Psychological stress and sleep
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Sleep is a naturally recurring state of mind and body, characterized by altered consciousness, relatively inhibited sensory activity, reduced muscle activity and inhibition of nearly all voluntary muscles during rapid eye movement (REM) sleep, and reduced interactions with surroundings. The correlation between psychological stress and sleep is complex and not fully understood. Sleep change depends on the type of stressor, sleep perception, related psychiatric conditions, environmental factors and physiological limits.
Types of stressorEdit
Stressors can be categorised into the Challenge/Hindrance stressor model. Challenge stressors, while unpleasant, allow for growth and achievement such as time pressure in a work context. Hindrance stressors are those that cause unnecessary burden and do not contribute to achievement such as poor work supervision. Self-reported quality of sleep reduces in relation to more hindrance stressors but not to challenge stressors. Sleep duration does not change in relation to the hindrance: challenge ratio and neither does increased stressful working hours effect self-reported sleep quality.
Sleep quality perceptionEdit
Insomnia is a common condition affecting up to a fifth of the population in many countries across the world and is often complicated by a number of psychiatric conditions. Paradoxical insomnia is the phenomenon of a discrepancy between reported sleep duration and objective measurement of sleep. In some cases however the stress and anxiety produced does, in fact, result in an objective reduction in quality of sleep.
Sleep can be broadly split into the lighter "rapid eye movement" (REM) and deeper "non-rapid eye movement" (NREM). Changes in sleep phase varies in animal models depending on the stressor but does not alter total sleep duration with the exception of novelty which reduces both REM and NREM. Conditioned fear for example reduces REM sleep whereas auditory stimulation increases it.
In humans, models of stress have been closely linked to the context depression. Changes in sleep patterns in depression are very close to those seen in acutely stressed animals; these changes can be used as a predictor for developing depression. Long-term/ chronic psychosocial stress is known to cause depression symptoms but the effect of chronic stress on sleep without the confounding factor of depression is unclear. Early life sleep disruption caused by stressors may affect neuroplasticity and synaptic connectivity potentially leading to the development of mood disorders. This poor sleep may become a stressor itself compounding the phenomenon.
In animal studies, psychologically stressed rats display an increase in total REM sleep and average length of REM phase duration (but not number of cycles). This change is mediated by cholinergic neurons as stressed animals' prolonged REM cycles can be reduced by using a cholinergic antagonist (atropine). One study found that auditory stimulation stressors act similarly by inhibiting the cholinergic reduction of REM sleep. Chronic mildly stressed rats display a reduction in inhibitory GABA receptors in the hypothalamus (increasing the release of stress hormones) and brain stem among others. Within the pedunculopontine tegmentum region, in the brainstem, reduced GABA imbibition of cholinergic neurons acts again in the same way in increases REM sleep duration.
The neuroendocrine hypothalamic-pituitary-adrenal axis is a system of hormones that culminates in the release of cortisol from the adrenal glands in response to acute stress and is also seen to regulate sleep patters. The reduction in GABA receptors in the hypothalamus seen in chronic stress reduces the inhibition of stress hormone release however does not appear to impact sleep patterns after exposure to a stressful social stimulus in animals.
Pre-natal and childhood stressEdit
Chronic maternal stress in pregnancy exposes the foetus to increased levels of glucocorticoid and inflammatory markers which in turn negatively effects the H-P-A axis and disrupts sleep regulation of the foetus. Up until the age of 2 years, children who have been exposed to pre-natal stress have shortened and disorganized sleeping patterns. During early childhood development the child's brain is particularity sensitive to adverse events such as family conflict, maternal post-natal depression or abuse. It is thought that it is via sensitization of the H-P-A axis that an abnormal stress response is developed in response to these events/ stressors which in turn causes emotional disorders and later life sleeping disorders. 
Observations have been made that there is an association between stress, sleep and Interleukin-6 proposing a possible mechanism for sleep changes.
During both chronic and acute phase sleep deprivation there are increases in the pro-inflammatory cytokine Interleukin-6 (IL-6). Not only is IL-6 influenced by the circadian rhythm but its effectiveness is increased by sleep itself as there is an increase in serum IL-6 receptor during sleep. After periods of long sleep deprivation the first post-deprivation sleep shows a marked drop in IL-6 and an increase in slow wave sleep / "deep sleep". Similarly napping during the day time has been shown to decrease IL-6 and reduce tiredness. When humans are injected with exogenous IL-6 they display an increase in fatigue and other sickness behaviour.
This IL-6 increase is also observed during times of increased psychological stress. In a laboratory setting, individuals exposed to psychological stressors have had raised IL-6 (and acute phase protein CRP) measured especially in those who displayed anger or anxiety in response to stressful stimulus. Just as the human body responds to inflammation-inducing illness with increased fatigue or reduced sleep quality, so too does it respond to psychological stress with a sickness behaviour of tiredness and poor sleep quality. While sleep is important for recovery from stress, as with an inflammatory illness, continuous and long term increases of inflammatory markers with its associated behaviours may be considered maladaptive. 
Since the American Civil War there has been multiple "war syndromes" reported such as 'irritable heart', 'effort syndrome' and 'Gulf War Syndrome'. Thought to be discrete and different from post-traumatic stress disorder (PTSD), these war syndromes have a range of physical symptoms but commonly feature sleep disturbances, tiredness, poor concentration and nightmares. The historic picture is unclear due to poor contemporary understanding of psychological illness and, in more modern conflicts, gathering data has been difficult due to operational priorities; no cause has been identified that isn't connected to psychological stress.
Sleep is often a core focus for both diagnosis and management of PTSD with 70% of PTSD patients reporting insomnia or sleep disturbances. When studied against controls, however, little difference was measured in the quality of sleep suggesting a paradoxical insomnia along with physiological H-P-A axis involvement and "fight or flight responses". Its is on this basis that CBT, a non-pharacological therapy, is justified along with pharmacological intervention.
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