Corticolimbic anatomical characteristics predetermine risk for chronic pain.
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ABSTRACT:
SUBMITTER: Vachon-Presseau E
PROVIDER: S-EPMC4939699 | biostudies-literature | 2016 Jul
REPOSITORIES: biostudies-literature
Publications
Corticolimbic anatomical characteristics predetermine risk for chronic pain.
Vachon-Presseau Etienne E Tétreault Pascal P Petre Bogdan B Huang Lejian L Berger Sara E SE Torbey Souraya S Baria Alexis T AT Mansour Ali R AR Hashmi Javeria A JA Griffith James W JW Comasco Erika E Schnitzer Thomas J TJ Baliki Marwan N MN Apkarian A Vania AV
Brain : a journal of neurology 20160505 Pt 7
SEE TRACEY DOI101093/BRAIN/AWW147 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Mechanisms of chronic pain remain poorly understood. We tracked brain properties in subacute back pain patients longitudinally for 3 years as they either recovered from or transitioned to chronic pain. Whole-brain comparisons indicated corticolimbic, but not pain-related circuitry, white matter connections predisposed patients to chronic pain. Intra-corticolimbic white matter connectivity analysis identified three seg ...[more]
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Project description:BackgroundA 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.MethodsResting-state functional magnetic resonance imaging data were acquired in 30 patients with chronic pain. Twenty-three patients completed EXP, and 6-month follow-up data were available in 20 patients (magnetic resonance imaging data in 17 patients). Pain-free control data were acquired at two time points (n = 29, n = 21). Seed-based resting-state functional connectivity (rsFC) analyses were performed, with seeds in the amygdala, hippocampus, and nucleus accumbens.ResultsPain relief after EXP was highly variable, with 60% of patients reporting a clinically relevant improvement. Amygdala rsFC with the middle frontal gyrus decreased significantly over time in patients but was not associated with pain relief. In contrast, greater pain relief was associated with greater decreases over time in hippocampus rsFC with the precuneus, which was related to reductions in catastrophizing (EXP therapeutic target) as well. Greater pain relief was also associated with lower pretreatment rsFC between nucleus accumbens and postcentral gyrus.ConclusionsWhile changes in hippocampus rsFC were associated with pain relief after EXP, pretreatment nucleus accumbens rsFC showed potential prognostic value. Our findings further support the importance of corticolimbic circuitry in chronic pain, emphasizing its relation to pain relief and identifying potential underlying mechanisms and prognostic factors, warranting further testing in independent samples.
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Project description:PurposeResearch into the pathophysiology of chronic prostatitis/chronic pelvic pain syndrome has primarily focused on markers of peripheral dysfunction. We present the first neuroimaging investigation to our knowledge to characterize brain function and anatomy in chronic prostatitis/chronic pelvic pain syndrome.Materials and methodsWe collected data from 19 male patients with chronic prostatitis/chronic pelvic pain syndrome, and 16 healthy age and gender matched controls. Functional magnetic resonance imaging data were obtained from 14 patients with chronic prostatitis/chronic pelvic pain syndrome as they rated spontaneous pain inside the scanner. Group differences (16 patients per group) in gray matter total volume and regional density were evaluated using voxel-based morphometry, and white matter integrity was studied with diffusion tensor imaging to measure fractional anisotropy. Functional and anatomical imaging outcomes were correlated with the clinical characteristics of chronic prostatitis/chronic pelvic pain syndrome.ResultsSpontaneous pelvic pain was uniquely characterized by functional activation within the right anterior insula, which correlated with clinical pain intensity. No group differences were found in regional gray matter volume, yet density of gray matter in pain relevant regions (anterior insula and anterior cingulate cortices) positively correlated with pain intensity and extent of pain chronicity. Moreover the correlation between white matter anisotropy and neocortical gray matter volume was disrupted in chronic prostatitis/chronic pelvic pain syndrome.ConclusionsWe provide novel evidence that the pain of chronic prostatitis/chronic pelvic pain syndrome is associated with a chronic pelvic pain syndrome specific pattern of functional brain activation and brain anatomical reorganization. These findings necessitate further investigations into the role of central mechanisms in the initiation and maintenance of chronic prostatitis/chronic pelvic pain syndrome.
