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.

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.

This study was designed to examine the effect of emotion on the nociceptive flexion reflex and pain ratings. To do so, 28 participants viewed pictures varying in emotional valence (unpleasant, neutral, pleasant) and electric stimulations were delivered during and in between pictures. Biceps femoris EMG resulting from the stimulations was used to quantify the nociceptive flexion reflex (spinal nociception), and pain ratings to the stimulations were used as an evaluative measure of supraspinal nociception. Manipulation checks suggested that pictures effectively manipulated emotion. Moreover, nociceptive flexion reflex magnitudes and pain ratings were modulated in a parallel manner. Specifically, viewing unpleasant pictures enhanced the nociceptive flexion reflex and pain, whereas viewing pleasant pictures inhibited the reflex and pain. Analyses suggested that emotional valence, but not arousal, mediated the effects of pictures.

This study tested the prospective effects of hope on depression and anxiety using a longitudinal design. A sample of 522 college students completed self-report measures of hope, depression, and anxiety at three time points, with 1-month delays between administrations. Structural equation modeling was employed to test two cross-lagged panel models of the reciprocal effects of the Agency and Pathways components of hope on depression and anxiety. Results indicated statistically significant negative effects for the Agency component of hope on later depression but no unique effect of the Pathways component of hope on depression. Likewise, Agency showed a statistically significant negative effect on later anxiety, but again Pathways had no significant influence on anxiety. In both cases, neither depression nor anxiety demonstrated any longitudinal effects on either the Agency or Pathways components of hope. Implications of these findings are discussed, along with potential directions for future research.

Despite the widespread use of the nociceptive flexion reflex (NFR) paradigm in clinical and experimental pain research, there is currently no consensus on how best to define NFR threshold. Accordingly, the present studies were designed to assess the accuracy and reliability of different NFR threshold scoring criteria. Study 1 compared 13 scoring criteria in their accuracy for identifying the presence of the NFR, then generated empirically derived cut-points for the best criteria, and examined the test-retest reliability of NFR thresholds derived from these cut-points. Study 2 evaluated the replicability of these findings in an independent sample. Results from the two studies suggested that standardized peak (NFR Interval Peak z score) and mean (NFR Interval z score) biceps femoris electromyogram (EMG) activity were accurate and reliable criteria for defining NFR threshold. Acknowledging that cut-points may need to be adjusted for different research designs, graphs depicting sensitivity and specificity across a range of cut-points have been provided to facilitate researcher's decision-making. It is hoped that the results of these studies will promote a standard NFR threshold assessment methodology, and further encourage the application of the NFR paradigm in the investigation of mechanisms and characteristics of both painful and non-painful diseases.

Prior research suggests emotional picture-viewing modulates motoric (nociceptive flexion reflex), autonomic (skin conductance response, heart rate acceleration), and subjective (pain rating) reactions to noxious electrodermal stimulation. The present study sought to determine whether emotional valence and arousal contribute to nociception modulation. To do so, pictures varying in emotional content (erotica, food, neutral, loss, attack) were chosen to manipulate emotional valence (pleasant=erotic and food; unpleasant=loss and attack) and arousal (low=food and loss; moderate=erotica and attack). Pictures were presented in pseudorandom order to elicit emotional processing while noxious electric stimulations were delivered to the sural nerve. Nociceptive flexion reflex (NFR) magnitude, skin conductance response (SCR), heart rate (HR) acceleration, and subjective pain ratings to each stimulation were measured, standardized, averaged by picture content, and analyzed. Results suggested that picture-viewing explained 52% of the variance in the multivariate combination of the nociceptive reactions and modulated them in parallel. Pleasant pictures inhibited reactions, whereas unpleasant pictures enhanced them. However, only erotica and attack pictures elicited significant modulation relative to neutral pictures, suggesting arousal also contributed. An exploratory multilevel analysis also supported this conclusion. Together, these data suggest emotional control of nociceptive reactions (ECON) is associated with a valence-by-arousal interaction. Implications of these findings for how emotional picture-viewing can be used to study supraspinal modulation are discussed.

Headache is a chronic disease that occurs with varying frequency and results in varying levels of disability. To date, the majority of research and clinical focus has been on the role of biological factors in headache and headache-related disability. However, reliance on a purely biomedical model of headache does not account for all aspects of headache and associated disability. Using a biopsychosocial framework, the current manuscript expands the view of what factors influence headache by considering the role psychological (i.e., cognitive and affective) factors have in the development, course, and consequences of headache. The manuscript initially reviews evidence showing that neural circuits responsible for cognitive-affective phenomena are highly interconnected with the circuitry responsible for headache pain. The manuscript then reviews the influence cognitions (locus of control and self-efficacy) and negative affect (depression, anxiety, and anger) have on the development of headache attacks, perception of headache pain, adherence to prescribed treatment, headache treatment outcome, and headache-related disability. The manuscript concludes with a discussion of the clinical implications of considering psychological factors when treating headache. Keywordsheadache; self-efficacy; locus of control; biopsychosocial; psychological; negative affect Headache is currently conceptualized as a chronic disorder with acute episodes of pain occurring intermittently lasting anywhere from minutes to days. For a significant number of patients, these attacks occur once a month or more and result in varied levels of disability. 1-4 Clinicians thus need to consider what factors influence the development, course, and severity of individual headache attacks and subsequent disability in order to minimize the frequency of attacks, reduce their severity, and limit their impact on functioning. To date, the overwhelming majority of research and clinical interest has focused on biological influences. These efforts have resulted in significant steps forward in the treatment and prevention of headache and its related disability; however, this research has also revealed that biological factors alone fail to account for all aspects of headache and disability. Psychological factors such as headache management locus of control and self-efficacy, and negative affect/emotional states can alter the likelihood of a headache attack being triggered, the perceived severity of headache pain, the impact headache has on functioning, and treatment prognosis. 5,6 Unfortunately, psychological factors are typically considered relevant only in cases where the patient presents

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