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 randomly 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 resulted 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.

This study evaluated the psychometric characteristics of the Beck Depression Inventory-II (BDI-II; A. T. Beck, R. A. Steer, & G. K. Brown, 1996) in a primary care medical setting. A principal-components analysis with Promax rotation indicated the presence of 2 correlated factors, Somatic-Affective and Cognitive, which explained 53.5% of the variance. A hierarchical, second-order analysis indicated that all items tap into a second-order construct of depression. Evidence for convergent validity was provided by predicted relationships with subscales from the Short-Form General Health Survey (SF-20; A. L. Stewart, R. D. Hayes, & J. E. Ware, 1988). A receiver operating characteristic analysis demonstrated criterion-related validity: BDI-II scores predicted a diagnosis of major depressive disorder (MDD), as determined by the Primary Care Evaluation of Mental Disorders (PRIME-MD) Patient Health Questionnaire (PHQ). This study demonstrated that the BDI-II yields reliable, internally consistent, and valid scores in a primary care medical setting, suggesting that use of the BDI-II in this setting may improve detection and treatment of depression in these medical patients.

These results are consistent with a motivational priming model that predicts that unpleasant affective states should enhance pain and that pleasant affective states should attenuate it.

Cancer therapy makes patients sick. The therapies that are available to clinicians allow them to successfully control nausea, emesis, and pain. However, this is not the case for a number of other symptoms that include fatigue, distractibility, poor memory, and diminished interest in previously pleasurable activities. These symptoms cluster during the course of cancer therapy and impair patient quality of life, limit therapy options, and do not always resolve at the cessation of treatment. It is possible to describe the intensity and temporal features of symptoms and assess their relationship with the inflammatory response that is associated with cancer and cancer therapy. At the preclinical level, sophisticated animal models still need to be deployed to study the causal role of inflammation in specific components of cancer-related symptoms. Various approaches can be optimally combined in a translational symptom research pathway to provide a framework for assessing in a systematic manner the neurobehavioral toxicity of existing and newly developed cancer therapies. Ultimately this knowledge will allow derivation of mechanism-based interventions to prevent or alleviate cancer-related symptoms.

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Shocked rats (Rattus norvegicus) often exhibit longer tail withdrawal latencies to radiant heat, which suggests that exposure to shock reduces pain. But at the same time, rats appear hyperreactive to shock, suggesting than pain is enhanced. Experiment 1 replicated these findings and showed that when tail movement was monitored, shocked rats were less responsive to heat and hyperreactive to shock even when the same behavioral criteria were used. When latency to vocalize was measured, shocked rats appeared hyperreactive to both test stimuli (Experiments 2 and 3). Prior exposure to shock also enhanced the acquisition of conditioned fear in a different context (Experiment 4) and the speed with which rats learned a response to avoid a thermal stimulus (Experiment 5). The results suggest that exposure to shock enhances pain.

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