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Project description:Background. Inter- and intra-individual fluctuations in pain intensity pose a major challenge to treatment efficacy, with a majority perceiving their pain relief as inadequate. Recent preclinical studies have identified circadian rhythmicity as a potential contributor to these fluctuations and therapeutic target. Methods. We therefore sought to determine the impact of these rhythms in people with chronic low back pain (CLBP) through a detailed characterization, including questionnaires to evaluate biopsychosocial characteristics, ecological momentary assessment (7-day e-diaries at 8:00/14:00/20:00) to assess pain fluctuations, and intra-day blood transcriptomics (8:00/20:00) to identify genes/pathways of interest. Results. While most individuals displayed constant or variable/mixed pain phenotypes, a distinct subset had daily fluctuations of increasing pain scores (>30% change in intensity over 12-hours in ≥4/7 days). This population had no opioid users, better biopsychosocial profiles, and differentially expressed transcripts relative to other pain phenotypes. The circadian-governed neutrophil degranulation pathway was particularly enriched among arhythmic individuals; the link between neutrophil degranulation and opioid use was further confirmed in a separate CLBP cohort. Conclusion. Our findings identify pain rhythmicity and the circadian expression of neutrophil degranulation pathways as indicators of CLBP outcomes, which may help provide a personalized approach to phenotyping biopsychosocial characteristics and medication use. This highlights the need to better understand the impact of circadian rhythmicity across chronic pain conditions.
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Project description:AbstractNeuroimaging is a powerful tool to investigate potential associations between chronic pain and brain structure. However, the proliferation of studies across diverse chronic pain syndromes and heterogeneous results challenges data integration and interpretation. We conducted a preregistered anatomical likelihood estimate meta-analysis on structural magnetic imaging studies comparing patients with chronic pain and healthy controls. Specifically, we investigated a broad range of measures of brain structure as well as specific alterations in gray matter and cortical thickness. A total of 7849 abstracts of experiments published between January 1, 1990, and April 26, 2021, were identified from 8 databases and evaluated by 2 independent reviewers. Overall, 103 experiments with a total of 5075 participants met the preregistered inclusion criteria. After correction for multiple comparisons using the gold-standard family-wise error correction ( P < 0.05), no significant differences associated with chronic pain were found. However, exploratory analyses using threshold-free cluster enhancement revealed several spatially distributed clusters showing structural alterations in chronic pain. Most of the clusters coincided with regions implicated in nociceptive processing including the amygdala, thalamus, hippocampus, insula, anterior cingulate cortex, and inferior frontal gyrus. Taken together, these results suggest that chronic pain is associated with subtle, spatially distributed alterations of brain structure.
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Project description:AbstractDecades of efforts in elucidating pain mechanisms, including pharmacological, neuroanatomical, and physiological studies have provided insights into how nociceptive information transmits from the periphery to the brain and the locations receiving nociceptive signals. However, little is known about which specific stimulus-dependent activated neurons, amongst heterogeneous neural environments, discriminatively evoke the cognate pain behavior. We here shed light on the population of neurons in the spinal cord activated by a painful stimulus to identify chronic pain-dependent activated neuronal subsets using Fos2A-iCreER (TRAP2) mice. We have found a large number of neurons activated by a normally nonpainful stimulus in the spinal cord of spinal nerve-ligated mice, compared with sham. Neuronal activation was observed in laminae I and II outer under heat hyperalgesia. A large number of neurons in laminae II inner were activated in both mechanical allodynia and heat hyperalgesia conditions, while mechanical allodynia tends to be the only stimulus that activates cells at lamina II inner dorsal region. Neuroanatomical analyses using spinal cell markers identified a large number of spinal inhibitory neurons that are recruited by both mechanical allodynia and heat hyperalgesia. Of interest, spinal neurons expressing calretinin, calbindin, and parvalbumin were activated differently with distinct pain modalities (ie, mechanical allodynia vs heat hyperalgesia). Chemogenetic inhibition of those activated neurons significantly and specifically reduced the response to the pain stimulus associated with the stimulus modality originally given to the animals. These findings support the idea that spinal neuronal ensembles underlying nociceptive transmission undergo dynamic changes to regulate selective pain responses.
