Consequence of sleep loss

The major consequence of acute or chronic sleep curtailment is excessive sleepiness. Excessive sleepiness is a subjective report of difficulty staying awake that is serious enough to impact social and vocational functioning and increase the risk for accident or injury. While self-imposed sleep restriction is a common cause of excessive sleepiness, disruption of the normal sleep cycle (as seen in shift work), underlying sleep disorders, medications, alcohol and substance use, and many medical and psychiatric disorders are important causes of excessive sleepiness.

We need to only look to our own experiences with acute or total sleep loss to recognize its consequences. After a poor night’s sleep, we feel tired, lethargic, and out of synch. The effects of chronic sleep deprivation may be less obvious but may have a greater overall impact on health and well-being. A discrepancy between hours of sleep obtained and hours of sleep required for optimal functioning is responsible for a state of sleep deprivation, which has widespread implications for quality of life, health, and safety. Since there can be considerable individual variability in total sleep need, the term sleep deprivation applies only to impaired functioning due to sleep loss.

Many of the neurocognitive symptoms of chronic sleep deprivation can mimic psychiatric symptoms, highlighting the importance of a comprehensive sleep evaluation for patients with mental health disorders. In a recent multiethnic, representative sample of U.S. adults, insufficient sleep/rest was shown to be positively associated with poor self-rated health (Geiger et al., 2012). Adults who sleep less than 6 hours per night are more likely to report fair to poor general health, mood disturbance, increase in pain syndromes/perception, impaired cognitive function and memory disturbance, and reduction in measures of overall quality of life (Grandner et al., 2010).

Short and long sleep duration (sleeping less than 6 hours per night or greater than 8 hours per night) is associated with up to a twofold increased risk of obesity, diabetes, hypertension, cardiovascular disease, stroke, depression, substance abuse, and all-cause mortality in multiple studies (NCSDR, 2011). Less than 6 hours of sleep per night is associated with impaired glucose tolerance, elevated cortisol levels, and alterations in sympathetic nervous system activity. Sleep deprivation may be linked to obesity since it is associated with dysregulation of leptin (a hormone that regulates satiety or feelings of fullness) and ghrelin (a hormone that regulates hunger). Less than 6 hours of sleep per night may also increase pro-inflammatory markers such as C-reactive protein, tumor necrosis factor, and interleukin (Luyster et al, 2012). All these problems are common pathways to the development of cardiovascular disease and diabetes. Mechanisms linking long sleep time with vascular and metabolic morbidities are unknown but may be related to cofounders such as depression, inactivity, low socioeconomic status, and overall poor general health (Luyster et al., 2012).

Sleep loss diminishes safety and results in the loss of lives and property. Sleep deprivation can produce psychomotor impairments equivalent to those induced by alcohol consumption at or above the legal limit. Daytime wakefulness in excess of 17 to 19 hours can produce psychomotor deficits equivalent to blood alcohol concentrations (BACs) between 0.05% and 0.1% (the legal limit in most states is 0.08%) (Williamson & Feyer, 2007; Insurance Institute for Highway Safety, 2012).

Acute or chronic sleep deprivation can result in episodes of microsleep lasting from a second up to 10 seconds when a tired person is trying to stay awake. Many of us have experienced this when sitting in a class or in a meeting; this can lead to lower capabilities and efficiency of task performance and increased risk for errors (Orzel-Gryglewska, 2010). Some of the most devastating environmental and human tragedies of our time can be linked to human error due to sleep loss and fatigue. The grounding of the Exxon Valdez, the nuclear meltdown at Three Mile Island, and the explosion of the Union Carbide chemical plant in India are prime examples. Sleepiness with driving has become a national epidemic. The 2011 NSF Sleep in America Poll indicates that an alarming 52% of respondents admit to driving while sleepy. An incredible statistic cites one third of Americans report falling asleep while driving once or twice a month (CDC, 2010).

Although researchers have tried to quantify the financial burden associated with sleep disruption, there is relatively little comprehensive data available on the economic burden of sleep-wake disorders; however, considering the prevalence, impact on overall health and quality of life, and the indirect costs associated with property loss and damage, the economic burden is likely in the billions of dollars (Skaer & Sclar, 2010). For example, a recent study estimated that chronic insomnia results in nearly $63.2 billion dollars in direct and indirect expenses annually (Kessler et al., 2011).

Formal training in sleep or sleep disorders within medical and nursing education is limited, and the number of trained clinicians and scientists continues to be insufficient (Institute of Medicine [IOM], 2006). Awareness among health care providers regarding the prevalence and burden of sleep disruption and the problem of inadequate sleep is underappreciated, and providers do not routinely screen for sleep disturbance or inquire about overall sleep quality (Sorscher, 2008). Consequently, sleep disturbances may not be recognized, diagnosed, managed, and treated.

