http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
generality of negative affect-induced pain modulation
Five studies built upon prior work that suggests negative affect can modulate pain. In Experiments 1 and 2 (between-subjects design), pain was tested before and after one of three emotion-induction manipulations that elicited negative affect. To elicit highly arousing negative affect, the shock manipulation exposed participants to surprising electrical stimulations. To elicit moderately arousing negative affect, the anticipation manipulation verbally threatened participants with shock (without exposure). A neutral condition just tested pain. To measure pain, Experiment 1 used pain ratings to a constant intensity and duration heat source (hand ipsilateral to shocks), and Experiment 2 used finger withdrawal to heat (contralateral to shocks). In Experiments 3-5 (within-subjects design), a conditioned fear paradigm was used to test the bilateral influence of highly arousing negative affect on finger withdrawal to fast-ramped heat (Exp 3), pain ratings to constant heat (Exp 4), and finger withdrawal to slow-ramped heat (Exp 5). It was hypothesized that low to moderately arousing negative affect would elicit hyperalgesia, whereas highly arousing negative affect would elicit hypoalgesia. Intense, highly arousing negative affect induced by shock and conditioned fear caused pain inhibition in every experiment, across three pain indices. Surprisingly, the anticipation manipulation resulted in a mild hypoalgesia in Experiment 1 and no group-level change in Experiment 2. Exploratory correlational analyses indicated that these unexpected results stemmed from individual differences in the affective state of participants. These analyses suggested that affect intensity, and not arousal alone, correlated with the direction of pain modulation. Low negative affect intensity caused no change in pain, moderate negative affect intensity caused hyperalgesia, and high negative affect intensity caused hypoalgesia. Physiological arousal correlated with the strength of the hypoalgesia, but not its occurrence. Furthermore, analyses suggest: (a) pain modulation occurs bilaterally, (b), negative affect-induced hypoalgesia is not mediated by diffuse noxious inhibitory controls (DNIC), and (c) positive affect may negate negative affect-induced hypoalgesia.
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Includes bibliographical references (leaves 118-129).