Sleep of good quantity and quality is considered a biologically important resource necessary to maintain homeostasis of pain-regulatory processes. To assess the role of chronic sleep disturbances in pain processing, we conducted laboratory pain testing in subjects with primary insomnia. Seventeen participants with primary insomnia (mean±SEM 22.6±0.9 years, 11 women) were individually matched with 17 healthy participants. All participants completed daily sleep and pain diaries over a 2-week period. Laboratory pain testing was conducted in a controlled environment and included (1) warmth detection threshold testing, (2) pain sensitivity testing (threshold detection for heat and pressure pain), and (3) tests to access pain-modulatory mechanisms (temporal summation and pain inhibition). Primary insomnia subjects reported experiencing spontaneous pain on twice as many days as healthy controls during the at-home recording phase (p<0.05). During laboratory testing, primary insomnia subjects had lower pain thresholds than healthy controls (p<0.05 for heat pain detection threshold, p<0.08 for pressure pain detection threshold). Unexpectedly, pain facilitation, as assessed with temporal summation of pain responses, was reduced in primary insomnia compared to healthy controls (p<0.05). Pain inhibition, as assessed with the diffuse noxious inhibitory control paradigm (DNIC), was attenuated in insomnia subjects when compared to controls (p<0.05). Based on these findings, we hypothesize that pain-inhibitory circuits in patients with insomnia are in a state of constant activation to compensate for ongoing subclinical pain. This constant activation ultimately results in a ceiling effect of pain-inhibitory efforts, as indicated by the inability of the system to adequately function during challenge.

Postpartum depression (PPD) is a serious public health problem affecting 10% to 15% of women during the first year after delivery with negative consequences for both mother and infant. There is a need for evidence-based interventions to treat this disorder. Thus, the purpose of this study was to systematically review the literature regarding group treatment for PPD to determine the current state of knowledge regarding the efficacy of this treatment modality for reducing depressive symptoms in postpartum women. A systematic search of published and unpublished literature using the electronic databases Medline, CINAHL, PsycINFO, Cochrane Database, Cochrane Central Register of Controlled Trials, Current Controlled Trials, and Dissertation Abstracts through March 2011, supplemented by hand searches, identified 11 studies which met inclusion criteria: six were randomized controlled trials and five were non-randomized trials which utilized non-equivalent control or comparison groups. All but one study showed statistically significant improvement in depression scores from pretreatment to post-treatment, suggesting that group treatment is effective in reducing PPD symptoms. The review provides initial support for the role of group therapy in the treatment of PPD; however, caution is advised in making generalized interpretations of the findings as there was considerable heterogeneity of the studies included and the quality of the studies was mixed. Overall, the review reveals significant gaps in the current evidence base for group treatment for PPD and recommendations for further research is discussed.

Background The nucleus accumbens (NAc) plays a key role in brain reward processes including drug seeking and reinstatement. Several anatomical, behavioral, and neurochemical studies discriminate between the limbic-associated shell and the motor-associated core regions. Less studied is the fact that the shell can be further subdivided into a dorsomedial shell (NAcDMS) and an intermediate zone (NAcINT) based on differential expression of transient c-Fos and long-acting immediate-early gene ΔFosB upon cocaine sensitization. These disparate expression patterns suggest that NAc shell subregions may play distinct roles in reward-seeking behavior. In this study, we examined potential differences in the contributions of the NAcDMS and the NAcINT to reinstatement of reward-seeking behavior after extinction. Methods Rats were trained to intravenously self-administer cocaine, extinguished, and subjected to a reinstatement test session consisting of either an intracranial microinfusion of amphetamine or vehicle targeted to the NAcDMS or the NAcINT. Results Small amphetamine microinfusions targeted to the NAcDMS resulted in statistically significant reinstatement of lever pressing, whereas no statistical difference was observed for microinfusions targeted to the NAcINT. No significant difference was found for vehicle microinfusions in either case. Conclusion These results suggest heterogeneity in the behavioral relevance of NAc shell subregions, a possibility that can be tested in specific neuronal populations in the future with recently developed techniques including optogenetics.