Partial sleep deprivation therapy combined with sertraline affects subjective sleep quality in major depressive disorder

BACKGROUND AND PURPOSE: Earlier studies have shown an association between mood disorders and sleep regulation. Total or partial sleep deprivation was demonstrated to have rapid antidepressive effects in depression. Depressive symptoms recur after one night of recovery sleep, but relapse is less when patients are receiving medication. In this study, we examined the subjective sleep quality changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. PATIENTS AND METHODS: Thirteen patients received six partial sleep deprivation therapies in addition to sertraline; the sleep schedule on deprivation nights started at 11:00 p.m. and ended at 3:00 a.m. Eleven patients were treated with sertraline monotherapy as a control group. Six nights of partial sleep deprivation were completed in the first two weeks. Subjective sleep quality was evaluated with the Pittsburgh Sleep Quality Index (PSQI); depression and the accompanying anxiety were also assessed at baseline and at the end of the fourth week. RESULTS: The late partial sleep deprivation (LPSD) group showed less increase in estimated sleep duration and less significant improvement in subjective sleep quality than the control group. Although decreased sleep latency and increased sleep efficiency are associated with the sleep deprivation, contrary results were found in our study. CONCLUSIONS: In conclusion, changes in subjective sleep quality could occur relative to the combined partial sleep deprivation therapy and to pharmacotherapy and must be differentiated from the rapid effects of sleep deprivation therapy and objective polysomnographic measures.     

Melatonin excretion, body temperature and subjective arousal during 64 hours of sleep deprivation

(1) Evidence has been presented, based on measurement of melatonin by radioimmunoassay in 12 healthy males, that the urinary excretion of melatonin follows a circadian pattern in humans during sleep deprivation when the subjects are exposed to light. (2) Melatonin excretion increased with increased sleep deprivation. (3) Melatonin excretion during recovery sleep did not differ from that during base line sleep. (4) Melatonin excretion did not react to psychosocial stress at trough times (as adrenaline did). (5) Self-rated fatigue and body temperature exhibited a circadian variation. (6) Peak fatigue and trough body temperature coincided temporally with the peak of melatonin excretion.     

A comparison of sleep deprivation and narcolepsy in terms of complex cognitive performance and subjective sleepiness

OBJECTIVES: (i) To expose 'normal sleepers' to a 32-h sleep deprivation protocol and evaluate the impact of this deprivation on a complex performance task i.e. the paced auditory serial addition test (PASAT). (ii) To compare these sleep deprivation performance findings with historical data on the impact of sleepiness secondary to narcolepsy on PASAT performance measures. (iii) To investigate the recuperative effects of a brief nap period on both sleepiness and PASAT performance for the sleep-deprived subjects. (iv) To compare these post-nap effects with historical data relating to the impact of napping on both sleepiness and PASAT performance for subjects with narcolepsy. BACKGROUND: Previous research has demonstrated that sleepiness induced by sleep deprivation in normal sleepers may lead to cognitive impairment across a range of performance tasks. Sleepiness secondary to narcolepsy has also been noted to impair cognitive function especially for complex processing tasks. Direct comparison of the effects of sleepiness on performance between non-pathological and pathological sleepiness states is confounded, however, by methodological differences in research design especially in relation to levels of induced sleepiness and performance task selection. The purpose of the current study was to undertake a sleep deprivation study that achieved a methodological match with published data evaluating the impact of sleepiness on cognitive performance for subjects with narcolepsy. This methodological matching allowed for a more precise comparison of the impact of sleepiness on performance between non-pathological and pathological sleepiness groups. RESULTS: Normal sleepers required a 32-h deprivation protocol to develop a subjective level of sleepiness that equated with that identified by subjects with narcolepsy. This induced sleepiness in normal sleepers did not result in any significant decrement in complex performance, a finding that was in contrast to the performance decrement previously found in subjects with narcolepsy with equivalent subjective sleepiness ratings. A 20-min nap produced more improvement in both arousal and cognitive processing performance for the subjects with narcolepsy than for the current sleep-deprivation cohort. CONCLUSION: This study identified significant differences in the impact of sleepiness on complex performance between non-pathological sleep-deprived subjects and subjects with narcolepsy. This paper explores these differences in relation to the potential for both quantitative and qualitative differences that exist in the nature of sleepiness between non-pathological and pathological sleepiness states.     

Association of subjective anxiety, depression, and sleep disturbance with quality-of-life ratings in adults with epilepsy

Purpose :  To determine the relative contributions of subjective anxiety, depression, sleep disturbance, and seizure-related variables to quality-of-life scores in adults with epilepsy, and the interrelationships among these factors.
Methods :  Consecutive adult patients with epilepsy attending neurology outpatient clinics were recruited. Patients completed the following scales: Hospital Anxiety and Depression Scale (HADS), Hamilton Anxiety Rating Scale, Medical Outcomes Study (MOS) Sleep Scale, Epworth Sleepiness Scale, and Quality of Life in Epilepsy Inventory-31 (QOLIE-31). Univariate and multivariate linear regression models were used to identify variables associated with QOLIE-31 overall score. Path analysis model was constructed to test for interrelations between the variables.
Results :  Two hundred forty-seven patients completed the questionnaires. By multivariate analysis, in order of degree of contribution, HADS anxiety subscale score, MOS Sleep Scale Sleep Problems Index score, HADS depression subscale score, number of current antiepileptic drugs used, and seizure freedom in the past 4 weeks, significantly correlated with QOLIE-31 overall score, accounting for 65.2% of the variance. Complex interrelationships were present between these factors. A general linear model to predict QOLIE-31 overall score in the presence of these factors was constructed.
Conclusion :  Subjective anxiety, depression, and sleep disturbance exerted greater effect than short-term seizure control on quality of life scores of patients with epilepsy. These factors should be considered simultaneously when evaluating effects of treatment on quality of life.     

