Area Of Allodynia Research Articles

Pain sensitivity and experimentally induced sensitisation in red haired females

Introduction and aim Pain sensitivity has been linked to the melanocortin-1 receptor (MC1R) gene. A mutation in MC1R can result in pale skin and red hair in humans and may modulate pain responses in general. Human studies have shown that women with non-functional MC1R's were sensitive to experimental induced cold and heat pain. A study demonstrated that females with red hair required higher dose of anesthesia than females with dark hair to experience analgesia to electrical stimulation. Moreover, women expressing non-functional MC1Rs display greater analgesia from opioid analgesia. If redheads in general respond differently to pain and analgesics, this is of clinical importance. The aim of this study was therefore to investigate pain sensitivity and experimentally induced sensitisation in red haired females. Method Twenty healthy females with pale skin and red hair (mean age 32 years, range 20–55) and 20 healthy females with blond/dark hair (mean age 31 years, range 20–51) participated in this study. The pain tolerance thresholds to heat and pressure stimulation were determined. Hyperalgesia was induced experimentally by applying 0.075% topical capsaicin cream for 30 min. The secondary pin-prick hyperalgesic area was estimated with a calibrated filament (von Frey hair, 15 g) and the area of allodynia by a soft brush. This was done 0, 30, 60, and 90 min after cream removal. Results Neither heat nor pressure pain tolerance thresholds were changed in the two groups. The secondary pin-prick hyperalgesic areas were significantly smaller for red haired females than blond/dark haired females ( P = 0.014). There were no significant differences in the allodynic areas. Discussion As the secondary hyperalgesic response evoked by topical capsaicin is a central phenomenon, the observed smaller pin-prick hyperalgesic area in the red haired females could indicate a central role of MCRs in development or maintenance of hyperalgesia. Central involvement of MC1Rs or dysfunction of peripheral MC1Rs activating central MC4Rs has been suggested to influence pain sensitivity. The difference observed between red haired and non-red haired females may have implications for pain management regimens as compounds interacting with sensitisation such as NMDA-antagonists or alpha-2-delta-ligands may exert different types of action in people with MC1R mutation. Conclusion The present study showed that red haired females were less sensitive to topical capsaicin induced pin-prick hyperalgesia compared with blond/dark haired females. Implications The smaller hyperalgesic area in redheads could be a manifestation of central anti-hyperalgesic involvement of MCRs and could have an influence on the treatment of pain as well as in studies investigating anti-hyperalgesic drugs.

Anesthesia Literature Review

Anesthesia Literature Review

Painful Medial Branch Neuroma Treated with Minimally Invasive Medial Branch Neurectomy

Case report. To report an unusual complication following lumbar facet radiofrequency denervation and describe a successful, minimally invasive treatment of a presumed medial branch neuroma. Radiofrequency medial branch neurotomy is a common procedure for the treatment of mechanical back pain. Deafferentation injury and neuroma formation is well known and reported following chemical, surgical, and cryoablation neurolysis; however, it is thought to be rare with radiofrequency ablation. When this problem is encountered, treatment options appear to be limited. Further radiofrequency ablations may be ineffective and indeed may cause further injury. A 17-year-old male who sustained a traumatic fracture of the right L3-4 facet joint presented with increasing back pain after multiple radiofrequency ablations of the medial branches of the L2 and L3 dorsal rami. The description of the back pain, initially nociceptive in nature, had become progressively neuropathic with clear focal areas of allodynia and hyperesthesia. Further medial branch radiofrequency denervation was found to be ineffective. Diagnostic block of the right medial branch of the L2 dorsal ramus provided the patient with total relief of pain. This was followed by a minimally invasive open surgical ablation of the L2 medial branch neuroma using three-dimensional, fluoroscopy-based image guidance. At 7 months of follow-up, the patient reported complete resolution of pain, discontinuation of all pain medications, and return to all previous physical activities. Deafferentation injury is a rare but recognized complication of chemical, surgical, and thermal neuroablation. This case report presents a rare instance of presumed neuroma formation following multiple radiofrequency ablations for the treatment of facet-generated mechanical back pain. Open and minimally invasive medial branch neurectomy resulted in complete resolution of pain and return to baseline function.

