Y. Guereca

The Influence of Placebo Analgesia Manipulations on Pain Report, the Nociceptive Flexion Reflex, and Autonomic Responses to Pain

Expectations for pain relief and experience/conditioning are psychological factors that contribute to placebo analgesia, yet few studies have studied the physiological mechanisms underlying their effects. This study randomized 133 participants to 4 groups: an expectation only (E-only) group, a conditioning only (C-only) group, an expectation plus conditioning (E+C) group, and a natural history (NH) control group. Painful electric stimulations were delivered before and after an inert cream was applied to the site of stimulation. Pain-related outcomes (pain ratings, nociceptive flexion reflex [NFR], skin conductance response, and heart rate acceleration) were recorded after each stimulation. NFR (a measure of spinal nociception) assessed if placebo analgesia inhibited spinal processing of pain. E+C was the only manipulation that significantly inhibited pain and skin conductance response. Surprisingly, NFR was facilitated in the E+C and E-only groups. No effects were noted for C-only. Mediation analysis suggested 2 descending processes were engaged during E+C that influenced spinal nociception: 1) descending facilitation and 2) descending inhibition that was also responsible for pain reduction. These results suggest that E+C manipulations produce the strongest analgesia and have a complex influence on spinal nociception involving both inhibitory and facilitatory processes. PERSPECTIVE: This study assessed whether placebo analgesia manipulations that include expectations, conditioning, or both modulate the NFR (measure of spinal nociception). Only the manipulation that involved expectations and conditioning inhibited pain, but both expectation manipulations facilitated NFR. This suggests a complex modulation of spinal neurons by placebo manipulations.

Is conditioned pain modulation disrupted in sexual assault survivors

 Conditioned Pain Modulation (CPM) -Test stimulus: electric stimulations at an intensity that was individually calibrated for each participant -Conditioning stimulus: painful 10° C cold water Introduction Sexual assault (SA) is defined as any form of sexual contact that occurs without the explicit consent of the recipient and ranges from unwanted touch to rape. SA is associated with increased chronic pain risk and numerous chronic pain conditions. Recent findings from our research group suggest that SA survivors exhibited hyperalgesia and difficulty engaging in descending modulation of spinal nociception (assessed via the nociceptive flexion reflex [NFR]) via emotional processes. To our knowledge, no study has examined the relationship between SA and conditioned pain modulation (CPM; pain inhibits pain). The present study examined the relationship between SA and CPM in a sample of SA survivors and a matched comparison group.

345) Is history of traumatic events associated with nociceptive flexion reflex (NFR) threshold

 Overview, Informed Consent & Eligibility Determination (Health Status Screening) -Two testing sessions were completed on separate days -Testing session and test order were counterbalanced -Informed consent obtained at beginning of first testing session  Life Events Checklist Administered -Self-report measure that indicated the number of traumatic events an individual has experienced in their lifetime  NFR Threshold Testing -Sensors and stimulating electrode applied to the left ankle over the sural nerve -Suprathreshold intensity assessed used during NFR magnitude testing  Heat Pain Threshold Testing Heat probe placed on the left volar forearm Pain threshold was defined as the temperature (in °C) at which point the individual reported they first felt the probe become painful (the average temperature of 4 trials)  Heat Pain Tolerance Testing Heat probe placed on left volar forearm Pain tolerance was defined as the temperature (in °C) at which point the individual reported they could no longer tolerate the pain from the heat (the average temperature of 4 trials) Introduction

346) Is resting blood pressure associated with emotional modulation of pain

Procedures These data were taken from a parent study investigating pain processing in Native American individuals Stimulating electrode was applied over the sural nerve of the left ankle  Resting blood pressure (systolic/diastolic) readings were taken before pain testing procedures began Emotional Controls of Nociception was among the experimental pain procedures assessed  Participants received electrocutaneous stimulations while viewing:  Unpleasant Pictures (e.g., injured bodies)  Neutral Pictures (e.g., household objects)  Pleasant Pictures (e.g., people in sexual acts) Introduction Blood pressure (BP) is associated with pain processing and pain modulation. For example, resting BP is associated with the effectiveness of conditioned pain modulation (i.e., pain inhibiting pain). To the best of our knowledge, however, no study has investigated the relationship between BP and the effectiveness of other forms of pain modulation systems. In an effort to expand this literature, the current study will investigate the relationship between the effectiveness of emotional controls of nociception [ECON] and resting blood pressure in healthy pain-free individuals.

