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Reliability and smallest detectable change of the Danish version of the Pain Self-Efficacy Questionnaire in patients with chronic low back pain.

Low back pain (LBP) is the leading cause of disability and a global public health concern. Studies indicate that pain self-efficacy is associated with the development of disability in chronic LBP (CLBP) patients. The Pain Self-Efficacy Questionnaire (PSEQ) is a commonly used questionnaire to assess pain self-efficacy in patients with CLBP. It is essential to examine the psychometric properties of the PSEQ in the population in which it is to be used. Thus, the aim of this study is to evaluate the reliability and smallest detectable change of the Danish version of the Pain Self-Efficacy Questionnaire (PSEQ-DK) in patients with CLBP before implementing it as an outcome measure in an inpatient rehabilitation context.

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Clinical Features and Treatment Response in Immune-Mediated Small Fiber Neuropathy with Trisulfated Heparin Disaccharide or Fibroblast Growth Factor Receptor 3 Antibodies.

Novel antibodies to trisulfated heparin disaccharide (TS-HDS) and fibroblast growth factor receptor 3 (FGFR-3) have been recently described in otherwise cryptogenic small fiber neuropathy (SFN) cases. Our goal was to further describe clinical features in such cases and to analyze treatment responses.

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Corticolimbic Circuitry in Chronic Pain Tracks Pain Intensity Relief Following Exposure In Vivo.

A subset of patients with chronic pain who receive exposure in vivo (EXP) treatment experience clinically relevant relief of pain intensity. Although pain relief is not an explicit therapeutic target, it is important to understand how and why this concomitant effect occurs in some patients but not others. This longitudinal study therefore aimed to characterize brain plasticity as well as to explore pretreatment factors related to pain relief.

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Social deprivation and paediatric chronic pain referrals in Ireland: a cross-sectional study.

Social deprivation is associated with a higher prevalence of chronic pain in children and an under-representation in specialist paediatric chronic pain programs. Our primary objective was to determine if there was a relationship between social deprivation and paediatric chronic pain referrals in Ireland. Secondary objectives included analysing for differences between deprivation groups in pain characteristics and function that are recorded at first clinic visit.

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Chronic pain severity, impact, and opioid use among patients with cancer: An analysis of biopsychosocial factors using the CHOIR learning health care system.

Despite the biopsychosocial underpinnings of chronic noncancer pain, relatively little is known about the contribution of psychosocial factors to chronic cancer pain. The authors aimed to characterize associations between biopsychosocial factors and pain and opioid use among individuals with chronic pain and cancer.

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Symptomatic Treatment of Pain-Related Pediatric Functional Gastrointestinal Disorders in a Biopsychosocial Construct, and a Validity Study of Rome III Criteria.

Our study aims to assess improvement with symptomatic treatment of pain-related functional gastrointestinal disorders (FGIDs) in a biopsychosocial construct and evaluate validity of Rome III criteria. Children with chronic abdominal pain diagnosed with an FGID or organic disease were followed for 1 year: 256/334 were diagnosed with an FGID and 78/334 were diagnosed with a possible organic disease due to alarm signs or not meeting Rome III criteria. After 1 year, 251 had true FGID and 46 had organic diseases. Ninety percent of FGID patients improved with symptomatic treatment over an average of 5.4 months. With a 95% confidence interval, Rome criteria predicted FGIDs with sensitivity 0.89, specificity 0.90, positive predictive value 0.98, and negative predictive value 0.59. We conclude that symptomatic treatment of pain-related FGIDs results in clinical improvement and could reduce invasive/expensive testing. Rome III criteria's high specificity and positive predictive value suggest they can rule in a diagnosis of FGID.

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The effect of social support in chronic back pain: number of treatment sessions and reported level of disability.

