Pain
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Chronic pain and mental health problems have both been identified as public health emergencies and co-occur at high rates. This prospective, longitudinal investigation examined whether chronic pain status, pain-related symptoms (intensity, interference), pain catastrophizing, and insomnia severity predicted first lifetime onset of depressive and/or anxiety disorders as well as suicidality in a cohort of youth with a parental history of mood and/or anxiety disorders. Participants included 145 youth ( Mage = 13.74 years; 64% female) who completed structured diagnostic interviews at baseline and at 9- and 18-month follow-up to assess depressive and anxiety disorders as well as suicidality. ⋯ Increased pain intensity and interference at baseline predicted increased severity of suicidality at follow-up. Insomnia severity predicted increased likelihood of anxiety disorder onset. The presence of chronic pain and elevated pain-related symptoms and insomnia are premorbid risk factors for the development of significant mental health disorders and issues in youth.
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Observational Study
Fibromyalgia predicts increased odds of pain-related addiction exacerbation among individuals with pain and opioid use disorder.
Fibromyalgia and opioid use disorder (OUD) are highly impactful chronic illnesses with substantially overlapping psychosocial, biological, and clinical features. Little previous research has examined interactions between fibromyalgia and OUD. Limiting such research has been the previous requirement of a clinical examination to diagnose fibromyalgia. ⋯ Although all participants had pain, those with fibromyalgia demonstrated significantly greater odds of acknowledging pain-related OUD exacerbations. Pain-related OUD Exacerbation Scale was found to have a single-factor solution, strong internal consistency, and construct validity. This study provides first evidence of fibromyalgia as a risk factor for pain-related exacerbation of OUD and introduces a new scale with promising psychometric properties to measure pain-related OUD exacerbation.
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Adverse childhood experiences (ACEs) are associated with altered ongoing and evoked pain experiences, which have scarcely been studied for the peripartum period. We aimed to investigate how ACEs affect pain experience in pregnancy and labor. For this noninterventional trial with a short-term follow-up, pregnant women were divided into a trauma group (TG) with ACEs (n = 84) and a control group (CG) without ACEs (n = 107) according to the Childhood Trauma Questionnaire. ⋯ While PPTs increased through delivery in the CG (clinical CPM), and this PPT change was positively correlated with the experimental CPM ( r = 0.55), this was not the case in the TG. The association of ACEs with increased peripartal pain affect and heightened risk for preexisting back pain suggest that such women deserve special care. The dissociation of impaired clinical CPM in women with ACEs and normal prepartum experimental CPM implies at least partly different mechanisms of these 2 manifestations of endogenous pain controls.
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Chronic pain is a prevalent disease with increasing clinical challenges. Genome-wide association studies in chronic pain patients have identified hundreds of common pathogenic variants, yet they only explained a portion of individual variance of chronic pain. With the advances in next-generation sequencing technologies, it is now feasible to conduct rarer variants studies in large-scale databases. ⋯ These 2 rare variants were then tested for replication in 3 other biobanks, and the strongest evidence was found for rs28364172 as an individual contributor. Transcriptional analyses of Slc13a1 in rodents showed substantial regulation of its expression in the dorsal root ganglia and the sciatic nerve in neuropathic pain assays. Our results stress the importance of the SLC13A1 gene in sulfate homeostasis in the nervous system and its critical role in preventing pain states, thus suggesting new therapeutic approaches for treating chronic pain in a personalized manner, especially in people with mutations in the SLC13A1 gene.