ClinicalTrials.gov: http://clinicaltrials.gov/show/NCT01359878. Published protocol: http://www.trialsjournal.com/content/pdf/1745-6215-13-110.pdf.

Inguinal hernia repair is associated with a 5%-30% incidence of chronic pain, but the pathogenesis remains unknown. We therefore evaluated pain and sensory dysfunction by quantitative sensory testing 6-12 mo after open hemiorrhaphy. Before sensory testing, all patients (n = 72) completed a short-form McGill Pain Questionnaire and a functional impairment questionnaire. Sensory dysfunction in the incisional area was evaluated by quantification of thermal and mechanical thresholds, by mechanical pain responses (von Frey/pressure algometry), and by areas of pinprick hypoesthesia and tactile allodynia. The incidence of chronic pain was 28% (20 of 72). Quantitative sensory testing and pressure algometry did not demonstrate differences between the pain and nonpain groups, except for a small but significant increase in pain response to von Frey hair and brush stimulation in the pain group. Hypoesthesia, or tactile allodynia, in the incisional area was observed in 51% (37 of 72) of the patients, but the incidence did not differ significantly between the pain group and the nonpain group (14 of 20 versus 23 of 52; P > 0.3). We concluded that cutaneous hypoesthesia, or tactile allodynia, is common after inguinal hemiotomy but has a low specificity for chronic postherniotomy pain. Factors other than nerve damage may be involved in the development of chronic posthemiotomy pain.

One of the oldest methods of pain relief following a burn injury is local application of ice or cold water. Experimental data indicate that cooling may also reduce the severity of tissue injury and promote wound healing, but there are no controlled studies in humans evaluating the anti-inflammatory or anti-hyperalgesic potential of early cooling after thermal injury. Twenty-four healthy volunteers participated in this randomized, single-blinded study. Following baseline measurements, which included inflammatory variables (skin temperature, erythema index) and sensory variables (thermal and mechanical detection thresholds, thermal and mechanical pain responses, area of secondary hyperalgesia), first degree burn injuries were induced on both calves by contact thermodes (12.5 cm(2), 47 degrees C for 7 min). Eight minutes after the burn injury, contact thermodes (12.5 cm(2)) were again applied on the burns. One of the thermodes cooled the burn (8 degrees C for 30 min) whereas the other thermode was a non-active dummy on the control burn. Inflammatory and sensory variables were followed for 160 min after end of the cooling procedure. The burn injury induced significant increases in skin temperature (P<0.0005), erythema index (P<0.0001), thermal pain responses (P<0.0005), mechanical pain responses (P<0.005) and secondary hyperalgesia, and significant decreases in heat pain threshold (P<0.0005) and mechanical pain threshold (P<0.0005). There were no post-cooling effects on skin temperature (P>0.5), erythema (P>0.9), heat pain threshold (P>0.5), thermal or mechanical pain responses (P>0.5) or the development of secondary hyperalgesia (P>0.4) compared with the control burn. However, a significant, albeit transient, increase in cold detection threshold was observed on the cooled burn side (P<0.0001). In conclusion, cooling with 8 degrees C for 30 min following a first degree burn injury in humans does not attenuate inflammatory or hyperalgesic responses compared with a placebo-treated control burn.

The study indicates that systemic administration of dexamethasone 2 hours before a burn injury does not reduce the inflammatory-mediated changes in quantitative sensory thresholds, pain perception, or skin erythema in humans.

Arthroscopic knee surgery did not modify nociceptive responses to a contralaterally applied experimental burn injury.