Pain
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The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (<15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (≥15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n=33) and chronic tension-type headache (n=22) sufferers. ⋯ When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days, denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.
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The communication of pain has received a great deal of attention in the pain literature; however, one form of pain communication--emotional disclosure of pain-related distress (e.g., sadness, worry, anger about pain)--has not been studied extensively. This study examined the extent to which this form of pain communication occurred during an observed conversation with one's spouse and also investigated the correlates and consequences of disclosure. Individuals with chronic pain (ICP) and their spouses (N=95 couples) completed several questionnaires regarding pain, psychological distress, and relationship distress as well as video recorded interactions about the impact of pain on their lives. ⋯ Furthermore, spouses were more likely to engage in invalidation after attempting more neutral or validating responses, suggesting an erosion of support when ICPs engaged in high rates of disclosure. Correlates of spousal invalidation included both spouses' helplessness catastrophizing, ICPs' affective distress about pain, and spouses' anxiety, suggesting that both partners' distress are implicated in maladaptive disclosure-response patterns. Findings are discussed in light of pain communication and empathy models of pain.
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Chronic pain is currently considered a public health problem with high costs to the individual and society. To improve prevention and treatment of chronic pain, epidemiologic studies are mandatory for assessing chronic pain. The aims of this study were to estimate the prevalence of chronic pain in the adult Danish population and to analyze associated factors such as diseases, immigration, and opioid use. ⋯ The study population consisted of 14,925 individuals in whom a high prevalence of chronic pain (26.8%, 95% confidence interval: 26.1 to 27.5) and a high prevalence of opioid consumption (4.5%) were observed. Other aspects of particular note: (1) a higher prevalence of chronic pain occurred among individuals with cardiovascular and chronic pulmonary diseases than among individuals with cancer; and (2) individuals with a non-Western background reported a higher pain prevalence, higher pain intensities, and more widespread pain than individuals with Danish background; however, opioids were more frequently used by native Danes. The prevalence of chronic pain as well as opioid use in Denmark are alarmingly high, and the relevance of opioid consumption is unknown.
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Peripheral nerve injury provokes heightened excitability of primary sensory afferents including nociceptors, and elicits ectopic activity in lesioned and neighboring intact nerve fibers. The major transmitter released by sensory afferents in the superficial dorsal horn of the spinal cord is glutamate. Glutamate is critically involved in nociceptive signaling and the development of neuropathic pain. ⋯ Treatment with the β-lactam antibiotic ceftriaxone increased the expression of glutamate transporter 1 (Glt1) in the dorsal horn after SNI, raised transmitter uptake, and lowered extracellular glutamate. Improving glutamate clearance prevented the facilitation of transmitter release by mGluR5 and attenuated neuropathic pain-like behavior. Balancing glutamate release and uptake after nerve injury should be an important target in the management of chronic neuropathic pain.
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Randomized Controlled Trial
Associations between daily chronic pain intensity, daily anger expression, and trait anger expressiveness: an ecological momentary assessment study.
Links between elevated trait anger expressiveness (anger-out) and greater chronic pain intensity are well documented, but pain-related effects of expressive behaviors actually used to regulate anger when it is experienced have been little explored. This study used ecological momentary assessment methods to explore prospective associations between daily behavioral anger expression and daily chronic pain intensity. Forty-eight chronic low back pain (LBP) patients and 36 healthy controls completed electronic diary ratings of momentary pain and behavioral anger expression in response to random prompts 4 times daily for 7 days. ⋯ Overlap with trait and state negative affect did not account for study findings. This study for the first time documents lagged within-day influences of behavioral anger expression on subsequent chronic pain intensity. Trait anger regulation style may moderate associations between behavioral anger expression and chronic pain intensity.