Impairment In Chronic Pain Patients Research Articles

Estimation of cognitive impairment in chronic pain patients and characteristics of estimated mild cognitive impairment.

Patients with chronic pain suffer from psychological effects such as anxiety due to the pain itself. Pain can not only impair activities of daily living (ADL) and quality of life (QOL), but also impair cognitive function. Therefore, in this study, we aimed to estimate the cognitive function of chronic pain patients using a deep neural network (DNN) model that has already been implemented in society. We investigated the characteristics of patients presumed to have mild cognitive impairment (MCI) and, at the same time, verified the relationship with the questionnaire commonly used in chronic pain research, which is administered by 43 university affiliated hospitals and medical institutions participating in the chronic pain research group of the Ministry of Health, Labor and Welfare in Japan (assessment batteries). The study included 114 outpatients from a multidisciplinary pain clinic, and we estimated their Mini-Mental State Examination (MMSE) scores based on age and basic blood test data (23 items). Furthermore, we classified the estimated MMSE scores of chronic pain patients into two groups based on a cutoff score of 27, which indicates MCI, and compared the blood data and assessment batteries. Additionally, we used a control group of 252 healthy adults aged 45 years or older who visited a dementia prevention outpatient clinic for comparison with the MMSE scores of chronic pain patients. The MMSE scores in chronic pain patients were below the cutoff for MCI. When classified into two groups based on the estimated MMSE score of 27 points, WBC, RBC, Hb, Hct, PLT, UA, BUN, creatinine, Triglyceride, and γ-GT were significantly higher in the blood data. In the MCI group, PDAS values were significantly lower. Furthermore, only in the non-MCI group, a significant correlation was found between the estimated MMSE value and BPI, PDAS, and Locomo. The estimated MMSE scores were significantly lower in chronic pain patients than in healthy adults (p = 0.04). Patients with chronic pain may exhibit cognitive impairment due to systemic metabolic disturbances. This suggests that chronic pain affects activities of daily living, resulting in systemic metabolic disorders.

Chronic Pain and Sleep Disturbances: A Dangerous Coexistence

Chronic Pain (CP) new definition has brought benefits to address the complexity of this syndrome. Quality of Life (QoL) and Functional Recovery (FR) represent fundamental issues of clinical outcomes, which go beyond mere pain relief. Such a definition recognizes the bidirectional association between CP and SD. Patients who suffer from CP always have Sleep Disturbances (SD). These patients may feel agitated during the night and tired in the morning, leading to a significant decrease in personal productivity. The two-way relationship between poor sleep and pain operates to maintain and amplify sleep inadequacy and growth and intensification of pain. There is a great need to increase awareness on the contribution of sleep quality to the severity of functional impairment in CP patients. CP disorders are not a simple exacerbation of acute pain. The negative effect of pain and sleep problems on quality of life outlines the necessity for investigating how the two conditions are associated and how to structure treatments and prevention strategies.

Unmet needs in the management of functional impairment in patients with chronic pain: a multinational survey.

Background: A survey of European Pain Federation 2019 attendees was conducted to identify unmet needs in chronic pain patients. Materials & methods: Four questions were asked focusing on functional impairment in chronic pain, including who are at increased risk and ways to better identify and manage these patients. Results: In total143 respondents indicated that key issues were lack of knowledge, lack of resources/time to assess and manage chronic painand lack of sufficient tools to identify patients at risk for functional impairment. Education and training of primary care physicians, simplified guidelines and practical tools for assessmentand use of multidisciplinary teams to treat chronic pain were recommended. Conclusion: There are many unmet needs in the management of functional impairment in chronic pain patients.

Detection of systemic inflammation in severely impaired chronic pain patients and effects of a multimodal pain rehabilitation program.

