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Mechanical hyperesthesia of human facial skin induced by tonic painful stimulation of jaw muscles.

The function of the somatosensory system in patients with painful temporomandibular disorders is still a matter of discussion. We wished to determine cutaneous sensitivity to innocuous mechanical stimuli in the orofacial region before, during (3 and 12 min) and after standardized experimental jaw-muscle pain. Twelve healthy subjects were exposed to tonic infusion of hypertonic (5%) and isotonic (0.9%) saline into the masseter muscle. All subjects experienced moderate pain with hypertonic saline, and the area of self-reported pain increased significantly from 3 min after infusion start to 12 min after infusion start (mean +/- SEM: 115+/-49%; P < 0.05). The psychophysical ratings of punctate von Frey hair stimulation were significantly increased 12 min after start of hypertonic saline infusion as compared to baseline and post-baseline ratings at the site of infusion (50+/-10%; P < 0.05) and at two adjacent facial sites (18+/-7%, 37+/-9%; P < 0.05). In contrast, isotonic saline infusion was associated with a significant decrease in ratings at post-baseline as compared to baseline ratings. The psychophysical ratings of a stroking cotton swab stimulation were not significantly affected by infusion of saline. These results in a human model of jaw-muscle pain are comparable to animal studies demonstrating increased size of cutaneous receptive fields and increased responsiveness of brain stem neurons to cutaneous mechanical stimuli. Similar hyperexcitability changes may be part of the pathophysiological mechanisms involved in painful temporomandibular disorders.

Adult↗

Spinal pharmacology of thermal hyperesthesia induced by incomplete ligation of sciatic nerve. I. Opioid and nonopioid receptors.

Mechanisms underlying the pain state in humans that follows incomplete injury to peripheral nerve are little understood. To gain better understanding of this phenomenon, this study evaluated the effects on the thermally evoked hind-paw withdrawal latency produced by the intrathecal administration of morphine, U-50 488H (U-50), (D-Pen2, D-Pen5)-enkephalin (DPDPE), ST-91, baclofen, muscimol, and 5'-N-ethylcarboxamide-adenosine (NECA) in normal rats and in rats with a hind paw rendered unilaterally hyperesthetic by the unilateral application of loose ligatures to the sciatic nerve. In the animals with one ligated nerve, the hind-paw latency for the ligated paw was typically 2-4 s less than that for the nonligated paw, at 7-11 days postoperatively. In normal rats prepared with chronic intrathecal catheters, dose-dependent increases in paw withdrawal latency were observed; the order of activity was: baclofen, ST-91, morphine, muscimol, DPDPE much greater than U50, NECA greater than or equal to 0. In the nonligated (nonhyperesthetic) paw of the lesioned animals, intrathecal agents also resulted in a dose-dependent increase in the paw withdrawal latency; the order of potency was: NECA, baclofen, morphine, ST-91, muscimol, DPDPE greater than U50 greater than or equal to 0. For both NECA and morphine, the median effective dose (ED50) values were significantly less in the nonhyperesthetic hind paw. For the hyperesthetic paw, the dose-response curves were parallel to those obtained concurrently in the nonhyperesthetic paw but were shifted significantly to the right by a factor of 3-5, with the rank order of activity in the hyperesthetic paw being baclofen, morphine, muscimol, DPDPE greater than ST-91, NECA, U50 greater than or equal to 0. These data indicate that 1) spinal receptor systems that alter thermal afferent processing in the normal animal are similarly active in the hyperesthetic paw of the lesioned animal; and 2) unexpectedly, despite similar predrug response latencies, certain receptor systems regulating the response in the nonhyperesthetic paw of the lesioned rat (morphine and NECA) show greater activity than in the nonlesioned rat.

Analgesics↗