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Project description:BACKGROUND:Chronic postsurgical pain (CPSP) after hernia repair research has mainly relied on unconfirmed self-reporting. We aimed to describe confirmed CPSP incidence, management, and quality of life (QoL) in a 2-year prospective study. METHODS:Multicenter study (GENDOLCAT) of 3890 patients undergoing 4 common surgical procedures in 23 hospitals to develop a risk model for CPSP; 2352 men underwent open hernia repair. Patients with pain were identified by telephone at 1 and 3 months and referred to the hospital 4 months after surgery for a physical examination to confirm CPSP. Three validated tools were used: the Brief Pain Inventory (BPI) for severity, analgesic use, and interference with activities; the SF-12 questionnaire for QoL (validated Spanish version), and the Douleur Neuropathique 4 (DN4). Patients with CPSP were called again at 1 and 2 years. RESULTS:In 1761 patients who underwent hernia repair and were eligible for physical examination for CPSP, the incidence of confirmed pain at 4 months was 13.6% (patient-reported pain, 6.2% at 1 year and 4.0% at 2 years). Neuropathic pain was diagnosed in 38.5% of the CPSP patients at 4 months. The incidences of neuropathic CPSP in patients with mesh or non-mesh repairs were similar (38.6 and 33.3%, respectively). SF-12 physical component scores changed little in all patients, whether or not they developed CPSP. The SF-12 mental component decreased significantly in all patients, but the decrease was clinically significant only in CPSP patients. CPSP interfered with activities (18%), work (15.6%), walking (15%) and mood (10.2%). At 2 years 52.1% of CPSP patients had moderate/intense pain and 28.2% took analgesics. CONCLUSION:CPSP affects QoL-related activities, and although it diminishes over the course of 2 years after surgery, many patients continue to have moderate/intense pain and take analgesics. CPSP and neuropathic pain rates seem to be similar after mesh and non-mesh repair. BPI and SF-12 mental component scores detect effects on QoL. TRIAL REGISTRATION:ClinicalTrials.gov NCT01510496.
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Project description:ObjectiveTo describe the clinical and psychosocial characteristics of chronic pain in cancer survivors referred to one Australian hospital's ambulatory pain clinic over a 7-year period (2013-19), and to compare cancer treatment-related pain with comorbid non-malignant pain.MethodRetrospective chart review including responses to standardized self-report questionnaires (Brief Pain Inventory, Depression Anxiety Stress Scale, Pain Self-Efficacy Questionnaire, Pain Catastrophizing Scale), routinely collected in all patients referred to pain clinics at Australian and New Zealand hospitals.ResultsOf 3510 new referrals during the study period, 267 (7.5%) had a history of cancer and 176 (5.0%) met the study's eligibility criteria. Their average age was 63 ± 13 years, with 55% female. Breast cancer survivors were commonest, followed by hematological, prostate, melanoma, and colorectal, a median of 3 years post-diagnosis. Pain was attributed to cancer treatment in 87 (49%), surgery being the commonest modality. Multimodal treatment (n = 89, 58%) was significantly commoner in the treatment-related pain group (p < 0.001). Average pain severity was moderate, as was pain-related disability and distress. Pain cognitions were often maladaptive (low pain self-efficacy, high pain catastrophizing), predicted by pre-existing anxiety and depression. Associations between pain cognitions and outcomes were medium-to-large. Differences between treatment pain and comorbid pain were small-to-medium. Their scores were similar to Australian pain clinic norms.ConclusionCancer treatment causes tissue damage, but pain-related distress and disability in survivors is associated with maladaptive pain cognitions. Survivors with poor pain outcomes should be evaluated for unhelpful thoughts and beliefs especially when they have pre-existing depression or anxiety.
