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Started first post as a very young junior doctor, coping with work and on-call and sleep deprivation. Worked in surgery and respiratory medicine. An unplanned pregnancy and subsequent turmoil. Worked in A&E then went to Mexico with partner, got engaged. Came back to do obstetrics and gynaecology and dermatology. Then went to Cornwall for GP training.
Sleep deprivation, which is a decrease in duration and quality of sleep, is a common problem in today’s life. Epidemiological and interventional investigations have suggested a link between sleep deprivation and overweight/obesity. Sleep deprivation affects homeostatic and non-homoeostatic regulation of appetite, with the food reward system playing a dominant role. Factors such as sex and weight status affect this regulation; men and individuals with excess weight seem to be more sensitive to reward-driven and hedonistic regulation of food intake. Sleep deprivation may also affect weight through affecting physical activity and energy expenditure. In addition, sleep deprivation influences food selection and eating behaviours, which are mainly managed by the food reward system. Sleep-deprived individuals mostly crave for palatable energy-dense foods and have low desire for fruit and vegetables. Consumption of meals may not change but energy intake from snacks increases. The individuals have more desire for snacks with high sugar and saturated fat content. The relationship between sleep and the diet is mutual, implying that diet and eating behaviours also affect sleep duration and quality. Consuming healthy diets containing fruit and vegetables and food sources of protein and unsaturated fats and low quantities of saturated fat and sugar may be used as a diet strategy to improve sleep. Since the effects of sleep deficiency differ between animals and humans, only evidence from human subject studies has been included, controversies are discussed and the need for future investigations is highlighted.
Sleep is essential for an adequate neurobiological functioning, being implicated in several cognitive functions. Even in healthy individuals, sleep deprivation can lead to a number of psychopathological changes, including perceptual distortions, hallucinations and delusions. Thus, the resulting clinical picture may be similar to a psychotic disorder.
Objectives
To present a clinical case of psychotic symptomatology induced by sleep deprivation.
Methods
Patient’s clinical file consultation and literature review using the search engine Pubmed® and the keywords: “sleep deprivation”, “sleep loss” and “psychosis”.
Results
We present the case of a 41-year-old woman with a history of an episode of mood changes with psychotic symptoms that was preceded by a period of total insomnia. No psychotropic drugs since then and no relapses. In May 2020, she was admitted in psychiatry department due to clinical picture composed by significant psychomotor slowing, drowsiness, slowed speech, verbal visual, tactile and auditory hallucinations accompanied by grandiose delusions. These symptoms were preceded by total insomnia with one week of duration. In the hospital was administered quetiapine 100mg and lorazepam 2.5mg to aid in the recovery of sleep deprivation and concomitantly aripiprazole 15mg was prescribed. The patient presented a rapid and significant clinical improvement. Currently, it is without any type of medication and without psychopathological changes.
Conclusions
The clinical picture present in this case report was triggered after a significant period of sleep deprivation. Thus, it illustrates the role that sleep has in the development of psychiatric symptomatology, sometimes difficult to differentiate from psychiatric disorders.
The challenge of identifying efficacious out-patient treatments for depression is amplified by the increasing desire to find interventions that reduce the time to sustained improvement. One potential but underexplored option is triple chronotherapy (TCT). To date, use of TCT has been largely restricted to specialist units or in-patients. Recent research demonstrates that it may be possible to undertake sleep deprivation in out-patient settings, raising the possibility of delivering TCT to broader populations of individuals with depression. Emerging evidence suggests that out-patient TCT is a high-benefit, low-risk intervention but questions remain about how to target TCT and its mechanisms of action. Like traditional antidepressants, TCT probably acts through several pathways, especially the synchronisation of the ‘master clock’. Availability of reliable and valid methods of out-patient measurement of intra-individual circadian rhythmicity and light exposure are rate-limiting steps in the wider dissemination of TCT.
