The journal of pain : official journal of the American Pain Society
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This study compared recalled average pain, assessed at the end of the day, with the average of real-time pain ratings recorded throughout the day among patients with osteoarthritis (OA). Participants (N = 157) with hand, hip, or knee OA completed electronic pain diaries on 1 weekend day and 1 weekday. Diaries included at least 7 pain ratings per day, immediately after waking and every 2 hours following, using a visual analog scale (VAS) scored as 1 to 100 (scores not seen by participants). At the end of each diary day, participants rated their average pain that day on the same VAS. Pearson correlations examined associations between recalled average pain and the average of real-time pain ratings that day. Mixed models, including interaction terms, examined whether associations between recalled and actual average pain ratings differed according to the following patient characteristics: joint site, age, race, gender, study enrollment site, and pain catastrophizing. Correlations between recalled and actual average pain ratings were r = .88 for weekdays and r = .86 for weekends (P < .0001). In mixed models, there were no significant interaction terms for any patient characteristics. In summary, patients with OA accurately recalled their average pain over a 1-day period, and this did not differ according to any patient characteristics examined. ⋯ This study showed that patients with OA accurately recalled their average pain over a single-day period, and this did not differ according to patient characteristics. Results of this study indicate that end-of-day recall is a practical and valid method for assessing patients' average pain during a day.
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Peripheral nerve injury leads to neuropathic pain, but the underlying mechanisms are not clear. The TRPV1 channel expressed by nociceptors is one receptor for noxious heat and inflammatory molecules. Lumbar 4 (L4) spinal nerve ligation (SNL) in mice induced persistent heat hyperalgesia 4 to 10 days after injury. The heat hypersensitivity was completely reversed by the TRPV1 antagonist A-425619. Furthermore, DRG neurons were isolated from the injured L4 ganglia or adjacent L3 ganglia 4 to 10 days after L4 SNL. Whole-cell patch-clamp recordings were performed and heat stimuli (22 degrees C to 50 degrees C/3 s) were applied to the soma. Neurons were classified by soma size and isolectin-B4 (IB4) binding. Among directly injured L4 neurons, SNL increased the percentage of small-diameter IB4-positive neurons that were heat-sensitive from 13% (naive controls) to 56% and conversely decreased the proportion of small IB4-negative neurons that were heat-sensitive from 66% (naive controls) to 34%. There was no change in IB4 binding in neurons from the injured ganglia. Surprisingly, in neurons from the adjacent L3 ganglia, SNL had no effect on the heat responsiveness of either IB4-positive or negative small neurons. Also, SNL had no effect on heat responses in medium-large-diameter neurons from either the injured or adjacent ganglia. ⋯ TRPV1 function is upregulated in IB4-positive sensory neurons, and TRPV1 is responsible for the behavioral heat hypersensitivity in the spinal nerve ligation model. Because IB4-positive neurons may contribute to the emotional perception of pain, TRPV1 antagonists, targeting both sensory and affective pain components, could have broad analgesic effects.