Sleep loss, a possible factor in augmenting manic episode

Barbini, Barbara; Bertelli, Sara; Colombo, Cristina; Smeraldi, Enrico

doi:10.1016/s0165-1781(96)02909-5

Cited by 132 publications

(71 citation statements)

References 6 publications

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“…Empirical studies have confirmed this view [Barbini et al, 1996;Leibenluft et al, 1996]. It was shown that reduced sleep duration predicted (hypo-)manic symptoms, and it was concluded that alterations of sleep towards decreasing sleep duration in subjects with bipolar depression should warrant immediate intensive treatment to avoid full-blown manic episodes.…”

Section: Sleep In Maniamentioning

confidence: 97%

Sleep and Sleep-Wake Manipulations in Bipolar Depression

Riemann

Voderholzer

Berger³

2002

Neuropsychobiology

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In the last 30 years, it has been convincingly demonstrated that sleep in major depression is characterized by disturbances of sleep continuity, a reduction of slow wave sleep, a disinhibition of REM sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period) and an increase in REM density. Furthermore, manipulations of the sleep-wake cycle like total or partial sleep deprivation or phase advance of the sleep period have been proven to be effective therapeutic strategies for patients with unipolar depression. The database concerning sleep and sleep-wake manipulations in bipolar disorder in comparison is not yet as extensive. Studies investigating sleep in bipolar depression suggest that during the depressed phase sleep shows the same stigmata as in unipolar depression. During the hypomanic or manic phase, sleep is even more curtailed, though subjectively not experienced as disturbing by the patients. REM sleep disinhibition is present as well. An important issue is the question, whether sleep-wake manipulations can also be applied in patients with bipolar depression. Work by others and our own studies indicate that sleep deprivation and a phase advance of the sleep period can be used to treat bipolar patients during the depressed phase. The risk of a switch into hypomania or mania does not seem to be more pronounced than the risk with typical pharmacological antidepressant treatment. For patients with mania, sleep deprivation is not an adequate treatment – in contrast, treatment strategies aiming at stabilizing a regular sleep-wake schedule are indicated.

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Section: Sleep In Maniamentioning

confidence: 97%

Sleep and Sleep-Wake Manipulations in Bipolar Depression

Riemann

Voderholzer

Berger³

2002

Neuropsychobiology

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“…Changes in mental functions A strong relationship was found between sleep time and the intensity of manic symptoms [117]. An animal model of mania could be obtained under conditions of the sleep deprivation experiment.…”

Section: Therapeutic Applications Of Sleep Restrictionmentioning

confidence: 98%

Consequences of sleep deprivation

Orzeł-Gryglewska¹

2010

International Journal of Occupational Medicine and Environmental Health

206

133

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This paper presents the history of research and the results of recent studies on the effects of sleep deprivation in animals and humans. Humans can bear several days of continuous sleeplessness, experiencing deterioration in wellbeing and effectiveness; however, also a shorter reduction in the sleep time may lead to deteriorated functioning. Sleeplessness accounts for impaired perception, difficulties in keeping concentration, vision disturbances, slower reactions, as well as the appearance of microepisodes of sleep during wakefulness which lead to lower capabilities and efficiency of task performance and to increased number of errors. Sleep deprivation results in poor memorizing, schematic thinking, which yields wrong decisions, and emotional disturbances such as deteriorated interpersonal responses and increased aggressiveness. The symptoms are accompanied by brain tissue hypometabolism, particularly in the thalamus, prefrontal, frontal and occipital cortex and motor speech centres. Sleep deficiency intensifies muscle tonus and coexisting tremor, speech performance becomes monotonous and unclear, and sensitivity to pain is higher. Sleeplessness also relates to the changes in the immune response and the pattern of hormonal secretion, of the growth hormone in particular. The risk of obesity, diabetes and cardiovascular disease increases. The impairment of performance which is caused by 20-25 hours of sleeplessness is comparable to that after ethanol intoxication at the level of 0.10% blood alcohol concentration. The consequences of chronic sleep reduction or a shallow sleep repeated for several days tend to accumulate and resemble the effects of acute sleep deprivation lasting several dozen hours. At work, such effects hinder proper performance of many essential tasks and in extreme situations (machine operation or vehicle driving), sleep loss may be hazardous to the worker and his/her environment.

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“…The strongest triggers of mania and/or worsening of manic symptomatology are factors associated with sleep deficits or deprivation [93][94][95][96][97][98][99][100][101] . Also, antidepressants, which reduce brain arousal as mentioned above, can induce a switch into mania.…”

Section: The Vigilance Regulation Model Of Affective Disorders and Adhdmentioning

confidence: 99%

Assessment of Wakefulness and Brain Arousal Regulation in Psychiatric Research

Sander¹,

Hensch²,

Wittekind³

et al. 2015

Neuropsychobiology

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tion of wakefulness to the environmental and situational needs so that the optimal balance between energy conservation and responsiveness can be obtained. Since one approach to the assessment of brain arousal regulation is the classification of EEG vigilance stages, a computer-based algorithm (Vigilance Algorithm Leipzig) has been introduced, allowing classification of EEG vigilance stages in EEG recordings under resting conditions. The time course of EEG vigilance stages in EEGs of 15-20 min duration allows estimation of the individual arousal regulation (hyperstable, adaptive, or unstable vigilance pattern). The vigilance model of affective disorders and attention-deficit/hyperactivity disorder links a disturbed arousal regulation to the pathogenesis of psychiatric disorders and accordingly helps to explain and possibly also predict treatment effects of pharmacological and nonpharmacological interventions for these conditions. AbstractDuring the last few decades, much knowledge has been gained about sleep being a heterogeneous condition with several distinct sleep stages that represent fundamentally different physiological states. The same applies for the wake state which also comprises distinct global functional states (called vigilance stages). However, various terms and concepts have been introduced describing different aspects of wakefulness, and accordingly several methods of assessment exist, e.g. sleep laboratory assessments (Multiple Sleep Latency Test, Maintenance of Wakefulness Test), questionnaires (Epworth Sleepiness Scale, Karolinska Sleepiness Scale), behavioural tasks (Psychomotor Vigilance Test) or electroencephalography (EEG)-based assessments (Alpha Attenuation Test, Karolinska Drowsiness Test). Furthermore, several theoretical concepts about the regulation of sleep and wakefulness have been put forward, and physiological correlates have been identified. Most relevant for healthy functioning is the regulation of brain arousal and the adap-

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Sleep loss, a possible factor in augmenting manic episode

Cited by 132 publications

References 6 publications

Sleep and Sleep-Wake Manipulations in Bipolar Depression

Sleep and Sleep-Wake Manipulations in Bipolar Depression

Consequences of sleep deprivation

Assessment of Wakefulness and Brain Arousal Regulation in Psychiatric Research

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