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      Sleep and circadian rhythm disruption in schizophrenia†

      , PhD , PhD, , PhD , PhD, FRS , FRCPsych

      The British Journal of Psychiatry

      Royal College of Psychiatrists

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          Abstract

          Background

          Sleep disturbances comparable with insomnia occur in up to 80% of people with schizophrenia, but very little is known about the contribution of circadian coordination to these prevalent disruptions.

          Aims

          A systematic exploration of circadian time patterns in individuals with schizophrenia with recurrent sleep disruption.

          Method

          We examined the relationship between sleep-wake activity, recorded actigraphically over 6 weeks, along with ambient light exposure and simultaneous circadian clock timing, by collecting weekly 48 h profiles of a urinary metabolite of melatonin in 20 out-patients with schizophrenia and 21 healthy control individuals matched for age, gender and being unemployed.

          Results

          Significant sleep/circadian disruption occurred in all the participants with schizophrenia. Half these individuals showed severe circadian misalignment ranging from phase-advance/delay to non-24 h periods in sleep-wake and melatonin cycles, and the other half showed patterns from excessive sleep to highly irregular and fragmented sleep epochs but with normally timed melatonin production.

          Conclusions

          Severe circadian sleep/wake disruptions exist despite stability in mood, mental state and newer antipsychotic treatment. They cannot be explained by the individuals' level of everyday function.

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          Most cited references 46

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          The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research.

          Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
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            Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia.

            Many risk genes interact synergistically to produce schizophrenia and many neurotransmitter interactions have been implicated. We have developed a circuit-based framework for understanding gene and neurotransmitter interactions. NMDAR hypofunction has been implicated in schizophrenia because NMDAR antagonists reproduce symptoms of the disease. One action of antagonists is to reduce the excitation of fast-spiking interneurons, resulting in disinhibition of pyramidal cells. Overactive pyramidal cells, notably those in the hippocampus, can drive a hyperdopaminergic state that produces psychosis. Additional aspects of interneuron function can be understood in this framework, as follows. (i) In animal models, NMDAR antagonists reduce parvalbumin and GAD67, as found in schizophrenia. These changes produce further disinhibition and can be viewed as the aberrant response of a homeostatic system having a faulty activity sensor (the NMDAR). (ii) Disinhibition decreases the power of gamma oscillation and might thereby produce negative and cognitive symptoms. (iii) Nicotine enhances the output of interneurons, and might thereby contribute to its therapeutic effect in schizophrenia.
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              Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire.

              The Primary Care Evaluation of Mental Disorders (PRIME-MD) was developed as a screening instrument but its administration time has limited its clinical usefulness. To determine if the self-administered PRIME-MD Patient Health Questionnaire (PHQ) has validity and utility for diagnosing mental disorders in primary care comparable to the original clinician-administered PRIME-MD. Criterion standard study undertaken between May 1997 and November 1998. Eight primary care clinics in the United States. Of a total of 3000 adult patients (selected by site-specific methods to avoid sampling bias) assessed by 62 primary care physicians (21 general internal medicine, 41 family practice), 585 patients had an interview with a mental health professional within 48 hours of completing the PHQ. Patient Health Questionnaire diagnoses compared with independent diagnoses made by mental health professionals; functional status measures; disability days; health care use; and treatment/referral decisions. A total of 825 (28%) of the 3000 individuals and 170 (29%) of the 585 had a PHQ diagnosis. There was good agreement between PHQ diagnoses and those of independent mental health professionals (for the diagnosis of any 1 or more PHQ disorder, kappa = 0.65; overall accuracy, 85%; sensitivity, 75%; specificity, 90%), similar to the original PRIME-MD. Patients with PHQ diagnoses had more functional impairment, disability days, and health care use than did patients without PHQ diagnoses (for all group main effects, P<.001). The average time required of the physician to review the PHQ was far less than to administer the original PRIME-MD (<3 minutes for 85% vs 16% of the cases). Although 80% of the physicians reported that routine use of the PHQ would be useful, new management actions were initiated or planned for only 117 (32%) of the 363 patients with 1 or more PHQ diagnoses not previously recognized. Our study suggests that the PHQ has diagnostic validity comparable to the original clinician-administered PRIME-MD, and is more efficient to use.
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                Author and article information

                Journal
                Br J Psychiatry
                Br J Psychiatry
                bjprcpsych
                The British Journal of Psychiatry
                Royal College of Psychiatrists
                0007-1250
                1472-1465
                April 2012
                1 April 2012
                : 200
                : 4
                : 308-316
                Affiliations
                Nuffield Laboratory of Ophthalmology, University of Oxford, John Radcliffe Hospital, Oxford
                Surrey Sleep Research Centre and Centre for Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford
                Nuffield Laboratory of Ophthalmology, University of Oxford, John Radcliffe Hospital, Oxford
                Institute of Neurology, University College London, The National Hospital for Neurology and Neurosurgery, London, UK
                Author notes
                Correspondence: Russell G. Foster, University of Oxford, Level 6, West Wing, The John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK. Email: russell.foster@ 123456eye.ox.ac.uk
                [†]

                See editorial, pp. [Related article:]273-274, this issue.

                Article
                10.1192/bjp.bp.111.096321
                3317037
                22194182
                Royal College of Psychiatrists

                Royal College of Psychiatrists, This paper accords with the Wellcome Trust Open Access policy and is governed by the licence available at http://www.rcpsych.ac.uk/pdf/Wellcome%20Trust%20licence.pdf

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                Clinical Psychology & Psychiatry

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