***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Expectations congruently influence , or bias ,  pain perception . Recent social psychological research reveals that individuals differ in the extent to which they believe in expectation biases and that individuals who believe in expectation biases may adjust for this bias in their perceptions and reactions . That is , idiosyncratic beliefs about expectations can moderate the influence of expectations on experience . Purpose Prior research has not examined whether idiosyncratic beliefs about expectations can alter the degree to which one 's expectations influence pain perception . Using a laboratory pain stimulus , we examined the possibility that beliefs about expectation biases alter pain responses following both pain- and placebo-analgesic expectations . Methods Participants ' beliefs about expectation biases were measured . Next , participants were r and omly assigned to receive either a pain expectation or a placebo-analgesia expectation prior to a cold-pressor task . After the task , participants rated their pain . Results Beliefs about expectation biases significantly influenced pain reports . Specifically , pain reports were more influenced by provided expectations the less participants believed in expectation biases ( i.e. , pain expectations result ed in more pain than analgesia expectations ) . Conclusions Beliefs about the expectation bias are an important and under-examined predictor of pain and placebo analgesia The power of placebos has long been recognized for improving numerous medical conditions such as Parkinson 's disease ( PD ) . Little is known , however , about the mechanism underlying the placebo effect . Using the ability of endogenous dopamine to compete for [11C]raclopride binding as measured by positron emission tomography , we provide in vivo evidence for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo . Our findings indicate that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system Rationale In a r and omised placebo-controlled clinical trial it is assumed that psychosocial effects of the treatment , regression to the mean and spontaneous remission are identical in the drug and placebo group . Consequently , any difference between the groups can be ascribed to the pharmacological effects . Previous studies suggest that side effects of drugs can enhance expectancies of treatment effects in the drug group compared to the placebo group , and thereby increase placebo responses in the drug group compared to the placebo group . Objectives The hypothesis that side effects of drugs can enhance expectancies and placebo responses was tested . Method Painful laser stimuli were delivered to 20 healthy subjects before and after administration of a drink with 0 or 4 mg/kg caffeine . The drink was administered either with information that it contained a painkiller or that it was a placebo .  Laser-evoked potentials and reports of pain , expectancy , arousal and stress were measured . Results Four milligrammes per kilogramme of caffeine reduced pain . Information that a painkiller was administered increased the analgesic effect of caffeine compared to caffeine administered with no drug information . This effect was mediated by expectancies . Information and expectancies had no effect on pain intensity when 0 mg/kg was administered . Conclusion The analgesic effect of caffeine was increased by information that a painkiller was administered . This was due to an interaction of the pharmacological action of the drug and expectancies . Hence , psychosocial effects accompanying a treatment can differ when an active drug is administered compared to a placebo Applying the self-fulfilling prophecy ( SFP ) approach to combating seasickness , the authors experimentally augmented the self-efficacy of naval cadets by telling them that they were unlikely to experience seasickness and that , if they did , it was unlikely to affect their performance at sea . Naval cadets ( N = 25 ) in the Israel Defense Forces were r and omly assigned to experimental and control conditions . At the end of a 5-day training cruise , experimental cadets reported less seasickness and were rated as better performers by naive training officers than were the control cadets . There was a nonsignificant tendency for the experimental effects to be stronger among cadets of lower initial self-efficacy , suggestive of behavioral plasticity . Reducing seasickness by verbally enhancing self-efficacy is discussed as an application of " verbal placebo . " These findings extend the generalizability of the SFP-at-work model and suggest new arenas for its practical application CONTEXT Placebo and nocebo effects , the therapeutic and adverse effects , respectively , of inert substances or sham procedures , represent serious confounds in the evaluation of therapeutic interventions . They are also an example of cognitive processes , particularly expectations , capable of influencing physiology . OBJECTIVE To examine the contribution of 2 different neurotransmitters , the endogenous opioid and the dopaminergic ( DA ) systems , to the development of placebo and nocebo effects . DESIGN AND SETTING Using a within-subject design , subjects twice underwent a 