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Biomedical subjects

Donald D Price

Publications and source records attributed to Donald D Price.

At least 55 records · Page 3Linked to original sources
PubMed2003

Sex differences in common pain events: expectations and anchors.

This study examined (1) the effects of sex-related stereotypes in commonly experienced, potentially painful events and (2) differences in events representing the worst pain sensation imaginable for the typical woman and the typical man. Undergraduates (63 women and 54 men) completed the Situational Pain Questionnaire as the typical woman would and as the typical man would. The participants also answered 2 open-ended questions regarding the worst pain sensation imaginable for the typical woman and for the typical man. Our findings demonstrate that sex-related stereotypes extend to common pain events and that men and women expected that men would report less pain for common pain events than women. This suggests a gender-role related learning history that is relatively consistent for both sexes. The worst pain sensation imaginable was perceived to be different for typical men and women. Both sexes chose injury as the class of events men would find most painful and childbirth and menstrual pain as the class of events women would find most painful. Implications of this finding for common pain scaling approaches are discussed. The results of this study were obtained from a fairly uniform group of undergraduate men and women, which may limit the generalizability of our findings.

Adolescent↗
PubMed2003

An examination of the relationships among recalled, expected, and actual intensity and unpleasantness of delayed onset muscle pain.

This investigation assessed the relationships among recalled, expected, and actual muscle pain intensity and unpleasantness during a period of 48 hours. We hypothesized that (1). specific expectations of pain after 24 hours would account for a significant amount of variance in actual pain, (2). recalled pain from the most recent episode of naturally occurring muscle pain would be significantly associated with expected pain, and (3). the accuracy of expectations (ie, the difference between expected and actual pain) would increase across time as the onset of muscle pain occurred. Ninety-five students completed 3 sessions. In Session 1, recalled muscle pain and expected muscle pain in the next 24 hours were collected before exercise. In Sessions 2 and 3, muscle pain during movement and expected pain in the next 24 hours were collected. Recalled muscle pain was associated with expectations at baseline, r values [equals].26 to.47, P [lt ].05. The accuracy of expected intensity increased during the study, t [equals] 3.20, P [lt ].01, and the accuracy of expected unpleasantness was associated with change in expected unpleasantness, r values [equals] [minus ].28, P [lt ].01. The amount of variance in actual intensity and unpleasantness accounted for by expectations increased up to 55% and 52%, respectively, during the study. Expected unpleasantness did not account for variance in actual intensity. Expected intensity accounted for 3% of the variance in actual unpleasantness, but only in the second 24-hour period. Thus, our hypotheses were generally supported, but unanticipated findings regarding changes across time in the relationships among recalled, expected, and actual muscle pain were also detected.

Adolescent↗
PubMed2003

Hypnosis phenomenology and the neurobiology of consciousness.

Recent developments in the philosophical and neurobiological studies of consciousness provide promising frameworks to investigate the neurobiology of hypnosis. A model of consciousness phenomenology is described to demonstrate that the experiential dimensions characterizing hypnosis (relaxation and mental ease, absorption, orientation and monitoring, and self-agency) reflect basic phenomenal properties of consciousness. Changes in relaxation-mental ease and absorption, produced by standard hypnotic procedures, are further associated with changes in brain activity within structures critically involved in the basic representation of the body-self and the regulation of states of consciousness. The combination of experiential and modern brain imaging methods offers a unique perspective on hypnotic phenomena and provides new observations consistent with the proposition that hypnosis is an altered state of consciousness.

Brain↗
PubMed2002

Hypnosis modulates activity in brain structures involved in the regulation of consciousness.