(329) Temporal habituation of heat pain? Parameters used for measuring temporal summation primarily lead to decreases in pain ratings

Animal studies have shown that dorsal horn neurons become hyperexcitable (ie, wind-up) in response to a repetitive, constant-intensity, noxious stimulus. Temporal summation of pain (eg, increased pain in response to a repetitive, constant-intensity painful heat pulse) is believed to reflect the psychophysical correlate of wind-up. We examined temporal summation of heat pain (TS-heat) using previously published procedures in 107 healthy, pain-free participants from the community. To assess TS-heat, participants received 5 blocks of 10 heat pulses from a Contact Heat Evoked Potential Stimulator (CHEPs) attached to the volar surface of the left forearm, and the thermode was moved in between blocks. Pulse peak was determined from a preliminary workup that determined the temperature that evoked pain of 45 out of 100. TS-heat was assessed after thermal sensory thresholds, but was randomized with three other pain tests (heat pain threshold/tolerance, electric pain tolerance, pressure pain threshold). Two pulse train parameters were attempted (between-subjects) with the same 3-s ISI: 1) from baseline of 35 C, each pulse reached peak temperature in 0.5-s, held peak for 0.5-s, and returned to baseline in 0.5-s, 2) from baseline of 39 C, each pulse reached peak temperature in 0.5-s, held peak for 0.75-s, and returned to baseline in 0.5-s. Three methods were used to calculate TS-pain: 1) TStrend=mean pain ratings across all 10 pulses, 2) TS10=10 th pain rating minus 1 pain rating, and 3) TSmax=max pain rating of pulses 2-10 minus 1 pain rating. Analyses examined whether train parameter, testing order, or calculation method had an effect on TS-heat. Analyses revealed habituation rather than summation in all cases except when TSmax was employed. Even then, average summation was minimal (change=1.3-2.7 on 100point scale) and non-significant. Results suggest these TS-heat proceduresmay primarily measure habituation processes. Further investigation of the underlying neural mechanisms of TS-heat is warranted.

Is blood glucose associated with descending modulation of spinal nociception as measured by the nociceptive flexion reflex

Objectives Prior research has shown a relationship between blood glucose levels and some forms of self-regulation (eg, executive function), with low blood glucose levels associated with impaired self-regulation. Further, engagement in self-regulation tasks depletes blood glucose. Given these relationships, the present study examined whether blood glucose is associated with another form of self-regulation, ie, descending pain modulatory processes. Methods Forty-seven (32 female) pain-free participants were recruited and completed testing. Blood glucose was measured from finger sticks and a digital meter before and after experimental pain tests. Pain tests included the nociceptive flexion reflex (NFR) threshold to assess descending modulation of spinal nociception, but also electric pain threshold to assess perceptual pain detection. The Stroop color word naming test was also assessed before and after pain testing to examine changes in executive function. Results Results indicated that mean blood glucose levels decreased after pain testing, but Stroop performance did not significantly change. Importantly, changes in blood glucose were correlated with NFR threshold, such that decreases in blood glucose were associated with lower NFR thresholds (reduced descending inhibition). Changes in blood glucose were unrelated to pain threshold or executive function. Conclusion This study suggests that glucose depletion may impair performance of descending inhibitory processes, without impacting the perceptual detection of pain (pain threshold). Although findings need to be replicated, maintaining adequate glucose levels may be necessary to support inhibition of spinal nociception.

Does placebo analgesia inhibit spinal nociceptive processing in healthy participants? A pilot study

Placebo analgesia is effective pain reduction evoked by an inert treatment mediated by psychological factors. Brain imaging studies suggest that supraspinal regions involved with descending modulation of pain are activated during placebo analgesia, however, evidence for inhibition of spinal nociception is mixed. A previous study failed to show that a physiological correlate of spinal nociception, the nociceptive flexion reflex (NFR), and subjective pain ratings were inhibited by placebo analgesia. However, the previous study used an expectation only manipulation, and a combination of expectation + conditioning (E + C) elicits greater placebo effects. The present study examined whether pain and NFR were inhibited by E + C placebo manipulation. Pain and NFR were tested after two cream applications. The placebo group (E + C) was told that the cream was a powerful painkiller (i.e., Lidocaine), and stimulus intensity was surreptitiously reduced after the 1st cream application. These data were collected as part of a pilot study on placebo analgesia.