Identification and Characterization of Unique Subgroups of Chronic Pain Individuals with Dispositional Personality Traits.

Objective. The current study attempted to identify and characterize distinct CP subgroups based on their level of dispositional personality traits. The secondary objective was to compare the difference among the subgroups in mood, coping, and disability. Methods. Individuals with chronic pain were assessed for demographic, psychosocial, and personality measures. A two-step cluster analysis was conducted in order to identify distinct subgroups of patients based on their level of personality traits. Differences in clinical outcomes were compared using the multivariate analysis of variance based on cluster membership. Results. In 229 participants, three clusters were formed. No significant difference was seen among the clusters on patient demographic factors including age, sex, relationship status, duration of pain, and pain intensity. Those with high levels of dispositional personality traits had greater levels of mood impairment compared to the other two groups (p < 0.05). Significant difference in disability was seen between the subgroups. Conclusions. The study identified a high risk group of CP individuals whose level of personality traits significantly correlated with impaired mood and coping. Use of pharmacological treatment alone may not be successful in improving clinical outcomes among these individuals. Instead, a more comprehensive treatment involving psychological treatments may be important in managing the personality traits that interfere with recovery.

The Long Term Role of Anxiety Sensitivity and Experiential Avoidance on Pain Intensity, Mood, and Disability among Individuals in a Specialist Pain Clinic.

Background. Anxiety sensitivity (AS) and experiential avoidance (EA) have been shown to have an interactive effect on the response an individual has to chronic pain (CP) potentially resulting in long term negative outcomes. Objective. The current study attempted to (1) identify distinct CP subgroups based on their level of EA and AS and (2) compare the subgroups in terms of mood and disability. Methods. Individuals with CP were recruited from an academic pain clinic. Individuals were assessed for demographic, psychosocial, and personality measures at baseline and 1-year follow-up. A cluster analysis was conducted to identify distinct subgroups of patients based on their level of EA and AS. Differences in clinical outcomes were compared using the Repeated Measures MANOVA. Results. From a total of 229 participants, five clusters were formed. Subgroups with lower levels of AS but similar high levels of EA did not differ in outcomes. Mood impairment was significantly greater among those with high levels of EA compared to lower levels (p < 0.05). Significant improvement in disability (p < 0.05) was only seen among those with lower levels of EA and AS. Conclusions. This cluster analysis demonstrated that EA had a greater influence on mood impairment, while both EA and AS levels affected disability outcomes among individuals with CP.

Psychological Distress in Out-Patients Assessed for Chronic Pain Compared to Those with Rheumatoid Arthritis.

Background. Patients diagnosed with chronic pain (CP) and rheumatoid arthritis (RA) represent two samples with overlapping symptoms, such as experiencing significant pain. Objectives. To compare the level of psychological distress among patients diagnosed CP attending a specialist pain clinic with those attending a specialist RA clinic. Measures. A cross-sectional study was conducted at an academic specialist chronic pain and rheumatology clinic. Participants. 330 participants included a CP group (n = 167) and a RA group (n = 163) completed a booklet of questionnaires regarding demographic characteristics, duration, and severity of their pain. Psychological and personality variables were compared between the CP and RA participants using a Multivariate Analysis of Covariance (MANCOVA). Results. Level of psychological distress based on the subscales of the DASS (depression, anxiety, and stress), PASS (escape avoidance, cognitive anxiety, fear of pain, and physiological anxiety), and PCS (rumination, magnification, and helplessness) was significantly higher in the CP group compared to the RA group. Categorization of individuals based on DASS severity resulted in significant differences in rates of depression and anxiety symptoms between groups, with a greater number of CP participants displaying more severe depressive and anxiety symptoms. Discussion and Conclusions. This study found greater levels of psychological distress among CP individuals referred to an academic pain clinic when compared to RA patients referred to an academic rheumatology clinic.

Does the treatment of spastic equinovarus deformity following stroke with botulinum toxin increase gait velocity? A systematic review and meta-analysis.