In this chapter, we briefly review the components of normal sleep, sleep regulation, and functions of sleep; give an overview of the most common sleep disturbances encountered in the clinical environment, with a focus on their relationship to psychiatric illness; and discuss the nurse’s role in the assessment and management of a patient presenting with sleep disturbance.

Normal sleep cycle

Sleep is a dynamic neurological process that involves complex interaction between the central nervous system and the environment. Behaviorally, sleep is associated with low or absent motor activity, a reduced response to environmental stimuli, and closed eyes. Neurophysiologically, sleep is categorized according to specific brain wave patterns, eye movements, and general muscle tone. Sleep is measured electrophysiologically through electroencephalogram (EEG) and consists of two distinct physiological states: non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

NREM sleep is divided into three stages (N1, N2, N3) according to criteria by the AASM (2005) and is characterized by progressive or deeper sleep. Stage 1 (N1) is a brief transition between wakefulness and sleep and comprises between 2% to 5% of total sleep time. The time it takes to fall to sleep is referred to as sleep latency. During stage 1 sleep, body temperature declines and muscles relax. Slow, rolling eye movements are common. People lose awareness of their environment but are generally easily aroused. Stage 2 (N2) sleep occupies 45% to 55% of total sleep time; heart rate and respiratory rate decline. Arousal from stage 2 sleep requires more stimuli than stage 1.

Stage 3 (N3) is known as slow wave sleep or delta sleep. Slow wave sleep is relatively short and constitutes only about 13% to 23% of total sleep time. It is characterized by further reduction in heart rate, respiratory rate, blood pressure, and response to external stimuli. The three stages of NREM sleep make up 75% to 80% of total sleep time. Stage 3 sleep is considered to be “restorative sleep,” as it is a time of reduced sympathetic activity.

REM sleep comprises 20% to 25% of total sleep time and is characterized by reduction and absence of skeletal muscle tone (muscle atonia), bursts of rapid eye movement, myoclonic twitches of the facial and limb muscles, reports of dreaming, and autonomic nervous system variability. The atonia in REM sleep is thought to be a protective mechanism to prevent the acting out of nightmares and dreams (Carskadon & Dement, 2011). Figure 19-1 shows the EEG patterns characteristic of these sleep stages.

In the adult, sleep normally begins with NREM sleep. Continuous EEG recordings of sleep demonstrate an alternating cycle between NREM and REM sleep. There are typically four to six cycles of NREM and REM sleep occurring over 90- to 120-minute intervals across the sleep period. There is also a distinct organization to sleep, with NREM predominating during the first half of the sleep period and REM sleep predominating during the second half. The shortest REM period occurs 60-90 minutes after sleep onset and lasts only for several minutes. The longest REM period occurs at the end of the sleep period and can last up to an hour. This is the reason why many people remember dreaming upon awakening in the morning (Carskadon & Dement, 2011).

The structural organization of NREM and REM sleep is known as sleep architecture and is often displayed graphically as a hypnogram. Figure 19-2 is a hypnogram depicting the normal progression of the stages of sleep in an adult. The visual depiction of sleep is helpful in identifying sleep continuity (i.e., the distribution of sleep and wakefulness across the sleep period), as well as changes in sleep that may occur as a result of aging, illness, or certain medications. Disruption of sleep stages as indicated by excessive amounts of stage 1 sleep, multiple brief arousals, and frequent shifts in sleep staging is known as sleep fragmentation. Figure 19-3 is a hypnogram of a patient with a complaint of insomnia, indicating multiple brief arousals.

The function of alternations between NREM and REM sleep is not yet understood, but irregular cycling, absent sleep stages, and sleep fragmentation are associated with many psychiatric disorders, sleep disorders, and medication effects. For example, in patients with depression, the latency to REM sleep is frequently reduced, as is the percentage of slow wave sleep. Patients with narcolepsy frequently enter sleep through REM sleep rather than NREM sleep. Benzodiazepines tend to suppress slow wave sleep whereas serotonergic drugs suppress REM sleep.

Sleep patterns

Sleep architecture changes over the lifespan. The percentage in each stage of sleep, as well as the overall sleep efficiency, or ratio of sleep duration to time spent in bed, varies according to age. For example, infants sleep 16 to 18 hours a day, enter sleep through REM (not NREM) sleep, and spend up to 50% of sleep time in REM sleep. The percentage of REM sleep decreases to 20% to 25% by age 3 and stays relatively constant throughout old age. The amount of slow wave sleep is maximal in young children and declines with age to almost none, particularly in men. This results in a tendency for middle-of-the-night awakenings and reduced sleep efficiency with age (Bliwise, 2011).

