Cases reported "Sleep Deprivation"

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1/6. Transient total sleep loss in cerebral Whipple's disease: a longitudinal study.

    A case with transient, almost complete sleep loss caused by cerebral manifestation of Whipple's disease (WD) is presented. Cerebral WD is rare and in most cases occurs after gastrointestinal infection. In our case, a progressive and finally almost complete sleep loss was the initial and predominant symptom. Polysomnographic studies in several consecutive nights and over 24 h showed a total abolition of the sleep-wake cycle with nocturnal sleep duration of less than 15 min. Endocrine tests revealed hypothalamic dysfunction with flattening of circadian rhythmicity of cortisol, TSH, growth hormone and melatonin. cerebrospinal fluid (CSF) hypocretin was reduced. [18F]deoxyglucose positron emission tomography (FDG-PET) revealed hypermetabolic areas in cortical and subcortical areas including the brainstem, which might explain sleep pathology and vertical gaze palsy. In the course of treatment with antibiotics and additional carbamazepine for 1 year, insomnia slowly and gradually improved. Endocrine investigations at 1-year follow-up showed persistent flattening of circadian rhythmicity. The FDG-PET indicated normalized metabolism in distinct regions of the brain stem which paralleled restoration of sleep length. The extent of sleep disruption in this case of organic insomnia was similar to cases of familial fatal insomnia, but was at least partially reversible with treatment.
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2/6. sleep deprivation in rapid-cycling bipolar affective disorder: case report.

    We describe a 4-month long hypomanic response to sleep deprivation in a patient with consistent (20-day cycles) rapid cycling. He subsequently reverted to very rapid cycling; however, sleep deprivation remained effective for each attack of depression. sleep deprivation treatment, its immediate but short-lived beneficial effect, may have a role in the treatment of the ultra-short depressions encountered in very rapid cycling.
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3/6. Modafinil as an adjunctive treatment to sleep deprivation in depression.

    sleep deprivation (SD) is a rapid-acting treatment for depression, but its clinical efficacy is hampered by high relapse rates after recovery sleep, and its effectiveness is reduced by the demanding effort needed for the patient to stay awake. To our knowledge, this is the first reported case of a successful treatment of depression with the combination of SD and the wakefulness-promoting agent modafinil. We suggest that modafinil may reinforce the action of SD, possibly by preventing daytime naps and microsleep, and may sustain the antidepressant effect of SD, possibly by stabilizing the resynchronization between the circadian clock and the sleep-wake cycle.
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4/6. Partial sleep deprivation to prevent 48-hour mood cycles.

    The course of a patient with the phenomenon of 48-h mood cycles, including her response to medication and to systematic partial sleep deprivation, is described. She had only a partial response to tranylcypromine alone. Partial sleep deprivation during the second half of alternate nights successfully prevented depressive mood cycles. Three to four weeks after discontinuing tranylcypromine she lost her ability to sustain this regimen. This case demonstrates an interaction between antidepressant medication and partial sleep deprivation in the prevention of depressive mood cycles.
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5/6. Abstinence from night sleep as a treatment for endogenous depressions. The earliest observations in a Danish mental hospital (1954) and an analysis of the causal mechanism.

    In the early 1950s before antidepressants were in use, I conceived the idea of treating patients with pure endogenous depressions by having them abstain from night sleep for two or more nights. The idea was based on several clinical observations: "It looks as if sleep as such has an unfortunate influence on the state of the depression and as if the organism itself resists the sleep rhythm during the period of depression." My first clinical experiment was conducted in June 1954 and was followed later by several others. At that time, I could not ascertain from the available literature whether this therapy had been tried elsewhere. The experiments completely confirmed that the hypothesis was correct--that the patients' condition had improved and that the treatment influenced the subcortical processes which determined the complaint. This led to studies on the transmitter function in the states of sleeping and waking, respectively, among healthy and sick people or, more precisely, the influence of darkness and light, respectively, on these functions. The studies appeared to confirm that therapy in which the patient is kept awake encourages the production of activating substances such as antidepressants. The most recent research on melatonin, which is formed in the corpus pineale, is briefly discussed. Provisional results seem to indicate that this substance has an inhibiting effect on vital brain functions in periods of darkness (periods of sleep) and thus contributes to the maintenance of the depression because melatonin is especially produced in the dark periods of the daily cycle. These investigations, though still at an experimental stage, suggest exciting possibilities, also for psychiatry.(ABSTRACT TRUNCATED AT 250 WORDS)
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6/6. Five variations of sleep deprivation in a depressed woman.

    Systematic variation in aspects of the sleep-wakefulness cycle of a depressed woman showed that recovery occurred reliably after 19 to 20 hours sustained wakefulness, unrelated to diurnal rhythm. depression returned during as little as 15 minutes sleep. The effect of sleep deprivation was a specific response, probably unrelated to REM sleep.
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