***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: & NA ; Conditioning procedures are used in many placebo studies because evidence suggests that conditioning‐related placebo responses are usually more robust than those induced by verbal suggestions alone . However , it has not been shown whether there is a causal relation between the number of conditioning trials and the resistance to extinction of placebo and nocebo responses . Here we test the effects of either one or four sessions of conditioning on the modulation of both non‐painful and painful stimuli delivered to the dorsum of the foot . Placebo and nocebo manipulations were obtained by pairing green or red light to a series of stimuli that were made lower or higher with respect to a yellow light associated with a series of control stimuli .  Subjects were told that the lights would indicate a treatment that would reduce or increase non‐painful and painful stimuli to the foot . They were r and omly assigned to either Group 1 or 2 . Group 1 underwent one session of conditioning and Group 2 received four sessions of conditioning . We found that one session of conditioning ( Group 1 ) induced nocebo responses , but not placebo responses in no pain condition . After one session of conditioning , we observed both nocebo and placebo responses to painful stimulation . However , these effects extinguished over time . Conversely , four sessions of conditioning ( Group 2 ) induced robust placebo and nocebo responses to both non‐painful and painful stimuli that persisted over the entire experiment . These findings suggest that the strength of learning may be clinical ly important for producing long‐lasting placebo effects The placebo and nocebo effect is believed to be mediated by both cognitive and conditioning mechanisms , although little is known about their role in different circumstances . In this study , we first analyzed the effects of opposing verbal suggestions on experimental ischemic arm pain in healthy volunteers and on motor performance in Parkinsonian patients and found that verbally induced expectations of analgesia/hyperalgesia and motor improvement/worsening antagonized completely the effects of a conditioning procedure . We also measured the effects of opposing verbal suggestions on hormonal secretion and found that verbally induced expectations of increase/decrease of growth hormone ( GH ) and cortisol did not have any effect on the secretion of these hormones . However , if a preconditioning was performed with sumatriptan , a 5-HT1B/1D agonist that stimulates GH and inhibits cortisol secretion , a significant increase of GH and decrease of cortisol plasma concentrations were found after placebo administration , although opposite verbal suggestions were given . These findings indicate that verbally induced expectations have no effect on hormonal secretion , whereas they affect pain and motor performance . This suggests that placebo responses are mediated by conditioning when unconscious physiological functions such as hormonal secretion are involved , whereas they are mediated by expectation when conscious physiological processes such as pain and motor performance come into play , even though a conditioning procedure is performed Learning processes such as respondent or Pavlovian conditioning are believed to play an important role in the development of chronic pain , however , their influence on the inhibition of pain has so far not been assessed in humans . The purpose of this study was the demonstration of Pavlovian conditioning of stress-induced analgesia  in humans and the determination of its opioid mediation . In a differential classical conditioning paradigm two different auditory stimuli served as conditioned stimuli and mental arithmetic plus white noise as unconditioned stimulus . Subsequent to four conditioning trials naloxone or placebo was applied in a double-blind fashion on two test days . Both pain threshold and pain tolerance showed conditioned stress-induced analgesia . Pain tolerance was affected by naloxone whereas pain threshold was not . The data of this study show that stress analgesia can be conditioned in humans and that it is at least partially mediated by the endogenous opioid system . Learning processes also influence pain inhibitory processes in humans and this effect might play a role in the development of chronic pain UNLABELLED Emotionally charged facial expressions ( happy , fear ) served as conditioned stimuli in a differential fear conditioning procedure . Expressions were presented in pseudo-r and om order on a computer monitor . For half of the participants , the fear expression was paired with an aversive electric stimulation ( UCS ) , whereas the happy expression was unpaired . The other participants had the opposite pairing . To assess the influence of conditioned fear on pain , expressions were shown again in the absence of the UCS and pain threshold was assessed during each expression . The latency of finger withdrawal from a radiant heat device was used to index pain threshold . Skin conductance response ( SCR ) and self-reported emotion were measured to assess fear conditioning . Consistent with preparedness theory , differential fear conditioning was only present when the fear expression was paired with the UCS . Moreover , pain threshold was only influenced by fear conditioning in persons for whom the fear expression was paired with the UCS . Specifically , finger withdrawal latencies were lower ( suggesting hyperalgesia ) during the fear expression than during the happy expression ; an effect that was not present before CS-UCS pairing . This work suggests that some stimuli are more readily associated with an aversive event and can lead to pain enhancement . PERSPECTIVE Although preliminary , these results suggest that fear-relevant environmental stimuli ( including facial expressions ) may provide important environmental cues during aversive events that influence the level of pain experienced We investigated the mechanisms underlying the activation of endogenous opioids in placebo analgesia by using the model of human experimental ischemic arm pain . Different types of placebo analgesic responses were evoked by means of cognitive expectation cues , drug conditioning , or a combination of both . Drug conditioning was performed by means of either the opioid agonist morphine hydrochloride or the nonopioid ketorolac tromethamine . Expectation cues produced placebo responses that were completely blocked by the opioid antagonist naloxone . Expectation cues together with morphine conditioning produced placebo responses that were completely antagonized by naloxone . Morphine conditioning alone ( without expectation cues ) induced a naloxone-reversible placebo effect . By contrast , ketorolac conditioning together with expectation cues elicited a placebo effect that was blocked by naloxone only partially . Ketorolac conditioning alone produced placebo responses that were naloxone-insensitive . Therefore , we evoked different types of placebo responses that were either naloxone-reversible or partially naloxone-reversible or , otherwise , naloxone-insensitive , depending on the procedure used to evoke the placebo response . These findings show that cognitive factors and conditioning are balanced in different ways in placebo analgesia , and this balance is crucial for the activation of opioid or nonopioid systems . Expectation triggers endogenous opioids , whereas conditioning activates specific subsystems . In fact , if conditioning is performed with opioids , placebo analgesia is mediated via opioid receptors , if conditioning is performed with nonopioid drugs , other nonopioid mechanisms result to be involved It is common clinical experience that anxiety about pain can exacerbate the pain sensation . Using event-related functional magnetic resonance imaging ( FMRI ) , we compared activation responses to noxious thermal stimulation while perceived pain intensity was manipulated by changes in either physical intensity or induced anxiety . One visual signal , which reliably predicted noxious stimulation of moderate intensity , came to evoke low anxiety about the impending pain . Another visual signal was followed by the same , moderate-intensity stimulation on most of the trials , but occasionally by discriminably stronger noxious stimuli , and came to evoke higher anxiety . We found that the entorhinal cortex of the hippocampal formation responded differentially to identical noxious stimuli , dependent on whether the perceived pain intensity was enhanced by pain-relevant anxiety . During this emotional pain modulation , entorhinal responses predicted activity in closely connected , affective ( perigenual cingulate ) , and intensity coding ( mid-insula ) areas . Our finding suggests that accurate preparatory information during medical and dental procedures alleviates pain by disengaging the hippocampus . It supports the proposal that during anxiety , the hippocampal formation amplifies aversive events to prime behavioral responses that are adaptive to the worst possible outcome Abstract Animal studies suggest that fear inhibits pain whereas anxiety enhances it ; however it is unclear whether these effects generalize to humans . The present study examined the effects of experimentally induced fear and anxiety on radiant heat pain thresholds .  Sixty male and female human subjects were r and omly assigned to 1 of 3 emotion induction conditions : ( 1 ) fear , induced by exposure to three brief shocks ; ( 2 ) anxiety , elicited by the threat of shock ; ( 3 ) neutral , with no intervention .  Pain thresholds were tested before and after emotion induction . Results suggest that findings from animal studies extend to humans : fear result ed in decreased pain reactivity , while anxiety led to increased reactivity . Pain rating data indicated that participants used consistent subjective criteria to indicate pain thresholds . Both subjective and physiological indicators ( skin conductance level , heart rate ) confirmed that the treatment conditions produced the targeted emotional states . These results support the view that emotional states modulate human pain reactivity 
    Output:
    
The existing literature suggests that classical conditioning can amplify pain .
No conclusions can be drawn about whether or not classical conditioning can elicit pain .