REM Sleep

Because most people awakened during an REM period report that they were dreaming, physicians have come to equate REM sleep with dream-filled sleep. Dreams that occur during REM sleep possess intellectual complexity, at least on a superficial level, and rich visual imagery.

Except for the eye movements and normal breathing, people in REM sleep remain immobile with paretic, flaccid, and areflexic muscles. EMGs recorded from chin and limb muscles, which are a standard placement, show no electric activity (Fig. 17-1). This paralysis is fortuitous because it prevents people from acting out their dreams.

FIGURE 17-1 Polysomnography of rapid eye movement (REM) sleep displays nine channels, each of which monitors a physiologic function. The EEG has low-voltage, fast activity similar to the EEG activity of awake individuals. The electro-oculogram (EOG) channel – ROC-LOC – reflects several REMs by large-scale, quick fluctuations. Electromyograms (EMGs) of the chin and right anterior tibialis muscles show virtually no activity, which indicates an absence of muscle movement and tone (flaccid paresis). The microphone detects a snore. The regular, undulating airway and diaphragm recordings indicate normal breathing and air movement.

In marked contrast to the flaccid muscle paralysis during REM sleep, autonomic nervous system (ANS) activity increases and produces generally increased but sometimes labile pulse and elevated blood pressure, raised intracranial pressure, increased cerebral blood flow, greater muscle metabolism, and, in men, erections. As though defying psychoanalytic interpretation, erections develop regardless of the content of boys’ and men’s dreams. The discrepancy between intense ANS activity and the immobile body led early researchers to describe REM sleep as “activated” or “paradoxical” sleep. In fact, REM-induced ANS activity has been implicated in the increased incidence of myocardial infarctions and ischemic strokes that strike between 6:00 and 11:00 AM.

The EEG also shows surprising activity during REM sleep. Aside from eye movement artifact, the REM-induced EEG appears similar to the EEG in wakefulness. Overall, REM sleep with its ANS activity and EEG patterns, except for the almost complete absence of EMG activity, resembles wakefulness far more than NREM sleep.

Nuclei in the pons generate the basic physical elements of REM sleep, and the peri-locus ceruleus, situated immediately adjacent to locus ceruleus, abolishes muscle tone (see Chapters 18 and 21). In other words, an active process, rather than simply relaxation, produces REM sleep’s characteristic paresis as well as the characteristic ocular movement.

On a biochemical level, REM sleep is accompanied by decreased activity of monoamine neurotransmitters: dopamine, norepinephrine, epinephrine, and serotonin; however, it is accompanied by an increase in acetylcholine (cholinergic) activity. For example, cholinergic agonists, such as arecoline, physostigmine, and nicotine, induce or enhance REM activity. Conversely, medications with anticholinergic side effects, including tricyclic antidepressants (TCAs), suppress it. In fact, most antidepressants suppress REM activity.

NREM Sleep

NREM sleep, in contrast to REM sleep, has three stages (N1–3) distinguishable primarily by progressively greater depths of unconsciousness and slower, higher-voltage EEG patterns. In addition, during early NREM sleep, eyes roll slowly and cognitive activity consists only of brief, rudimentary, and readily forgotten thoughts or notions. Unlike individuals’ ability to recall dreams that occur during their REM sleep, they have little or no recall of any thought content that might develop during their NREM sleep.

Other distinguishing features of NREM sleep relate to the motor system. Individuals in NREM sleep have conspicuous repositioning movements of their body, relatively normal muscle tone, and preserved deep tendon reflexes. Their chin and limb muscles display readily detectable EMG activity (Fig. 17-2).

FIGURE 17-2 The polysomnogram of N1 stage sleep, which neurologists previously called stage l nonrapid eye movement sleep, shows low-voltage, 7-Hz activity. The ROC-LOC channel shows occasional slow ocular movement (i.e., no rapid eye movement activity). The chin electromyogram shows continual low-voltage activity that reflects persistent muscle tone.

Also contrary to individuals in REM sleep, those in NREM sleep have a generalized decrease in ANS activity. The decreased ANS activity typically leads to hypotension and bradycardia. Similarly, cerebral blood flow and oxygen metabolism fall to about 75% of the awake state and reach the level produced by light anesthesia.

