This section follows the system in the International Classification of Sleep Disorders, Revised (ICSD-2), which groups sleep complaints by primary symptomatology: insomnia, or disorders of initiating and maintaining sleep; hypersomnia, or disorders of EDS (Excessive Daytime Sleep); parasomnias; and circadian rhythm disorders. The section also comprises a brief discussion of sleep alterations associated with psychiatric disorders, substance use, medical conditions, and the reproductive cycle.
INSOMNIA
General Considerations
Insomnia is the complaint of difficulty initiating or maintaining sleep or of nonrestorative sleep (not feeling well rested after sleep that is adequate in amount). Insomnia is more common in women than in men; more common with age; and often associated with medical and psychiatric disorders or use of alcohol, drugs, and medication.
Clinical Findings
Transient insomnia is much more common than chronic (>1 month) insomnia. It generally results from acute stress. Many such cases resolve without intervention. PSG abnormalities have been documented in acute bereavement. However, persistent insomnia should raise the consideration of depression, adjustment disorder, or other psychiatric disorders. Psychophysiologic insomnia is a “disorder of somatized tension and learned sleep-preventing associations that result in a complaint of insomnia” (ICSD-2 1997). All patients with chronic insomnia probably develop learned sleep-preventing associations, such as marked overconcern with the inability to sleep. The frustration, anger, and anxiety associated with trying to sleep or maintain sleep serve only to arouse them further as they struggle to sleep. These patients can acquire aversive associations with their bedrooms, often sleeping better in other places such as in front of the television set, in a hotel, or in the sleep laboratory. Psychophysiologic insomnia can become chronic.
Differential Diagnosis
Because chronic insomnia is so commonly caused by medical, psychiatric, or substance use comorbidity or in association with medication, the clinician should always look carefully for other conditions and treat the primary disorder. Although 780.59 Breathing-Related Sleep Disorder is classified as a hypersomnia, apneic episodes can cause insomnia. Insomnia can also be associated with sleep-related movement disorders, for example, restless legs syndrome (RLS) and PLMs (discussed separately).
Treatment
Nonpharmacologic treatment includes education about sleep hygiene (Table 36–4, Stimulus-Control Treatment) as well as identifying and correcting faulty beliefs—for example, the fear of not being able to function at all without 8 hours of uninterrupted sleep.
Table 36–4 Stimulus-Control Treatment
Keep bedtimes and awakening constant, even on the weekends. |
Do not use the bed for watching television, reading a book, or working. If sleep does not begin within a period of time, say, 30 minutes, leave the bed and do not return until drowsy. |
Avoid napping. |
Exercise regularly (3–4 times per week) but try to avoid exercising in the early evening if this tends to interfere with sleep. |
Discontinue or reduce alcohol, caffeine, cigarettes, and other substances that may interfere with sleep. |
“Wind down” before bed with quiet or relaxing activities. |
Maintain a cool, comfortable, and quiet sleeping environment. |
Sleep restriction therapy involves gradually improving sleep consolidation (minimizing interruptions of the nocturnal sleep period) by limiting the time patients spend in bed. Many insomniac patients underestimate actual sleep time (“sleep state misperception”) and have poor sleep efficiency (SE). If the patient reports sleeping 6 hours per night, he or she is required to limit time in bed to 6 hours or slightly more. This simple maneuver usually produces mild sleep deprivation, shortens sleep latency, and increases SE. As sleep becomes more consolidated, the patient is allowed gradually to increase time in bed. It may be helpful to counsel for acute stressors and break the “vicious cycle” of psychophysiological insomnia.
Weighted blankets are popular, but safety concerns have been raised about small children and the elderly.
Meditation is good for sleep problems. The author (C.P. Clark) does not endorse a particular cell phone “app” but has many patients who like Calm. The author encourages looking at the meditation videos on YouTube in the Generation Calm series on anxiety, sleep, physical symptoms (intended for those produced by anxiety but useful for other problems such as side effects, and chronic pain) and recommends the wholesome newsletter as well. (Clare Roberts, PhD, ongoing)
Psychopharmacologic Interventions
Benzodiazepines (BZDs) have been for many years the most widely prescribed true sedative–hypnotics, being safer than barbiturates. They generally reduce sleep latency, minutes awake after sleep onset, SWS, and REM while increasing stage 2. The choice of BZD depends on onset and duration of action (in relation to the timing of sleep complaints) and anxiolytic properties if needed. In the absence of substance abuse history or concomitant abuse of other substances, short-term use of BZDs to treat insomnia is usually safe and effective. The long-term efficacy is not clear; physiologic tolerance can occur.
