patients. Methods By using a resting‐state functional magnetic resonance imaging approach, the resting‐state functional connectivity (RS‐Fc) of both visual and sensorimotor networks in 20 complex MwA patients was compared with 20 simple visual MwA patients and 20 migraine without aura patients. Results Complex MwA patients showed a significantly higher RS‐Fc of the left lingual gyrus, within the visual network, and of the right anterior insula, within the sensorimotor network, compared to both simple visual MwA and migraine without aura patients (p < 0.001). The abnormal right anterior insula RS‐Fc was able to discriminate complex MwA patients from simple aura MwA patients as demonstrated by logistic regression analysis (area under the curve 0.83). Conclusion Our findings suggest that higher extrastriate RS‐Fc might promote cortical spreading depression onset representing the neural correlate of simple visual aura that can propagate to sensorimotor regions if an increased insula RS‐Fc coexists, leading to complex aura phenotypes.

Applying a biopsychosocial model to migraine: rationale and clinical implications

“…Interestingly, the same technique also showed a heightened connection between sensory areas and areas regulating affective processes including the limbic system [ 25 – 28 ], which is implied in pain processing and in the regulation of emotional life. This may explain migraineurs’ susceptibility to external triggers causing sensory overload; those triggers may modify brain circuits functioning [ 29 – 31 ]. Individuals with migraine show a decreased threshold for several sensory stimuli, including sensory, pain, thermal, visual, auditory, and olfactory ones, which well correlates with the symptoms of increased sensitivity to light, noise, and odors reported by migraineurs not only during, but also between their attacks.…”

The Functional Network of the Visual Cortex Is Altered in Migraine

“…A recent study showed an increased FC between area V5 and the lower middle frontal gyrus in the symptomatic hemisphere during migraine attacks for MwA patients [ 34 ]. The MwA patients experiencing somatosensory, dysphasic, and motor symptoms (the so-called complex auras) showed a significantly higher FC of the left lingual gyrus, within the visual network, and of the right anterior insula, within the sensorimotor network, when compared to both the simple visual MwA and MwoA patients [ 62 ]. Whether the lateralized visual functional network is related to unilateral visual auras and/or visually triggered unilateral migraine attacks remains to be investigated.…”

Visual stimulation and frequency of focal neurological symptoms engage distinctive neurocognitive resources in migraine with aura patients: a study of resting-state functional networks

“…All of these regions are part of multiple neurocognitive networks that have previously been linked to MwA pathogenesis [10][11][12][13][14][15][16][17], and their dysfunction may explain why MwA patients appear to have more pronounced cognitive abnormalities than migraine without aura [18].…”

“…The precentral gyri, middle frontal gyri, and superior and inferior temporal gyri are the most noteworthy extrastriate regions that were discovered to be functionally related following visual stimulation [ 8 ]. All of these regions are part of multiple neurocognitive networks that have previously been linked to MwA pathogenesis [ 10 – 17 ], and their dysfunction may explain why MwA patients appear to have more pronounced cognitive abnormalities than migraine without aura [ 18 ]. According to this research, neurocognitive networks may exhibit altered functional connectivity in response to visual stimulation in the context of a state of impaired visual information processing, such as in MwA patients.…”