Neuropsychological and neuroanatomical sequelae of chronic non-malignant pain and opioid analgesia.

BACKGROUND: The pervasive disease of chronic pain is a common challenge for the clinical rehabilitation professional. Concurrent with physical and emotional symptoms, pain-related cognitive impairment has been reported. Although opioid analgesics are frequently prescribed, concern exists that opioids possess adverse cognitive effects of their own. OBJECTIVES: To review the neuropsychological and neuroanatomical sequelae of chronic non-malignant pain and opioid therapy, to clarify roles and benefits of neuropsychological assessment in a chronic pain population, and to provide recommendations for clinical practice and future research. METHODS: This non-systematic review sought to provide a comprehensive synthesis of relevant neurobiology, neuroimaging, neuropsychological, and rehabilitation research literatures. We included citations from seminal and current texts as well as relevant original and review articles from 1980-2012 in PubMed and PubMedCentral online research databases. DISCUSSION AND SUMMARY/CONCLUSIONS: To date, evidence from opioid studies suggests only mild deficits in specific cognitive domains (e.g., memory, attention/concentration) and only under specific conditions (e.g., dose escalations). Additionally, neuroimaging and neuropsychological evidence suggests that pain itself results in cognitive sequelae. Methodological improvements in future research will allow for better delineation of the contributing effects of pain and opioids, with an overall goal of improving evidence-based clinical treatment recommendations.

Catastrophizing, acceptance, and interference: laboratory findings, subjective report, and pain willingness as a moderator.

OBJECTIVE: The present study investigated the effects of both catastrophizing and the pain willingness component of acceptance on interference in daily activities and task performance during experimentally induced ischemic pain. In addition, the potential moderating role of pain willingness on the relationship between catastrophizing and degree of pain interference was also examined. DESIGN: Sixty-seven persons with chronic low back pain completed measures of catastrophizing, acceptance, and daily pain interference. Participants underwent an ischemic pain induction procedure during which a Stroop-like task was administered. MAIN OUTCOME MEASURES: Self-reported pain interference and observed performance on a Stroop-like task during induced pain. RESULTS: The pain willingness component of acceptance and catastrophizing both contributed significantly to self-reports of pain interference. However, levels of pain willingness had an effect much stronger than the negative effects associated with catastrophizing with respect to observed pain interference during induced pain. Results also indicated that pain willingness serves as a moderator in the relationship between catastrophizing and task performance during induced pain. CONCLUSION: The pain willingness factor of acceptance and catastrophizing both appear to be strong predictors for self-reported pain interference. During an objective assessment of pain interference, however, pain willingness shows a stronger effect and attenuates the negative impact of catastrophizing on task functioning.

Depressive symptoms and pain evaluations among persons with chronic pain: catastrophizing, but not pain acceptance, shows significant effects.

Cognitive factors such as catastrophic thoughts regarding pain, and conversely, one's acceptance of that pain, may affect emotional functioning among persons with chronic pain conditions. The aims of the present study were to examine the effects of both catastrophizing and acceptance on affective ratings of experimentally induced ischemic pain and also self-reports of depressive symptoms. Sixty-seven individuals with chronic back pain completed self-report measures of catastrophizing, acceptance, and depressive symptoms. In addition, participants underwent an ischemic pain induction procedure and were asked to rate the induced pain. Catastrophizing showed significant effects on sensory and intensity but not affective ratings of the induced pain. Acceptance did not show any significant associations, when catastrophizing was also in the model, with any form of ratings of the induced pain. Catastrophizing, but not acceptance, was also significantly associated with self-reported depressive symptoms when these two variables were both included in a regression model. Overall, results indicate negative thought patterns such as catastrophizing appear to be more closely related to outcomes of perceived pain severity and affect in persons with chronic pain exposed to an experimental laboratory pain stimulus than does more positive patterns as reflected in measures of acceptance.

Systemic lupus erythematosus in three ethnic groups. X. Measuring cognitive impairment with the cognitive symptoms inventory.

OBJECTIVE: To determine the factor structure of the Cognitive Symptoms Inventory (CSI) in patients with systemic lupus erythematosus (SLE) participating in a multiethnic longitudinal study of outcome, the Lupus in Minority populations, Nature versus nurture (LUMINA) study. METHODS: LUMINA patients of Hispanic (n = 48), African American (n = 64), and Caucasian (n = 44) ethnicity who had a study visit (enrollment or followup) between January 1 and September 30, 2000 were included. Patients completed the CSI, a 21-item self-report measure of cognitive function. Sociodemographic, clinical, immunologic, psychosocial, and behavioral variables were ascertained per protocol and as previously described. Data were analyzed with SPSS. The factor structure of the CSI was determined using the principal axis method with oblique rotation as decided by Gorsuch. All factors having an Eigenvalue greater than 1 were considered. A 4-factor solution was derived that accounted for 42.6% of the common variance. The correlations between patient factor scale scores and variables from the demographic, clinical, psychosocial, and behavioral domains were then examined. RESULTS: The four factors and their respective variance are, Attention/Concentration (28.8%), Pattern Recognition/Activity Management (5.7%), Intermediate Memory (4.7%), and Initiation of Executive Functions (3.4%); each factor correlated with the total CSI score. Overall, patients' factor scale scores were positively and significantly correlated with other measures of cognitive dysfunction such as the Systemic Lupus Activity Measure (neuromotor domain) or the Systemic Lupus International Collaborating Clinics Damage Index (neurocognitive impairment), as well as with measures of fatigue, maladaptive coping skills, poor mental functioning, poor social support, and helplessness. They were, however, not correlated with sociodemographic or clinical variables. CONCLUSIONS: In addition to demonstrating that the CSI can be used to measure cognitive impairment in patients with SLE in the research setting, we have determined a 4-factor solution for the CSI that appears to have adequate metric properties. At present, the CSI may best be used as a screen for difficulties in daily activities involving intermediate memory, concentration, attention, and executive function. Nevertheless, further work with the CSI items and factor scales is necessary to establish internal and test-retest reliability of the factor scales; and provide additional evidence of the convergent and predictive validity of these scales in larger samples of patients from each ethnic subgroup.

Is fibromyalgia a neurologic disease?

Fibromyalgia (FM) is characterized by abnormal pain sensitivity in response to diverse stimuli as well as persistent widespread pain and other symptoms such as fatigue and sleep disturbance. Progress has been made in identifying factors that contribute to the etiopathogenesis of abnormal pain sensitivity, but there is no single model of pathophysiology or treatment of FM that has gained wide acceptance among health care professionals. We review the literature on the etiopathogenesis of abnormal pain sensitivity in FM and describe an explanatory model that serves as a source of testable hypotheses in our laboratory. This model posits that interactions of exogenous (e.g., environmental stressors) and endogenous (e.g., neuroendocrine dysfunction) abnormalities in genetically predisposed individuals lead to a final common pathway, i.e., alterations in central nervous system function and neuropeptide production that underlie central sensitization and abnormal pain sensitivity. This model also suggests that efforts to develop and evaluate treatments for FM should focus on interventions with direct or indirect effects on central functions that influence pain sensitivity.