While botulinum toxin-A (BT-A) has been used to treat lower-limb focal spasticity successfully, its effect on characteristics of gait has not been well defined. The objective of this systematic review was to establish the treatment effect associated with the use of BT-A for equinovarus to improve gait velocity following stroke, using a meta-analytic technique. Relevant studies were identified through a literature search encompassing the years 1985 to November 2009. Studies were included if (i) the sample was composed of adult subjects recovering from either first or subsequent stroke, presenting with spastic equinovarus deformity of the ankle preventing full active dorsiflexion, and (ii) subjects who received BT-A were compared with subjects who had received a placebo, or (iii) in the absence of a placebo-controlled condition, subject had received BT-A and was assessed before and after treatment. A standardized mean difference (SMD) ± standard error and 95% confidence interval (CI) for gait velocity between the treatment and control group was calculated for each study, using Hedges's g, and the results pooled. Eight trials, five randomized controlled trials, and three single group intervention studies were included. Data representing 228 subjects were available for pooled analysis. Treatment with BT-A was associated with a small improvement in gait velocity (Hedge's g = 0.193 ± 0.081; 95% CI: 0.033 to 0.353, P < 0.018) representing an increase of 0.044 meters/s. The use of BT-A for lower-limb post-stroke equinovarus because of spasticity was associated with a small, but statistically significant increase in gait velocity.

A systematic review of the therapeutic interventions for heterotopic ossification after spinal cord injury.

STUDY DESIGN: Systematic review. OBJECTIVE: To conduct a systematic review of the effectiveness of interventions used to prevent and treat heterotopic ossification (HO) after spinal cord injury (SCI). SETTING: St Joseph's Parkwood Hospital, London, Ontario, Canada. METHODS: MEDLINE, CINAHL, EMBASE and PsycINFO databases were searched for articles addressing the treatment of HO after SCI. Studies were selected by two reviewers and were only included for analysis if at least 50% of the subjects had an SCI, there were at least three SCI subjects and if the study subjects participated in a treatment or intervention. Study quality was assessed by two independent reviewers using the Downs and Black evaluation tool for all studies, as well as the PEDro assessment scale for randomized control trials only. Levels of evidence were assigned using a modified Sackett scale. RESULTS: A total of 13 studies met the inclusion criteria. The selected articles were divided into prevention or treatment of post-SCI HO. Nonsteroidal anti-inflammatory drugs (NSAIDs), warfarin, and pulse low-intensity electrogmagnetic field (PLIMF) therapy were reviewed as prophylactic measures. Bisphosphonates, radiotherapy and excision were reviewed as treatments of post-SCI HO. CONCLUSIONS: Pharmacological treatments of HO after SCI had the highest level of research evidence supporting their use. Of these, NSAIDs showed greatest efficacy in the prevention of HO when administered early after an SCI, whereas bisphosphonates were the intervention with strongest supportive evidence once HO had developed. Of the non-pharmacological interventions, PLIMF was supported by the highest level of evidence; however, more research is needed to fully understand its role.

Elevated serum titers of proinflammatory cytokines and CNS autoantibodies in patients with chronic spinal cord injury.

This study characterized the proinflammatory cytokines, interleukin-2 (IL-2) and tumor necrosis factor alpha (TNFalpha), the antiinflammatory cytokines, IL-4 and IL-10, autoantibodies specific for GM1 ganglioside (anti-GM1), IgG and IgM, and myelin-associated glycoprotein (anti-MAG), in the sera of infection-free, chronic (>12 months), traumatically injured SCI patients (n = 24). Healthy able-bodied subjects (n = 26) served as controls. The proinflammatory cytokines and anti-GM1 antibodies were of particular interest as they have been implicated in an autoimmune "channelopathy" component to central and peripheral conduction deficits in various chronic neuroinflammatory diseases. Antibody and cytokine titers were established using enzyme-linked immunosorbent assays (ELISA). The mean anti-GM(1) (IgM) titer value for the SCI group was significantly higher (p < 0.05) than controls. The SCI group also demonstrated significantly higher titers (p < 0.05) of IL-2 and TNF alpha than controls. No differences were found between the SCI group and control group mean levels of IL-4 or IL-10. Overall, the serum of 57% of SCI patients contained increased levels of autoantibodies or proinflammatory cytokines relative to control values. These results provide preliminary support for the hypothesis that chronic immunological activation in the periphery occurs in a subpopulation of chronic SCI patients. It remains to be established whether elevated serum titers of proinflammatory cytokines and autoantibodies against GM1 are beneficial to the patients or whether they are surrogate markers of a channelopathy that compounds the neurological impairment associated with traumatic axonopathy or myelinopathy.