This chapter looks at the state of sleep and its biology. it begins by looking at what comprises the state of sleep, and examines comparatively which, and how, other animals sleep. It looks at circadian rhythms, and how the sleep--wake cycle is controlled, with melatonin manufactured by the pineal gland. There is emphasis on the electrophysiology of sleep (sleep EEG), and a description of the stages of sleep and how they are characterised by different EEG profiles, particularly the distinction between REM and non-REM sleep. The neurology of sleep looks at the role of structures such as the brainstem and reticular activating system, and the effect of damage at different levels of the brain on sleeping behaviour. The psychopharmacology of sleep looks at the changing role of neurotransmitters throughout the day and night, and in dreaming and dreamless sleep. The chapter then examines the range of sleep disorders, including problems getting to sleep, as well as sleep walking and sleep talking. It then looks at the effects of sleep deprivation. The chapter concludes with a discussion of why we sleep, covering the possible evolutionary functions of sleep, with focus on the role of sleep in learning and memory consolidation.
Energy deficit is common during prolonged periods of strenuous physical activity and limited sleep, but the extent to which appetite suppression contributes is unclear. The aim of this randomised crossover study was to determine the effects of energy balance on appetite and physiological mediators of appetite during a 72-h period of high physical activity energy expenditure (about 9·6 MJ/d (2300 kcal/d)) and limited sleep designed to simulate military operations (SUSOPS). Ten men consumed an energy-balanced diet while sedentary for 1 d (REST) followed by energy-balanced (BAL) and energy-deficient (DEF) controlled diets during SUSOPS. Appetite ratings, gastric emptying time (GET) and appetite-mediating hormone concentrations were measured. Energy balance was positive during BAL (18 (sd 20) %) and negative during DEF (–43 (sd 9) %). Relative to REST, hunger, desire to eat and prospective consumption ratings were all higher during DEF (26 (sd 40) %, 56 (sd 71) %, 28 (sd 34) %, respectively) and lower during BAL (–55 (sd 25) %, −52 (sd 27) %, −54 (sd 21) %, respectively; Pcondition < 0·05). Fullness ratings did not differ from REST during DEF, but were 65 (sd 61) % higher during BAL (Pcondition < 0·05). Regression analyses predicted hunger and prospective consumption would be reduced and fullness increased if energy balance was maintained during SUSOPS, and energy deficits of ≥25 % would be required to elicit increases in appetite. Between-condition differences in GET and appetite-mediating hormones identified slowed gastric emptying, increased anorexigenic hormone concentrations and decreased fasting acylated ghrelin concentrations as potential mechanisms of appetite suppression. Findings suggest that physiological responses that suppress appetite may deter energy balance from being achieved during prolonged periods of strenuous activity and limited sleep.
Aging is marked by cognitive decline, which in the case of Alzheimer’s disease is associated with tremendous global economic burden. Identifying modifiable risk factors for cognitive decline is therefore of paramount importance. In this chapter, we describe how aging compromises sleep quality and sleep architecture at a rate that parallels normal age-related cognitive decline. We argue that understanding the neurocognitive functions of sleep – frontal lobe restoration, memory consolidation, and metabolite clearance – and how such functions change in later life will be key to informing why some older individuals maintain healthy cognitive functioning and other older individuals do not. Critically, by investigating how sleep, cognition, and aging interact, researchers and clinicians can develop sleep-related treatments that target preventing, or at least ameliorating, pathologies such as Alzheimer’s disease.
Both sleep and motor activity have a bidirectional relationship with depression. The existing literature on motor activity during therapeutic sleep deprivation in depressed patients is inconsistent and fragmentary. In the present study we measured motor activity continuously during 40 hours of sleep deprivation in depressed patients.
Method
Thirty-four inpatients suffering from a major depression (DSM-IV) underwent sleep deprivation with a continuous waking period of 40 hours. Motor activity of the patients was continuously recorded using an actigraph on the non-dominant wrist. The effect of sleep deprivation was assessed by the Hamilton Depression Scale (six-item version), thus separating the group into responders and non-responders to sleep deprivation.
Results
We found no significant differences in motor activity between responders and non-responders on the day before sleep deprivation. During the night, responders to sleep deprivation exhibited a higher motor activity and less periods of rest. On the day after sleep deprivation, responders exhibited a higher activity, too.
Conclusions
Motor activity levels differ between the two groups, thus giving more insight into possible mechanisms of action of the therapeutic sleep deprivation. We suggest that higher motor activity during the night prevents naps and leads to better response to sleep deprivation.
