Comparison of somatosensory cortex excitability between migraine and “strict-criteria” tension-type headache: a magnetoencephalographic study

Abstract

Tension-type headache (TTH) and migraine are both common types of headaches. Despite distinct symptoms, TTH and migraine are highly comorbid and exhibit many clinical similarities. This study enrolled consecutive patients with TTH and age- and sex-matched patients with migraine and healthy controls to investigate whether TTH and migraine are similar in brain excitability change assessed by magnetoencephalography. Patients with TTH were excluded if they reported any headache features or associated symptoms of migraine. In response to paired-pulse electrical stimulations, the gating responses obtained from the contralateral primary somatosensory cortex differed between groups. The first response, which reflected the preactivation excitability, was smaller in the migraine group (29.54 ± 2.31 pAm) compared with the TTH group (79.76 ± 8.36, P < 0.001) and controls (59.95 ± 4.26, P = 0.006). The gating ratio (ie, the ratio of the second vs first response strength) was 0.76 ± 0.03 in controls, 0.88 ± 0.03 in the migraine group, 0.93 ± 0.03 in the TTH group, with a significant increase in TTH (P = 0.003 vs controls) suggesting central disinhibition. The area under the receiver operating characteristic curve of the first response strength in differentiating between TTH and migraine was 0.85 ± 0.44, indicating excellent discrimination. In conclusion, TTH and migraine are different clinical entities in view of somatosensory cortex excitability. The preactivation excitability assessed through somatosensory gating is a potential marker for differentiating between TTH and migraine.

Misperception of Visual Verticality in Patients with Primary Headache Disorders: A Systematic Review with Meta-Analysis

“…The somatosensory system plays an important role in PHD physiopathology processes. In this regard, disruptions of the somatosensory temporal discrimination threshold have been observed during migraine attacks [ 64 ], distinguishing migraine and TTH as two different clinical entities [ 65 ]. In the case of TTH, excitability of deep nociceptors of upper cervical structures triggers headache attacks, contributing to the sensitization process responsible for TTH chronification.…”

Neuromagnetic Amygdala Response to Pain-Related Fear as a Brain Signature of Fibromyalgia

“…During responses to UCSs, distributed source activities of MEG signals recorded from the entire head surface were estimated using depth-weighted minimum norm estimates (MNEs) [ 39 – 41 ], which accurately resolve source localizations even for the activities of deep generators [ 42 , 43 ]. The neural dynamics of cortical and subcortical sources were calculated using a deep brain model that defines neural generators according to anatomical and electrophysiological priors for neocortex and subcortical structures [ 43 ].…”

Individual Pain Sensitivity is Associated With Resting-state Cortical Activities in Healthy Individuals but Not in Patients With Migraine: A Magnetoencephalography Study

“…Notably, in consistent with our ndings, Schwedt and Chong [61] examined the correlations between heat pain thresholds and cortical thickness using functional MRI, and revealed a signi cant negative correlation in healthy subjects but not in patients with migraine. In part, this dissociation may re ect the heightened cortical excitability [26,27] and abnormal resting-state cortical oscillations and connectivity in pain-related regions [28][29][30] in patients with migraine. Speci cally, in a resting-state condition, patients with migraine were associated with enhanced gamma power in the frontal and temporal regions [62,63] and reorganized functional connectivity in the default mode, salience, or sensorimotor network [29,64], implying that the functions of the resting brain were reshaped by clinical pain.…”

“…Furthermore, we recruited patients with episodic migraine (EM) to determine whether the study ndings are exclusive to patients with pain disorder. We selected EM here because patients with EM have been characterized as having an aberrant pain sensitivity threshold [25], heightened cortical excitability [26,27], and altered resting-state cortical oscillations and connectivity in pain-related regions [28][29][30]. Moreover, whether the underlying pain sensitivity mechanism is reshaped for pain disorder remains uncertain.…”