Nevertheless, important hypothalamic–pituitary (neuroendocrine) activity accompanies NREM sleep. For example, the daily secretion of growth hormone occurs almost entirely during NREM sleep, about 30–60 minutes after sleep begins. In another endocrine surge, serum prolactin secretions rise to their highest level about the same time. Cortisol concentration is also sleep-dependent, but its secretion occurs in 5–7 discrete late nighttime episodes, which accumulate to yield the day’s highest cortisol concentration at about 8:00 AM.

Overall, N3 sleep, often called slow-wave sleep, probably provides most of the physical recuperation derived from a night’s sleep. As if the immediate role of sleep were to revitalize the body, this sleep phase occurs predominantly in the early night, almost as soon as people fall asleep. After “squeezing” it into the beginning of the night, remaining sleep lightens and allows more dreams, i.e., sleep shifts to N1, N2, and REM sleep.

Patterns

After going to bed, people usually fall asleep within 10–20 minutes. That interval, sleep latency, is inversely related to sleepiness: the greater the sleepiness, the quicker people fall asleep and the shorter the interval. Neurologists sometimes refer to sleepiness as “sleep pressure” and have correlated it with serum concentrations of adenosine. In other words, the concentration of adenosine, which is a nucleoside, rises with sleep pressure and the degree of sleepiness.

During daytime, sleep latency shrinks to its shortest duration during the afternoon, at approximately 4:00 PM. However, numerous psychologic and physical factors may alter it. In fact, short sleep latencies characterize several sleep disorders (Box 17-1).

The ratio of the total time asleep to the time in bed, expressed as a percentage, defines sleep efficiency. Reduced sleep efficiency, ratios considerably lower than 1.0, characterizes numerous disorders.

Once asleep, normal individuals enter NREM sleep and pass in succession through its three stages. After 90–120 minutes of NREM sleep, they enter the initial REM period. Abnormalities in the interval between falling asleep to the first REM period, the REM latency, characterize several sleep disorders, particularly narcolepsy (Box 17-2).

The NREM–REM cycle repeats throughout the night with a periodicity of approximately 90 minutes. REM periods develop four or five times in total, but in the latter half of the night, they lengthen and occur more frequently (Fig. 17-3). Also, in the latter half, when the tendency toward REM sleep peaks, body temperature falls to its lowest point (the nadir). The final REM period typically merges with awakening. Consequently, people can most easily recall their final dream, which may incorporate surrounding morning household activities. In addition, because of residual REM influence, men’s erections often persist on awakening.

FIGURE 17-3 In the conventional representation of a normal night’s sleep pattern – its sleep architecture or hypnogram – the first rapid eye movement (REM) period starts approximately 90 minutes after sleep begins and lasts about 10 minutes. Later in the night, REM periods recur more frequently and have longer duration. Nonrapid eye movement (NREM) sleep progresses through its three stages (N1–N3).

Without external clues, an “internal biological clock,” centered in the suprachiasmatic nucleus of the hypothalamus, would set the daily (circadian) sleep–wake cycle at 24.5–25 hours (Fig. 17-4). This nucleus also sets the circadian hormone and metabolic rhythms. When individuals are forced to rely exclusively on their internal biologic clock, as when they volunteer for experiments that isolate them from their environment and its cues, such as living in caves for months, they gradually lengthen their circadian cycle to almost 25 hours and fall asleep later each day.

FIGURE 17-4 When healthy young adults are allowed to sleep and arise at will in rooms protected from time cues, such as clocks, daylight, daytime sounds, and delivery of meals on a fixed schedule, i.e., “free run,” they typically go to sleep later each day (delay their sleep phase) and extend their sleep–wake (circadian) cycle to 24.5– 25 hours, as shown here.

Adults average 7.5–8 hours of total sleep time, but with a broad range of 4–10 hours. Genetic and personal factors tend to set each individual’s total sleep requirement; however, environmental light–dark cycles, work schedules, and social demands usually override it. As they age, individual’s sleep time decreases.

Intrinsic Sleep Disorders

The intrinsic sleep disorders classification includes important, discrete, and well-established neurophysiologic disturbances. Patients typically come to medical attention because of EDS.

Narcolepsy

Narcolepsy, the most dramatic of the Intrinsic Disorders, emerges in 90% of patients between their adolescence and 30th year. In fact, its onset peaks in the teenage years. Young people with narcolepsy often remain undiagnosed or misdiagnosed as lazy, neurotic, or depressed. It affects young men and women equally.