The notion of consciousness is at the core of an ongoing debate on the existence and nature of hypnotic states. Previously, we have described changes in brain activity associated with hypnosis (Rainville, Hofbauer, Paus, Duncan, Bushnell, & Price, 1999). Here, we replicate and extend those findings using positron emission tomography (PET) in 10 normal volunteers. Immediately after each of 8 PET scans performed before (4 scans) and after (4 scans) the induction of hypnosis, subjects rated their perceived level of "mental relaxation" and "mental absorption," two of the key dimensions describing the experience of being hypnotized. Regression analyses between regional cerebral blood flow (rCBF) and self-ratings confirm the hypothesized involvement of the anterior cingulate cortex (ACC), the thalamus, and the ponto-mesencephalic brainstem in the production of hypnotic states. Hypnotic relaxation further involved an increase in occipital rCBF that is consistent with our previous interpretation that hypnotic states are characterized by a decrease in cortical arousal and a reduction in cross-modality suppression (disinhibition). In contrast, increases in mental absorption during hypnosis were associated with rCBF increases in a distributed network of cortical and subcortical structures previously described as the brain's attentional system. These findings are discussed in support of a state theory of hypnosis in which the basic changes in phenomenal experience produced by hypnotic induction reflect, at least in part, the modulation of activity within brain areas critically involved in the regulation of consciousness.

Analysis of Variance↗
PubMed2002

Irritable bowel syndrome as a common precipitant of central sensitization.

Animal models of neuropathic pain have significantly advanced our knowledge of abnormalities in central pain processing mechanisms in chronic pain disorders. New neuroimaging techniques using functional magnetic resonance imaging and positron emission tomography scanning are beginning to provide insight into cortical participation in the processing of pain. Irritable bowel syndrome (IBS) is one of the most common gastrointestinal disorders seen by physicians. Visceral hypersensitivity or decreased pain thresholds to distension of the gut is considered to be a biologic marker for IBS and is present in most patients with this gastrointestinal disorder. Patients with IBS also have many extraintestinal symptoms consistent with a central hyperalgesic state. Recent studies suggest that patients with IBS may also have cutaneous hyperalgesia similar to that seen in other chronic pain disorders such as fibromyalgia. This suggests that abnormalities of central nociceptive processing are present in IBS.

Animals↗
PubMed2002

Gender role expectations of pain: relationship to experimental pain perception.

The primary purpose of this study was to investigate the influence of an individual's Gender Role Expectations of Pain (GREP) on experimental pain report. One hundred and forty-eight subjects (87 females and 61 males) subjects underwent thermal testing and were asked to report pain threshold, pain tolerance, VAS ratings of pain intensity and unpleasantness, and a computerized visual analogue scales (VAS) rating of pain intensity during the procedure. Subjects completed the GREP questionnaire to assess sex-related stereotypic attributions of pain sensitivity, pain endurance, and willingness to report pain. Consistent with previous research, significant sex differences emerged for measures of pain threshold, pain tolerance, and pain unpleasantness. After statistically controlling for age, GREP scores were significant predictors of threshold, tolerance, and pain unpleasantness, accounting for an additional 7, 11, and 21% of the variance, respectively. Sex remained a significant predictor of pain tolerance in hierarchical regression analyses after controlling for GREP scores. Results provide support for two competing but not mutually exclusive hypotheses related to the sex differences in experimental pain. Both psychosocial factors and first-order, biological sex differences remain as viable explanations for differences in experimental pain report between the sexes. It appears that GREP do play a part in determining an individual's pain report and may be contributing to the sex differences in the laboratory setting.

Adolescent↗
PubMed2002

Enhanced temporal summation of second pain and its central modulation in fibromyalgia patients.

We have previously shown that fibromyalgia (FMS) patients have enhanced temporal summation (windup) and prolonged decay of heat-induced second pain in comparison to control subjects, consistent with central sensitization. It has been hypothesized that sensory abnormalities of FMS patients are related to deficient pain modulatory mechanisms. Therefore, we conducted several analyses to further characterize enhanced windup in FMS patients and to determine whether it can be centrally modulated by placebo, naloxone, or fentanyl. Pre-drug baseline ratings of FMS and normal control (NC) groups were compared with determine whether FMS had higher pain sensitivity in response to several types of thermal tests used to predominantly activate A-delta heat, C heat, or cold nociceptors. Our results confirmed and extended our earlier study in showing that FMS patients had larger magnitudes of heat tap as well as cold tap-induced windup when compared with age- and sex-matched NC subjects. The groups differed less in their ratings of sensory tests that rely predominantly on A-delta-nociceptive afferent input. Heat and cold-induced windup were attenuated by saline placebo injections and by fentanyl (0.75 and 1.5 microg/kg). However, naloxone injection had the same magnitudes of effect on first or second pain as that produced by placebo injection. Hypoalgesic effects of saline placebo and fentanyl on windup were at least as large in FMS as compared to NC subjects and therefore do not support the hypothesis that pain modulatory mechanisms are deficient in FMS. To the extent that temporal summation of second pain (windup) contributes to processes underlying hyperalgesia and persistent pain states, these results indirectly suggest that these processes can be centrally modulated in FMS patients by endogenous and exogenous analgesic manipulations.