The lack of sleep is a significant problem in the modern world. The structure of the economy means that 24 hour working is required from some of us, sometimes because we are expected to be able to respond to share-price fluctuations on the other side of the planet, sometimes because we are expected to serve kebabs to people leaving nightclubs, and sometimes because lives depend on it. The immediate effect is that we feel groggy; but there may be much more sinister long-term effects of persistent sleep deprivation and disruption, the evidence for which is significant, and worth taking seriously. If sleeplessness has a serious impact on health, it represents a notable public health problem. In this article, I sketch that problem, and look at how exploiting the pharmacopoeia (or a possible future pharmacopoeia) might allow us to tackle it. I also suggest that using drugs to mitigate or militate against sleeplessness is potentially morally and politically fraught, with implications for social justice. Hence, whatever reasons we have to use drugs to deal with the problems of sleeplessness, we ought to be careful.
Introduction: Sleep deprivation negatively affects cognitive and behavioural performance. Emergency Medicine (EM) residents commonly work night shifts and are then expected to perform with competence. This study examines the impact of night shifts on EM resident performance in simulated resuscitation scenarios. Methods: A retrospective cohort study was completed at a single Canadian academic centre where residents participate in twice-annual simulation-based resuscitation objective structured clinical examinations (OSCEs). OSCE scores for all EM residents between 2010-2016 were collected, as well as post-graduate year (PGY1-5), gender, and shift schedules. OSCEs were scored using the Queen’s Simulation Assessment Tool (QSAT) evaluating four domains: primary assessment, diagnostic actions, therapeutic actions and communication, and an overall global assessment score (GAS). A night shift was defined as a late evening (beyond 23:00) or overnight shift within the three days before an OSCE. A mixed effects linear regression model was used to model the association between night shifts and OSCE scores while adjusting for gender and PGY. Results: A total of 136 OSCE scores were collected from 56 residents. PGY-5 residents had 37.1% (31.3 to 34.0%; p<0.01) higher OSCE scores than those in PGY-1 with an average increase of 8.8% (7.5 to 10.1%; p<0.01) per year. Working one or more night shifts in the three days before an OSCE reduced the total and communication scores by an average of 3.8% (p=0.04) and 4.5% (p=0.04) respectively. We observed a significant gender difference in the effects of acute shift work (p=0.03). Working a night shift one night prior to an OSCE was not associated with total score among male residents (p=0.33) but was associated with a 6.1% (-11.9 to -0.2; p=0.04) decrease in total score among female residents. This difference was consistent across PGY and was primarily due to an 8.5% (-15.5 to -1.6%; p=0.02) decrease in communication scores and a 6.7% (-13.1 to -0.3%; p=0.04) reduction in GAS. Conclusion: Proximity to night shifts significantly impaired the performance of EM trainees in simulated resuscitation scenarios, particularly in the domain of communication. For female residents, the magnitude of difference in total scores after working such shifts one night prior to a resuscitation OSCE was approximately equal to the difference seen between residents one year apart in training.
Unequivocal results demonstrating a causal relationship between a disturbance in circadian rhythms and depression have not yet been reported (reviews). However, acute mood changes, such as the antidepressive effect of sleep deprivation, diurnal variations of mood and their interrelationship, are commonly put forward as evidence of the importance of circadian dysregulations in affective disorders. The purpose of the present study is to obtain more insight in the mechanisms underlying these mood changes. The results will be discussed in the context of a recently postulated non-chronobiological explanation.
Earlier studies have suggested that the relationship between diurnal variation of mood and the response to total sleep deprivation (TSD) is clear and unambiguous: improvement of mood during the day prior to TSD (a positive diurnal variation) is followed by a positive response (mood improvement) to TSD, while no improvement or deterioration of mood during the day prior to TSD (a negative diurnal variation) may result in no, or even a negative, TSD response (for references see Van den Hoofdakker). However, these conclusions were based on the results from cross-sectional studies, comparing single TSD effects across individuals. Comparison of sleep deprivation effects within individuals, however, revealed that the course of mood during the day prior to TSD is irrelevant for the TSD response. Accordingly, a favourable response to TSD appeared to be related to the patient's propensity to show diurnal mood variations per se, irrespective of their direction.