Background and aims Recent research indicates a previously unknown low-grade systemic or neurogenic inflammation in groups of chronic pain (CP) patients. Low-grade inflammation may have an important role in symptoms that have previously not been well depicted: widespread pain, tiredness and cognitive dysfunctions frequently seen in severely impaired CP patients. This study aimed to investigate the plasma inflammatory profile in a group of very complex CP patients at baseline and at a 1-year follow-up after participation in a cognitive behavior therapy (CBT)-based multimodal pain rehabilitation program (PRP). Methods Blood samples were collected from 52 well-characterized CP patients. Age- and sex-matched healthy blood donors served as controls. The samples were analyzed with a multiple Proximal Extension Analysis allowing a simultaneous analysis of 92 inflammation-related proteins consisting mainly of cytokines, chemokines and growth-factors. At follow-up, 1-year after participation in the RPR samples from 28 patients were analyzed. The results were confirmed by a multi-array technology that allows quantitative estimation. Results Clear signs of increased inflammatory activity were detected in the CP patients. Accepting a false discovery rate (FDR) of 5%, there were significant differences in 43/92 inflammatory biomarkers compared with the controls. In three biomarkers (CXCL5, SIRT2, AXIN1) the expression levels were elevated more than eight times. One year after the PRP, with the patients serving as their own controls, a significant decrease in overall inflammatory activity was found. Conclusions Our results indicate that the most impaired CP patients suffer from low-grade chronic systemic inflammation not described earlier with this level of detail. The results may have implications for a better understanding of the cluster of co-morbid symptoms described as the "sickness-syndrome" and the wide-spread pain seen in this group of patients. The decrease in inflammatory biomarkers noted at the follow-up after participation in the PRP may reflect the positive effects obtained on somatic and psycho-social mechanisms involved in the inflammatory process by a rehabilitation program. Besides the PRP, no major changes in medication or lifestyle factors were implemented during the same period. To our knowledge, this is the first study reporting that a PRP may induce inflammatory-reducing effects. Further studies are needed to verify the objective findings in CP patients and address the question of causality that remains to be solved. Implications The findings offer a new insight into the complicated biological processes underlying CP. It may have implications for the understanding of symptoms collectively described as the "sickness-syndrome" - frequently seen in this group of patients. The lowering of cytokines after the participation in a PRP indicate a new way to evaluate this treatment; by measuring inflammatory biomarkers.

Identifying characteristics of the most severely impaired chronic pain patients treated at a specialized inpatient pain clinic

Background and aimsPatients suffering from chronic nonmalignant pain constitute a heterogeneous population in terms of clinical presentation and treatment results. Few data are available about what distinguishes different groups in this huge population of patients with chronic persistent pain (CPP). A subgroup that is poorly studied, consists of the most severely impaired chronic pain patients. At the Uppsala University Hospital Pain Clinic, there is a specialized department accepting the most complex patients for rehabilitation. In the endeavour to improve and evaluate treatment for this subgroup, a better understanding of the complex nature of the illness is essential. This prospective study aimed to describe the characteristics of this subgroup of patients with CPP. MethodsSeventy-two consecutive patients enrolled in the Uppsala programme were evaluated. We collected data on demographics, type of pain and experienced symptoms other than pain using a checklist of 41 possible symptoms. Psychiatric comorbidity was assessed by a psychiatrist using a structured clinical interview. Quality of life (QoL), pain rating and medication/drug/alcohol usage were measured by validated questionnaires: SF-36, NRS, DUDIT and AUDIT. Concerning physical functioning and sick leave, a comparison was made with data from the Swedish Quality Register Registry for pain rehabilitation (SQRP). ResultsThe cohort consisted of 61% women and the average age was 45 (range 20–70) years. For this cohort, 74% reported being on sick leave or disability-pension. In the SQRP 59% were on sick leave at the time they entered the rehabilitation programmes [1]. On average, the study-population reported 22 symptoms other than pain, to be at a high rate of severity. Patients treated in conventional pain-rehabilitation programmes reported a mean of 10 symptoms in average. Symptoms reported with the highest frequency (>80%), were lethargy, tiredness, headache and difficulties concentrating. Seventy-six percent were diagnosed with a psychiatric disorder. Sixty-nine fulfilled the criteria for depression or depression/anxiety disorder despite that most (65%) were treated with psychotropic medication. Alcohol/drug abuse was minimal. Seventy-one percent were on opioids but the doses were moderate (<100mg) MEq. The pain rating was ≥7 (out of a maximum of 10) for 60% of the patients. ConclusionThis study describes what makes the subgroup of pain patients most affected by their pain special according to associated factors and comorbidity We found that they were distinguished by a high degree of psychiatric comorbidity, low physical functioning and extreme levels of symptom preoccupation/hypervigilance. Many severe symptoms additional to pain (e.g. depression/anxiety, tiredness, disturbed sleep, lack of concentration, constipation) were reported. The group seems hypervigilant, overwhelmed with a multitude of different symptoms on a high severity level. ImplicationsWhen treating this complex group, the expressions of the illness can act as obstacles to achieve successful treatment outcomes. The study provides evidence based information, for a better understanding of the needs concerning these pain patients. Our result indicates that parallel assessment and treatment of psychiatric comorbidities and sleep disorders combined with traditional rehabilitation, i.e. physical activation and cognitive reorganization are imperative for improved outcomes.