The most salient feature of narcolepsy, EDS, takes the form of brief, irresistible sleep episodes (attacks). The attacks initially mimic normal daytime naps because they typically occur when patients are bored, comfortable, and engaged in monotonous activities. Each attack usually lasts less than 15 minutes and can be easily interrupted by noise or movement.

As narcolepsy progresses, sleep attacks evolve into episodes that clearly differ from normal naps. They then have a relatively abrupt onset and, more strikingly, take place when patients are standing, during a lively interchange, or in the middle of activities that require constant attention, including driving. Multiple attacks occur daily. Each may cause momentary amnesia, confusion, and autonomic changes.

Despite their not appearing as normal naps, sleep attacks are not peculiar to narcolepsy. Sleep attacks may also be a manifestation of sleep deprivation, sleep apnea, Parkinson disease, or, ironically, dopamine agonist treatment for Parkinson disease.

The other cardinal features of narcolepsy, cataplexy, sleep paralysis, and sleep hallucinations, which all reflect disordered REM sleep, usually develop after sleep attacks have become frequent. In total, the symptoms form the narcoleptic tetrad:

• EDS with sleep attacks

• Cataplexy

• Sleep paralysis

• Hallucinations on falling asleep (hypnagogic hallucinations) or during sleep (sleep-related hallucinations).

Narcolepsy may occur with or without cataplexy, i.e., narcolepsy with cataplexy and narcolepsy without cataplexy. Even when cataplexy complicates narcolepsy, it appears about 4 years into the illness. Depending on the diagnostic criteria, age of the patients, and duration of their narcolepsy, surveys have reported a wide variability of the proportion of narcolepsy patients who have cataplexy. Most surveys give a figure of 10–70%. In any case, with the comorbidity far below 100%, neurologists do not require cataplexy for a diagnosis of narcolepsy.

Cataplexy consists of attacks, typically lasting 30 seconds or less, occurring one to four times daily, of sudden weakness precipitated by emotional situations. Patients remain alert during an attack, but immediately afterwards they may have a sleep attack.

Cataplexy-induced weakness tends to be symmetric and proximal. For example, the neck, trunk, hips, knees, or shoulders may suddenly lose their strength. Sometimes the eyelids, jaw, or face weaken alone or in combination with the trunk and limbs. The most common pattern is sudden but brief weakness of the legs or merely the knees. Physicians and patients could easily dismiss attacks when they involve only jaw dropping open or head nodding. In its most sensational form of cataplexy, which rarely occurs, patients’ entire body musculature suddenly becomes limp and they collapse to the floor.

The most common precipitant of an attack is hearing or telling a joke. Other situations or emotions that commonly provoke it are surprise, anger, fear, and arousal.

Whether a group of muscles or the entire musculature weakens, affected muscles become flaccid and areflexic – as in REM sleep. Nevertheless, also as in REM sleep, patients breathe normally and retain full ocular movement.

Sleep paralysis and hypnagogic hallucinations – other components of the tetrad – affect about 50% of narcolepsy with cataplexy patients. They develop several years after the onset of narcolepsy. In other words, only 10% of narcolepsy patients display the full narcoleptic tetrad. Sleep paralysis and sleep hallucinations may be present on awakening (hypnopompic) or while falling asleep (hypnagogic). In sleep paralysis, patients are unable to move or speak for as long as several minutes on awakening or when falling asleep, but they remain cognizant of their surroundings, breathe, and move their eyes. This situation may terrify the patients who vainly attempt to scream or move about. Although sleep paralysis is a characteristic feature of narcolepsy, it is not diagnostic because it may occur in sleep-deprived individuals and anyone with REM deprivation.

During hypnopompic or hypnagogic hallucinations, patients essentially experience vivid dreams while in a twilight state, but they are technically awake. Hypnopompic or hypnagogic hallucinations qualify as an organic cause of visual hallucinations (see Chapters 9 and 12). As with the other features of narcolepsy, hypnopompic or hypnagogic hallucinations represent REM sleep intruding into people’s wakefulness or at least the transition into wakefulness (Fig. 17-5).

FIGURE 17-5 A narcoleptic attack begins when the electroencephalogram channel shows the low-voltage fast activity of rapid eye movement sleep. The absence of chin electromyogram activity indicates that muscles are flaccid. After several seconds, REMs begin.

In addition to the narcolepsy tetrad, multiple, brief, spontaneous awakenings interrupt nighttime sleep. These interruptions cause inadequate nighttime sleep that exacerbates the EDS.