In 1975 van den Burg and van den Hoofdakker hypothesized that depressed patients might be ‘overaroused.’ This suggestion is consistent not only with their seminal observations on the antidepressant effects of total sleep deprivation in depression, but with the short, fragmented, and shallow sleep of depressed patients, lowered arousal thresholds, hyperactivity of the hypothalamus-pituitary adrenal (HPA) axis, and elevated core body temperature commonly found in some patients during the sleep period.
Based on previous studies demonstrating detrimental effects of reduced alertness on attentional orienting our study seeks to examine covert and overt attentional orienting in different arousal states. We hypothesized an attentional asymmetry with increasing reaction times to stimuli presented to the left visual field in a state of maximally reduced arousal. Eleven healthy participants underwent sleep deprivation and were examined repeatedly every 4 hr over 28 hr in total with two tasks measuring covert and overt orienting of attention. Contrary to our hypothesis, a reduction of arousal did not induce any asymmetry of overt orienting. Even in participants with profound and significant attentional asymmetries in covert orienting no substantial reaction time differences between left- and right-sided targets in the overt orienting task could be observed. This result is not in agreement with assumptions of a tight coupling of covert and overt attentional processes. In conclusion, we found differential effects of lowered arousal induced by sleep deprivation on covert and overt orienting of attention. This pattern of results points to a neuronal non-overlap of brain structures subserving these functions and a differential influence of the norepinephrine system on these modes of spatial attention. (JINS, 2015, 21, 545–557)
The present study aimed to assess the adequacy of energy, macronutrients and water intakes of ultra-endurance runners (UER) competing in a 24 h ultra-marathon (distance range: 122–208 km). The ad libitum food and fluid intakes of the UER (n 25) were recorded throughout the competition and analysed using dietary analysis software. Body mass (BM), urinary ketone presence, plasma osmolality (POsmol) and volume change were determined at pre- and post-competition time points. Data were analysed using appropriate t tests, with significance set at P <0·05. The total energy intake and expenditure of the UER were 20 (sd 12) and 55 (sd 11) MJ, respectively (control (CON) (n 17): 12 (sd 1) and 14 (sd 5) MJ, respectively). The protein, carbohydrate and fat intakes of the UER were 1·1 (sd 0·4), 11·3 (sd 7·0) and 1·5 (sd 0·7) g/kg BM, respectively. The rate of carbohydrate intake during the competition was 37 (sd 24) g/h. The total water intake of the UER was 9·1 (sd 4·0) litres (CON: 2·1 (sd 1·0) litres), while the rate of water intake was 378 (sd 164) ml/h. Significant BM loss occurred at pre- to post-competition time points (P =0·001) in the UER (1·6 (sd 2·0) %). No significant changes in POsmol values were observed at pre- (285 (sd 11) mOsmol/kg) to post-competition (287 (sd 10) mOsmol/kg) time points in the UER and were lower than those recorded in the CON group (P <0·05). However, plasma volume (PV) increased at post-competition time points in the UER (10·2 (sd 9·7) %; P <0·001). Urinary ketones were evident in the post-competition samples of 90 % of the UER. Energy deficit was observed in all the UER, with only one UER achieving the benchmark recommendations for carbohydrate intake during endurance exercise. Despite the relatively low water intake rates recorded in the UER, hypohydration does not appear to be an issue, considering increases in PV values observed in the majority (80 %) of the UER. Population-specific dietary recommendations may be beneficial and warranted.
The objective of our study was to explore the association between sleep deprivation and obesity among shift workers.
Design
A cross-sectional study was conducted. Obesity was defined as BMI ≥30 kg/m2. Time of sleep was categorized as: >5 h of continuous sleep/d; ≤5 h of continuous sleep/d with some additional rest (sleep deprivation level I); and ≤5 h of continuous sleep/d without any additional rest (sleep deprivation level II). Sociodemographic, parental and behavioural variables were evaluated by means of a standardized pre-tested questionnaire. Potential confounding factors were controlled for in the multivariable model.
Setting
A poultry-processing plant in southern Brazil.
Subjects
Nine hundred and five shift workers (63 % female).
Results
Obesity was more prevalent in the participants who were female, aged 40 years and older, who had less schooling and reported excess weight in both parents. Sleep deprivation levels I and II were associated with increased income, number of meals consumed throughout the day and nightshift work. All of the workers who exhibited a degree of sleep deprivation worked the night shift. After controlling for potential confounding factors, the prevalence ratios of obesity were 1·4 (95 % CI 0·8, 2·2) and 4·4 (95 % CI 2·4, 8·0) in the workers with sleep deprivation levels I and II, respectively, compared with the reference group.