Detection of systemic inflammation in severely impaired chronic pain patients, and effects of a CBT-ACT-based multi-modal pain rehabilitation program

Abstract Aims A few previous studies indicate an ongoing of low-grade systemic inflammation in chronic pain patients (CPP) [1, 2]. In the present study we investigated the plasma inflammatory profile in severely impaired chronic pain patients. In addition we studied if there were any alterations in inflammation patterns at one-year follow up, after the patients had taken part in a CBT-ACT based 4 weeks in-hospital pain rehabilitation program (PRP). Methods Blood samples were collected from 52 well characterized chronic pain patients. Plasma from matched healthy blood donors were used as controls. At one year after the treatment program, 28 of the patients were available for follow up. Instead of only analyzing single inflammation-related substances, we used a new multiplex panel enabling the simultaneous analysis of 92 inflammation-related proteins, mainly cytokines and chemokines (Proseek Inflammation, Olink, Uppsala, Sweden). Multivariate statistics were used for analysis. Results Clear signs of increased inflammatory activity were detected in the pain patients. Accepting a false discovery rate (FDR) of 5%, there were significant differences in 43 of the 92 inflammatory biomarkers. The expression of 8 biomarkers were 4 times higher in patients compared to controls. Three biomarkers, CXCL5, SIRT2, AXIN1 were more than 8 times higher. The conventional marker for inflammation, CRP, did not differ. Of the 28 patients available for follow up one year after the intervention, all showed lower levels of the inflammatory biomarker initially raised. Conclusions The results indicate that CPP suffer from a low grade of chronic systemic inflammation, not detectable by CRP analysis. This may have implications for the general pain hypersensitivity, and other symptoms, often described in this group of patients. We conclude that inflammatory plasma proteins may be measureable molecular markers to distinguishes CPP from pain free controls, and that a CBT-ACT pain rehab program seem to decrease this inflammatory activity.

Mechanisms of cognitive impairment in chronic pain patients can now be studied preclinically by inducing cognitive deficits with an experimental animal model of chronic neuropathic pain

There is accumulating clinical evidence indicating that chronic ain may impair various aspects of cognition, such as attention, orking memory, decision-making and executive function (for a eview see e.g. [1]). The mechanisms underlying the chronic painssociated cognitive impairment are still poorly known. Human tudies allow unequivocal assessments of cognition and pain, but echanistic studies can be performed only to a limited extent in umans. In contrast, experimental animal studies allow controlled nvasive studies assessing molecular and cellular level mechanisms, hile the weakness of animal studies is that cognition and pain eed to be indirectly evaluated by assessing motor behavior in arious cognition-demanding tasks.

Memory impairment in chronic pain patients and the related neuropsychological mechanisms: a review.

