The journal of pain : official journal of the American Pain Society
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This study examined the factor structure of the Children's Depression Inventory (CDI) among children and adolescents with chronic pain using exploratory and confirmatory factor analysis in a large, multisite sample of treatment-seeking youth. Participants included 1,043 children and adolescents (ages 8-18) with a range of chronic pain complaints who presented for initial evaluation at 1 of 3 tertiary care pediatric chronic pain clinics across the United States. They completed the CDI and reported on pain intensity and functional disability. Factor analysis was conducted using a 2-step (exploratory and confirmatory) approach. Results supported a 5-factor model for the CDI with good fit to the data. The distribution and item-total correlations of the somatic items (eg, pain complaints, fatigue) were explored in this sample. Results indicate that the CDI is a useful tool for assessing depressive symptoms in youth with chronic pain, but some caution is warranted in interpreting the clinical significance of scores in light of the overlap of specific symptoms common to both pain and depression. ⋯ The CDI can be considered a valid tool for assessing mood symptoms in children with chronic pain. Caution is encouraged when interpreting the clinical significance of scores due to symptom overlap between chronic pain and depression.
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An inverse association between resting blood pressure (BP) and acute pain sensitivity is well documented. Whether BP-related hypoalgesia differs by gender is unclear from prior work. Whether it increases proportionally with BP throughout the full BP range is also unknown. We examined BP-related hypoalgesia in a general population sample (n = 10,371, aged 30-87) of equal gender distribution reflecting the extremely low through hypertensive BP range. Resting BP was assessed and individuals participated in a standardized cold pressor test, providing pain ratings every 9 seconds. For systolic BP (SBP), a significant SBP × Gender interaction was observed on mean pain ratings (P < .001). Females displayed significant BP-related hypoalgesia (P < .001), with males showing a 38% smaller effect (P < .001). A similar DBP × Gender interaction was also observed (P < .05). Spline regression indicated a significant (P < .001) change in slope of the SBP-pain association at 140 mmHg. Among individuals with lower resting SBP (<140/90), increasing hypoalgesia with increasing SBP levels was observed (P < .001), with no further increases in those with higher BP (≥140/90; P > .10). This is the first large-scale study to confirm past results suggesting that BP-related hypoalgesia differs by gender; that is, females exhibited greater hypoalgesia. BP-related hypoalgesia appears subject to ceiling effects in the hypertensive BP range. ⋯ Females show greater BP-related hypoalgesia than males, highlighting gender differences in endogenous antinociceptive systems. Extent of BP-related hypoalgesia does not increase further once resting pressures reach the hypertensive range, suggesting persistent maximal demands on these antinociceptive systems among hypertensive individuals.
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Ultraviolet-B (UV-B) irradiation is a well-established inflammatory pain model inducing mechanical and thermal hyperalgesia, presumably mediated by released mediators that sensitize sensory nerve endings. Here, we used additional electrical stimulation to investigate axonal hyperexcitability. The lower leg of 13 volunteers was irradiated with 3-fold the minimum erythema UV-B dose and sensitization was recorded at days 1, 3, 7, and 14. Maximum heat pain (47°C, 5 seconds) developed at day 1 (visual analog scale [VAS: 0-100]; 59), was reduced at day 3 (VAS 43, P < .002), and was back to normal at day 7 (VAS 18). Mechanical impact pain (8 m/s), pinprick (150 mN), and pressure (100 kPa) hyperalgesia were maximum throughout days 1 to 3 (VAS 16, 8, and 12, respectively, P < .001) and back to normal at day 7. Suprathreshold transcutaneous electrical stimuli (1.5-fold pain threshold) were delivered in trains of 10 pulses at frequencies of 5 to 100 Hz. Electrical pain thresholds (determined at 2 Hz) decreased significantly (P < .002) and suprathreshold electrical pain increased by about 70% at days 1 to 3 after irradiation (VAS 36, P < .002). Electrical hyperalgesia did not correlate with mechanical sensitization but with reduced heat pain threshold and increased tonic heat pain (r = -.46 and .53; P < .05 and < .01), indicating that axonal hyperexcitability might contribute to heat hyperalgesia. Released inflammatory mediators (eg, prostaglandins) might sensitize both heat transducer molecules and axonal ion channels and receptors, which would explain the simultaneous development and close correlation between heat hyperalgesia and axonal hyperexcitability. ⋯ Local inflammation by UV-B irradiation sensitizes not only sensory endings, but also axons. Increased axonal excitability could contribute to inflammatory hyperalgesia by facilitating spike generation and increasing peak discharge frequencies of nociceptors. Thus, axonal channels and receptors crucial for this sensitization need to be identified to provide new therapeutic targets.
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This study investigated observational learning of pain-related fear and subsequent extinction after first-hand exposure to the feared stimulus. Moreover, the specific contingencies that are learned when observing others in pain were explored. A differential fear-conditioning paradigm was used, showing video models displaying either a painful (CS+ color; aversively conditioned stimulus) or a neutral (CS- color; neutrally conditioned stimulus) facial expression in the presence of a colored warm water task (WWT; observation phase). In 1 condition (open WWT cover), the model's hand was immersed in the colored liquid, while in the other condition (closed WWT cover), no contact was displayed between the model and the liquid. During exposure, participants subsequently immersed their own hand into each WWT with equal temperatures. Results revealed successful acquisition of pain-related fear. Participants with higher levels of pain catastrophizing, intolerance of uncertainty, trait fear of pain, or dispositional empathy were more prone to develop pain-related fear. Pain-related fear extinguished quickly after direct exposure to both WWTs. Contingencies between the color of the WWT and either the painful facial expressions or the assumed properties of the colored liquid were learned in both conditions. Clinical implications and limitations of the current study are discussed, providing avenues for future research in observational learning of pain-related fear. ⋯ Pain-related fear promotes the development as well as the continuation of chronic pain. A better understanding of the acquisition and extinction of this fear may help to improve pain treatment programs. Furthermore, we intended to identify individuals who are more prone to develop pain-related fear.
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This study investigated putative mechanisms of impaired spinal opioid antinociception such as a downregulation of mu-opioid receptor (MOR) number, coupling, and efficacy in rats with advanced (12 weeks) streptozotocin (STZ)-induced diabetes. Intravenous injection of STZ (45 mg/kg) in Wistar rats led to selective degeneration of insulin-producing pancreatic ß-cells, elevated blood glucose, and mechanical hyperalgesia. In these animals, dose-dependent and naloxone-reversible intrathecal fentanyl antinociception was significantly impaired and associated with a loss in MOR immunoreactivity of calcitonin gene-related peptide-immunoreactive (CGRP-IR) sensory nerve terminals, membrane-bound MOR binding sites, and MOR-stimulated G protein coupling within the dorsal horn of the spinal cord. Intrathecal delivery of nerve growth factor (NGF) in diabetic animals normalized spinal MOR number and G protein coupling and rescued spinal fentanyl-induced antinociception. These findings identify for the first time a loss in functional MOR on central terminals of sensory neurons as a contributing factor for the impaired spinal opioid responsiveness during advanced STZ-induced diabetes that can be reversed by NGF. Moreover, they support growing evidence of a distinct regulation of opioid responsiveness during various painful states of disease (eg, arthritis, cancer, neuropathy) and may give novel therapeutic incentives. ⋯ In diabetic neuropathy a loss in sensory neuron mu-opioid receptor number and coupling contributes to impaired spinal opioid antinociception that can be reversed by NGF. These findings support growing evidence of a distinct regulation of opioid responsiveness during various painful diseases and may give novel therapeutic incentives.