20-minute st and ardized pain challenge , in the absence and presence of a placebo with expected analgesic properties . Studies were conducted in a university hospital setting . PARTICIPANTS Twenty healthy men and women aged 20 to 30 years recruited by advertisement . MAIN OUTCOME MEASURES Activation of DA and opioid neurotransmission by a pain stressor with and without placebo  ( changes in the binding potential of carbon 11 [11C]-labeled raclopride and [ 11C ] carfentanil with positron emission tomography ) and ratings of pain , affective state , and anticipation and perception of analgesia . RESULTS  Placebo-induced activation of opioid neurotransmission was detected in the anterior cingulate , orbitofrontal and insular cortices , nucleus accumbens , amygdala , and periaqueductal gray matter . Dopaminergic activation was observed in the ventral basal ganglia , including the nucleus accumbens . Regional DA and opioid activity were associated with the anticipated and subjectively perceived effectiveness of the placebo and reductions in continuous pain ratings . High placebo responses were associated with greater DA and opioid activity in the nucleus accumbens . Nocebo responses were associated with a deactivation of DA and opioid release . Nucleus accumbens DA release accounted for 25 % of the variance in placebo analgesic effects . CONCLUSIONS Placebo and nocebo effects are associated with opposite responses of DA and endogenous opioid neurotransmission in a distributed network of regions . The brain areas involved in these phenomena form part of the circuit typically implicated in reward responses and motivated behavior Placebo analgesia and reward processing share several features . For instance , expectations have a strong influence on the subsequent emotional experience of both . Recent imaging data indicate similarities in the underlying neuronal network . We hypothesized that placebo analgesia is a special case of reward processing and that placebo treatment could modulate emotional perception in the same way as does pain perception . The behavioral part of this study indicates that placebo treatment has an effect on how  subjects perceive unpleasant pictures . Furthermore , event-related fMRI demonstrated that the same modulatory network , including the rostral anterior cingulate cortex and the lateral orbitofrontal cortex , is involved in both emotional placebo and placebo analgesia . These effects were correlated with the reported placebo effect and were predicted by the amount of treatment expectation induced on a previous day . Thus , the placebo effect may be considered to be a general process of modulation induced by the subjects ' expectations Identifying patients who are potential placebo responders has major implication s for clinical practice and trial design . Catechol-O-methyltransferase ( COMT ) , an important enzyme in dopamine catabolism plays a key role in processes associated with the placebo effect such as reward , pain , memory and learning . We hypothesized that the COMT functional val158met polymorphism , was a predictor of placebo effects and tested our hypothesis in a subset of 104 patients from a previously reported r and omized controlled trial in irritable bowel syndrome ( IBS ) . The three treatment arms from this study were : no-treatment ( “ waitlist ” ) , placebo treatment alone ( “ limited ” ) and , placebo treatment “ augmented ” with a supportive patient-health care provider interaction . The primary outcome measure was change from baseline in IBS-Symptom Severity Scale ( IBS-SSS ) after three weeks of treatment . In a regression model , the number of methionine alleles in COMT val158met was linearly related to placebo response as measured by changes in IBS-SSS ( p = .035 ) . The strongest placebo response occurred in met/met homozygotes treated in the augmented placebo arm . A smaller met/met associated effect was observed with limited placebo treatment and there was no effect in the waitlist control . These data support our hypothesis that the COMT val158met polymorphism is a potential biomarker of placebo response OBJECTIVE We investigated the effects of pain anxiety and a placebo/nocebo/neutral intervention on ice water-induced pain .  DESIGN We divided 72 volunteers into high- and low-anxiety groups before r and omly assigning them to experimental and control subgroups . METHOD Participants completed preimmersion tests of pain anxiety , pain worry , and mood . We scored first immersion pain behavior , experience , and intensity . Each subgroup then received an instruction design ed to elicit a positive ( placebo ) , negative ( nocebo ) , or neutral response . After repeating the pain worry test , we gathered second immersion pain scores , and participants repeated the mood test , completed the treatment credibility measure , and were debriefed . OUTCOME MEASURES We used the Pain Anxiety Symptom Scale ; self-rating Likert-type scales for pain worry , pain intensity , and pain-coping ; the Multiple Affect Adjective Checklist ( mood ) ; timed measurements for pain threshold and pain tolerance ; and a treatment credibility scale . RESULTS Pain anxiety and the placebo interventions significantly altered participants ' pain scores , with