Mary W. Meagher

Fear and anxiety: divergent effects on human pain thresholds

Abstract 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.

Psychometric evaluation of the Beck Depression Inventory-II with primary care medical patients.

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.

Pain and Emotion: Effects of Affective Picture Modulation

Objective and Methods Two experiments examined the impact of viewing unpleasant, pleasant, and neutral photographic slides on cold-pain perception in healthy men and women. In each experiment, participants viewed one of three slide shows (experiment 1 = fear, disgust, or neutral; experiment 2 = erotic, nurturant, or neutral) immediately before a cold-pressor task. Skin conductance and heart rate were recorded during the slide shows, whereas visual analog scale ratings of pain intensity and unpleasantness thresholds and pain tolerance were recorded during the cold-pressor task. Results Viewing fear and disgust slides decreased pain intensity and unpleasantness thresholds, but only the fear slides decreased pain tolerance. In contrast, viewing erotic, but not nurturant, slides increased pain intensity and unpleasantness threshold ratings on the visual analog scale in men, whereas neither nurturant nor erotic slides altered pain tolerance. Conclusions 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.

The role of emotion in pain modulation

Although most agree that emotion can alter pain, little well-controlled research has been conducted to examine this issue. The present review provides psychological and physiological rationales for considering the influence of emotion on pain, followed by an overview of recent work in this area. We conclude that the pain-modulating effects of emotion are best characterized by an interaction between valence and arousal. Positive emotions lead to pain reduction as long as a minimal threshold of arousal is attained. However, negative emotions only lead to pain inhibition when they are highly arousing. Negative emotions coupled with low-to-moderate arousal facilitate pain.

Negative affect: effects on an evaluative measure of human pain

Prior work indicates that exposure to fear‐inducing shock inhibits finger‐withdrawal to radiant heat in humans (hypoalgesia), whereas anxiety induced by threat of shock enhances reactivity (hyperalgesia; Pain 84 (2000) 65–75). Although finger‐withdrawal latencies are thought to reflect changes in pain sensitivity, additional measures of pain are needed to determine whether pain perception is altered. The present study examined the impact of negative affect on visual analog scale (VAS) ratings of fixed duration thermal stimuli. One hundred twenty‐seven male and female human subjects were randomly assigned to one of three emotion‐induction conditions: (1) negative affect induced by exposure to three brief shocks; (2) negative affect elicited by the threat of shock without presentation; and (3) neutral affect, with no intervention. VAS ratings were tested before and after emotion‐induction. Results suggest that both negative affect manipulations reduced pain. Manipulation checks indicated that the emotion‐induction treatments induced similar levels of fear but with different arousal levels. Potential mechanisms for affect induced changes in pain are discussed.

Translational approaches to treatment-induced symptoms in cancer patients

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.

Shock-induced hyperalgesia: III. Role of the bed nucleus of the stria terminalis and amygdaloid nuclei.

Rats exposed to a few moderately intense (1 mA) shocks subsequently exhibit lower vocalization thresholds to shock and thermal stimuli. They also exhibit facilitated learning in a Pavlovian conditioning paradigm. Together, these results suggest that shock exposure can enhance pain (hyperalgesia). The present study examined the role of the amygdala and bed nucleus of the stria terminalis (BNST), 2 systems that have been implicated in the induction and maintenance of negative affective states. Experiment 1 showed that lesions of the central, but not the basolateral, amygdala eliminate shock-induced hyperalgesia as measured by a decrease in vocalization thresholds to shock. Experiment 2 revealed that central nucleus lesions also prevent shock-induced sensitization of the vocalization response to heat. Anterior, but not posterior, BNST lesions had a similar effect.

The Effects of Restraint Stress on the Neuropathogenesis of Theiler's Virus Infection: I. Acute Disease

Restraint stress was found to have a profound effect on the acute phase of Theilers virus infection. Increased mortality rates were observed in restrained CBA mice infected with the BeAn strain of Theilers virus. In addition, restrained mice developed higher CNS viral titers than infected/nonrestrained mice. Thymic atrophy was observed in both infected and uninfected restrained mice. Decreased microgliosis, perivascular cuffing, and astrocytosis were observed in restrained mice compared to nonrestrained infected mice at 7 days postinfection. Restraint-stressed mice also developed decreased numbers of lymphocytes and increased numbers of neutrophils in the blood. The mechanism proposed for these alterations involves stress-induced corticosterone, which causes immunosuppression, decreased trafficking of inflammatory cells in the CNS, and, consequently, increased viral replication.

Chronic restraint stress during early Theiler's virus infection exacerbates the subsequent demyelinating disease in SJL mice.

Chronic restraint stress, administered during early infection with Theilers virus, was found to exacerbate the acute central nervous system (CNS) viral infection and the subsequent demyelinating phase of disease (an animal model of Multiple Sclerosis (MS)) in SJL male and female mice. During early infection, stressed mice displayed decreased body weights and spontaneous activity; while increased behavioral signs of illness and plasma corticosterone (CORT) levels. During the subsequent chronic demyelinating phase of disease, previously stressed mice had greater behavioral signs of the chronic phase, worsened rotarod performance, and increased inflammatory lesions of the spinal cord. In addition, mice developed autoantibodies to myelin basic protein (MBP), proteolipid protein peptide (PLP139-151), and myelin oligodendrocyte glycoprotein peptide (MOG33-55).

Impact of shock on pain reactivity: II. Evidence for enhanced pain.

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.