This study provides a comprehensive review of the literature on memory impairment and the potential effective factors in patients with chronic pain. A literature search of databases PubMed, EMBASE, SpringerLink, and PsycINFO until September 2012 was conducted using the keywords ‘memory’ and ‘chronic pain’. The study emphasises on publications over the past 20 years. Memory impairment in chronic pain patients is substantial, but the aspects of memory (e.g. working memory, long-term memory, and autobiographical memory) in chronic pain patients and the potentially related factors (e.g. age, level of education, pain conditions, emotion, neural network, and use of analgesics) are modest. Memory impairment is interpreted with the attention-narrowing hypothesis and the capacity-reduction hypothesis. The currently available data and theory have explained memory impairment in chronic pain patients, but many controversies remain. Future research should focus on the subclinical characteristics of chronic pain, enlarging the sample size, and emphasise on the experimental intervention method and the cognitive neuroscience method.

The Evaluation of Permanent Impairment in Chronic Pain Patients

Pain is one of the most common causes of disability and work loss. However, patients with chronic pain have not been regarded as impaired persons in the Republic of Korea because of a lack of objective findings in those patients and difficulties in validating their genuine suffering and quantitative evaluation of pain. Here, the difficulties in the evaluation of impairment in chronic pain patients are discussed. In addition, guidelines for rating impairment in chronic pain patients, which are under development by the Korean Academy of Medical Sciences, are introduced.(Korean J Pain 2007; 20: 1-7)

Does cognitive change predict the outcome of cognitive-behavioural pain management?

Does cognitive change predict the outcome of cognitive-behavioural pain management? The psychometric properties of the Pain Cognitions Questionnaire (PCQ: Boston et al. , 1990), a brief self-rated measure of spontaneously occurring pain-related cognitions, were examined in a sample of 833 severely impaired chronic pain patients who completed it prior to and at several points following discharge from an inpatient cognitive-behavioural pain management programme. Principal components analysis allowed the identification of a two-factor structure which remained stable in this population across all points of assessment. The first factor (11 items) was labelled 'positive self statements'; the second (12 items), 'lack of mastery over pain'. Both factors showed adequate reliability (test-retest and internal consistency) and sensitivity to treatment-induced change; and preliminary support was obtained for criterion-related validity. The PCQ was then used to examine an underlying assumption of cognitive-behavioural therapies (CBT), viz that cognitive change mediates successful treatment outcome. Regression modelling was used to examine the extent to which change in PCQ scores from pre- to post-treatment was predictive of a range of outcomes including pain, depression, medication use and general functioning (Sickness Impact Profile scores) at one-month follow-up after controlling for pre-treatment levels of relevant variables. Results were broadly, though weakly, supportive of the cognitive hypothesis, with cognitive change accounting for up to 15% of outcome variance.

Estimating premorbid intelligence: Evaluating the revisions to the Oklahoma premorbid intelligence estimate formulae (OPIE vs. OPIE-R) with other premorbid indicators among Schizophrenic, brain-injured, and non-neurologically impaired chronic pain patients

Estimating premorbid intelligence: Evaluating the revisions to the Oklahoma premorbid intelligence estimate formulae (OPIE vs. OPIE-R) with other premorbid indicators among Schizophrenic, brain-injured, and non-neurologically impaired chronic pain patients

Estimating premorbid intelligence: Evaluating the revisions to the Oklahoma premorbid intelligence estimate formulae (OPIE vs. OPIE-R) with other premorbid indicators among Schizophrenic, brain-injured, and non-neurologically impaired chronic pain patients

Estimating premorbid intelligence: Evaluating the revisions to the Oklahoma premorbid intelligence estimate formulae (OPIE vs. OPIE-R) with other premorbid indicators among Schizophrenic, brain-injured, and non-neurologically impaired chronic pain patients

Opiate reduction in chronic pain patients: A comparison of patient-controlled reduction and staff controlled cocktail methods

