2015
DOI: 10.1093/pm/pnv044
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Can Pain or Hyperalgesia Be a Classically Conditioned Response in Humans? A Systematic Review and Meta-Analysis

Abstract: The existing literature suggests that classical conditioning can amplify pain. No conclusions can be drawn about whether or not classical conditioning can elicit pain. Rigorous experimental conditioning studies with nociceptive unconditioned stimuli are needed to fill this gap in knowledge.

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Cited by 46 publications
(70 citation statements)
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“…Findings support a distinct contribution of these limbic regions during anticipation in line with previous evidence documenting their role in pain‐related fear learning and memory processes, and in classically conditioned nocebo responses . In addition, they lend further support for the role of conditioned pain‐related anticipation as a mechanism in central pain modulation . In line with this assumption, we observed a strikingly similar activation pattern in response to cues that previously signaled highly intense stimulation and subsequent distension with overlapping neural activation particularly in a fronto‐limbic network involving pACC, dlPFC and caudate.…”
Section: Discussionsupporting
confidence: 90%
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“…Findings support a distinct contribution of these limbic regions during anticipation in line with previous evidence documenting their role in pain‐related fear learning and memory processes, and in classically conditioned nocebo responses . In addition, they lend further support for the role of conditioned pain‐related anticipation as a mechanism in central pain modulation . In line with this assumption, we observed a strikingly similar activation pattern in response to cues that previously signaled highly intense stimulation and subsequent distension with overlapping neural activation particularly in a fronto‐limbic network involving pACC, dlPFC and caudate.…”
Section: Discussionsupporting
confidence: 90%
“…9 In addition, they lend further support for the role of conditioned pain-related anticipation as a mechanism in central pain modulation. 14,15 In line with this assumption, we observed a strikingly similar activation pattern in response to cues that previously signaled highly intense stimulation and subsequent distension with overlapping neural activation particularly in a fronto-limbic network involving F I G U R E 5 Region-of-interest (ROI) analyses of differential anticipatory neural activation during test [CS High > CS Low ]. Enhanced differential neural responses to cues predicting high intensity distensions in anterior PFC, thalamus and bilateral pACC, dlPFC, and caudate (all p FWE <.05).…”
Section: Discussionsupporting
confidence: 72%
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“…Indeed, a modern conceptualisation of pain (e.g. Moseley and Butler, 2015b) holds that pain is the end product of a complex evaluative process that is usually, but not necessarily, triggered by noxious stimuli (see Harvie et al (2015), Moseley (2004), and Moseley and Arntz (2007) for experimental evidence of the dissociation between nociception from pain and Madden et al (2015) for a systematic review of associative learning of pain). Thus, pain and lower reflex thresholds are more likely to reflect epiphenomena in much the same way as has been proposed for pain and motor control (Moseley, 2013).…”
Section: Generalising Across Clinical Pain Conditionsmentioning
confidence: 99%