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Aims of the study were to: Implement supported self-management for chronic primary orofacial pain in a clinical setting. Evaluate its impact on consultation rates, pain-severity, interference-with-life and patient experience.
Learn More >Migraine is three times more prevalent in people with bipolar disorder or depression. The relationship between schizophrenia and migraine is less certain although glutamatergic and serotonergic neurotransmission are implicated in both. A shared genetic basis to migraine and mental disorders has been suggested but previous studies have reported weak or non-significant genetic correlations and five shared risk loci. Using the largest samples to date and novel statistical tools, we aimed to determine the extent to which migraine's polygenic architecture overlaps with bipolar disorder, depression, and schizophrenia beyond genetic correlation, and to identify shared genetic loci. Summary statistics from genome-wide association studies were acquired from large-scale consortia for migraine (n cases=59,674; n controls=316,078), bipolar disorder (n cases=20,352; n controls=31,358), depression (n cases=170,756; n controls=328,443) and schizophrenia (n cases=40,675, n controls=64,643). We applied the bivariate causal mixture model to estimate the number of disorder-influencing variants shared between migraine and each mental disorder, and the conditional/conjunctional false discovery rate method to identify shared loci. Loci were functionally characterised to provide biological insights. Univariate MiXeR analysis revealed that migraine was substantially less polygenic (2.8K disorder-influencing variants) compared to mental disorders (8.1K-12.3K disorder-influencing variants). Bivariate analysis estimated that 0.8K (0.3K), 2.1K (SD = 0.1K) and 2.3K (SD = 0.3K) variants were shared between bipolar disorder, depression and schizophrenia, respectively. There was also extensive overlap with intelligence (1.8K, SD = 0.3K) and educational attainment (2.1K, SD = 0.3K) but not height (1K, SD = 0.1K). We next identified 14 loci jointly associated with migraine and depression and 36 loci jointly associated with migraine and schizophrenia, with evidence of consistent genetic effects in independent samples. No loci were associated with migraine and bipolar disorder. Functional annotation mapped 37 and 298 genes to migraine and each of depression and schizophrenia, respectively, including several novel putative migraine genes such as L3MBTL2, CACNB2, SLC9B1. Gene-set analysis identified several putative gene-sets enriched with mapped genes including transmembrane transport in migraine and schizophrenia. Most migraine-influencing variants were predicted to influence depression and schizophrenia, although a minority of mental disorder-influencing variants were shared with migraine due to the difference in polygenicity. Similar overlap with other brain-related phenotypes suggests this represents a pool of 'pleiotropic' variants which influence vulnerability to diverse brain-related disorders and traits. We also identified specific loci shared between migraine and each of depression and schizophrenia, implicating shared molecular mechanisms and highlighting candidate migraine genes for experimental validation.
Learn More >Spinal cord stimulation (SCS) has become a common treatment modality for chronic pain of various etiologies. Over the past two decades, significant technological evolution has occurred in the SCS space, and this includes high-frequency (10 kHz) stimulation. Level I evidence exists reporting superiority of 10 kHz SCS over traditional SCS, however, conflicting reports have been published. The primary objective was to report site-collected real-world patient reported percentage improvement in pain scale (PR-PIPS) with traditional SCS and 10 kHz SCS from a single, academic medical center.
Learn More >To describe interictal brain structural and metabolic differences between patients with episodic migraine (EM), chronic migraine (CM) and healthy controls (HC).
Learn More >Reliable, clinic-friendly screening for Chronic postsurgical pain (CPSP) risk is unavailable. Within a prospective, observational study, we evaluated Pediatric Pain Screening Tool (PPST), a concise 9-item questionnaire, as a preoperative screening tool to identify those at higher risk for CPSP (NRS>3/10 beyond three months post-surgery) and poor function (disability/FDI/quality of life/PedsQL)) after spine fusion and Nuss procedures. Incidence of CPSP was 34.86% (38/109). We confirmed PPST scale stability, test re-test reliability (ICC=0.68;p<0.001); PPST measures were positively correlated with known CPSP risk factors (p<0.001) (preoperative pain (SCC:0.672), CASI (SCC:0.357), PROMIS pain interference (SCC:0.569), PROMIS depression (SCC:0.501), PedsQL (SCC:-0.460) and insomnia severity index (SCC0.567). Preoperative PPST and PPST physical sub-scores (median(IQR) were higher in CPSP (2(0.5,4), 1(0,2)) compared to non-CPSP ((1(0,3), 0(0,1.5)) groups (p=0.026, p=0.029) respectively. PPST scores/sub-scores positively correlated with higher FDI at 6 months but only PPST total and PPST psychosocial subscore correlated with higher FDI at 12 months. Based on ROC, optimal PPST cutoff for CPSP was 2 (63.9% sensitivity, 64.7% specificity). CPSP risk was high (48.94% risk) if PPST ≥ 2 (n=47) and medium (22.81%) if PPST<2 (n=57) after spine/pectus surgery. General and risk-strata specific, targeted psychosocial non-pharmacological interventions, need to be studied. Findings need validation in diverse, larger cohorts. CLINICALTRIALS.GOV IDENTIFIER: NCT02998138 PERSPECTIVE: The article supports Pediatric Pain Screening Tool, a simple 9-item questionnaire, as a preoperative screening tool for chronic post-surgical pain (CPSP) and function 6-12 months after spine/pectus surgeries. PPST measures correlate with known risk factors for CPSP. Risk stratification and targeted preventive interventions in high-risk subjects are proposed.