This study compares the effectiveness of two methods of opiate reduction in 108 chronic pain patients during a 4 week inpatient pain management programme, and at 1-month and 6-month follow-up. Patients chose either the patient-controlled reduction (PCR) or cocktail reduction method, aiming to complete withdrawal by discharge. Use of opiates and other drugs was recorded, and psychological measures taken, at admission, at discharge, and at follow-ups. Patients who opted for the cocktail reduction method started at higher morphine equivalents ( P < 0.001), were less confident in their ability to cope without medication ( P < 0.05), and rated their everyday activities as more disrupted by pain ( P < 0.05). At discharge, 89% of the cocktail group were abstinent from opiates compared with 68% of the PCR group ( P < 0.05). By 1-month follow-up, the advantage of the cocktail method had disappeared, with no significant differences between the two groups in mean opiate dose, nor in the proportion of abstinent patients. This was the result of a greater return to opiate use in the cocktail group, with abstinence rates remaining unchanged in the PCR group. By 6-month follow-up, abstinence rates for the groups were equivalent, with 55% of patients remaining off opiates. By this stage, however, non-abstinent cocktail group patients were taking significantly larger doses of opiates than PCR patients ( P < 0.05), although in both groups, the dose was well below admission level. Admission opiate dose level was the best predictor both of abstinence at discharge and of subsequent opiate dose level in non-abstinent patients. This study demonstrates that both reduction methods can produce substantial reduction in opiate use by severely impaired chronic pain patients with long medication histories.

The effects of a cognitive-behavioral pain management programme on the quality of work and employment status of severely impaired chronic pain patients.

This study examined changes in employment status and quality of work in 109 chronic pain patients who underwent a cognitive-behavioural pain management course; 68% of patients were female, mean age was 45 years, mean pain chronicity 10.7 years, 70% had spinal pain, and mean impairment on the Sickness Impact Profile was 26%. Twenty-six per cent of patients were employed at pre-treatment; the remaining 74% had been unemployed for 4.3 years on average. Measures of work status and quality, mood, pain, self-efficacy and walking performance were taken before admission, and at 1-, 6-, and 12-month follow-ups. Among employed patients quality of work scores improved by 35% from pre- to post-treatment (p < 0.01). Thirty per cent of previously unemployed patients returned to work during the 1-year follow-up, although employment status fluctuated greatly during this period. Non-workers were generally more impaired than workers on most measures, but the same measures did not differentiate between those who successfully returned to work and those who remained unemployed.

Description of a brief scale to measure functional impairment in chronic pain patients

The acute myeloid leukemia 1 (AML1, RUNX1) transcription factor is a key regulator of hematopoietic differentiation both in embryonic stem cells and mature hematopoietic progenitors. The RUNX1 protein is thought to play a role in the control of progression through the cell cycle. We have shown that post-transcriptional regulation of RUNX1 activity occurs, in part, through phosphorylation. To investigate whether transit through the cell cycle is associated with changes in the phosphorylation of RUNX1, we have derived phospho-specific antibodies against three of the five major phosphorylation sites in the transcriptional activation domain of RUNX1, S276, S303 and S462. Using these antibodies we demonstrate that treatment of Jurkat T-cells with nocodazole, a G2/M blocking compound, causes an increase in phosphorylation of these three amino acids. By elutriating the Jurkat cells, we are able to demonstrate that these amino acids are normally phosphorylated at the G2/M phase of the cell cycle. Using in vivo inhibitors and in vitro assays this phosphorylation appears to be dependent on Cdk1. We find that RUNX1 degradation occurs at the G2/M–G1 transition and is regulated by both Cdc20 and phosphoryation, suggesting that the anaphase promoting complex plays a role in modifying the level of this protein. Regulation of the extent of phosphorylation of RUNX1 may play a role in controlling the degradation of the protein, implying that additional E3 ligases may also be involved.

Validation of a german pain description-scale as screening instrument for psychologic impairment in chronic pain patients

Validation of a german pain description-scale as screening instrument for psychologic impairment in chronic pain patients