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Abstract
Sleep is a state of unconsciousness in which the brain is relatively more responsive to internal than external stimuli.
Mechanism of sleep:
Withdrawal of sensory awareness is believed to be a factor in sleep, but an active initiation mechanism that facilitates brain withdrawal is also recognized.
The ”switch” for sleep is considered to be the ventro-lateral preoptic nucleus (VLPO) of the anterior hypothalamus. This area becomes active during sleep and uses the inhibitory neuro-transmitters GABA and galanin to initiate sleep by inhibiting the arousal regions of the brain.
Waking usually transitions into light NREM sleep.
STAGES OF SLEEP:
Normal sleep is divided into non–rapid eye movement (NREM) and rapid eye movement (REM) sleep.
NREM sleep:
NREM sleep is further divided into progressively deeper stages of sleep: stage N1, stage N2, and stage N3 (deep or delta-wave sleep). As NREM stages progress, stronger stimuli are required to result in an awakening.
NREM sleep is controlled by complex initiating and maintenance mechanisms, the extent of which is not fully elaborated. Probably no single sleep-generating center exists.
NREM is an active state that is maintained partly through oscillations between the thalamus and the cortex.
Although the functions of NREM sleep remain speculative, several theories have been put forth. One theory proposes that decreased metabolic demand facilitates replenishment of glycogen stores. Another theory, which utilizes neuronal plasticity, suggests that the oscillating depolarizations and hyperpolarizations consolidate memory and remove redundant or excess synapses.
REM sleep:
Stage R sleep (REM sleep) has tonic and phasic components. The phasic component is a sympathetically driven state characterized by rapid eye movements, muscle twitches, and respiratory variability. Tonic REM is a parasympathetically driven state with no eye movements. The REM period length and density of eye movements increases throughout the sleep cycle.
REM sleep is generated by the cholinergic mediated ”REM- on neurons” in the mesencephalic and pontine cholinergic neurons.
REM-off neurons” are the monoadrenergic locus ceruleus and serotonergic raphe neurons.
PTSD
Posttraumatic stress disorder (PTSD) is a debilitating anxiety disorder seen in 25-30% of individuals experiencing a traumatic event.
Athough initial theorists proposed that PTSD represents a normative response to exposure to extreme stressors, it soon became evident that only minority of individuals who experience a traumatic event will develop the disorder. Thus while most individuals are able to cope with the stressor and maintain or regain homeostasis, a small but significant minority of persons fail to recover and exhibits prolonged and abnormal behavior and physiological responses to the traumatic experience, as manifested in the symptoms of PTSD.
It is estimated that 70-87% of patients with PTSD experience sleep disruption. Specifically, the traumatic event is persistently re-experienced in recurrent distressing dreams or nightmares, and the patient has ongoing symptoms of increased arousal, manifesting as difficulty in falling or staying asleep. Other sleep problems, such as periodic limb movement disorder and sleep-disordered breathing, also appear to be more prevalent in patients with PTSD than in the general population.
The symptoms of PTSD are believed to reflect stress-induced changes in neurobiological systems and/or an inadequate adaptation of neurobiological systems to exposure to severe stressors. Consequently, much research has been focused on elucidating alterations in stress-regulating neurobiological systems in patients with PTSD. Neurobiological systems that have been implicated in the pathophysiology of PTSD include the hypothalamic-pituitary-adrenal (HPA) axis, as well as various neurotransmitters and neuropeptides that comprise a network of brain regions that regulate fear and stress responses, including the prefrontal cortex, hippocampus, amygdala, and brainstem nuclei. More recently, there have been attempts to link the identified neurobiological changes to the specific features that constitute PTSD, such as altered mechanisms of learning and extinction, sensitization to stress, and arousal.
Furthermore, there have been efforts to understand whether certain neurobiological changes in PTSD reflect preexisting vulnerability factors rather than consequences of trauma exposure or correlates of PTSD.