ABSTRACT
To translate and validate the Pittsburgh Sleep Quality Index [PSQI], a standardized self-administered questionnaire for the assessment of subjective sleep quality into the Urdu language. Validation study. Mayo Hospital, Lahore, from March to April 2012. The PSQI was translated into Urdu following standard guidelines. The final Urdu version [PSQI-U] was administered to 200 healthy volunteers comprising medical students, nursing staff and doctors. Inter-item correlation was assessed by calculating Cronbach alpha. Correlation of component scores with global score was assessed by calculating Spearman correlation coefficient. Correlation between global PSQI-U scores at baseline with global scores for each PSQI-U and PSQI-E at 4-week interval was evaluated by calculating Spearman correlation coefficient. Moreover, scores on individual items of the scale at baseline were compared with respective scores after 4-week by t-test. One hundred and eighty five [185] participants completed the PSQI-U at baseline. The Cronbach alpha for PSQI-U was 0.56. Scores on individual components of the PSQI-U and composite scores were all highly correlated with each other [all p-values < 0.01]. Composite scores for PSQI-U at baseline and PSQI-E at 4-week interval were also highly correlated with each other [Spearman correlation coefficient 0.74, p-value < 0.01] indicating good linguistic interchangeability. Composite scores for PSQI-U at baseline and at 4-week interval were positively correlated with each other [Spearman correlation coefficient 0.70, p < 0.01] indicating good test-retest reliability. The PSQI-U is a valid and reliable instrument for the assessment of sleep quality. It shows good linguistic interchangeability and test-retest reliability in comparison to the original English version when applied to individuals who speak the Urdu language. The PSQI-U can be a tool either for clinical management or research
ABSTRACT
The purpose of this article is to review the evidence linking depression with inflammation, to examine the bi-directional relationship between the neuro-humeral circuitry of depression and the inflammatory response, and point out new treatment implications of these ideas. The evidence available is in areas of genetic links, association of depression with raised inflammatory markers such as Tumour Necrosis Factor [TNF]-alpha, Interleukin [IL]-1, IL-6, co-morbidity of depression with inflammatory medical illnesses, administration of cytokines leading to depression, and the recognition that anti-depressants have anti-inflammatory and neuro-protective properties. Inflammatory response and mood regulation constitute a system of bi-directional communication such that inflammatory cytokines can penetrate the CNS and influence behavior. Activation of the CNS cytokine network leads to a cascade of effects such as disturbed metabolism of amino acids, neurotoxicity, diminished neurotrophic support, decreased neurogenesis, impaired negative feedback regulation of HPA axis function and glucocorticoid resistance. Treatment implications include strategies to screen for patients with increased inflammatory activity, possible treatment with anti-inflammatory agents, and the recognition of new target areas for antidepressant medications. A literature search for articles published during the last ten years was conducted using various combinations of key words ['depression', 'inflammation', 'cytokines', 'immune system', 'interleukins'] utilizing the databases Google Scholar and PubMed. An outline of the most relevant aspects of the role of inflammatory processes in depression was created. Major papers, including other review articles, were identified in accordance with our outline. These articles were subsequently hand searched and reviewed individually for further references of significance. The inflammatory response leading to formation of inflammatory cytokines plays a significant role in the pathophysiology of depression, and this has important implications with regards to new and personalized treatment of depression