Adult↗
PubMed2002

A comparison of placebo effects in clinical analgesic trials versus studies of placebo analgesia.

A previous meta-analysis of clinical analgesic trial studies showed generally low magnitudes of placebo analgesia (N. Engl. J. Med. 344 (2001) 1594). However, as studies included in their analysis used only placebo as a control condition, we conducted two meta-analyses, one in which 23 studies used only placebo as a control condition, and one in which 14 studies investigated placebo analgesic mechanisms. Magnitudes of placebo analgesic effects were much higher in the latter (mean effect size=0.95) as compared to the former (mean effect size=0.15) and were significantly different (P=0.003). This difference as well as differences in effect sizes within studies of placebo mechanisms may be parsimoniously explained by differences in expected pain levels produced by placebo suggestions and by conditioning. Furthermore, some of the studies of placebo analgesic mechanisms indicate that the magnitude of placebo analgesia is higher when the placebo analgesic effect is induced via suggestion combined with conditioning than via suggestion alone or conditioning alone. Based on these findings, we suggest that placebo analgesic effects are most optimally conceptualized in terms of perception of the placebo agent, and therefore a new definition of placebo response is proposed.

Analgesia↗
PubMed2002

Racial/ethnic differences in the experience of chronic pain.

The purpose of this study was to examine racial/ethnic-related differences in a four-stage model of the processing of chronic pain. The subjects were 1557 chronic pain patients (White=1084, African American=473) evaluated at a pain management clinic at a large southeastern university medical center. Using an analysis of covariance controlling for pain duration and education, African American patients reported significantly higher levels of pain unpleasantness, emotional response to pain, and pain behavior, but not pain intensity than Whites. Differences were largest for the unpleasantness and emotion measures, particularly depression and fear. The groups differed by approximately 1.0 visual analogue scale unit, a magnitude that may be clinically significant. Racial/ethnic differences in the linear relationship between stages were also tested using structural equation modeling and LISREL-8. The results indicate differences in linear associations between pain measures with African Americans showing a stronger link between emotions and pain behavior than Whites.

Adult↗
PubMed2002

Integrating experiential-phenomenological methods and neuroscience to study neural mechanisms of pain and consciousness.

Understanding the nature of pain at least partly depends on recognizing its inherent first person epistemology and on using a first person experiential and third person experimental approach to study it. This approach may help to understand some of the neural mechanisms of pain and consciousness by integrating experiential-phenomenological methods with those of neuroscience. Examples that approximate this strategy include studies of second pain summation and its relationship to neural activities and brain imaging-psychophysical studies wherein sensory and affective qualities of pain are correlated with cerebral cortical activity. The experiential paradigm of offers the possibility of improved designs and methods for investigating neural mechanisms underlying pain and consciousness.

Brain↗
PubMed2002

Central neural mechanisms that interrelate sensory and affective dimensions of pain.

The perception of pain is highly complex, and requires neural integration from a variety of routes. Spinal pathways to the amygdala, hypothalamus, reticular formation, medial thalamic nuclei, and limbic cortical structures transmit information involved arousal, bodily regulation, and emotional responses. Other, albeit indirect, pathways can carry signals to these same structures, for example, from spinal pathways to somatosensory thalamic and cortical areas, and from these to cortical limbic structures. Indirect cortico-limbic pathways integrate nociception with information about the status of the body and indirect routes must culminate in the prioritization of emotions and responses to pain.

Animals↗
PubMed2001

Hypersensitivity to visceral and cutaneous pain in the irritable bowel syndrome.