Regulation of sleep

Although the regulation of sleep and wakefulness is not completely understood, it is believed to be a complex interaction between two processes, one that promotes sleep—known as the homeostatic process, or sleep drive—and one that promotes wakefulness, known as the circadian process, or circadian drive. The homeostatic process, is dependent on the number of hours a person is awake. The longer the period of wakefulness, the stronger the sleeps drive. During sleep, the sleep drive gradually dissipates.

Circadian drives are near-24-hour cycles of behavior and physiology generated and influenced by endogenous and exogenous factors and are wake-promoting. The exogenous factors are various clues from the environment known as zeitgebers (time-givers) that help set our internal clock to a 24-hour cycle. The strongest external cue for wakefulness is light whereas darkness is the cue for sleep. Other environmental cues include the timing of social events, such as meals, work, or exercise (Czeisler et al., 2011).

A master biological clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. This clock regulates not only sleep but also a host of other biological and physiological functions within the body. Information about the lighting conditions of the external environment is relayed to the SCN from the retina. The SCN also receives information from the thalamus and the midbrain. These two pathways transmit photic and nonphotic information to the circadian clock through an expansive network. In addition to regulating sleep/wake cycles, they also exert control over endocrine regulation, body temperature, metabolism, autonomic regulation, psychomotor and cognitive performance, attention, memory, and emotion (Czeisler et al., 2011).

In addition to the circadian and homeostatic processes, several neurotransmitter systems are responsible for sleep and wakefulness. The neurotransmitters responsible for wakefulness are dopamine, norepinephrine, serotonin, acetylcholine, histamine, glutamate, and hypocretin; sleep-promoting neurotransmitters include adenosine, gamma–aminobutyric acid (GABA), and galanin (Carney et al., 2011). Any medication that crosses the blood-brain barrier may have effects on sleep and wakefulness through modulation of these neurotransmitters.

It is important to appreciate the neurotransmitters involved in sleep and wakefulness; many of the medications used in psychiatry manipulate these neurotransmitter systems. For example, amphetamines—which promote wakefulness—increase the release of dopamine and norepinephrine. Caffeine (methylxanthine)—which promotes alertness—functions by blocking adenosine. Patients newly started on selective serotonin reuptake inhibitors (SSRIs) frequently report difficulty sleeping when beginning treatment with one of these agents.

Functions of sleep

Despite remarkable advances in the understanding of sleep disorders and the biological and physiological process of sleep, very little is known about the true function of sleep. Most of the information regarding the function of sleep comes to us from animal models of sleep deprivation and human models of partial sleep deprivation. Based on these models, several theories are proposed and include brain tissue restoration, body restoration (NREM sleep), energy conservation, memory reinforcement and consolidation (REM sleep), regulation of immune function, metabolism and regulation of certain hormones, and thermoregulation (Bonnet, 2011).

Sleep requirements

Sleep architecture and efficiency may change over time, but there is little change in the amount of sleep required once we reach adulthood. Sleep requirement varies considerably from individual to individual and to some degree is probably genetically mediated. While most adults require 7 to 8 hours of sleep for optimal functioning, there is a small percentage of individuals defined as long sleepers (requiring 10 or more hours per night) and short sleepers (requiring less than 5 hours per night). The amount of sleep required is the amount necessary to feel fully awake and able to sustain normal levels of performance during the periods of wakefulness and is known as the basal sleep requirement.

For many people, there is a misconception regarding sleep need and a tendency to allow circumstances to dictate the amount of sleep obtained. The most accurate way to determine sleep requirements is to establish a routine bedtime and allow oneself to sleep undisturbed without an alarm for several days. This is usually best accomplished during an extended period of leisure time, such as during a vacation. The average of several nights’ sleep undisturbed is a good estimate of the basal sleep requirement.

Hypersomnolence disorders

Hypersomnolence disorders are associated with excessive daytime sleepiness and have a prevalence of more than 15% in the general population (Ohayon et al., 2012). Hypersomnolence disorders are chronic (3 months or more) and begin in young adulthood (Ali et al., 2009). The patient with hypersomnolence reports recurrent periods of sleep or unintended lapses into sleep, frequent napping, a prolonged main sleep period of greater than 9 hours, non-refreshing non-restorative sleep regardless of amount of time slept, and difficulty with full alertness during the wake period. Excessive sleepiness significantly impairs social and vocational functioning by impacting the person’s ability to participate in and enjoy relationships and function in the workplace. Cognitive impairment is common as is an increased risk for accident or injury associated with the sleepiness.

Treatment for hypersomnolence disorders focuses on maintaining a regular sleep-wake schedule with an ample sleep opportunity. Some individuals will improve if they allow for an extended sleep opportunity of 10 or more hours. Pharmacotherapy with long-acting amphetamine-based stimulants such as methylphenidate and non-amphetamine-based stimulants such as modafinil are helpful.

