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9 results

  • The temporal dynamics of sleep disturbance and psychopathology in psychosis: a digital sampling study

  • Nicholas Meyer, Dan W. Joyce, Chris Karr, Maarten de Vos, Derk-Jan Dijk, Nicholas C. Jacobson, James H. MacCabe
  • Journal:
    Psychological Medicine / Volume 52 / Issue 13 / October 2022
    Published online by Cambridge University Press:
    12 January 2021, pp. 2741-2750
    Print publication:
    October 2022
    • Article
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  • Background

    Sleep disruption is a common precursor to deterioration and relapse in people living with psychotic disorders. Understanding the temporal relationship between sleep and psychopathology is important for identifying and developing interventions which target key variables that contribute to relapse.

    Methods

    We used a purpose-built digital platform to sample self-reported sleep and psychopathology variables over 1 year, in 36 individuals with schizophrenia. Once-daily measures of sleep duration and sleep quality, and fluctuations in psychopathology (positive and negative affect, cognition and psychotic symptoms) were captured. We examined the temporal relationship between these variables using the Differential Time-Varying Effect (DTVEM) hybrid exploratory-confirmatory model.

    Results

    Poorer sleep quality and shorter sleep duration maximally predicted deterioration in psychosis symptoms over the subsequent 1–8 and 1–12 days, respectively. These relationships were also mediated by negative affect and cognitive symptoms. Psychopathology variables also predicted sleep quality, but not sleep duration, and the effect sizes were smaller and of shorter lag duration.

    Conclusions

    Reduced sleep duration and poorer sleep quality anticipate the exacerbation of psychotic symptoms by approximately 1–2 weeks, and negative affect and cognitive symptoms mediate this relationship. We also observed a reciprocal relationship that was of shorter duration and smaller magnitude. Sleep disturbance may play a causal role in symptom exacerbation and relapse, and represents an important and tractable target for intervention. It warrants greater attention as an early warning sign of deterioration, and low-burden, user-friendly digital tools may play a role in its early detection.

  • Chapter 19 - Clock polymorphisms associated with human diurnal preference

  • from Section 3 - Sleepphysiology and homeostasis
  • Edited by Paul Shaw, Mehdi Tafti, Michael J. Thorpy
  • Book:
    The Genetic Basis of Sleep and Sleep Disorders
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 197-207

  • Summary

    The principal classes of glia in the mature brain are astrocytes, microglia and oligodendrocytes. According to the Benington-Heller hypothesis, astrocytic glycogen, which acts as a reserve glucose store for neurons, is depleted during wakefulness and restored during non-rapid-eye-movement (NREM) sleep. Cerebral microglia and oligodendrocytes cells secrete a number of substances in vitro known to influence sleep or brain activity in sleep. As sleep deprivation is associated with an increase in markers of cellular stress, it has been proposed that substances secreted by microglia may play a central role in sleep regulation. An important future area of investigation is to determine the anatomic locations where glial cells exert their effects on sleep and/or brain activity. Glia is dispersed widely in subcortical and cortical brain areas including regions known to trigger sleep and wakefulness. Astrocytic adenosine is likely to be a key mediator of sleep behavior and brain activity.

  • Chapter 31 - Delayed sleep phase disorder, circadian genes, sleep homeostasis and light sensitivity

  • from Section 7 - Circadian rhythm sleep disorders
  • Edited by Paul Shaw, Mehdi Tafti, Michael J. Thorpy
  • Book:
    The Genetic Basis of Sleep and Sleep Disorders
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 327-334

  • Summary

    This chapter focuses on long-term memory and its relationship to sleep with an emphasis on the role of sleep during memory consolidation. Declarative memory consolidation relies on the reactivation of the initially labile memory traces in the hippocampal formation as the temporary store, which drives memory reactivation in the cortex for long-term storage. Procedural memory of acquired skills is most often tested with regard to the effects of sleep. Regions critical for the consolidation of procedural memory are the cerebellum, striatum and motor cortex. Aside from pure memory consolidation, an added consideration for emotional memory is the effect of sleep on emotional salience. Long-term memory is dependent on the various sleep stages for consolidation. Aging is accompanied by general decline in memory and cognitive function. Many neurodegenerative diseases have profound deficits on systems critical for long-term memory consolidation and sleep regulation.

  • Chapter 21 - Neuroimaging the effects of light on non-visual brain functions

  • from Section 3 - Neuroimaging, sleep loss, and circadian misalignment
  • Edited by Eric Nofzinger, University of Pittsburgh, Pierre Maquet, Université de Liège, Belgium, Michael J. Thorpy
  • Book:
    Neuroimaging of Sleep and Sleep Disorders
    Published online:
    05 March 2013
    Print publication:
    07 March 2013, pp 171-178

  • Summary

    This chapter reviews the functional brain imaging studies, using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), that have examined neural activity patterns between non-rapid eye movement (NREM) sleep and wakefulness, and within NREM sleep in association with phasic neuronal oscillations. It explores recent fMRI data investigating the relationship between these rhythms and the processing of external stimulation during sleep. In order to further explore this relationship between external stimulation and NREM sleep phasic activity, brain responses to pure tones delivered during NREM sleep were evaluated in a recent event-related fMRI study. In the fMRI study, the relationship between auditory stimulation and slow waves was also explored. It is well known that external stimulation during NREM sleep can trigger a slow wave on electroencephalographic (EEG) recordings: such evoked slow waves, especially during stage N2, are also termed K-complexes.

  • Sleep and circadian rhythm disruption in schizophrenia

  • Katharina Wulff, Derk-Jan Dijk, Benita Middleton, Russell G. Foster, Eileen M. Joyce
  • Journal:
    The British Journal of Psychiatry / Volume 200 / Issue 4 / April 2012
    Published online by Cambridge University Press:
    02 January 2018, pp. 308-316
    Print publication:
    April 2012
    • Article
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      • Open access
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  • 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.