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BACKGROUND - The default network is a set of brain regions that exhibit a reduction in BOLD response during attention-demanding cognitive tasks, and distinctive patterns of functional connectivity that typically include anti-correlations with a fronto-parietal network involved in attention, working memory, and executive control. The function of the default network regions has been attributed to introspection, self-awareness, and theory of mind judgments, and some of its regions are involved in episodic memory processes.
RESULTS - Using the method of psycho-physiological interactions, we studied the functional connectivity of several regions in a fronto-parietal network involved in a paired image discrimination task involving transitive inference. Some image pairs were derived from an implicit underlying sequence A>B>C>D>E, and some were independent (F>G, H>J, etc). Functional connectivity between the fronto-parietal regions and the default network regions depended on the presence of the underlying sequence relating the images. When subjects viewed learned and novel pairs from the sequence, connectivity between these two networks was higher than when subjects viewed learned and novel pairs from the independent sets.
CONCLUSIONS - These results suggest that default network regions were involved in maintaining the internal model that subserved discrimination of image pairs derived from the implicit sequence, and contributed to introspective access of an internal sequence model built during training. The default network may not be a unified entity with a specific function, but rather may interact with other functional networks in task-dependent ways.
OBJECTIVES - We examined whether "state" anger regulation-inhibition or expression-among chronic low back pain (CLBP) patients would affect lower paraspinal (LP) muscle tension following anger-induction, and whether these effects were moderated by trait anger management style.
METHOD - Eighty-four CLBP patients underwent harassment, then they regulated anger under one of two conditions: half expressed anger by telling stories about people depicted in pictures, whereas half inhibited anger by only describing objects appearing in the same pictures. They completed the anger-out and anger-in subscales (AOS; AIS) of the anger expression inventory.
RESULTS - General Linear Model procedures were used to test anger regulation condition by AOS/AIS by period interactions for physiological indexes. Significant three-way interactions were found such that: a) high trait anger-out patients in the inhibition condition appeared to show the greatest LP reactivity during the inhibition period followed by the slowest recovery; b) high trait anger-out patients in the expression condition appeared to show the greatest systolic blood pressure (SBP) reactivity during the expression period followed by rapid recovery.
CONCLUSIONS - Results implicate LP muscle tension as a potential physiological mechanism that links the actual inhibition of anger following provocation to chronic pain severity among CLBP patients. Results also highlight the importance of mismatch situations for patients who typically regulate anger by expressing it. These CLBP patients may be at particular risk for elevated pain severity if circumstances at work or home regularly dictate that they should inhibit anger expression.
Despite frequent use of the term symptom distress in the pain literature, symptom distress is often confused with symptom intensity and psychological distress, contributing to inadequate assessment of symptoms and less than ideal symptom management. In this article we address these issues and propose a hybrid model, combining Price's interaction of pain sensation, pain unpleasantness, and secondary pain affect model with an information processing model. Recommendations on methods and techniques to reduce this confusion would assist healthcare professionals and researchers to better distinguish among these terms as they manage patient symptoms and design symptom management studies. Thus, the purpose of this article is to examine the terms symptom distress, symptom intensity, and psychological distress using pain as the example symptom.
(c) 2007 Wiley Periodicals, Inc.
A tendency to manage anger via direct expression (anger-out) is increasingly recognized as influencing responses to pain. Elevated trait anger-out is associated with increased responsiveness to acute experimental and clinical pain stimuli, and is generally related to elevated chronic pain intensity in individuals with diverse pain conditions. Possible mechanisms for these links are explored, including negative affect, psychodynamics, central adipose tissue, symptom specific muscle reactivity, endogenous opioid dysfunction, and genetics. The opioid dysfunction hypothesis has some experimental support, and simultaneously can account for anger-out's effects on both acute and chronic pain. Factors which may moderate the anger-out/pain link are described, including narcotic use, gender, and genetic polymorphisms. Pain exacerbating effects of trait anger-out are contrasted with the apparent pain inhibitory effects of behavioral anger expression exhibited in anger-provoking contexts. Conceptual issues related to the state versus trait effects of expressive anger regulation are discussed.
Anger management style is related to both acute and chronic pain. Recent research suggests that individuals who predominantly express anger (anger-out) may report heightened chronic pain severity due in part to endogenous opioid antinociceptive dysfunction. If exogenous opioids serve to remediate opioid deficits, we predicted that regular use of opioid analgesics by chronic pain patients would alter these relationships such that anger-out would be related to chronic pain severity only among opioid-free patients. For 136 chronic pain patients, anger management style, depression, anxiety, pain severity, and use of opioid and antidepressant medication was assessed. Results of hierarchical multiple regressions to predict chronic pain severity showed: (a) a significant Anger-out x Opioid use interaction such that high Anger-out was associated with high pain severity only among patients not taking opioids; (b) controlling for depressed affect and anxiety did not affect this association; (c) the Anger-out x Antidepressant use interaction was nonsignificant; (d) Anger-in did not interact with use of any medication to affect pain severity. Results are consistent with an opioid-deficit hypothesis and suggest that regular use of opioid medications by patients high in anger expression may compensate for an endogenous opioid deficit, and mitigate the effects of elevated anger expression on chronic pain intensity.