SEATTLE, WA—Endogenous pain regulatory function is impacted by sleep duration, according to data presented at SLEEP 2015, by M.M. Hand, of Johns Hopkins University School of Medicine in Baltimore, MD.
It is well-documented that poor sleep negatively impacts clinical pain — a phenomenon corroborated in laboratory testing, where shortened sleep duration or poor sleep quality is shown to amplify sensitivity to quantitative sensory testing methods, said Hand. Response of endogenous pain-regulatory systems to sleep may mediate this connection.
To test this hypothesis, Hand and her group employed naloxone (0.1mg/kg), an opioid antagonist, to probe endogenous opioid function and investigate its effect on pain report in 32 healthy individuals with differing sleep patterns (20 with <6.5 hours and 12 with ≥6.5 hours per night). The mean age of patients was 25.4 years (standard deviation [SD], 5.2). The sleep groups were matched in sex, age, and psychological characteristics (eg, pain catastrophizing and reactivity).
The researchers applied at 10% topical cream of capsaicin to the dorsum of the non-dominant hand and utilized a thermode to maintain a constant temperature of 40oC for 90 minutes. Pain ratings were obtained every five minutes, using a scale from 0–100. They compared the reactions of the two sleep groups to capsaicin pain under both naloxone and saline conditions.
Analyses revealed a main effect of the drug (P=0.015), with responses during the naloxone session generally rated as less intense than during the saline session. They also observed a drug-by-sleep interaction (P=0.038), with participants who slept less reporting significant pain increase in the naloxone condition, compared to longer sleepers, suggesting a potential protective effect of increased sleep on the experience of pain.
The researchers added that animal models suggest that naloxone may be a potential microglia inhibitor, which can also impact the sleep-pain relationship.
This article originally appeared on MPR