Preparedness Theory Classical Conditioning

Preparedness Theory Classical Conditioning-16
Exploratory analyses did not reveal any influence of individual differences.Thirty of the 34 participants were unaware of the contingencies between stimuli. The results of this study provide no evidence that allodynia can be induced in healthy humans using a classical conditioning procedure with simultaneous timing. Associative learning has been proposed as a mechanism behind the persistence of pain after tissue healing.

Exploratory analyses did not reveal any influence of individual differences.Thirty of the 34 participants were unaware of the contingencies between stimuli. The results of this study provide no evidence that allodynia can be induced in healthy humans using a classical conditioning procedure with simultaneous timing. Associative learning has been proposed as a mechanism behind the persistence of pain after tissue healing.

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After healing, once nociception has diminished or ceased altogether, the informational value of the non-nociceptive input could be sufficient to drive the perseveration of pain.

Clinically, this mechanism is very well endorsed: the vast majority of clinicians believe that pain can be a classically conditioned response to non-nociceptive stimuli in the absence of nociception [8].

However, that study could not distinguish between direct modulation of pain and a change in pain threshold secondary to changes in arousal and valence, leaving the question of classically conditioned pain unanswered.

In the current study, we aimed to use a classical conditioning paradigm to induce allodynia to a somatosensory stimulus in healthy humans.

Chronic pain is a societal problem: It affects 35.5% of people [1], exerts a substantial burden both financially [2] and socially [3], and according to years lived with disability, it is humanity’s most burdensome health condition [4].

Despite real advances in our understanding of physiology, genetics, brain function, and comorbidities, how acute pain transitions to chronic pain remains to be elucidated.

We hypothesized that pairing of one non-nociceptive somatosensory stimulus (CS ) with painful nociceptive heat (UShigh) and another (CS-) with nonpainful heat (USlow) would result in a lower pain threshold to subsequent trials of heat that were paired with the CS than to trials that were paired with the CS-.

Our secondary aim was to investigate whether such pairing would alter subsequent perception of the CS relative to the CS-.

Screening exclusion criteria were: pain at the time of testing, use of analgesic medication on the day of testing, a current chronic pain problem, a sensation problem, diagnosed peripheral vascular disease, diabetes mellitus, a neurological problem, or a previous or current psychiatric diagnosis.

Volunteers were not eligible if they had completed previous classical conditioning experiments in our laboratory.

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