| S-EPMC9796565 | biostudies-literature
Project description:The COVID-19 pandemic has affected millions of individuals worldwide. Pain has emerged as a significant post-COVID-19 symptom. This study investigated the incidence, characteristics, and risk factors of post-COVID chronic pain (PCCP) in Thailand. A cross-sectional study was conducted in participants who had been infected, including those hospitalized and monitored at home by SARS-CoV-2 from August to September 2021. Data were collected for screening from medical records, and phone interviews were done between 3 to 6 months post-infection. Participants were classified into 1) no-pain, 2) PCCP, 3) chronic pain that has been aggravated by COVID-19, or 4) chronic pain that has not been aggravated by COVID-19. Pain interference and quality of life were evaluated with the Brief Pain Inventory and EuroQol Five Dimensions Five Levels Questionnaire. From 1,019 participants, 90% of the participants had mild infection, assessed by WHO progression scale. The overall incidence of PCCP was 3.2% (95% CI 2.3-4.5), with 2.8% (95% CI 2.0-4.1) in mild infection, 5.2% (95% CI 1.2-14.1) in moderate infection and 8.5% (95% CI 3.4-19.9) in severe infection. Most participants (83.3%) reported pain in the back and lower extremities and were classified as musculoskeletal pain and headache (8.3%). Risk factors associated with PCCP, included female sex (relative risk [RR] 2.2, 95% CI 1.0-4.9) and greater COVID-19 severity (RR 3.5, 95% CI 1.1-11.7). Participants with COVID-19-related exacerbated chronic pain displayed higher pain interferences and lower utility scores than other groups. In conclusion, this study highlights the incidence, features, and risk factors of post-COVID chronic pain (PCCP) in Thailand. It emphasizes the need to monitor and address PCCP, especially in severe cases, among females, and individuals with a history of chronic pain to improve their quality of life in the context of the ongoing COVID-19 pandemic.
| S-EPMC10786369 | biostudies-literature
Project description:ObjectivesDetermine pain prevalence and clinical characteristics in patients with advanced chronic disease and identify breakthrough pain frequency.DesignObservational, descriptive, cross-sectional study.LocationThree primary care teams and one intermediate care hospital.ParticipantsAll patients with advanced chronic disease.Main measurementsA semi-structured interview was performed to collect demographic, clinical, and specific variables of pain using validated scales. Patient location (home, nursing home or hospital) and advanced chronicity trajectory (organ failure, oncological disease, dementia, or multimorbidity) were recorded. Pain was assessed based on the Brief Pain Inventory (BPI) and, in cases of disabling dementia, using the Pain Assessment in Advanced Dementia (PAINAD). A statistical descriptive, comparative analysis between variables was performed using the R software.ResultsOf all patients selected, 223 (60.4%) were included. Prevalence of pain: 83.9% (n=187), with no differences based on location or trajectory. Significant differences in pain intensity based on location (P=.0046) (moderate-severe in patients at home, moderate in hospital patients, and mild in nursing home patients) and on trajectory (P<.0001) (moderate-severe in patients with organ failure and multimorbidity, moderate in patients with cancer, and mild in patients with dementia). Global functional impact of pain was mild-moderate, emotional impact was severe in 41.5% of patients (n=51), and breakthrough pain was observed in 8.6% (n=13).ConclusionsPain must always be explored and assessed in patients with advanced chronicity, since it was highly prevalent in all locations and trajectories, being particularly intense in patients at home with organ failure and multimorbidity. Breakthrough pain was found in non-oncological trajectories.
| S-EPMC10505975 | biostudies-literature