Non-BZD hypnotics include zolpidem, zaleplon, eszopiclone (the S-isomer of zopiclone), ramelteon, and suvorexant (Table 36–5). Compared to BZDs, these drugs tend to have less risk of misuse, rebound insomnia, and withdrawal symptoms and can generally be given to recovering addicts. Zolpidem can be taken in doses larger than described. Aside from ramelteon, these are GABAA receptor agonists, which probably explains their less marked motor and cognitive side effects. Onset and duration of action should be considered. Some non-BZDs can cause morning “hangovers” if taken too late in the night. Controlled-release zolpidem has been approved by the U.S. Food and Drug Administration (FDA) and has shown efficacy in long-term use as well.
Table 36–5 Non-benzodiazepine Hypnotics
Generic | Trade | Half-life (h) | Onset | Dose, Adult (mg) | Mechanism |
|---|---|---|---|---|---|
Zolpidem | Ambien | 1.5–2.4 | Fast | 5–10 | GABAA agonist |
Zaleplon | Sonata | 1 | Fast | 5–10 | GABAA agonist |
Eszopiclone | Lunesta | 5–7 | Medium | 2–3 | GABAA agonist |
Ramelteon | Rozerem | 1–2.6 | Fast | 8 | Melatonin agonist |
Suvorexant | Belsomra | 8 | Medium | 5,10,15,20 | Inhibitor of Orexin A and B |
Ramelteon, a selective melatonin (MEL) agonist (active at MT1 and MT2 sites), does not bind to GABA receptors, nor does it possess activity within the brain reward system. It is being marketed as “addiction proof”; if this claim stands the test of time, it will provide an important option for many patients in recovery. Its rapid onset of action and melatonergic mechanisms appear promising for initial insomnia, especially in the context of a delayed circadian phase.
Suvorexant is an inhibitor of orexin A and orexin B. Orexin, aka hypocretin, is a hormone that promotes wakefulness. There is concern that suvorexant may be habit forming.
Other medications prescribed for insomnia in the absence of psychiatric comorbidity include trazodone, other sedating antidepressants, and the more sedating atypical antipsychotics.
Over-the-counter (OTC) sleeping pills usually consist of or contain histamine 1 antagonists (e.g., diphenhydramine). Their efficacy is dubious. “Natural” remedies include valerian and MEL; the latter has been used for many years and probably does have some efficacy.
More recently, particularly in some jurisdictions, some cannabis products (cannabidiol [CBD], cannabinol [CBN], and cannabigerol [CBG]) have sedative, anxiolytic, and analgesic properties, although one internet site describes CBN as “mildly intoxicating.” Contamination of cannabis products, especially with tetrahydrocannabinol (THC, which produces the “high”) is a big problem, and labels must be read cautiously. CBD is FDA-approved as Epidiolex, which is used in two types of epilepsy in small children.
The author wishes to thank Amrit Ahluwalia, MD for his recommendation of www.lazarusnaturals.com, a highly pure source of cannabidoids. The author (C.P. Clark) does not recommend THC or CBN because of the risks of severe psychiatric problems. Caution: any cannabinoid will potentially show as positive on a tox screen. While laws and interpretation of the law are changing throughout the nation, there is no protection for workers taking medicinal cannabinoids of any type under national law. This may affect VA workers, federal contractors, etc. The author thanks Marian Birge, Esq, of Garcia and Birge for her scholarly review of the current legal situation.
Complications/Adverse Outcomes of Treatment
The liability for tolerance, withdrawal, and abuse must be considered in regard to all the BZDs, although many patients with anxiety disorder and insomnia take them long-term without misuse, particularly after proper patient education and supervision. However, withdrawal from prolonged high-dose BZDs can cause seizures, psychosis, delirium, or even death. Rebound insomnia can also occur even with well-planned tapering.
The “war on drugs” increasingly leads many clinicians to prescribe medication with less favorable safety profiles than BZDs (e.g., risk of priapism with trazodone and metabolic complications with atypical antipsychotics). Elderly patients are particularly vulnerable to the anticholinergic side effects of antihistamines.
