Changes in pain and quality of life in depressed individuals with spinal cord injury: does type of pain matter?

OBJECTIVE: To examine the association of neuropathic and nociceptive pain severity and interference with quality of life (QoL) in persons with spinal cord injury (SCI) who underwent a randomized controlled 12-week trial of an antidepressant to treat depression. A secondary objective was to assess the effect of changes in pain on mobility and physical independence. DESIGN: Multivariable ANCOVA models controlling for relevant demographic covariates, treatment condition, and baseline pain and QoL were used. SETTING: Six rehabilitation centers. PARTICIPANTS: Of the 133 persons who were randomized into the trial, 108 provided pain severity and interference ratings through follow-up. INTERVENTIONS: Not applicable. OUTCOME MEASURES: The Satisfaction with Life Scale and the physical and mental component summary scores of the 12-Item Short-Form Health Survey (SF-12). Secondary outcome measures included the mobility and physical independence subscales of the Craig Handicap Assessment and Reporting Technique (CHART). RESULTS: Broadly, few associations between pain and QoL were evident. Results revealed relationships between lower baseline nociceptive pain interference and higher satisfaction with life and mental health-related QoL at 12 weeks. Similarly, lower neuropathic pain interference was associated with change in physical independence, but unrelated to mobility. CONCLUSIONS: Pain interference over time may be differentially related to QoL outcomes based on the type of pain following SCI, but overall, there were no extensive relationships between pain and QoL in this sample of depressed persons with SCI.

Mental health and outcomes in primary total joint arthroplasty.

A consecutive series of 640 total joint arthroplasty patients was interviewed before surgery and at a minimum of 2 years following surgery. Statistical analyses were conducted to examine the effect of psychological distress and other patient characteristics on outcomes (Western Ontario and McMaster Universities Osteoarthritis Index, Short Form 36, and Quality of Well-Being index). Before and after surgery, distressed subjects had significantly lower scores than nondistressed subjects for most dependent measures (P range, .05 ≤ .001). All mean outcomes improved by follow-up in both groups (P ≤ .001) except mental health scores of nondistressed subjects. Stepwise regression analysis found that low baseline mental health score, non-Hispanic ethnicity, and fewer years since procedure were the strongest predictors of worse Western Ontario and McMaster Universities Osteoarthritis Index scores at follow-up. Although the magnitude of improvement is similar to nondistressed subjects, distressed patients do not achieve comparable functional and psychosocial outcomes.

Assessing the progression of mild cognitive impairment to Alzheimer's disease: current trends and future directions.

With the advent of advances in biomarker detection and neuropsychological measurement, prospects have improved for identifying and tracking the progression of Alzheimer's disease (AD) from its earliest stages through dementia. While new diagnostic techniques have exciting implications for initiating treatment earlier in the disease process, much work remains to be done to optimize the contributions of the expanding range of tools at the disposal of researchers and clinicians. The present paper examines recent work in cerebrospinal fluid biomarkers, magnetic resonance imaging, positron emission tomography, neuropsychological measures, and functional assessment. The strengths and weaknesses of current methodologies are explored and discussed. It is concluded that AD from its mild cognitive impairment state through dementia represents a continuous process, and that progression over time can best be accomplished by interval-level variables. Biomarkers that are most sensitive to early AD may not be the most optimal for monitoring longitudinal change, and it is likely that multivariate models incorporating cognitive measures, functional variables and biomarker data will be the most fruitful avenues for future research.

Oxytocin attenuates atherosclerosis and adipose tissue inflammation in socially isolated ApoE-/- mice.