In children, EDS, whether from sleep deprivation, narcolepsy, or other disorder, leads to somewhat different symptoms than in adults. For example, instead of being merely sleepy, children typically develop inattention and “paradoxical hyperactivity” (increased, usually purposeless, activity). Children with narcolepsy also have behavioral, cognitive, and scholastic impairments that resemble learning disabilities or attention deficit hyperactivity disorder. When combined with cataplexy (see later), these children may appear to have a behavioral disorder.

Neurologists use the multiple sleep latency test (MSLT) to support a clinical diagnosis of narcolepsy. Using PSG recording techniques, the MSLT determines both sleep latency and REM latency during five “nap opportunities” offered at 2-hour intervals during daytime. The MSLT shows that, in contrast to normal adults who might take a nap, those with narcolepsy fall asleep on two or more nap opportunities and do so almost immediately. In fact, narcolepsy patients typically take only 8 minutes or less to fall asleep and have SOREMP during at least two naps.

Although sensitive for the diagnosis of narcolepsy, MSLT abnormalities are not specific. The MSLT shows shortened sleep latency and SOREMPs in EDS from almost any cause. To reduce false-positive results, patients suspected of having narcolepsy should first undergo a PSG, mostly to exclude sleep apnea and sleep deprivation.

A complementary test, the maintenance of wakefulness test (MWT), measures daytime sleepiness by assessing an individual’s ability to remain awake. Subjects undergoing the MWT attempt to remain awake in a quiet, dark room while sitting still for four 40-minute periods at 2-hour intervals during daytime. Those who fall asleep have EDS. However, such a determination does not constitute a diagnosis of a particular disorder.

Narcolepsy probably results from an interaction of a genetic predisposition and environmental factors. First-degree relatives have a 10–40-fold increased risk of developing the illness, but the concordance rate between monozygotic twins is only 25%. Almost 90% of patients with cataplexy as well as narcolepsy carry a certain major histocompatibility complex, designated human leukocyte antigen (HLA) DQB1*0602, on chromosome 6. Despite the antigen’s prevalence among narcolepsy patients, the antigen is neither sufficient nor necessary to diagnose narcolepsy-cataplexy because approximately 25% of the asymptomatic general population also carries it and most carriers do not have the illness. Curiously, antistreptococcal antibody titers are elevated in narcolepsy-cataplexy patients.

In a major medical advance that has located narcolepsy’s physiologic basis, studies have shown close association between narcolepsy and a deficiency in a pair of polypeptide excitatory neurotransmitters, hypocretin 1 and 2, which are also known as orexin A and B.

Hypocretin normally maintains wakefulness and activity and stimulates the appetite. It is also associated with arousal and, during sleep, increased REM and decreased NREM activity. Different research groups named hypocretin for its location in the hypothalamus, and orexin for orexis (Greek, appetite).

Cells in the hypothalamus synthesize hypocretin. These cells, which are the only ones in the central nervous system (CNS) that synthesize hypocretin, project to several brainstem centers involved with sleep regulation, particularly the hypothalamus and locus ceruleus. They also secrete some hypocretin into the cerebrospinal fluid (CSF).

Distinctive findings in narcolepsy-cataplexy consist of degeneration of hypocretin-synthesizing cells in the hypothalamus and the resulting absence or near absence of hypocretin in the CSF. Low levels of CSF hypocretin correlate much more closely with narcolepsy with cataplexy than narcolepsy without cataplexy. Curiously, in both conditions serum hypocretin concentrations remain normal, which suggests that cells outside the CNS also synthesize it. Narcolepsy with the characteristic hypocretin deficiency also occurs in an autosomal recessive inheritance pattern in certain families of ponies and dogs. Their members serve as laboratory models of the disorder.

The primary goal in the treatment of narcolepsy is for the patient to remain awake during critical times, particularly when driving, attending school, and working. In one approach, methylphenidate (Ritalin) and amphetamines, which enhance adrenergic and dopaminergic activity, reduce EDS and the naps. The major problem with this approach is the potential for abuse. For example, even from the beginning, individuals may falsely report symptoms of narcolepsy-cataplexy in order to secure these stimulants. Individuals may then use or sell their drugs to others. Another potential problem is that stimulants induce tolerance and may create psychiatric side effects.