A functional magnetic resonance imaging navigated repetitive transcranial magnetic stimulation study of the posterior parietal cortex in normal pain and hyperalgesia

Noxious stimuli activate a complex cerebral network. During central sensitization to pain, activity in most of these areas is changed. One of these areas is the posterior parietal cortex (PPC). The role of the PPC during processing of acute pain as well as hyperalgesia and tactile allodynia remains elusive. Therefore, we performed a functional magnetic resonance imaging (fMRI) based, neuro-navigated, repetitive transcranial magnetic stimulation (rTMS) study in 10 healthy volunteers. Firstly, pin-prick hyperalgesia was provoked on the right volar forearm, using the model of electrically-induced secondary mechanical hyperalgesia. fMRI was performed during pin-prick stimulation inside and outside the hyperalgesic areas. Secondly, on four different experimental sessions, the left and right individual intraparietal BOLD peak-activations were used as targets for a sham-controlled 1 Hz rTMS paradigm of 10 min duration. We measured psychophysically the (i) electrical pain stimulus intensity on an 11-point numeric pain rating scale (NRS, 0–10), the (ii) area of hyperalgesia, and the (iii) area of dynamic mechanical allodynia. Sham stimulation or rTMS was performed 16 min after induction of pin-prick hyperalgesia and tactile allodynia. Compared to sham stimulation, no significant effect of rTMS was observed on pain stimulus intensity and the area of allodynia. However, a reduction of the hyperalgesic area was observed for rTMS of the left PPC (P<0.05). We discuss the role of the PPC in central sensitization to pain, in spatial discrimination of pain stimuli and in spatial-attention to pain stimuli.

Natural history of sensory function after herpes zoster

The natural history of sensory function in the first 6 months after herpes zoster (HZ) was determined in a cohort of 94 subjects at elevated risk for developing post-herpetic neuralgia (PHN). All four visits included ratings of pain and sensory symptoms, mapping areas of altered sensation and allodynia, and quantitative thermal and mechanical sensory testing. The last three visits included the capsaicin response test. Sensory thresholds in distant control skin were stable. Mirror-image skin was persistently hyperesthetic to warming and mechanical stimuli and hyperalgesic to heat compared to distant control skin. HZ skin showed deficits in all thermal modalities. Sensory recovery was limited and selective. Allodynia area and severity, hyperalgesia to von Frey hair, and cold detection threshold improved, but deficits to warmth and heat pain did not. Capsaicin on HZ skin significantly aggravated pain and allodynia in the majority of subjects at 6–8 weeks after HZ onset. At study entry, eventual PHN subjects had significantly more impairment in detecting warmth and cold, a larger area of altered sensation, a larger area of allodynia, and more severe allodynia. The results support the study hypothesis that severity of initial injury predicts PHN, especially impaired cold sensation in HZ skin. The hypothesis that PHN develops because of a failure to recover normal neural function was not supported. Sensory recovery proceeded at the same rate in eventual pain-free and eventual PHN subjects and is not a requirement for pain resolution. Early interventions that reduce neural injury or enhance recovery should be of benefit.

Validation, reproducibility and safety of trans dermal electrical stimulation in chronic pain patients and healthy volunteers.

BackgroundSurrogate pain models have been extensively tested in Normal Human Volunteers (NHV). There are few studies that examined pain models in chronic pain patients. Patients are likely to have altered pain mechanisms. It is of interest to test patient pain responses to selective pain stimuli under controlled laboratory conditions.MethodsThe Institutional Ethic Committee approved the study. 16 patients with chronic neuropathic radiculopathy and 16 healthy volunteers were enrolled to the study after obtaining informed consent. During electrical stimulation (150 minutes for volunteers and 75 minutes for patients) the following parameters were measured every 10 minutes:Ongoing pain: Visual Analogue Scale (VAS) and Numeric Rate Scale (NRS)Allodynia (soft foam brush)Hyperalgesia (von Frey monofilament 20 g)FlareFor each endpoint, the area under the curve (AUC) was estimated from the start of stimulation to the end of stimulation by the trapezoidal rule. The individual AUC values for both periods were plotted to show the inter- and intra-subject variability. For each endpoint a mixed effect model was fitted with random effect subject and fixed effect visit. The estimate of intra-subject variance and the mean value were then used to estimate the sample size of a crossover study required to have a probability of 0.80 to detect a 25% change in the mean value. Analysis was done using GenStat 8th edition.ResultsEach endpoint achieved very good reproducibility for patients and NHV. Comparison between groups revealed trends towards:Faster habituation to painful stimuli in patientsBigger areas of hyperalgesia in patientsSimilar area of allodynia and flare (no statistical significance)ConclusionThe differences demonstrated between patients and NHVs suggest that the electrical stimulation device used here may stimulate pathways that are affected in the pathological state.

