Pain
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Randomized Controlled Trial
Pulsed radiofrequency adjacent to the cervical dorsal root ganglion in chronic cervical radicular pain: a double blind sham controlled randomized clinical trial.
Cervical radicular pain affects approximately 1 on 1000 adults per year. Although many treatment modalities are described in the literature, the available evidence for efficacy is not sufficient to allow definitive conclusions on the optimal therapy to be made. The effect of pulsed radiofrequency treatment for this type of patients was evaluated in a prospective audit that showed satisfactory pain relief for a mean period of 9.2 months, justifying a randomized sham controlled trial. ⋯ The need for pain medication was significantly reduced in the pulsed radiofrequency group after six months. No complications were observed during the study period. These study results are in agreement with the findings of our previous clinical audit that pulsed radiofrequency treatment of the cervical dorsal root ganglion may provide pain relief for a limited number of carefully selected patients with chronic cervical radicular pain as assessed by clinical and neurological examination.
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Review Meta Analysis Comparative Study
Systematic review of observational (behavioral) measures of pain for children and adolescents aged 3 to 18 years.
Observational (behavioral) scales of pain for children aged 3 to 18 years were systematically reviewed to identify those recommended as outcome measures in clinical trials. This review was commissioned by the Pediatric Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (www.immpact.org). In an extensive literature search, 20 observational pain scales were identified for review including behavior checklists, behavior rating scales, and global rating scales. ⋯ No observational measures were recommended for assessing chronic or recurrent pain because the overt behavioral signs of chronic pain tend to habituate or dissipate as time passes, making them difficult to observe reliably. In conclusion, no single observational measure is broadly recommended for pain assessment across all contexts. Directions for further research and scale development are offered.
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Biopsychosocial models of chronic pain that recognize psychological and environmental factors as important aspects of adjustment to pain have been proposed for understanding chronic pain and related suffering in persons with multiple sclerosis (MS), but such models have not been empirically tested. The objective of this study was to test such a model by evaluating the associations of several psychosocial variables (i.e., pain-related catastrophizing, perceived social support, pain beliefs, and pain coping) with pain intensity, pain interference with functioning, and psychological functioning in persons with chronic pain and MS, after controlling for demographic and disease-related factors. Participants were 125 community-dwelling persons with MS and pain who completed a mailed questionnaire that included measures of pain intensity and interference, psychological functioning, catastrophizing, social support, and pain beliefs and coping. ⋯ These variables explained an additional 22% of the variance in pain-related interference (p<.001) and 43% of the variance in psychological functioning (p<.001), after adjusting for demographic and MS-related variables and average pain intensity. Catastrophizing was consistently and independently associated with all criterion measures, whereas social support, pain beliefs, and pain coping were associated with some criterion measures but not others. The results provide empirical support for a biopsychosocial understanding of chronic pain in MS and suggest that specific psychosocial factors (e.g., catastrophizing) may be important regarding adjustment to pain in persons with MS.
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Cyclin-dependent kinase 5 (Cdk5) is a unique member of the CDK family. It is predominantly expressed in postmitotic neurons and has been implicated in neuronal plasticity. The present study showed that Cdk5 and p35 were expressed in primary sensory and dorsal horn neurons, while p25, an N-terminal truncated derivative of p35, could only be detected in the dorsal horn neurons. ⋯ Intrathecal pretreatment with Roscovitine, a specific inhibitor of Cdk5 activity, and intrathecal delivery of the DN-Cdk5(N144) gene both alleviated CFA-induced heat hyperalgesia but not mechanical allodynia. In contrast, overexpression of Cdk5, p35 or p25 in primary sensory and dorsal horn neurons significantly enhanced heat hyperalgesia. We conclude that Cdk5/p35 and Cdk5/p25 complexes in primary sensory and dorsal horn neurons may potentially be involved in nociceptive transmission after inflammation and may be employed in synaptic plasticity underlying pain hypersensitization.