Conclusions
These results show a strong association between sleep deprivation and obesity in shift workers and that sleep deprivation may be a direct consequence of working at night.
During sleep deprivation, the homeostatic sleep drive does not build up as high in the long sleepers as in the short sleepers due to allostatic effects from prior sleep history, and at least in part as a consequence of genetic make-up, there are large individual differences in the cognitive deficits caused by sleep deprivation. A frequently overlooked aspect of trait vulnerability to sleep loss is that ranking of individuals in terms of magnitude of their vulnerability depends on the task they perform. Despite an ongoing, worldwide search for predictors of trait vulnerability to sleep loss, reliable biomarkers have not yet been identified. Handful of genetic polymorphisms has been found to modulate individual vulnerability to sleep deprivation. In summary, healthy adults exhibit systematic individual differences both in sleep duration and in cognitive impairment due to sleep loss.
This chapter reviews the techniques currently applied to study brain function during sleep deprivation (SD) as opposed to the consequence of SD. It provides a bird's eye view of functional imaging studies performed on healthy young adult volunteers to date and comment on how this research has evolved the conceptualization of how SD modulates behavior. The first functional imaging studies involving SD utilized positron emission tomography (PET). Based on the initial findings, cognitive domain and task difficulty was proposed as determinants of the neural response to SD. It was postulated that changes in dopamine signaling in the SD state contributed to the change in functional connectivity, an idea reprised when discussing risky decision making in SD. The interaction of SD and circadian effects, including the effects of chronotype, could be a further target of functional neuroimaging studies, including the effect of countermeasures such as naps and stimulants.
Functional MRI provides a reproducible, non-invasive, and flexible means to study inter-individual variation in performance impairment in the setting of sleep deprivation (SD). An important long-term goal of studying inter-individual differences in responses to SD is to elucidate phenotypes that predict how an individual perform in an operational setting after being sleep deprived. The seemingly contradictory findings regarding the benefit of greater activation in areas of the brain led one to examine whether evaluating shifts in activation across states would prove a reliable marker of inter-individual variability in behavior. The thalamus plays an important part in mediating arousal and attention, which in turn have substantial effects on behavioral performance. Thalamic activation is less reliably reproducible across scan sessions than frontoparietal activation. More complex decision making tasks, where different strategies may be engaged, allow some latitude regarding which neural circuits are engaged and are potentially less at risk of use-dependent effects.
Extensive electroencephalographic (EEG) sleep studies have demonstrated increases in rapid eye movement (REM) sleep and changes in non-rapid eye movement (NREM) sleep in depression. Preclinical evidence shows that REM sleep is generated in the brainstem. It also shows that NREM sleep is characterized by slower frequency, higher amplitude thalamocortical electrical oscillations. The alterations in NREM sleep in depressed patients may lead to impaired restoration of prefrontal cortex function during NREM sleep. Functional neuroimaging studies of sleep extend the preclinical understanding of the mechanisms of sleep/wake regulation by providing potential links between neural systems involved in emotional behavior and those involved in sleep. The notion of hyperarousal in paralimbic structures in depressed patients has received further support from an extensive literature describing the functional neuroanatomical correlates of the antidepressant response to sleep deprivation in depressed patients. Patients with schizophrenia are known to have severely disturbed subjective sleep.
Deficits in attention are a central mechanism through which performance in higher cognitive domains such as memory may be affected in sleep deprivation (SD). This chapter reviews how different facets of attention and information processing are compromised in sleep-deprived persons. It discusses the link between behavioral alterations and concurrently observed shifts in task-related functional magnetic resonance imaging (fMRI) signal as well as how imaging can reveal alterations in processing not evident in overt behavior. Complimenting attention's enhancement effects is its ability to suppress irrelevant distractors. This ability is impaired by SD. The perceptual load theory of attention provides a useful framework for evaluating SD-induced change in visual information processing. Reduced engagement of frontoparietal regions that mediate top-down control of attention has been demonstrated in experiments evaluating visual short-term memory (VSTM), preparatory attention, and selective attention.