Unravelling central-pain mechanisms in patients with temporomandibular disorders
(2023)
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- Abstract
- Temporomandibular disorders (TMDs) can substantially reduce one’s quality of life and lead to both persistent pain and psychological distress. However, TMDs are often overlooked and poorly understood. There are wide variations in the severity, duration, and distribution of pain in individuals with TMDs. These variations are believed to be better explained by central sensitization – that is, the enhanced sensitivity of neurons in the central nervous system – than by the extent of tissue damage or biomechanical dysfunctions in the masticatory system. The objective of this thesis is to improve the understanding of central-pain mechanisms in persistent TMDs and unravel the potential role of central sensitization. We will focus specifically on temporomandibular myalgia (TMDm), which is the most common subtype of TMDs. First, we seek, examine, and summarize the best available evidence on central sensitization and persistent TMDm. We find that, on average, individuals with persistent TMDm have an increased mechanical temporal summation in the upper limb but few other somatosensory abnormalities that are believed to reflect central sensitization. Second, we investigate the reliability of a promising experimental model to study central sensitization in humans. This model, called high-frequency electrical stimulation (HFS), induces secondary mechanical hyperalgesia. Based on animal studies, secondary mechanical hyperalgesia can confidently be attributed to central sensitization. We identify the most reliable features of secondary mechanical hyperalgesia induced by HFS. We also demonstrate that HFS is suitable to discriminate or compare individuals with respect to their propensity to develop central sensitization. Third, we assess the impact of HFS-induced central sensitization on pressure pain thresholds. Central sensitization induced by HFS does not alter pressure pain thresholds. While derived from an experimental model, this finding contradicts the common view that a widespread decrease in pressure pain thresholds reflects central sensitization. Fourth, we compare the propensity of individuals with persistent TMDs and healthy controls to develop secondary mechanical hyperalgesia after HFS. We find that TMDs are associated with a higher propensity to develop secondary mechanical hyperalgesia on the volar forearm. This thesis moves away from the use of central sensitization as an umbrella term that encompasses many mechanisms. Instead, we precisely characterize the few somatosensory abnormalities that accompany TMDs: increased mechanical temporal summation and a higher propensity to develop secondary mechanical hyperalgesia. These somatosensory abnormalities and their clinical significance are not yet fully understood. Future work is required to unravel the specific cognitive, behavioural, molecular, genetic, immune and neural mechanisms that mediate the somatosensory abnormalities associated with temporomandibular disorders. Doing so will help gain a better understanding of TMDs’ pathophysiology.
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Citations
Cayrol, T. (2023). Unravelling central-pain mechanisms in patients with temporomandibular disorders. https://hdl.handle.net/2078.5/102780