Pain
-
Cross-sectional research in clinical samples, as well as experimental studies in healthy adults, suggests that the experiences of pain and sleep are bi-directionally connected. However, whether sleep and pain experiences are prospectively linked to one another on a day-to-day basis in the general population has not previously been reported. This study utilizes data from a naturalistic, micro-longitudinal, telephone study using a representative national sample of 971 adults. ⋯ Results suggested that hours of reported sleep on the previous night was a highly significant predictor of the current day's pain frequency (Z=-7.9, p<.0001, in the structural equation model); obtaining either less than 6 or more than 9h of sleep was associated with greater next-day pain. In addition, pain prospectively predicted sleep duration, though the magnitude of the association in this direction was somewhat less strong (Z=-3.1, p=.002, in the structural equation model). Collectively, these findings indicate that night-to-night changes in sleep affect pain report, illuminating the importance of considering sleep when assessing and treating pain.
-
Comparative Study
C-fiber spontaneous discharge evoked by chronic inflammation is suppressed by a long-term infusion of lidocaine yielding nanogram per milliliter plasma levels.
Nociceptors innervating inflamed tissue acquire an abnormal spontaneous discharge that is believed to be at least part of the reason for the persistent spontaneous pain, allodynia, and hyperalgesia that accompany inflammation. Recent studies suggest that patients with chronic inflammatory pain may obtain an analgesic effect with transdermal application of lidocaine that yields very low plasma levels (130-225 ng/ml). The aim of this study was to investigate whether a 7-day exposure to such low plasma levels of lidocaine had an effect on inflammation-evoked spontaneous discharge in the rat. ⋯ Lidocaine infusion had no effect on the incidence of spontaneous discharge in muscle or cutaneous A-fibers. Lidocaine infusion reduced mechano-hyperalgesia but had no effect on mechano-allodynia or heat-hyperalgesia. We conclude that the analgesic effects seen clinically with transdermal lidocaine administration yielding low plasma levels may be due to a systemic drug action on spontaneously active C-fibers.
-
Comparative Study
Increased bias to report heat or pain following emotional priming of pain-related fear.
Emotional and attentional factors have been identified to play a significant role in modulating pain perception with negative emotions increasing pain sensitivity. Recent studies suggest that fearful images may activate the attentional components of fear driven behaviours and facilitate an attentional bias or sensitivity toward noxious stimuli. The current investigation examines whether priming of pain-related fear will affect performance by increasing sensitivity to punctuate heat stimuli. ⋯ The results indicated a significant facilitation of heat and pain perception at varying temperatures following emotional priming. In particular, there was an increase in the bias toward reporting a heat stimulus following emotional priming. The findings emphasise the efficacy of the visual dot probe task as a method of priming and provide a possible method for probing hypervigilance in chronic pain patients.
-
Comparative Study
Role of spinal serotonin 5-HT2A receptor in 2',3'-dideoxycytidine-induced neuropathic pain in the rat and the mouse.
Several lines of evidence suggest that descending serotoninergic facilitatory pathways are involved in neuropathic pain. These pathways may involve 5-HT2A receptors known to play a role in spinal and peripheral sensitization. The implication of this receptor in neuropathy was investigated in a model of peripheral neuropathy induced by 2',3'-dideoxycytidine, a nucleoside analogue with reverse transcriptase inhibitory properties used in HIV/AIDS therapy. ⋯ Four days after 2',3'-dideoxycytidine administration, rats had developed thermal allodynia as well as mechanical hyperalgesia and allodynia, which dose-dependently decreased after epidural injection of MDL 11,939, a 5-HT2A receptor antagonist. Moreover, 5-HT2A receptor knock-out mice did not develop 2',3'-dideoxycytidine-induced neuropathy whereas their control littermates displayed a neuropathy comparable to that observed in rats. Our data show that 2',3'-dideoxycytidine-induced neuropathy is associated with alterations of nociceptive and non-nociceptive peripheral cells and that the 5-HT2A receptor is involved in the peripheral sensitization of nociceptors as well as in a wide central sensitization of dorsal horn neurons.