Pain
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This study presents the sociodemographic distribution of tooth pain and the dental care utilization of affected individuals. Data for adults 20 years of age and over were derived from the 1989 National Health Interview Survey's supplements on dental health, orofacial pain, and health insurance (n=33073). Prevalence of tooth pain by socioeconomic status (SES) and adjusted odds ratios of reporting tooth pain in the past 6 months and of having no dental visits in the past year among persons reporting pain in the previous 6 months were computed taking into account the survey's complex sample design. ⋯ In the younger age group, tooth pain was more likely to be reported by those with low SES than it was by those with high SES; in the older age group, tooth pain was more likely reported by non-Hispanic blacks than it was by non-Hispanic whites or Hispanics. Of those reporting pain, younger and older non-Hispanic blacks and persons with lower educational attainment were more likely not to have a dental visit in the previous 12 months. Persons with low SES characteristics were more likely to report tooth pain and to endure their pain without the benefit of dental care while the pain was present.
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A total of 68 neurons were recorded from the ventro-postero-lateral nucleus of thalamus (VPL) in rats with a unilateral chronic constriction injury (CCI) of the sciatic nerve (n=20), sham operation (n=24) and naive rats (n=24), and effects of the lesion of dorsal column (DC) pathway [DC lesion or DC+gracile nucleus lesions] on VPL nucleus neuronal activities were studied. In the VPL nucleus contralateral to the CCI (receiving input from the injured nerve), response latencies of low threshold mechanoreceptive (LTM) and wide dynamic range (WDR) neurons to electrical stimulation of the sciatic nerve were significantly longer than that in the contralateral VPL nucleus receiving input from the sham-operated side (P<0.05). In contrast, response latencies of LTM and WDR neurons to DC stimulation were not different between the sham operated and CCI sides (0.05). ⋯ The decrease in noxious stimulus-evoked responses of WDR neurons in the VPL nucleus contralateral to the CCI side after DC and DC+gracile nucleus lesions was greater than that in the VPL nucleus contralateral to the sham operated side and naive animals. These results indicated that DC and DC+gracile nucleus lesions produced selective and stronger effect on noxious responses of VPL nucleus WDR neurons receiving input from the site of nerve injury. The findings suggest that the gracile nucleus-thalamic pathway conveys, or modulates, nociceptive information to the VPL nucleus following peripheral nerve injury, resulting in an increase in VPL nucleus response to noxious stimuli that contributes to the development of mechanical hyperalgesia.
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The rostral ventromedial medulla (RVM) is critical for the modulation of dorsal horn nociceptive transmission. Three classes of RVM neurons (ON, OFF, and NEUTRAL) have been described that have distinct responses to noxious stimuli and mu opioid receptor (MOR) agonists. The present study in barbiturate anesthetized rats investigated the effects of the delta 2 opioid receptor (DOR2) agonist, [D-Ala2]deltorphin II (DELT), microinfused into the RVM on the tail flick reflex and activity of RVM neurons. ⋯ The activity of NEUTRAL cells was not affected. The antinociceptive effects and corresponding changes in ON and OFF cell activity produced by DELT were antagonized by the DOR2 antagonist, naltriben methanesulfonate, administered at the same site. These DOR2 mediated effects on noxious stimulation-evoked changes in RVM neuronal activity are similar to those reported for MOR agonists and suggest that both DOR2 and MOR produce analgesia through activation of OFF cells.
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We tested the ability of lithium (Li(+)) to block heat hyperalgesia, cold allodynia, mechanical allodynia and mechanical hyperalgesia in rats experimentally subjected to painful peripheral neuropathy. Chronic constrictive injury (CCI) to the sciatic nerve induced persistent hyperalgesia and allodynia. Intrathecal injection of Li(+) (2.5-40 micromol) into the region of lumbar enlargement dose-dependently reduced heat hyperalgesia, cold allodynia and mechanical allodynia for 2-6 h after injection, but had no effect on mechanical hyperalgesia. ⋯ Intrathecal injection of myo-inositol (2.5 mg) significantly reversed both the anti-hyperalgesic and anti-allodynic effect of Li(+). These findings suggest that intrathecal Li(+) suppresses neuropathic pain response in CCI rats through the intracellular phosphatidylinositol (PI) second messenger system in spinal cord neurons. Lithium (Li(+)) has already found widespread clinical application; these results suggest that its therapeutic utility may be extended to include treatment of neuropathic pain syndromes resulting from peripheral nerve injury.
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Complex regional pain syndromes (causalgia and RSD) can be relieved by blockade of the sympathetic efferent activity. The mechanisms of sympathetically maintained pain (SMP) are unclear. So far an adrenergic interaction between sympathetic vasoconstrictor neurons and nociceptors has been proposed. Alternatively, a cholinergic coupling of sympathetic sudomotor neurons and nociceptors is possible. ⋯ Cutaneous sympathetic sudomotor activity does not influence capsaicin induced pain and mechanical hyperalgesia.