OBJECTIVE: To determine the effect of exogenous oxytocin (OT) administration on inflammation and atherosclerosis in socially isolated apoE(-/-) mice. Hyperlipidemic animals housed in isolated or stressful social environments display more extensive atherosclerosis than those in an affiliative social environment. The neurohypophyseal peptide OT may be involved in both affiliative social behavior and cardiovascular homeostasis, suggesting a role in mediating the benefits of positive social interactions on atherosclerosis. METHODS: A total of 43, 12-week-old, apoE(-/-) mice were surgically implanted with osmotic minipumps containing OT (n = 23) or vehicle (n = 20). Blood samples were taken at baseline and after 6 weeks and 12 weeks of treatment. After 12 weeks of treatment, animals were killed, and samples of adipose tissue were dissected from a subset of OT-treated (n = 12) and vehicle-treated (n = 12) animals and incubated in culture media for 6 hours. Media samples were analyzed for interleukin (IL)-6 concentration corrected by sample dry weight. Aortas were dissected, formalin-fixed, and stained with oil-red O for en face quantification of lesion area. t tests were used to compare group means on measures of percent lesion area and IL-6 concentrations. RESULTS: There were no group differences in plasma lipids. Adipose tissue samples taken from OT-treated animals secreted significantly less IL-6 over 6 hours (p < .01). OT-treated animals displayed significantly less atherosclerosis in the thoracic aorta (p < .05). CONCLUSIONS: These results indicate that peripheral OT administration can inhibit atherosclerotic lesion development and adipose tissue inflammation, suggesting a potential role for this neuropeptide in mediating the benefits of stable group housing on atherosclerosis.

Oxytocin attenuates NADPH-dependent superoxide activity and IL-6 secretion in macrophages and vascular cells.

Oxytocin is synthesized and released in the heart and vasculature, tissues that also express oxytocin receptors. Although it has been established this intrinsic cardiovascular oxytocin system is important in normal homeostatic cardiac and vascular regulation, a role for this system in cardiovascular pathophysiology has not been investigated. The current study examined the influence of oxytocin on mechanisms in atherogenesis, oxidative stress, and inflammation in cultured human vascular cells, THP-1 monocytes, and macrophages. Oxytocin receptor protein and mRNA expression, NADPH-dependent superoxide activity, and interleukin-6 secretion were measured. Results demonstrated oxytocin receptor protein and mRNA in THP-1 monocytes and macrophages. Incubation of cells at physiological levels of oxytocin significantly decreased basal and stimulated NADPH-dependent superoxide activity in vascular cells, monocytes, and macrophages by 24-48%. Oxytocin also attenuated interleukin-6 secretion from stimulated THP-1 macrophages and endothelial cells by 56 and 26%, respectively. These findings suggest that oxytocin attenuates vascular oxidative stress and inflammation, two important pathophysiological processes in atherosclerosis. The fact that oxytocin receptors are found in monocytes and macrophages, and oxytocin decreases both superoxide production and release of a proinflammatory cytokine from these cells, suggests a potentially larger role for oxytocin in the attenuation of disease.

The effect of social environment on markers of vascular oxidative stress and inflammation in the Watanabe heritable hyperlipidemic rabbit.

OBJECTIVE: Previous research demonstrated that social environment can influence progression of atherosclerosis in the Watanabe Heritable Hyperlipidemic (WHHL) rabbit. This study examined the effect of social environment on markers of oxidative stress and inflammation to clarify the physiological pathways potentially responsible for the influence of social environment on disease. METHODS AND RESULTS: WHHL rabbits were assigned to 1 of 3 social groups: an unstable group, in which unfamiliar rabbits were paired daily, with the pairing switched each week; a stable group, in which littermates were paired daily; and an individually-caged group. The stable group engaged in more affiliative social behavior than the unstable group. The unstable group showed more agonistic behavior compared with the stable group and higher C-reactive protein levels than the individually caged group. The individually caged group was behaviorally sedentary, had higher 24-hour urinary catecholamine levels than the other groups, and exhibited higher NAD(P)H-oxidase activity in the aortic arch relative to the stable group. CONCLUSIONS: The results suggest that social environment creates distinct behavioral contexts that can affect markers of inflammation and oxidative stress early in the development of atherosclerosis. Specifically, physical inactivity associated with individual caging affects indices of oxidative stress and inflammation. These pathophysiological markers may help to explain behaviorally related differences in the extent of atherosclerosis observed in prior studies.