Different Anesthetic Techniques Associated with Different Incidences of Chronic Post-thoracotomy Pain: Low-Dose Remifentanil Plus Presurgical Epidural Analgesia is Preferable to High-Dose Remifentanil with Postsurgical Epidural Analgesia

To investigate the relationships between 2 anesthetic techniques, or the extent of allodynia around the surgical wound, and the occurrence of chronic post-thoracotomy pain. Prospective, randomized study. A single-institution, university hospital. Thirty-eight patients who underwent elective thoracotomy under general anesthesia. High-dose remifentanil (average effect-site concentration 5.61 +/- 0.84 ng/mL) with epidural analgesia started and at the end of surgery or low-dose remifentanil (average effect site concentration 1.99 +/- 0.02 ng/mL) with epidural analgesia with 0.5% ropivacaine started at the beginning of anesthesia. Pain intensity and the extent of allodynia around the wound were measured during the hospital stay. The presence and intensity of residual pain were assessed 1, 3, and 6 months after surgery and at the end of the study (6-13 months, average 9 months). A DN4 neuropathic pain diagnostic questionnaire was conducted at the same times. In the high-dose group, the area with allodynia was three times larger than the area in the low-dose group. The increased allodynia was associated with a higher incidence of chronic pain (RR: 2.7-4.2) 3 and 6 months after surgery and at the end of the study (median follow-up: 9.5 months). High-dose remifentanil (0.14-0.26 microg/kg/min) without epidural analgesia during surgery is associated with a large area of allodynia around the wound. These patients develop a much higher incidence of chronic pain than those receiving low-dose remifentanil with epidural analgesia during surgery.

Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain

Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain

Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain

Allodynia is a common, troublesome feature of neuropathic pain conditions. In a previous study of postherpetic neuralgia we observed that repeated tactile stimulation appeared to reduce the size of the area of allodynia in some patients. We have undertaken a pragmatic clinical study to characterise this phenomenon in neuropathic pain patients with a range of different aetiologies. Neuropathic pain patients with a discrete area of tactile allodynia were recruited ( n = 20). We assessed the sensitive area using punctate and dynamic tactile stimuli, and thermal quantitative sensory testing. On two separate testing visits, the patients had repeated (10× over 1 min) noxious heat or cotton bud strokes applied to the affected site or contralaterally. Tactile stimulation of the affected area evoked pain (median 7 NRS) and a reduction (>30%) in the area of allodynia in 9/18 patients (maximum −48 ± 9%, after 20 min), although the intensity of allodynic pain was unchanged. This effect persisted for over 1 h and was present the following day in all patients tested ( n = 5/5). No subjects showed an increase in area after allodynic stimulation. There was no change in heat pain threshold at a distant site following allodynic stimulation, suggesting no activation of diffuse noxious inhibitory control. Repeated thermal noxious stimulation (median NRS 7) could also elicit changes (>30%) in the area of allodynia in some patients (reductions in 7/20, increases in 3/20). Thus, we have found that a brief period of homotopic painful stimulation can reduce the area of allodynia in around half of patients with established neuropathic pains.

Mirror box therapy added to cognitive behavioural therapy in three chronic complex regional pain syndrome type I patients: a pilot study

Complex regional pain syndrome type I is a disorder of the extremities with disability and pain as the most prominent features. This paper describes the results of cognitive behavioural therapy combined with mirror box therapy in three patients with chronic complex regional pain syndrome type I. Before, during and at follow-up the following measurements were assessed: pain (visual analogue scale, 0-100), range of motion, muscle strength, and the areas of allodynia and of hyperalgesia. Furthermore, patients were asked for their feelings and thoughts about mirror box therapy and about the affected limb. Pain at rest, pain after measuring allodynia/hyperalgesia and pain after measuring strength decreased. Range of motion improved in two patients. Strength improved in one patient. The area of hyperalgesia increased for all three patients, whereas the area of allodynia remained stable in two patients and decreased in one patient. Two patients felt that their affected limb still belonged to them, one did not. Cognitive behavioural therapy combined with mirror box therapy for patients with chronic complex regional pain syndrome type I may facilitate rehabilitation. Measuring whether the affected limb still belongs in the patient's body scheme could be of prognostic value in the treatment of chronic complex regional pain syndrome type I patients.