Electroencephalography during sleep of patients with panic disorder

Sleep electroencephalograms (EEGs) of subjects with primary panic disorder were compared to those of normal controls matched for age and sex. Significant differences were found between patients and controls in sleep latency, sleep efficiency, and stage 2 sleep duration. No differences were found between the two groups in REM latency. Because depressed patients are known to have reduced latency to REM sleep, these data add support to the hypothesis that panic disorder and depression are distinct disorders.     

Human sleep spindle characteristics after sleep deprivation

OBJECTIVE: Sleep spindles (12-15 Hz oscillations) are one of the hallmarks of the electroencephalogram (EEG) during human non-rapid eye movement (non-REM) sleep. The effect of a 40 h sleep deprivation (SD) on spindle characteristics along the antero-posterior axis was investigated. METHODS: EEGs during non-REM sleep in healthy young volunteers were analyzed with a new method for instantaneous spectral analysis, based on the fast time frequency transform (FTFT), which yields high-resolution spindle parameters in the combined time and frequency domain. RESULTS: FTFT revealed that after SD, mean spindle amplitude was enhanced, while spindle density was reduced. The reduction in spindle density was most prominent in the frontal derivation (Fz), while spindle amplitude was increased in all derivations except in Fz. Mean spindle frequency and its variability within a spindle were reduced after SD. When analyzed per 0.25 Hz frequency bin, amplitude was increased in the lower spindle frequency range (12-13.75 Hz), whereas density was reduced in the high spindle frequency range (13.5-14.75 Hz). CONCLUSIONS: The observed reduction in spindle density after SD confirms the inverse homeostatic relationship between sleep spindles and slow waves whereas the increase in spindle amplitude and the reduction in intra-spindle frequency variability support the hypothesis of a higher level of synchronization in thalamocortical cells when homeostatic sleep pressure is enhanced.     

Clinical effects of sleep fragmentation versus sleep deprivation

Common symptoms associated with sleep fragmentation and sleep deprivation include increased objective sleepiness (as measured by the Multiple Sleep Latency Test); decreased psychomotor performance on a number of tasks including tasks involving short term memory, reaction time, or vigilance; and degraded mood. Differences in degree of sleepiness are more related to the degree of sleep loss or fragmentation rather than to the type of sleep disturbance. Both sleep fragmentation and sleep deprivation can exacerbate sleep pathology by increasing the length and pathophysiology of sleep apnea. The incidence of both fragmenting sleep disorders and chronic partial sleep deprivation is very high in our society, and clinicians must be able to recognize and treat Insufficient Sleep Syndrome even when present with other sleep disorders.     

Neurocognitive consequences of sleep deprivation

Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.     

Diagnostic applications of sleep deprivation

Four cases are described in which observation of the response to forty hour sleep deprivation was used in resolving the differential diagnosis between depression and dementia. In each case it was possible to conduct psychometric assessment of cognitive ability during the period of improvement of the clinical state. The utility of this approach and some of the difficulties associated with its use are discussed.     

Total sleep deprivation and Parkinson disease

Twelve Parkinson disease (PD) patients were submitted to a single night of total sleep deprivation (SD). Disease duration had a median of 5.1 years and all were using either anticholinergic or L-Dopa or the combination of both drugs. After SD there was an improvement of rigidity, bradykinesia, gait and posture disturbances and functional disability that remained significant for 2 weeks. No effect was observed on tremor. Concerning depressive symptoms, a significant difference was noted, that remained for one week. These results suggest that SD may be an useful procedure to improve PD symptomatology. It is discussed a possible change of dopaminergic receptors, induced by SD, to explain the improvement.     

Metabolic and endocrine effects of sleep deprivation

Sleep deprivation has multiple effects on endocrine and metabolic function. In particular, sleep restriction is accompanied by increased cortisol levels in the afternoon and early evening and a shorter quiescent period compared with extended sleep periods. Those alterations could facilitate central and peripheral disturbances that are associated with glucocorticoid excess, such as memory deficits, and are similar to those observed in aging. Thus, chronic sleep loss could contribute to acceleration of the aging process. Sleep restriction is also associated with an impairment of carbohydrate tolerance, similar to that observed in individuals with clinically significant impaired glucose tolerance. Thus, chronic sleep deprivation may increase the risk for diabetes. Finally, sleep plays an important role in energy balance. Partial sleep deprivation was found to be associated with a decrease in plasma levels of leptin and a concomitant increase in plasma levels of ghrelin; subjective ratings of hunger and appetite also increased (the appetite for protein-rich foods was not significantly affected). Moreover, a remarkable correlation was found between the increase in hunger and the increase in the ghrelin:leptin ratio. Thus, the neuroendocrine regulation of appetite and food intake appears to be influenced by sleep duration, and sleep restriction may favor the development of obesity.