Irritable bowel syndrome (IBS) is one of the most common gastrointestinal illnesses and is characterized by altered visceral perception. Previous studies in IBS have failed to demonstrate altered somatic or cutaneous perception. The aims of the study were to determine whether IBS patients have visceral hypersensitivity and cutaneous heat-induced hyperalgesia restricted to lumbosacral dermatomes, consistent with a localized segmental mechanism. Twelve patients (ten women, two men) with IBS and 17 control subjects (13 women, four men) rated pain intensity and unpleasantness to distension of the rectum (35, 55 mmHg) and thermal stimulation (45, 47 degrees C) of the hand and foot. Patients with IBS demonstrated cutaneous allodynia/hyperalgesia to thermal pain applied to the hand and foot. The cutaneous hyperalgesia was pronounced in the lower extremity yet present in the upper extremity to a lesser extent. Psychological testing revealed the IBS patients report more state anxiety and a greater number of somatic symptoms that significantly correlated with most of the pain measures. However, they did not differ from controls on several personality trait measures. These results suggest that patients with IBS have visceral hyperalgesia and cutaneous hyperalgesia that is distributed over a considerable rostral-caudal distance yet optimally expressed in lumbosacral dermatomes. This distribution is consistent with patterns of spinal hyperexcitability observed in experimentally induced persistent pain conditions.

Adult↗
PubMed1996

Continuous co-administration of dextromethorphan or MK-801 with morphine: attenuation of morphine dependence and naloxone-reversible attenuation of morphine tolerance.

N-Methyl-D-aspartate (NMDA) receptor antagonists have been repeatedly shown to attenuate the development of opiate tolerance and dependence in rodents. In the present experiments, continuous subcutaneous infusion of either MK-801 (0.01 mg/kg/h but not 0.005 mg/kg/h) or DM (0.133, 0.67 and 1.33 mg/kg/h) reliably prolonged the antinociceptive effect of continuous subcutaneous infusion of morphine sulfate (2.0 mg/kg/h), indicating attenuation of the development of morphine tolerance. Furthermore, this prolonged antinociception was completely reversible by naloxone (10 mg/kg, i.p.). Doses of MK-801 and DM that were equipotent in attenuating morphine tolerance (0.01 mg/kg/h and 1.33 mg/kg/h, respectively) revealed different profiles of effects, however, on locomotor activity and naloxone-precipitated abstinence/withdrawal symptoms. With regard to locomotor activity, rats having received continuous (48 h) subcutaneous infusion of morphine sulfate and MK-801, but not rats having received morphine sulfate and DM, displayed a reliable and striking increase in locomotor activity as compared with rats having received morphine alone. With regard to naloxone-precipitated withdrawal symptoms, continuous (48 h) subcutaneous co-infusion of either MK-801 (0.01 mg/kg/h) or DM (1.33 mg/kg/h) with morphine attenuated naloxone-precipitated hyperalgesia as compared with rats infused with morphine alone. MK-801 (0.01 mg/kg/h) was more effective than DM (0.133, 0.67, or 1.33 mg/kg/h), however, in reducing other naloxone-precipitated withdrawal symptoms (teeth chattering, jumping and wet dog shakes). The effects of MK-801 on all withdrawal symptoms were confounded, however, by the appearance of flaccidity following naloxone administration to rats having received MK-801 and morphine. These results extend previous observations by showing that the prolonged antinociception observed following co-administration of morphine and an NMDA antagonist is completely naloxone-reversible, supporting the notion that this antinociception reflects prolongation of an opioid receptor-mediated effect. The different profiles of side effects associated with MK-801 and DM, however, suggest that (1) attenuation of naloxone-precipitated withdrawal symptoms by MK-801 may be an artifact of toxicity, and (2) DM may prove clinically useful for the prevention of morphine tolerance, given its lack of observable side effects when administered concurrently with morphine to rodents.

Animals↗
PubMed1996

Assessing the stages of pain processing: a multivariate analytical approach.

A four-stage model of pain processing was proposed, consisting of pain sensation intensity, pain unpleasantness (stage 1 affect), suffering (stage 2 affect), and pain behavior. We studied 506 chronic pain patients (230 male and 276 female) using a multivariate statistical technique (LISREL) in order to demonstrate the structural relationship among multiple indicators of pain processing; and to characterize these stages in terms of their interactions. A strong relationship was revealed between the majority of the underlying indicators of each pain processing stage. A linear stage sequence best fitted the relationship between the four stages. Successive stages did not have recursive effects on earlier pain components. A confirmatory LISREL analysis was conducted with an additional sample of 502 chronic pain patients. In this replication analysis the structural equation model consisted of pain intensity, unpleasantness (stage 1 affect), emotional suffering (stage 2 affect), and pain behavior. This study extends the validation of these pain dimensions, as well as the validity of the measure(s) of each separate stage.