461 Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain

461 Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain

Effects of oral pregabalin and aprepitant on pain and central sensitization in the electrical hyperalgesia model in human volunteers

Central sensitization is an important mechanism of neuropathic pain; its human models could be useful for early detection of efficacy of novel treatments. The electrical hyperalgesia model invokes central sensitization by repetitive stimulation of the skin. To assess its predictive value, we have investigated pregabalin, a standard neuropathic pain treatment, and aprepitant, an NK(1) antagonist, as an example of a drug class active in animal models but not in neuropathic pain patients. Furthermore, we explored if combinations of either of these drugs with the COX-2 inhibitor parecoxib could improve its efficacy. This was a double-blind, two-period, placebo-controlled study using incomplete block design. Thirty-two healthy volunteers received either oral pregabalin (titrated to 300 mg) or aprepitant (titrated to 320 mg), or matching placebo over 6 days before testing. Sensitization was assessed over 3 h; at 2 h, subjects received either parecoxib (40 mg) or saline i.v. Pregabalin significantly reduced the areas of punctate mechanical hyperalgesia and dynamic touch allodynia vs placebo (both P < 0.0001); no significant reduction in the area of hyperalgesia or allodynia vs placebo was observed with aprepitant. In the pregabalin + parecoxib treated group, the area of allodynia was significantly reduced (P < 0.0001) and the area of hyperalgesia insignificantly attenuated (P = 0.09) vs placebo + parecoxib; no efficacy improvement was observed with aprepitant + parecoxib. The model can serve to predict analgesic efficacy in early human development and investigate the mechanism of action. The model could also be used to explore efficacy of analgesic combinations to provide a rationale for patient studies.

Activation of Naloxone-Sensitive and -Insensitive Inhibitory Systems in a Human Pain Model

We investigated naloxone effects in a model of electrically induced pain and hyperalgesia. In a double-blind, placebo-controlled, cross-over study, 15 volunteers underwent four 150-minute sessions of high-current-density electrical stimulation of their forearms. After 60 minutes, naloxone or placebo was given intravenously (increasing plasma concentrations of 0.1, 1, and 10 ng/mL; 30 minutes each) in 3 of the 4 sessions. Pain ratings and areas of mechanical hyperalgesia were assessed at regular intervals during all sessions. The low doses of naloxone did not cause any significant change of pain rating of areas of hyperalgesia. In terms of intrasession effects, pain ratings and areas of hyperalgesia significantly decreased during the sessions to 62% (pain rating), 70% (area of punctuate hyperalgesia), and 82% (area of allodynia) of the initial values. Naloxone (10 ng/ml) reversed these decreases. In terms of between-session effects, the time course of pain ratings remained constant from session to session. In contrast, the areas of punctate hyperalgesia successively decreased to 60% of initial value at the fourth repetition. The session effect was not reversed by naloxone. High-current-density electrical stimulation provokes central sensitization, but in addition inhibitory systems are activated that are only partly naloxone-sensitive. Perspective Endogenous inhibitory systems are of major importance for clinical pain conditions, but are not reflected in traditional human pain models. Here we show activation of a naloxone-sensitive short-term and a naloxone-insensitive long-term inhibitory system in a new model of electrically induced pain and hyperalgesia.

Tactile allodynia in patients with postherpetic neuralgia: Lack of change in skin blood flow upon dynamic stimulation

Tactile allodynia is a common, troublesome feature of neuropathic pain. Allodynia has been proposed to involve abnormal Aβ-afferent coupling in the dorsal horn resulting in C-fibre activation and increased skin blood flow (SBF). Thus, changes in SBF could provide an objective measure of allodynia. We searched for this mechanism in patients with postherpetic neuralgia (PHN) with varying degrees of cutaneous sensory loss. We mapped the allodynic area in PHN patients using cotton buds and von Frey hairs. Quantitative thermal testing was performed to assess small fibre function in the affected and mirror-image areas. At a subsequent visit the area of allodynia was remapped. Then the SBF in the affected and control areas was quantified before and after allodynic stimulation using laser Doppler imaging and subsequent single point continuous monitoring to detect rapid changes. We enrolled 10 PHN patients (medians: age 77 yrs, duration 20 months, ongoing pain 5). The allodynic area (range 11–546 cm 2) was stable across the sessions. Thermal testing showed similar ( n=5) or reduced ( n=5) warmth and pain sensation in the affected versus control area. Following allodynic stimulation (median evoked pain-5) we saw no changes in SBF using either imaging (repeated measures ANOVA, P=0.73) or single point monitoring. This was the case for all patients regardless of the degree of sensory impairment in the affected dermatome. In conclusion, in a representative population of PHN patients we found no evidence of changes in SBF in response to allodynic stimulation. Hence, SBF measurements are not suitable for assessing allodynia.

