The journal of pain : official journal of the American Pain Society
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People with intellectual disabilities (IDs) have a higher risk of painful medical conditions. Partly because of the impaired ability to communicate about it, pain is often undertreated. To strengthen pain assessment in this population, we conducted a systematic review to identify behavioral pain indicators in people with IDs by using Embase, PubMed, PsycINFO, CINAHL, and Cochrane. Inclusion criteria were 1) scientific papers; 2) published in the last 20 years, that is, 1992 to 2012; 3) written in English, 4) using human subjects, 5) intellectual disabilities, 6) pain, 7) behavior, and 8) an association between observable behavior and pain experience. From 527 publications, 27 studies were included. Pain was acute in 14 studies, chronic in 2 studies, both acute and chronic in 2 studies, and unspecified in 9 studies. Methodological quality was assessed with the Mixed Methods Appraisal Tool. Of the 14 categories with behavioral pain indicators, motor activity, facial activity, social-emotional indicators, and nonverbal vocal expression were the most frequently reported. Most of the behavioral pain indicators are reported in more than 1 study and form a possible clinical relevant set of indicators for pain in people with IDs. Determination of a behavioral pattern specific for pain, however, remains a challenge for future research. ⋯ This review focuses on categories of behavior indicators related to pain in people with IDs. The quality of evidence is critically discussed per category. This set of indicators could potentially help clinicians to recognize pain in this population, especially when unique individual pain responses are also identified.
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The purpose of this study was to develop and validate a brief, clinically relevant, multidimensional interview to assess pain burden among children and adolescents with sickle cell disease (SCD). The Sickle Cell Disease Pain Burden Interview-Youth (SCPBI-Y) was developed using a panel of experts, patients, and caregivers. Validation was undertaken with children and youth with SCD, ages 7 to 21 years (N = 129), recruited from 4 urban children's hospitals. Participants were recruited from inpatient (n = 62) and outpatient (n = 67) settings. The SCPBI-Y demonstrated strong internal consistency reliability, cross-informant concordance (child-caregiver), and test-retest reliability (outpatient setting). Moderate construct validity was found with validated measures of functional ability, pain, and quality of life. The SCPBI-Y demonstrated construct validity using a contrasted group approach between youth in inpatient versus outpatient settings and by severity of SCD symptoms, suggesting that youth in inpatient settings and with higher disease severity exhibited greater pain burden. Discriminant validity was found between SCPBI-Y and mood. Our preliminary findings suggest that the SCPBI-Y is a valid and reliable multidimensional interview that can be used in different clinical settings to evaluate pain burden among children and adolescents with SCD. ⋯ Multifaceted pain assessments are salient in providing optimal care to children and adolescents with SCD; however, current evaluations are lengthy and cumbersome to administer clinically. The current study introduces and validates a brief, clinically useful multidimensional interview to evaluate pain burden specific to youth with SCD.
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Chronic pain, chronic fatigue, and depressive mood are prevalent conditions in people with spinal cord injury (SCI). The objective of this research was to investigate the relationship between these conditions in adults with SCI. Multivariate analysis of variance, contingency analyses, and hierarchical regression were used to determine the nature of the relationship, as well as the contribution to this relationship of self-efficacy, a potential mediator variable. Seventy participants with SCI living in the community completed an assessment regimen of demographic and psychometric measures, including validated measures of pain, fatigue, depressive mood, and self-efficacy. Results indicated that participants with high levels of chronic pain had clinically elevated depressive mood, confusion, fatigue, anxiety and anger, low vigor, and poor self-efficacy. Participants with high chronic pain had 8 times the odds of having depressive mood and 9 times the odds of having chronic fatigue. Regression analyses revealed that chronic pain contributed significantly to elevated depressive mood and that self-efficacy mediated (cushioned) the impact of chronic pain on mood. Furthermore, both chronic pain and depressive mood were shown to contribute independently to chronic fatigue. Implications of these results for managing chronic pain in adults with SCI are discussed. ⋯ The relationship between pain, negative mood, fatigue, and self-efficacy in adults with SCI was explored. Results support a model that proposes that chronic pain lowers mood, which is mediated (lessened) by self-efficacy, whereas pain and mood independently increase chronic fatigue. Results provide direction for treating chronic pain in SCI.
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We examined changes in intraepidermal nerve fibers (IENFs) to differentiate patients with diabetic neuropathy (DN) and diabetic neuropathic pain (DN-P) from those with DN without pain (DN-NOP). Punch skin biopsies were collected from the proximal thigh (PT) and distal leg (DL) of normal subjects, patients with type 2 diabetes without evidence of DN (DM), or DN-P and DN-NOP patients. Protein gene product 9.5-positive (PGP+) immunohistochemistry was used to quantify total IENF, and growth-associated protein 43 (GAP43) for regenerating IENF. Compared to normal subjects and patients with type 2 diabetes without evidence of DN, both DN-P and DN-NOP have reduced PGP+ IENF densities in DL and PT. Although GAP43+ IENF densities were also reduced in DL for both DN-P and DN-NOP, the GAP43+ IENF densities in PT of DN-P remained at the control levels. Higher GAP43/PGP ratios were detected in DN-P compared to DN-NOP in the DL and PT. In parallel, increased numbers of axonal swellings per PGP+ fiber (axonal swelling/PGP) were detected in DN-P compared to normal subjects, patients with type 2 diabetes without evidence of DN, and DN-NOP in the DL. These axonal swellings were positive for tropomyosin-receptor-kinase A and substance P, suggesting that they are associated with nociception. ⋯ Among patients with DN, the ratios of GAP43/PGP and axonal swelling/PGP are likely to differentiate painful from painless phenotypes.
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Multiple physiological and psychological regulatory domains may contribute to the pathophysiology of pain in temporomandibular disorder (TMD) and other bodily pain conditions. The purpose of this study was to evaluate the relationship between multisystem dysregulation and the presence of TMD pain, as well as the presence of different numbers of comorbid pain conditions in TMD. Secondary data analysis was conducted in 131 non-TMD (without comorbid pain) controls, 14 TMD subjects without comorbid pain, 78 TMD subjects with 1 comorbid pain, and 67 TMD subjects with multiple comorbid pain conditions who participated in a TMD genetic study. Twenty markers from sensory, autonomic, inflammatory, and psychological domains were evaluated. The results revealed that 1) overall dysregulation in multiple system domains (OR [odds ratio] = 1.6, 95% confidence interval [CI] = 1.4-1.8), particularly in the sensory (OR = 1.9, 95% CI = 1.3-2.9) and the psychological (OR = 2.1, 95% CI = 2.1-2.7) domains, were associated with increased likelihood of being a painful TMD case; and 2) dysregulations in individual system domains were selectively associated with the increased odds of being a TMD case with different levels of comorbid persistent pain conditions. These outcomes indicate that heterogeneous multisystem dysregulations may exist in painful TMD subgroups, and multidimensional physiological and psychological assessments can provide important information regarding pathophysiology, diagnosis, and management of pain in TMD patients. ⋯ The concurrent assessment of multiple physiological and psychological systems is critical to our understanding of the pathophysiological processes that contribute to painful TMD and associated comorbid conditions, which will ultimately guide and inform appropriate treatment strategies that address the multisystem dysregulation associated with complex and common persistent pain conditions.