Articles: pain-threshold.
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This study examined masseter and temporalis pain-pressure thresholds in 29 patients with chronic bilateral myogenous temporomandibular disorder and in 11 controls. Patients with evidence of temporomandibular joint pathosis were omitted. The influence of time, facial side, muscle site, and side of greatest spontaneous pain on pain-pressure thresholds was measured. ⋯ Mean pain-pressure thresholds in patients differed over the four sessions, which is consistent with recent reports of fluctuating levels of pain in patients with temporomandibular disorders. Additional findings included significant pain-pressure threshold differences among muscle sites in patients and controls, and lower patient pain-pressure thresholds relative to controls. Within- and between-session reliability was adequate for patients (r = .85 and r = .75, respectively) and controls (r = .90 and r = .75, respectively).
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The optimal treatment of pain requires an understanding of the mechanisms involved. Pain is a sensory end-point that can be generated by a number of dissimilar processes. Consequently, the concept of treating pain as a unitary symptom is obsolete. ⋯ Clinical pain is more than a reflection of sustained peripheral input and it is, to a large extent, the expression of changes produced in the CNS, including the phenomenon of central sensitization. We need to treat both the disease/injury process in the periphery and the changes it induces or triggers in the CNS. Prevention of central sensitization will substantially eliminate the hyperalgesia and allodynia that patients find so distressing, and it offers new possibilities for the development of novel analgesics or antihypersensitivity drugs.
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Twenty-four healthy human subjects provided thresholds for their perception of pressure, sharpness, and pain. Mechanical forces were applied to the dorsal surface of the digits with flat-tipped probes of various sizes. Thresholds (expressed as force) increased with increasing probe size, as previously described. ⋯ In contrast, only 6% of subjects showed significant increases in sharpness or pressure thresholds over the same period. Thus, whereas most subjects exhibited stable pain thresholds, approximately one-fourth showed significant increases in pain threshold over time. We conclude that for evaluating regional dysesthesia or hemidysesthesia, a right-left difference in pain thresholds will provide a more sensitive and reliable measure than absolute pain threshold.
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The gate control theory of pain (Melzack and Wall, 1965) suggests that tactile stimuli can decrease the perception of pain. We have found the reverse effect: Heat at levels that induce pain can substantially suppress tactile sensitivity, independently of shifts in attention or arousal. Ten human observers were stimulated by a tonic, pain-producing heat stimulus and vibrotactile stimuli (1, 10, and 100 Hz) coincidentally presented to the right thenar eminence. ⋯ The changes are not attributable to attentional or arousal shifts, since they were not associated with changes in auditory thresholds. Furthermore, the changes occurred just below the subjects' pain thresholds (where nociceptors are presumably activated). This over-twofold diminution of vibrotactile sensitivity suggests that heat stimuli capable of inducing pain can significantly diminish taction, perhaps through a "touch gate" in a manner similar to the gate control theory proposed for pain.
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It is reported that intrathecal (it) injection of low dose of dynorphin (Dyn) induces no analgesia while high dose of Dyn induces analgesia and might lead to hindlimb paralysis and loss of reflex via NMDA receptor. We hypothesized that NMDA receptor antagonists may reveal kappa analgesic-potential of subliminal dose of Dyn. ⋯ Combination of Dyn A- (1-13) 5 nmol or U50488H 100 nmol, a kappa receptor agonist with either DL-2-amino-5-phosphonovaleric acid (5 and 10 nmol) or kynurenic acid (25 and 50 nmol) it induced synergistic analgesia, which was reversed by nor-binaltorphimine 15 nmol, a kappa receptor antagonist. It is concluded that kappa opioid receptor agonists and NMDA receptor antagonists synergistically induce analgesia via interaction with their receptors.