Narcolepsy/hypocretin deficiency

The classic symptoms of narcolepsy/hypocretin deficiency include irresistible attacks of refreshing sleep, cataplexy, hypnagogic hallucinations, and sleep paralysis. Cataplexy is defined as brief episodes of bilateral loss of muscle tone with maintained consciousness. This usually happens along with a strong emotion such as anger, frustration, or laughter. Symptoms may last for up to several minutes, and recovery is generally immediate and complete. Hypnagogic hallucinations may be auditory, visual, and tactile and occur at sleep onset. Sleep paralysis is an inability to move or speak during the transition from sleep to wakefulness. Hynagogic hallucinations and sleep paralysis are quite frightening and may be misdiagnosed as psychiatric symptoms, frequently delaying the identification and treatment of the patient with narcolepsy/hypocretin deficiency.

Additional symptoms of narcolepsy/hypocretin deficiency include disturbed nighttime sleep with multiple middle-of-the-night awakenings and automatic behaviors characterized by memory lapses. Narcolepsy/hypocretin deficiency is distinguished from primary hypersomnia or other hypersomnia disorders in that patients with narcolepsy/hypocretin deficiency generally feel refreshed upon awakening but within 2 or 3 hours begin to feel sleepy again. Individuals with other hypersomnia disorders generally do not feel rested or refreshed regardless of the amount of sleep obtained. Hypocretin measurements in cerebrospinal fluid provide an objective basis for diagnosis (Gever, 2012). Treatment is through lifestyle modifications and long-acting stimulant medication.

Breathing-related sleep disorders

The most common disorder of breathing and sleeping is obstructive sleep apnea hypopnea syndrome (OSAHA), which is characterized by repeated episodes of upper airway collapse and obstruction that result in sleep fragmentation. Patients maintain respiratory effort against an obstructed airway. Essentially, patients with obstructive sleep apnea are not able to sleep and breathe at the same time. Typical symptoms include loud, disruptive snoring, witnessed apnea episodes, and excessive daytime sleepiness. Obesity is an important risk factor for obstructive sleep apnea. Diagnosis is determined by clinical evaluation and polysomnography. Treatment is with continuous positive airway pressure (CPAP) therapy.

Additional breathing-related sleep disorders include central sleep apnea and sleep-related hypoventilation. Central sleep apnea is the cessation of respiration during sleep without associated ventilatory effort and is caused by instability of the respiratory control system. Central sleep apnea is seen in older individuals, those with advanced cardiac or pulmonary disease, or those with neurological disorders. Sleep-related hypoventilation is associated with sustained oxygen desaturation during sleep in the absence of apnea or respiratory events and is seen in individuals with morbid obesity, lung parenchymal disease, or pulmonary vascular pathology.

Circadian rhythm sleep disorder

Circadian rhythm sleep disorders occur when there is a misalignment between the timing of the individual’s normal circadian rhythm and external factors that affect the timing or duration of sleep. Diagnosis is determined by clinical evaluation, sleep diaries, and actigraphy. Treatment is with aggressive lifestyle management strategies aimed at adapting to or modifying the required sleep schedule. Examples include delayed sleep phase type, advanced sleep phase type, irregular sleep-wake type, free-running type, jet lag type, and shift work type.

Disorders of arousal

Unusual or undesirable behaviors of sleep that occur during sleep-wake transitions or during certain stages of sleep are known as disorders of arousal.

Sleepwalking, or somnambulism, consists of a sequence of complex behaviors that begin in the first third of the night during NREM sleep and usually progress (without full consciousness or later memory) to leaving the bed and walking about. The individual may dress, go to the bathroom, leave the house, and, in some extreme cases, drive a car. Because of the possibility of accident or injury, a sleep specialist should always evaluate somnambulism. Polysomnography is sometimes indicated to rule out the possibility of an underlying disorder of sleep fragmentation. Treatment consists of instructing the patient and family regarding safety measures, such as alarms or locks on windows and doors and gating stairways. Attention to sleep hygiene, limiting alcohol prior to bed, obtaining adequate amounts of sleep, and stress reduction are helpful. Benzodiazepines are frequently prescribed when the risk for accident or injury is likely.

Confusional arousals consist of mental confusion or confused behavior during or following arousal from slow wave sleep but also upon attempted awakening from sleep in the morning. Patients may sometimes state that they are not sure they are awake or asleep. Sleepwalking is sometimes difficult to distinguish from confusional arousals because the sleepwalker may frequently seem disoriented. As with sleepwalking, treatment is focused on lifestyle management, safety measures, and gentle reassurance of the confused individual during an episode.