Trigeminal Nociceptive Evaluation in TMD Patients by studying CO2-Laser Evoked Potentials and Masseter Laser Silent Periods
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[[|Italian]]Trigeminal Nociceptive Evaluation in TMD Patients by studying CO2-Laser Evoked Potentials and Masseter Laser Silent Periods
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Article by Antonietta Romaniello
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The term temporomandibular dysfunction (TMD) refers to a group of painful syndromes affecting the masticatory muscles and the temporomandibular joint (TMJ). Nosographic classifications of TMD vary widely as they may involve different pathophysiological mechanisms, and the etiological factors are often unknown Many of the hypotheses proposed to explain its pathophysiology and etiology remain largely unproven. Electromyographic (EMG) alterations of the voluntary or reflex activity of the masticatory muscles have often been found in association with TMD; however, EMG studies have neither provided reliable criteria nor clarified the pathogenesis of this controversial syndrome.
Recent studies have contradicted the hypothesis of muscle hyperactivity or a state of central nervous system hyperactivity in TMD patients. Studies aimed at evaluating the somatosensory system in TMD patients have yielded conflicting results regarding the extent and detection of somatic sensitivity alterations, reporting hypersensitivity, hyposensitivity, or no alterations at all. An experimental study conducted on healthy volunteers has recently shown that tonic experimental pain in the trigeminal territory reduces CO2 laser-evoked potentials (LEPs) and laser silent periods (LSPs). Since the laser stimulus selectively activates small-caliber afferents (A-delta and C fibers) and evaluates nociceptive afferents function, the authors concluded that tonic pain induces hypoexcitability of the trigeminal nociceptive system.
The primary aim of this study was to test the hypothesis that a well-defined group of TMD patients with unilateral chronic craniofacial pain exhibits hyposensitivity to phasic nociceptive stimuli applied in the trigeminal area. Secondly, we investigated whether brainstem reflex circuits mediating LSP are modulated by chronic craniofacial pain.
Modulation of Laser-Evoked Potentials (LEPs): It has been hypothesized that the degree of organic involvement relative to psychological involvement in different chronic pain conditions might explain the contrasting results obtained in various studies. Patients with painful paraplegia, neuropathic pain, and low back pain exhibit an increase in the perceptual threshold for painful stimuli compared to controls. Conversely, pain conditions where psychological factors are believed to be predominant, such as fibromyalgia, or psychiatric pain, tend to be associated with a reduction in the perceptual threshold. In TMD patients, Maixner et al. described increased sensitivity to experimental pain and suggested that pain associated with TMD may be considered a psychological disorder associated with an alteration in central inhibitory mechanisms, which consequently induces facilitation of nociceptive system activity. Conversely, a study conducted by Cruccu et al. on TMD patients did not confirm a state of central hyperactivity, as TMD patients had normal excitability of the brainstem reticular formation and corticoreticular projections. It is likely that experimental differences, such as the use of different types of experimental nociceptive stimuli and the stimulation of different areas, could result in different findings in various studies.
Modulation of Laser Silent Period (LSP): Recently, it has been demonstrated that LSP is strongly suppressed by tonic experimental trigeminal pain, both muscular and cutaneous. In this study, the absence of LSP in 12 out of 15 patients suggests a marked hypoactivity of the brainstem pathways mediating LSP. LSP was suppressed to a considerably greater extent than LEPs. It is possible that the reflex pathway is subject to dual inhibition: one mediated by a mechanism similar to that involved in LEPs (see the previous section) and another mediated by a segmental inhibition mechanism that acts on the brainstem LSP reflex circuit. Segmental inhibition can occur presynaptically, on the primary afferent fiber, or postsynaptically in the interneuronal circuit. Several studies have demonstrated presynaptic depolarization (PAD) in the trigeminal nucleus after a conditioning trigeminal stimulus. However, while PAD may play a role in the modulation of LSP, the presynaptic inhibition mechanism alone is not sufficient to explain the bilateral suppression of LSP in our patients with unilateral pain. More likely, the pain-induced inhibitory effect occurred at the interneuronal level, along the central reflex pathway. At this level, the pain-induced effect can have a bilateral impact, as it has been demonstrated that a conditioning painful stimulus can induce contralateral segmental inhibition on dorsal horn neurons, both on nociceptive-specific neurons and wide-dynamic-range neurons.
Conclusion, this study demonstrated that in TMD patients with unilateral chronic pain, both nociceptive inputs directed to the cortex and the brainstem nociceptive reflex circuit are inhibited. While these results suggest a dysfunction of the nociceptive system that mediates and integrates phasic nociceptive inputs, it is not possible to assert whether this dysfunction plays a role in the pathophysiology of TMD or if it is rather a consequence of chronic pain.
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