A single dose of gabapentin reduces acute pain and allodynia in patients with herpes zoster

This randomized, double-blind, placebo-controlled crossover study measured the effect of a single dose of oral gabapentin (900 mg) on pain and allodynia associated with herpes zoster. Pain severity decreased by 66% with gabapentin compared to 33% with placebo. Reductions in allodynia area and severity, and overall pain relief, were also greater with gabapentin.

The effect of venlafaxine on ongoing and experimentally induced pain in neuropathic pain patients: a double blind, placebo controlled study

Background and aim The aim of this randomized double blind placebo controlled study was to investigate the effectiveness and the safety of venlafaxine XR 75 and 150 mg on ongoing pain and on quantitative sensory tests in 60 patients with neuropathic pain for 8 weeks. Methods Evaluation parameters consisted of ongoing pain intensity (VAS), patient satisfaction, side effects, global efficacy and tolerance. Quantitative sensory measurements taken from the affected area before and after the drug treatment included pin-prick hyperalgesia, allodynia, detection and pain thresholds to electrical and heat stimuli, temporal summation of repetitive electrical and heat stimuli. Results A total of 55 patients completed the study. VAS scores decreased significantly compared to the baseline measurements in all groups. There was no significant difference between the groups regarding pain intensity and escape medication. The areas of allodynia and pin-prick hyperalgesia decreased significantly in venlafaxine groups compared to the placebo. There was no significant difference between the groups regarding the detection thresholds (electrical and heat). The pain threshold and the summation threshold to electrical stimuli and the summation threshold to heat stimuli increased significantly following treatment in both venlafaxine groups. In addition, the degree of the temporal summation to electrical and heat stimuli decreased significantly following treatment in both venlafaxine groups compared to the placebo. Conclusion The study showed significant effect of venlafaxine in the manifestations of hyperalgesia and temporal summation, but not on the ongoing pain intensity. Furthermore, the quantitative sensory tests provided complementing information to the clinical measures.

Effect of pre-emptive ketamine on sensory changes and postoperative pain after thoracotomy: comparison of epidural and intramuscular routes

In this study we have evaluated the efficacy of ketamine via i.m. and epidural routes for the control of post-thoracotomy pain. The study was randomized, double blinded and placebo controlled. With the approval of the Faculty Ethics Committee, 60 patients undergoing elective thoracotomy were randomized into three equal groups. Group IM had i.m. ketamine 1 mg kg(-1) in 2 ml plus epidural normal saline; Group EPI had epidural ketamine 1 mg kg(-1) in 10 ml plus i.m. normal saline; Group C had epidural normal saline 10 ml plus i.m. normal saline 10 ml. Anaesthesia was standardized. Postoperative analgesia was maintained with epidural patient-controlled analgesia using bupivacaine and morphine. Visual analogue scale values and analgesic consumption were evaluated at 2, 4, 6, 8, 10, 12, 24 and 48 h after surgery. The areas of allodynia, pin-prick hyperalgesia and pressure hyperalgesia were measured at 48 h, and days 15 and 30 in all groups. Intraoperative fentanyl requirement was significantly lower in Group EPI than Group C. The morphine and bupivacaine requirements were significantly lower in Group EPI than the other two groups in the postoperative period. There was reduced pin-prick hyperalgesia and touch allodynia in the EPI group. There were no side-effects attributable to ketamine. The results of the present study demonstrate that pre-emptive epidural ketamine is effective in reducing intra- and postoperative analgesic requirements, hyperalgesia and touch allodynia.