best-to-worse scores reported by the low pain-anxiety/placebo , high anxiety/placebo , low anxiety/neutral , low anxiety/nocebo , high anxiety neutral , and high anxiety/nocebo groups . The high pain-anxiety group demonstrated the greatest response to the placebo/nocebo intervention in the expected directions in pain , worry , and anxious mood scores and in decreased self-confidence in managing pain ( this was also negatively affected by the nocebo in each pain-anxiety group ) . CONCLUSION This study demonstrates that the interaction of the personality variable of pain anxiety with the placebo/nocebo response has an impact on pain , worry , and mood OBJECTIVE This experiment tested the hypothesis that differences in subjects ' expectations about the impairing effect of alcohol on cognitive performance predict their responses to alcohol and to a placebo . METHOD Twenty-seven male social drinkers were r and omly assigned to one of three treatment groups : alcohol ( 0.62 g/kg ) , placebo , or no treatment control . All groups practice d a Rapid Information Processing Task that measured cognitive performance by the speed of information processed . After practice , they rated the degree of impairment they expected alcohol to have on their performance , and then performed the task under their different treatments . RESULTS Alcohol slowed ( i.e. , impaired ) information processing compared with placebo and no treatment . In addition , those who expected more impairment performed more poorly under alcohol , and under the placebo when alcohol was expected . When no beverage was received , no expectancy-performance relationship was obtained . CONCLUSIONS The findings call attention to expectancies as an important factor that may contribute to individual differences in cognitive functioning under alcohol and placebo OBJECTIVE Prior investigations have failed to find reliable personality differences in  placebo responding . The present study tests the hypothesis that personality and situational variables interact to determine placebo responding . METHODS Optimists and pessimists were r and omly assigned to one of three conditions . In the first condition , the participants were told that they were to ingest a pill that would make them feel unpleasant ( deceptive-expectation group ) . In the second condition , the participants were told that they were to ingest a pill that would make them feel either unpleasant or was an inactive substance ( conditional-expectation group ) . Finally , a third group was told they were to ingest a pill that was inactive ( control group ) . RESULTS Pessimists were more likely than optimists to follow a negative-placebo expectation when given a deceptive expectation , but not when given a conditional expectation . CONCLUSION The personality variable optimism-pessimism relates to placebo responding when individuals are given a deceptive but not a conditional expectation . This suggests that personality and situational variables interact to determine placebo responding & NA ; This study reports how placebo analgesia was produced by conditioning whereby the intensity of electric stimulation was surreptitiously reduced in order to examine the contribution of psychological factors of suggestibility and expectancy on placebo analgesia . This strategy was used in order to manipulate expectancy for pain reduction . The magnitudes of the placebo effects were estimated after a manipulation procedure and during experimental trials in which stimulus intensities were reset to original baseline levels . Individual differences in suggestibility , verbal expectancy for drug efficacy and manipulation procedure for pain reduction were tested as possible mediators of placebo analgesia . The following dependent variables were measured : ( a ) subjective expectancy for drug efficacy in pain relief , ( b ) expected pain intensity and unpleasantness , ( c ) concurrent pain intensity and unpleasantness and ( d ) remembered pain intensity and unpleasantness . Statistically significant  placebo effects on sensory and affective measures of pain were obtained independently of the extent of the surreptitious lowering of stimulus strength during manipulation trials . The pairing of placebo administration with painful stimulation was sufficient to produce a generalized placebo analgesic effect . However , verbal expectancy for drug efficacy and individual differences in suggestibility were found to contribute significantly to the magnitude of placebo analgesia . The highest placebo effect was shown by the most pronounced reductions in pain ratings in highly suggestible subjects who received suggestions presumed to elicit high expectancy for drug efficacy . The results also demonstrated that placebo  effects established on remembered pain were at least twice as great as those obtained on concurrent placebo effects . This was mainly because baseline pain was remembered as being much more intense than it really was . Moreover , remembered placebo effects , like the concurrent placebo 
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PRs mainly appear to be moderated by expectations of how the symptom might change after treatment , or expectations of how symptom repetition can be coped with .