Pain modulation profiles in temporomandibular disorders with migraine and fibromyalgia

TL;DR

The study found that people with temporomandibular disorders and additional pain conditions like migraine and fibromyalgia have reduced pain inhibition abilities.

Contribution

This study identifies distinct pain modulation profiles in TMD patients with comorbid pain conditions.

Findings

TMD patients with migraine or fibromyalgia showed significantly reduced pain inhibition compared to healthy controls.

Increasing comorbidities were linked to weaker conditioned pain modulation.

TMD patients without comorbidities had intact endogenous pain modulation.

Abstract

Background: Temporomandibular disorders (TMD) frequently occur with
other pain conditions, and existing research has yielded mixed results regarding
the presence or absence of endogenous pain modulation (EPM). This study aimed to
investigate EPM in TMD patients with comorbid migraine and fibromyalgia (FM) in
the non-trigeminal innervated area. Methods: Conditioned pain modulation
(CPM) and temporal summation (TS) were assessed in healthy controls (n = 30), TMD
without comorbidity (n = 30), migraine (n = 30), TMD with migraine (n = 30), and
TMD with migraine + FM (n = 19). Based on the TS and CPM responses, participants
were categorized into pain modulation profiles (PMP, I–IV). Results: In
serial stimulation, patients with migraine, TMD + migraine, and TMDs + migraine +
FM showed significantly reduced pain inhibition compared with controls
(p = 0.003, p < 0.001, and p = 0.001, respectively),
while TMD patients without comorbidity exhibited intact modulation. Increasing
comorbidities were also linked to weaker CPM (single stimulation: R =
−0.312, p < 0.001; serial stimulation: R = −0.344, p
< 0.001). The PMP categorization demonstrated distinctions among the study
population, although further subgroup analysis proved challenging.
Conclusions: TMD patients without comorbid pain exhibited intact EPM in
non-painful areas. However, when these individuals experience comorbid pain
conditions, their ability to modulate pain may be compromised due to the pain
amplification and central sensitization associated with multiple comorbid pain
conditions.

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