Intrathecal, but not intravenous adenosine reduces allodynia in patients with neuropathic pain

Intrathecal adenosine reduces allodynia from intradermal capsaicin in human volunteers, and reduces hypersensitivity to mechanical stimuli in animals with nerve injury. Although both intrathecal and intravenous adenosine have been reported to relieve pain in patients with neuropathic pain, there are no controlled trials of this therapy. In order to determine the effect of adenosine, seven patients with chronic neuropathic pain and stable areas of mechanical hyperalgesia and allodynia were recruited. Using a double-blind, cross-over design, patients were studied on two occasions – once with intrathecal adenosine, 2 mg and once with intravenous adenosine, 2 mg, using saline by the alternate route. Areas of hyperalgesia and allodynia and pain from von Frey stimulation in the area of allodynia were determined up to 24 h after drug injection. Intrathecal, but not intravenous adenosine reduced area of allodynia by approximately 25% ( P<0.05) from 2 to 24 h after injection. Intrathecal adenosine reduced pain from von Frey filament stimulation in the area of allodynia by approximately 20% ( P<0.05). Ongoing pain was unaffected by adenosine by either route. Intrathecal, but not intravenous adenosine, caused backache in five of seven patients, lasting 6 h. These results indicate that intrathecal adenosine reduces allodynia and pain from stimulation in the area of allodynia, whereas the same dose of adenosine intravenously was ineffective. Given the modest effect and common side effects, the role for intrathecal adenosine as a sole agent for the treatment of neuropathic pain may be limited.

Central origin of secondary mechanical hyperalgesia.

The contribution for the development of secondary mechanical hyperalgesia by peripheral mechanisms has not been fully elucidated. We have reevaluated the effects of local anesthetics on electrically evoked flare reaction and mechanical hyperalgesia in human skin. We applied 2% lidocaine via intradermal microdialysis fibers at a length of 10 cm for 110 min to the volar forearm to establish a narrow and stable "anesthetic strip." After 60 min of lidocaine perfusion, transdermal electrical stimulation (1 Hz, 50 mA) was applied at a distance of 1 cm from the microdialysis fibers for 30 min. The areas of allodynia and punctate hyperalgesia were marked at the end of the stimulation period. The flare reaction was assessed by laser Doppler scanner and infrared thermography. Total protein content of the dialysate collected at the stimulating electrode was measured photometrically. We found no increase in protein content during electrical stimulation. Flare area (12.4 +/- 2.3 vs. 3.5 +/- 1.2 cm2) and intensity (426 +/- 24 vs. 257 +/- 21 PU) were significantly reduced beyond the lidocaine strip. The mean temperature increase in the area beyond the lidocaine strip was significantly reduced (1.1 +/- 0.1 vs. 0.2 +/- 0.1 degrees C) and did not differ from control areas. In contrast, allodynia (7.4 +/- 0.7 and 8.6 +/- 0.9 cm) and punctate hyperalgesia (7.6 +/- 0.7 and 8.6 +/- 0.9 cm) developed symmetrically on both sides of the anesthetic strip. Allodynia subsided 4 min after the end of the electrical stimulation. We conclude that the development of allodynia and punctate hyperalgesia in human skin is centrally mediated, whereas the axon reflex vasodilation is of peripheral origin.

Analgesic effects of dexamethasone in burn injury

Background and Objectives: Glucocorticoids are well-known adjuvant analgesics in certain chronic pain states. There is, however, a paucity of data on their analgesic efficacy in acute pain. Therefore, the aim of the study was to examine the analgesic effects of dexamethasone in a validated burn model of acute inflammatory pain in humans. Methods: Twenty-two volunteers were investigated in a double-blind, randomized, placebo-controlled cross-over study. Intravenous dexamethasone 8 mg or placebo was administered on 2 separate study days. Two hours after drug administration, a first-degree burn injury was produced on the medial aspect of the nondominant calf (12.5 cm2, 47°C for 7 minutes). Quantitative sensory testing included pain ratings to thermal and mechanical stimuli (visual analog scale [VAS]), assessments of thermal and mechanical detection thresholds, and areas of allodynia and secondary hyperalgesia. Results: The burn injury induced significant increases in erythema (P < .0001) and hyperalgesia (P < .001) in both groups. Pain ratings and development of tactile allodynia during the burn did not differ between dexamethasone and placebo treatments (P > .6). There were no significant differences between treatments in regard to skin erythema (P > .8), thermal or mechanical thresholds (P > .2), thermal or mechanical pain response (P > .2), or mechanical secondary hyperalgesia (P > .2). Dexamethasone had no analgesic effects in normal skin. Conclusions: 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. Reg Anesth Pain Med 2002;27:254-260.