Abstract

Not only are some clinical conditions experienced as more painful than others, but the variability in pain ratings of patients with the same disease or trauma is enormous. Available evidence indicates that to a large extent these differences reflect individual differences in pain sensitivity. Pain sensitivity can be estimated only through the use of well-controlled experimental pain stimuli. Such estimates show substantial heritability but equally important environmental effects. The genetic and environmental factors that influence pain sensitivity differ across pain modalities. For example, genetic factors that influence cold pressor pain have little impact on phasic heat pain and visa versa. Individual differences in pain sensitivity can complicate diagnosis, among other reasons because low sensitivity to pain may delay self-referral. Inclusion of patients with reduced pain sensitivity can attenuate treatment effects in clinical trials, unless controlled for. Measures of pain sensitivity are predictive of acute postoperative pain, and there is preliminary evidence that heightened pain sensitivity increases risk for future chronic pain conditions. At this time, however, it is unclear which experimental pain modalities should be used as predictors for future pain conditions. Careful assessment of each individual's pain sensitivity may become invaluable for the prevention, evaluation, and treatment of pain. Large individual differences in pain sensitivity can complicate diagnosis and pain treatment and can confound clinical trials. Pain sensitivity may also be of great importance for the development of clinical pain. Thus, assessment of pain sensitivity may be relevant for the prevention, evaluation, and treatment of acute and chronic pain.

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