Difference between revisions of "Trigeminal Nociceptive Evaluation in TMD Patients by studying CO2-Laser Evoked Potentials and Masseter Laser Silent Periods"

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.

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