In a newer, superior approach, the nonamphetamine medication modafinil (Provigil) and its long-acting, r-enantiomer version armodafinil (Nuvigil) promote wakefulness without causing excitation or nighttime insomnia. Moreover, unlike stopping amphetamines and other stimulants, stopping them does not lead to EDS or a rebound in NREM sleep. In other words, they do not merely keep people awake by postponing sleep. Modafinil interacts with multiple neurotransmitters, including dopamine, serotonin, and gamma-aminobutyric acid (GABA).

Despite their help in counteracting narcolepsy and keeping patients awake, these medicines have little effect on cataplexy. Instead, a rapid-acting hypnotic, oxybate (Xyrem), also known as gamma-hydroxybutyrate (GHB) or the “date rape drug,” reduces cataplexy. In addition, it increases slow-wave sleep. Illicitly prepared oxybate has caused many complications, including profound amnesia, coma, seizures, and, with continued use, addiction (see Chapter 21). Even a pharmaceutical preparation in narcolepsy-cataplexy patients may lead to sleepwalking, enuresis, confusion, and sleepiness. It may also lead to depression in predisposed patients. However, it does not seem to lead to addiction or, on stopping it, rebound insomnia.

Whether or not patients use these medicines, they should arrange for regular, strategically placed daytime naps after meals and during the late afternoon (“nap therapy”). The naps should be brief because short naps provide as much rest and recuperation as long ones. Patients should also maintain regular nighttime sleep schedules.

Sleep-Disordered Breathing (Sleep Apnea)

Multiple, 10-second to 2-minute interruptions in breathing (apnea) during sleep characterize sleep apnea, which specialists call sleep-disordered breathing but which neurologists persist in calling sleep apnea. It is one of the most common physiologic causes of EDS. As though the brain interrupts sleep in order to breathe, five or more episodes of apnea each hour produce partial awakenings (“microarousals”). Patients remain unaware of the awakenings because they are so brief and incomplete. Nevertheless, the awakenings lead to restless sleep and subsequent EDS.

As breathing resumes at the end of an apneic episode, patients briefly snore loudly. That snoring, an audible signature of the disorder, represents a resuscitative mechanism. In practice, loud nighttime snoring in individuals with irresistible daytime napping and EDS constitutes a diagnosis of sleep apnea.

During the day, because of their EDS, sleep apnea patients succumb to relatively brief and unrefreshing naps. Between attacks, patients are often physically fatigued as well as lethargic. In a potentially misleading scenario, sleep apnea patients may describe their symptoms as chronic fatigue rather than chronic sleepiness.

Sleep apnea includes an obstructive and central variety. In the obstructive variety, fat-laden or flabby soft tissues of the pharynx, congenital deformities, hypertrophied tonsils or adenoids, or other pharyngeal abnormalities block the airway. Neuromuscular disorders, such as bulbar poliomyelitis, can also interfere with the airway by producing weakness of the pharynx.

The central variety, which is less common, results from reduced or inconsistent CNS ventilatory effort or congestive heart failure. Patients who have survived lateral medullary infarctions and other injuries to the medulla (see Chapter 2), which houses the respiratory drive center, are susceptible to central sleep apnea.

Both varieties of sleep apnea can produce arterial blood oxygen desaturation (hypoxia) with oxygen saturation as low as 40%, cardiac arrhythmias, and pulmonary and systemic hypertension. Thus, sleep apnea constitutes a risk factor for stroke. It also causes or predisposes patients to the metabolic syndrome, headache, and symptoms of depression.

Directly or indirectly, sleep apnea causes sleepiness to the point of befuddlement, forgetfulness, and sometimes confusion during the day. The sleepiness alone predisposes patients to motor vehicle accidents and impairs their ability to work and fulfill social responsibilities. Thus, sleep apnea, technically speaking, qualifies as a cause of dementia. Sleep apnea develops predominantly but not exclusively in middle-aged men with hypertension and obesity. However, about 30% of patients are not obese. In addition, sleep apnea may develop in older children, adolescents, and young adults.

Children have a different presentation than adults. Instead of complaining about EDS, children have attention deficits, hyperactivity, learning disabilities, and even aggression. They usually have enlarged tonsils and adenoids obstructing their airway, which cause their snoring and restless, agitated sleep. Also unlike adults with the disorder, they are not obese. Children with Down syndrome, because of the architecture of their neck and large tongue, are particularly prone to this disorder.

