Chronic Pain and Psychiatric Conditions

Johnston, Keira J. A.; Huckins, Laura

doi:10.1159/000527041

Cited by 21 publications

(9 citation statements)

References 401 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Novel brain disorder-associated genes identified by stress-interactive models were enriched in pathways associated previously with stress-dependent disorder risk, such as N-acetylneuraminate catabolism in Alzheimer’s disease (p=4.48×10 -3 ), previously implicated in immune-mediated memory deficits 85 , nutrient absorption and metabolism (vitamin transmembrane transport, p=1.49×10 -2 , lipid digestion, p=1.56×10 -2 ) in anorexia nervosa, synaptic transmission (L-glutamate import, p=3.5×10 -3 , presynaptic vesicle fusion, p=1.81×10 -2 ) in ADHD 86 , and sensory perception of pain 87 in PTSD 88 (p=6.66×10 -3 ) and chronic pain (p=1.01×10 -2 ) ( Figure 5E ).…”

Section: Resultsmentioning

confidence: 99%

Common genetic variation impacts stress response in the brain

Seah,

Signer,

Deans

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

To explain why individuals exposed to identical stressors experience divergent clinical outcomes, we determine how molecular encoding of stress modifies genetic risk for brain disorders. Analysis of post-mortem brain (n=304) revealed 8557 stress-interactive expression quantitative trait loci (eQTLs) that dysregulate expression of 915 eGenes in response to stress, and lie in stress-related transcription factor binding sites. Response to stress is robust across experimental paradigms: up to 50% of stress-interactive eGenes validate in glucocorticoid treated hiPSC-derived neurons (n=39 donors). Stress-interactive eGenes show brain region- and cell type-specificity, and, in post-mortem brain, implicate glial and endothelial mechanisms. Stress dysregulates long-term expression of disorder risk genes in a genotype-dependent manner; stress-interactive transcriptomic imputation uncovered 139 novel genes conferring brain disorder risk only in the context of traumatic stress. Molecular stress-encoding explains individualized responses to traumatic stress; incorporating trauma into genomic studies of brain disorders is likely to improve diagnosis, prognosis, and drug discovery.Graphical Abstract

show abstract

Section: Resultsmentioning

confidence: 99%

Common genetic variation impacts stress response in the brain

Seah,

Signer,

Deans

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…The degree of awareness or conscientiousness, understood as one of the classic personality dimensions, appears to be inversely related to chronic low-intensity inflammation, as measured by levels of the glycoprotein interleukin-6 [57]. Additionally, the borderline personality pattern appears to be significantly correlated genetically with chronic pain [58]. Overall, however, the data collected so far do not allow us to associate inflammatory imbalance with personality traits [59].…”

Section: Aetiological Role Of Inflammatory Processesmentioning

confidence: 86%

Psychobiology and Treatment of Personality Disorders and Related Prominent Traits

Bertolín-Guillén

2024

PPD

View full text Add to dashboard Cite

Introduction: This theoretical narrative perspective will focus on pointing out the psychobiological factors which are involved in the genesis and treatment of personality prominent traits and disorders. Material and method: After a suitable search, mainly in PubMed and Psyc Info Journal databases, the number of selected quality publications is n= 95. The reduced sample sizes and numerous research designs that are merely exploratory or observational are its main limitations. Results and discussion: Regarding the psychopathology of personality neurodevelopment, environmental and genetic factors as well as neurotransmitter impairments are confirmed to be involved. Of interest are the endophenotypic perspective, endocannabinoid system and hypothalamus-regulated endocrine axes, among others. Neuroimmunology predicts important clinical and therapeutic innovations, but they are not a reality yet. It has been suggested that only with psychological interventions of various types is there symptomatic improvement as well as a favourable effect on stress-related epigenetic mechanisms. Psychopharmacotherapy continues to be useful, mainly off-label, with antipsychotics, anticonvulsants and opioid antagonists. Conclusions: In the absence of support from convincing qualified evidence, both users and health physicians usually prefer any type of psychological intervention to tackle complex personality clinical dysfunctions, without excluding complementary psychopharmacotherapy.

show abstract

“…On the other hand, bipolar disorder has been reported to be highly comorbid with chronic pain [109, 10,92]. There is evidence from two studies that it is genetically correlated with multisite pain [59,19], which is defined in both studies as the count of chronic pain sites across the body, using self-report in the UKBB. We used the same dataset and questionnaire, but we did not construct a phenotype using the count of pain sites, because as a measure of pain widespreadness it was of limited utility for determining shared cross-condition genetic risk (see [127] for a detailed discussion of our reasons).…”

Section: Discussionmentioning

confidence: 99%

Genetic relationships between chronic pain, psychopathologies, and neuroticism

Zorina-Lichtenwalter

Bango

Čeko

et al. 2023

Preprint

View full text Add to dashboard Cite

Chronic pain and psychiatric conditions have consistently demonstrated substantial overlap in risk factors, epidemiology, and effective treatments. Previous work has identified cross-condition latent factors underlying shared genetic risk for several distinct psychiatric conditions and pain conditions. Here, we sought to examine the relationships between these latent genetic factors to determine biological mechanisms common to both pain and psychiatric conditions. We combined two previously published genetic structural equation models. The first model consisted of 24 pain conditions and their two latent factors: General and Musculoskeletal pain-specific. The second model consisted of 11 psychiatric conditions and their four latent factors: Externalizing, Internalizing, Compulsive Thought, and Psychotic Thought. The combined model of six factors and 35 conditions allowed us to estimate correlations between all factors and between conditions of one domain (pain) and factors of the other (psychiatric). We then added three measures of neuroticism (depressive affect subscale, worrying subscale, and total neuroticism score) to this model to examine correlations with all conditions and factors and test for possible explanation of pain-mental disorder relationships by neuroticism. We found that genetic associations between pain and psychiatric conditions were selective to the General Pain factor (and not Musculoskeletal) and Internalizing and Externalizing, but not Thought disorder factors. Neuroticism was associated with pain conditions to the extent that they loaded onto the General Pain factor (i.e., were associated with other pain conditions). Neuroticism also explained a substantial proportion of shared genetic variance between General Pain and Externalizing and between General Pain and Internalizing factors. Overall, the genetic risks shared among chronic pain and psychiatric conditions and neuroticism suggest shared biological mechanisms and underscore the importance of clinical assessment and treatment programs that leverage these commonalities.

show abstract

Chronic Pain and Psychiatric Conditions

Cited by 21 publications

References 401 publications

Common genetic variation impacts stress response in the brain

Common genetic variation impacts stress response in the brain

Psychobiology and Treatment of Personality Disorders and Related Prominent Traits

Genetic relationships between chronic pain, psychopathologies, and neuroticism

Contact Info

Product

Resources

About