Chronic back pain is characterized by its duration and poor response to medical interventions and is a major health problem. Treatment up-take, adherence, and social support are key issues and are vital for recovery and functionality. However, there is limited research on the role of social support and treatment uptake and adherence for chronic back pain. The aim of this study was to explore the impact of social support in terms of treatment uptake and adherence in chronic back pain patients in Australia. Two hundred and one adult men and women completed a battery of questionnaires that assessed levels of social support and disability and treatment uptake and adherence. Stepwise multiple regression predicting treatment participation, produced a significant model that included participant's age and level of social support and accounted for 14% of the variance, (2,179) = 14.10,  < 0.001, adj  = 0.14. Life control, affective distress and level of social support scores accounted for 26% of the variance in disability levels (3,179) = 21.42,  < 0.001, adj  = 0.26. The findings indicated that age, social support had a significant positive effect on the number of treatment sessions attended by participants and that life control, affective distress, and level of social support were negatively related to disability levels. The findings support interdisciplinary approaches, including social interventions as important part of any chronic back pain treatment. Implications for rehabilitation Chronic back pain does not respond well to traditional rehabilitation methods based on the Medical Model. Social support has a significant impact on treatment adherence and disability. This study measures perceived social support from an emotional and instrumental perspective. Social support interventions as part of a multidisciplinary approach would be beneficial in the experience of chronic back pain.

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Elevated dietary ω-6 polyunsaturated fatty acids induce reversible peripheral nerve dysfunction that exacerbates comorbid pain conditions.

Chronic pain is the leading cause of disability worldwide and is commonly associated with comorbid disorders. However, the role of diet in chronic pain is poorly understood. Of particular interest is the Western-style diet, enriched with ω-6 polyunsaturated fatty acids (PUFAs) that accumulate in membrane phospholipids and oxidise into pronociceptive oxylipins. Here we report that mice administered an ω-6 PUFA-enriched diet develop persistent nociceptive hypersensitivities, spontaneously active and hyper-responsive glabrous afferent fibres and histologic markers of peripheral nerve damage reminiscent of a peripheral neuropathy. Linoleic and arachidonic acids accumulate in lumbar dorsal root ganglia, with increased liberation via elevated phospholipase (PLA)2 activity. Pharmacological and molecular inhibition of PLA2G7 or diet reversal with high levels of ω-3 PUFAs attenuate nociceptive behaviours, neurophysiologic abnormalities and afferent histopathology induced by high ω-6 intake. Additionally, ω-6 PUFA accumulation exacerbates allodynia observed in preclinical inflammatory and neuropathic pain models and is strongly correlated with multiple pain indices of clinical diabetic neuropathy. Collectively, these data reveal dietary enrichment with ω-6 PUFAs as a new aetiology of peripheral neuropathy and risk factor for chronic pain and implicate multiple therapeutic considerations for clinical pain management.

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Chronic pain-related cortical neural activity in patients with complex regional pain syndrome.

Quantitative objective measurement of chronic pain is important. We elucidated chronic pain-related cortical neural activity and neural connectivity among pain-related brain regions in complex regional pain syndrome (CRPS). Resting-state magnetoencephalography recordings were performed. Cortical current density and neural connectivity, revealed by amplitude envelope correlation (AEC), were estimated on standardized brain magnetic resonance imaging. Intra-experiment pain was assessed subjectively using a visual analogue scale (VAS). The correlation between current density and VAS scores was calculated for the occipital areas and pain-related cortices. Current density in the primary (SI) and secondary (SII) somatosensory cortex and precuneus in both hemispheres was negatively correlated with the pain VAS score. The AEC and VAS values were significantly correlated for the SII and the precuneus and for the SII and insular cortex in the alpha frequency band in the right hemisphere. In the theta frequency band, the AEC and VAS values correlated for the SII and posterior cingulate cortex in the right hemisphere. Our results suggested that disruption of pain processes and functions in the default mode network occurs in CRPS. Our method targeting the neural mechanism of pain has the potential to offer a clinically objective means of evaluating it.

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Vitamin D deficiency exacerbates UV/endorphin and opioid addiction.

The current opioid epidemic warrants a better understanding of genetic and environmental factors that contribute to opioid addiction. Here we report an increased prevalence of vitamin D (VitD) deficiency in patients diagnosed with opioid use disorder and an inverse and dose-dependent association of VitD levels with self-reported opioid use. We used multiple pharmacologic approaches and genetic mouse models and found that deficiencies in VitD signaling amplify exogenous opioid responses that are normalized upon restoration of VitD signaling. Similarly, physiologic endogenous opioid analgesia and reward responses triggered by ultraviolet (UV) radiation are repressed by VitD signaling, suggesting that a feedback loop exists whereby VitD deficiency produces increased UV/endorphin-seeking behavior until VitD levels are restored by cutaneous VitD synthesis. This feedback may carry the evolutionary advantage of maximizing VitD synthesis. However, unlike UV exposure, exogenous opioid use is not followed by VitD synthesis (and its opioid suppressive effects), contributing to maladaptive addictive behavior.

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