In both children and adults, the combination of EDS and snoring is the classic indication for performing a PSG. In sleep apnea, the PSG shows periods of apnea, arousals, and hypoxia. It detects intermittent loss of air flow despite chest and diaphragm respiratory movements and episodic loud snoring (Fig. 17-6). Because of sleep deprivation, sleep latency and REM latency both shorten and SOREMPs appear. During nighttime sleep, apnea episodes occur in either phase but more frequently during REM sleep because that sleep phase reduces muscle tone.

FIGURE 17-6 In sleep apnea, the polysomnogram shows that oxygen saturation falls during a period of nonrapid eye movement sleep. Hypoxia then triggers a partial arousal, indicated by faster electroencephalogram activity. Diaphragmatic movements reach a crescendo and loud snoring begins. After strenuous diaphragm movements, air moves through the nasal airway and oxygen saturation improves.

Successful treatment of sleep apnea eliminates or markedly reduces EDS and its systemic physiologic manifestations, including hypertension. Moreover, cognitive impairments respond to treatment, which qualifies sleep apnea as a reversible cause of dementia.

The initial management of sleep apnea, in most cases, attempts to have patients lose weight, give up smoking, and stop using hypnotics and alcohol. If those strategies do not alleviate the problem, physicians prescribe ventilation by nasal continuous positive airway pressure (CPAP). Although the device is cumbersome, CPAP remains the most reliable treatment. Other devices that might secure a patent airway include a tongue retainer and mandibular advancement prosthesis. Modafinil may help because it reduces EDS. Gastric bypass and other bariatric surgeries often benefit these patients because obesity is so often comorbid. Physicians should avoid prescribing benzodiazepines and opioid analgesics because they depress respirations. Tonsillectomy and adenoidectomy alleviate sleep apnea in children.

Periodic Limb Movement Disorder

Periodic limb movement disorder consists of regular (periodic), episodic stereotyped movements of the legs or, less often, arms during sleep. Most often individuals with periodic limb movements repetitively jerk both feet upward (dorsiflex at the ankle) in brief (0.5–5.0-second) thrusts. When the movements are confined to the legs, neurologists call the disorder periodic leg movements. In a more extensive variation, all the limbs simultaneously jerk. Whatever the pattern, the feet always move and EMG leads of the PSG show regular muscle contractions.

Movements take place at 20–40-second intervals, for episodes of 10 minutes to several hours primarily, but not exclusively, during stages of NREM sleep (Fig. 17-7). Periodic limb movements generally do not arouse patients. Thus, the movements rarely lead to EDS.

FIGURE 17-7 In periodic limb movements, approximately 30-second intervals of synchronous anterior tibialis contractions cause the patient’s ankles to dorsiflex and the electromyogram activity.

The disorder usually develops in individuals older than 55 years. It occurs in close association with RLS, with use of antidepressants, withdrawal from various medications, and the onset of certain medical illnesses, particularly anemia and uremia. A genetic variation on chromosome 6 is a risk factor. A disorder of dopamine physiology in either the brain or spinal cord may give rise to periodic limb movements.

Despite the frequent comorbidity of RLS and periodic movements, these conditions differ in many respects. Periodic limb movements occur at regular intervals, appear only during sleep, and do not arise as a response to either dysesthesias or an urge.

Neurologists usually do not treat periodic movements unless RLS is also present because they do not interrupt sleep, cause EDS, or create other problems. On the other hand, the movements may disrupt the sleep of a bed partner who may then develop EDS. When the movements require treatment, benzodiazepines and dopaminergic medications suppress them.

Extrinsic Sleep Disorders

Superimposed on a supposedly normal brain, outside factors, such as personal obligations, substances, or disruptions from the environment, cause extrinsic sleep disorders. In the most common subcategory, regularly taking a hypnotic, stimulant, or alcohol, for example, causes insomnia and its almost invariable sequela, EDS. The use of these substances for their hypnotic effect defines the condition; however, cutting a fine line, frank addiction, such as alcoholism, excludes it. The PSG generally shows short sleep latency, disrupted sleep, and fragmented or suppressed REM phases. Briefly put, people who take bedtime alcohol-containing drinks (“nightcaps”) rapidly reach deep sleep, but when their body metabolizes the alcohol in several hours, the person awakes in the early morning, which results in shortened, fragmented, and restless sleep.

Circadian Rhythm Disorders