Learn More >The aim of the present study was to investigate the role of cognitive processing biases in Type 2 diabetes (T2D) and chronic pain, two conditions that are highly co-morbid. The final sample comprised 333 individuals (86 with T2D and chronic pain, 65 with chronic pain, 76 with T2D, 106 without any form of diabetes or pain). Participants completed questionnaires assessing pain and diabetes-related outcomes, as well as measures of interpretation bias, attentional bias, and attentional bias variability. In a 2 (pain status) x 2 (T2D status) x 3 (bias valence) ANOVA design, interpretation biases were found to be stronger in individuals with chronic pain than individuals without pain, although there were no differences according to T2D status. No group differences in attentional biases were found. Among individuals with T2D, greater interpretation bias was associated with better blood glucose control, but also greater fear of hypoglycaemia. For individuals with chronic pain, greater interpretation bias and attentional bias variability was associated with worse pain outcomes.. Whilst interpretation bias may be present in chronic pain, it also appears to indicate better glycaemic control in individuals with T2D. These findings suggest a more dynamic approach to understanding cognitive bias is needed, to consider when these biases are more or less adaptive, so that they can be better harnessed to improve outcomes for individuals with T2D who experience chronic pain. Perspective: These findings suggest that cognitive biases can be associated with psychopathology in chronic pain and in T2D, but can also potentially be adaptive in those with T2D. Diabetes management interventions may require a careful balance between promoting sufficient concern to motivate engagement in adaptive diabetes self-management, whilst also minimising fear of hypoglycaemia.
Learn More >Chronic pain and depression are highly comorbid and difficult-to-treat disorders. We previously showed this comorbidity is associated with higher depression severity, lower antidepressant treatment effectiveness and poorer prognosis in the Australian Genetics of Depression Study.
Learn More >Calcitonin gene-related peptide plasma levels have frequently been determined as a biomarker for primary headaches. However, published data is often inconsistent resulting from different methods that are not precisely described in most studies.
Learn More >Little is known about the factors that influence providers' perceptions of patient risk for aberrant opioid use. Patient gender may interact with prior opioid misuse to influence these perceptions. We asked 131 physicians to view videos and vignettes for 8 virtual patients with chronic pain. Gender (male/female) and previous prescription opioid misuse (present/absent) varied across patients; the vignettes were otherwise balanced on demographic and clinical characteristics. For each patient, providers assessed four risk domains: opioid-related adverse events, opioid misuse/abuse, opioid addiction, and opioid diversion. Results indicated a significant gender-by-misuse interaction for risk of opioid misuse/abuse. When previous misuse behaviors were absent, providers rated men at higher risk; there was no gender difference when previous misuse behaviors were present. A significant gender-by-misuse interaction was found for risk of opioid-related adverse events. Providers perceived men to be higher risk when previous misuse behaviors were absent; there was no gender difference when previous misuse behaviors were present. A significant gender-by-misuse interaction was found for risk of opioid addiction. Providers rated women at higher risk when previous misuse behaviors were present, and men at higher risk when previous misuse behaviors were absent. There were significant main effects of gender and misuse for risk of opioid diversion. Providers rated men and those with previous misuse behaviors at higher risk. These results demonstrate that patient gender and previous opioid misuse have unique and interactive effects on provider perceptions of prescription opioid-related risks. Studies are needed to identify the mechanisms underlying these effects, such as gender-based stereotypes about risk-taking and drug abuse.
Learn More >Pain specialists treat patients with headache and interface with those who use opioids more so than neurologists and headache specialists. We assessed headache medicine knowledge and needs of pain specialists.
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