Abstract
In this study we used nitroglycerin (NTG)-induced migraine attacks as a translational human disease model. Static and dynamic functional connectivity (FC) analyses were applied to study the associated functional brain changes. A spontaneous migraine-like attack was induced in five episodic migraine (EM) patients using a NTG challenge. Four task-free functional magnetic resonance imaging (fMRI) scans were acquired over the study: baseline, prodromal, full-blown, and recovery. Seed-based correlation analysis (SCA) was applied to fMRI data to assess static FC changes between the thalamus and the rest of the brain. Wavelet coherence analysis (WCA) was applied to test time-varying phase-coherence changes between the thalamus and salience networks (SNs). SCA results showed significantly FC changes between the right thalamus and areas involved in the pain circuits (insula, pons, cerebellum) during the prodromal phase, reaching its maximal alteration during the full-blown phase. WCA showed instead a loss of synchronisation between thalami and SN, mainly occurring during the prodrome and full-blown phases. These findings further support the idea that a temporal change in thalamic function occurs over the experimentally induced phases of NTG-induced headache in migraine patients. Correlation of FC changes with true clinical phases in spontaneous migraine would validate the utility of this model.
Highlights
Episodic migraine, a disease with a complex pathophysiology, has been a challenge to study because of the nature of the timing of the disease [1,2]
Advanced neuroimaging techniques, including resting state functional magnetic resonance imaging, which allows to assess changes in static and dynamic functional connectivity (FC) when the brain is at “rest”, have emerged as a leading non-invasive candidate to investigate the disease-induced neural dysfunction associated with migraine
The final dataset consists of five subjects (3 males, 2 females, average age 33.4 ± 7.1 years) affected by episodic migraine (EM) without aura according to ICHD III criteria [22], mean onset of disease was at 13.2 years old (±4.2 years) and the average disease duration is 20.2 ± 7.2 years
Summary
A disease with a complex pathophysiology, has been a challenge to study because of the nature of the timing of the disease [1,2]. The overall output of these studies suggests that migraine attacks represent a disorder of the brain sensory processing Under this condition, several brain regions cyclically modify their functional coupling producing the complex phenomenology experienced by the patient [9]. Several brain regions cyclically modify their functional coupling producing the complex phenomenology experienced by the patient [9] In this framework, the thalamus emerges as a pivotal point of relay in the migraine cycle both from a structural perspective, for the ascending nociceptive information, via the trigemino-thalamocortical pathway from lower brain areas to various cortical regions, and from a functional perspective [10], when considering the abnormal thalamocortical connection dynamics in migraine ictal and inter-ictal phases, [11], accounting for the alteration within the salience network (SN). The thalamus is a site of central sensitisation in migraine pathophysiology [12]
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