Why Look in the Brain for Answers to Temporomandibular Disorder Pain?

Abstract

Temporomandibular disorder (TMD) patients often exhibit widespread clinical pain, as well as greater sensitivity to experimental pain than pain-free controls, suggesting a role of central pathophysiologic mechanisms in TMD. Moreover, TMD is more prevalent among women, which may be related to the higher sensitivity of women to experimental pain. Women also exhibit greater temporal summation of heat pain compared to men. Temporal summation, the increase in pain intensity upon repetitive noxious stimulation of constant intensity, at a high frequency is centrally mediated. Thus, greater temporal summation in women indicates that their central nociceptive processing is upregulated compared to men. Recent studies in our research center sought further evidence for upregulation of central nociceptive processing in females compared to males and in TMD patients compared to healthy controls, assessing group differences in temporal summation of mechanically evoked pain, and aftersensations following repetitive noxious stimulation. Sixteen series of 10 repetitive, sharp, mechanical stimuli were applied to the fingers of 25 female TMD patients, 25 healthy women, and 25 healthy men, with a computer-controlled small probe. All subjects rated the pain intensity or the unpleasantness evoked by the 1st, 5th and 10th stimulus in the series, and the aftersensations 15 s and 1 min after the last stimulus on visual-analog scales. TMD patients exhibited greater temporal summation of pain and unpleasantness, stronger aftersensations, and more frequent painful aftersensations than controls. Healthy females showed greater temporal summation of pain intensity and unpleasantness, higher intensity and unpleasantness of aftersensations, and more frequent painful aftersensations than males. Greater temporal summation of pain and aftersensations from digital stimulation of TMD patients than controls suggest a generalized hyperexcitability of the central nociceptive system in this patient group. Such hyperexcitability may contribute to the development and/or maintenance of chronic TMD pain. Moreover, greater temporal summation of pain and aftersensations in healthy females than males indicate that their central processing of nociceptive input may be more easily upregulated into pathological hyperexcitability, possibly accounting for the predominance of TMD among women.

Influence of craniomandibular and cervical pain on the activity of masticatory muscles in individuals with Temporomandibular Disorder

“…Nociceptive impulses from the head and neck muscles can produce a continuous afferent bombardment for the caudal trigeminal nucleus (20) and generate pain in the orofacial region (21) . The nociceptive input can be adjusted to a condition of pathological hyperexcitability and contribute to the development or maintenance of chronic pain, but also increase the likelihood of other pain disorders (22) . The results of this study showed that individuals with TMD showed greater asymmetry in the activation of the AT muscle during mastication's AP .…”

Different Pain, Different Brain: Thalamic Anatomy in Neuropathic and Non-Neuropathic Chronic Pain Syndromes

“…TMD are characterized by throbbing, tender, continuous pain and result from or are initiated by activation of nociceptors in the temporomandibular joint and/or muscles of mastication (Sarlani and Greenspan, 2005;Ro, 2008;Sessle et al, 2008;Manfredini and Nardini, 2010). In contrast, trigeminal neuralgia is characterized by intermittent periods of sharp, electricity-like, shooting pain that results primarily from compression of the trigeminal root entry zone by an arterial vessel (Meaney et al, 1995;Hamlyn, 1997).…”

“…Furthermore, VP thalamic stimulation can produce pain (Lenz et al, 1993;Davis et al, 1996) and increased thalamic bursting activity and biochemical changes indicative of neuronal loss occur in patients with pain after spinal cord injury (Lenz et al, 1989;Pattany et al, 2002). In direct contrast to neuropathic pain conditions, pain associated with temporomandibular disorders (TMD) results primarily from the activation of peripheral nociceptors (Sarlani and Greenspan, 2005;Ro, 2008;Sessle et al, 2008;Manfredini and Nardini, 2010) and, furthermore, is associated with thalamic gray matter volume increases (Younger et al, 2010). Given this, it is possible that the thalamus plays differential roles in the maintenance and/or generation of different forms of chronic pain.…”

Pain and Plasticity: Is Chronic Pain Always Associated with Somatosensory Cortex Activity and Reorganization?

“…All TMD patients were examined and diagnosed using the Research Diagnostic Criteria for TMD (Dworkin and LeResche, 1992) and all PTN patients were diagnosed using the Liverpool Criteria (Nurmikko and Eldridge, 2001). TMD is thought to result primarily from the activation of peripheral nociceptors (Sarlani and Greenspan, 2005;Ro, 2008;Manfredini and Nardini, 2010), although it may also contain a small neuropathic component. In contrast, PTN is commonly associated with a structural lesion or systematic disease and may result from direct trauma to the nerve.…”