Adolescent↗
PubMed1995

Hypnotic analgesia reduces R-III nociceptive reflex: further evidence concerning the multifactorial nature of hypnotic analgesia.

Mechanisms of hypnotic analgesia were investigated by examining changes in the R-III, a nociceptive spinal reflex, during hypnotic reduction of pain sensation and unpleasantness. The R-III was measured in 15 healthy volunteers who gave VAS-sensory and VAS-affective ratings of an electrical stimulus during conditions of resting wakefulness, suggestions for hypnotic analgesia, and attempted suppression of the reflex during non-hypnotic conditions. The H-reflex was also measured to monitor and control for general changes in alpha-motoneuron excitability. Hypnotic sensory analgesia was related to reduction in the R-III after controlling for changes in the H-reflex (R2 = 0.51, P < 0.003), suggesting that hypnotic sensory analgesia is at least in part mediated by descending antinociceptive mechanisms that exert control at spinal levels in response to hypnotic suggestion. The relationship between hypnotic affective analgesia and reduction in R-III approached significance (R2 = 0.26; P = 0.053). Reduction in R-III was 67% as great and accounted for 51% of the variance in reduction of pain sensation. In turn, reduction in pain sensation was 75% as great and accounted for 77% of the variance in reduction of unpleasantness. The results suggest that 3 general mechanisms may be involved in hypnotic analgesia. The first, implicated by reductions in R-III, is related to spinal cord antinociceptive mechanisms. The second, implicated by reductions in pain sensation over and beyond reductions in R-III, may be related to brain mechanisms that serve to prevent awareness of pain once nociception has reached higher centers, as suggested by Hilgard.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Experimental mononeuropathy reduces the antinociceptive effects of morphine: implications for common intracellular mechanisms involved in morphine tolerance and neuropathic pain.

Recent evidence suggests that hyperalgesia and morphine tolerance, two seemingly unrelated phenomena, have in common certain neural substrates such as activation of the N-methyl-D-aspartate (NMDA) receptor and the subsequent intracellular activation of protein kinase C and nitric oxide. Should common cellular elements be involved in hyperalgesia and morphine tolerance, these cellular and intracellular commonalities might be expected to result in interactions between these two phenomena. Indeed, our previous studies have shown that thermal hyperalgesia develops when animals are made tolerant to the antinociceptive effects of morphine. In this study, we examined the hypothesis that reduction of morphine antinociception occurs following unilateral ligation of the rats's sciatic nerve, a procedure which produces symptoms of a neuropathic pain syndrome including thermal hyperalgesia. When tested using the paw-withdrawal test on day 8 (D8) after either nerve ligation or sham operation, a single intrathecal treatment with 10 micrograms morphine sulfate (30 min after administration) produced significant antinociception in sham-operated rats but not in nerve-injured ones. These results also were obtained when thermal hyperalgesia was reversed in nerve-injured rats by the non-competitive NMDA receptor antagonist MK-801. Consistently, 8 days after sciatic nerve ligation but not after a sham operation, an approximately 6-fold rightward shift occurred in the morphine antinociceptive dose-response curve. This rightward shift of the morphine antinociceptive dose-response curve did not occur at 24 h after either nerve ligation or sham operation. In addition, once daily treatment with 10 nmol MK-801 from D2 to D7 after nerve ligation prevented both the development of thermal hyperalgesia and the rightward shift of the morphine antinociceptive dose-response curve on D8. The results indicate that the antinociceptive effects of morphine are reduced in nerve-injured rats in the absence of daily exposure to morphine and that the NMDA receptor activation may have a critical role in mechanisms of this phenomenon. These data provide further evidence indicating that interactions do occur between neural mechanisms underlying thermal hyperalgesia and morphine tolerance.

Analgesics, Opioid↗