Many people think “natural” products are safer, not knowing that the FDA classifies them as dietary supplements and does not regulate them as closely as “manufactured” pharmaceuticals. Serious problems have resulted from unsafe processing (e.g., L-tryptophan byproducts causing an eosinophilia-myalgia syndrome). Recently, an analysis of MEL tablets bought at “reputable” pharmacies, supermarkets, and health food stores found widely varying actual doses of MEL as well as adulterants such as CBD. Potential drug interactions are less well known for complementary medicine products, particularly in regard to botanicals, which contain multiple chemical compounds. Recent evidence suggests that MEL can harm the balance of the “gut microbiome” and potentially cause or at least worsen inflammation. The authors recommend avoiding MEL in patients with inflammatory bowel disease; prudence might suggest caution in patients with gastrointestinal symptoms (Luiz da Silva et al, 2023).
Prognosis
Prognosis depends on the underlying cause of insomnia as well as the prevention of secondary complications such as substance misuse in the context of self-medication.
RESTLESS LEGS SYNDROME/PLMS IN SLEEP
General Considerations/Clinical Findings
Restless leg syndrome (RLS) and PLMs are often discussed together because they overlap in presentation and symptoms. RLS is an uncomfortable “creeping, crawling” sensation or “pins and needles feeling” (described as similar to akathisia by patients who have had both) in the limbs, especially in the legs. RLS tends to occur during waking and at sleep onset, whereas PLMs occur during sleep. Patients with RLS sometimes also have PLMs, but patients with PLMs often do not have RLS. For most patients with RLS, being recumbent increases leg discomfort and leads to difficulty sleeping. Further sleep disruption may occur if movement of the affected limb becomes the only way to relieve the dysesthesia.
PLMs are involuntary, rhythmic (roughly every 20–40 seconds over periods up to hours) twitches, typically ankle dorsiflexion. Each movement may lead to a brief arousal; PLMs can provoke tremendous sleep fragmentation, yet patients commonly are not consciously aware of the movements and may present with hypersomnia alone. They may present after accidentally kicking their bedmates or drastically disarranging the bed linens. PLMs increase with age, the prevalence being about 30% over 50 years and 50% over 65.
Differential Diagnosis
The differential diagnosis of RLS and PLMs includes akathisia, neurologic diseases (e.g., neuropathies, myelopathies, spinal cord problems) as well as systemic illness (e.g., anemia, nutritional/metabolic disturbances, cancer, and particularly chronic renal disease with dialysis). Similar symptoms can result from the discontinuation of illicit substances or medications, particularly antidepressants.
Treatment
Treatment should include correcting underlying disorders (e.g., iron deficiency anemia) and (if possible) discontinuing the medications that cause RLS and PLMs. Most treatments reduce either the muscle activity or the sleep disruption. Treatment generally involves one of three drug categories: dopaminergic agents (e.g., ropinirole, pramipexole), GABAergic agents (e.g., baclofen, gabapentin and other anticonvulsants); while BZDs and opiates are effective, they are simply not prudent given the current war on drugs situation. It is not uncommon to have to switch from one drug class to another after a previously effective medication loses efficacy; conversely, it can be helpful to switch to a previously effective medication in a different drug class.
Some sleep experts consider dopaminergic agents the treatment of choice for RLS, although their long-term effects have not been well studied, even in nonpsychiatric populations. Ropinirole (the only FDA-approved RLS treatment) and pramipexole (previously used in Parkinson disease [PD]) have more benign side effects than older agents (e.g., levodopa/carbidopa) and fewer peripheral side effects. Anticonvulsants may be an option, particularly if psychiatric comorbidity (e.g., psychosis) is a relative contraindication to dopaminergic agents.
Prognosis
Prognosis depends on the underlying cause, the degree of sleep disruption, and the extent to which treatment complications can be prevented.
HYPERSOMNIAS
General Considerations/Clinical Findings
The term hypersomnia encompasses pathologically increased sleep duration (e.g., the patient with atypical depression who sleeps 14 hours a day), “sleep attacks” (abrupt involuntary onset of sleep), EDS, or a combination of these. It is important to note that hypersomnia or EDS can also be associated with poor nocturnal sleep (such as sleep disrupted by PLMs in sleep or other parasomnias) and with circadian rhythm disorders. The most common cause of EDS in the general population is chronic lack of sleep. It is important to differentiate between fatigue and EDS.
Treatment
The treatment of hypersomnia depends on diagnosis. When possible, treatment should attempt to correct an aspect of the pathophysiology itself. Supportive therapy may help patients adjust to the illness and its social sequelae (e.g., being fired for falling asleep on the job).
Prognosis
Prognosis depends on the nature of the underlying disorder, neurological causes of hypersomnia other than narcolepsy being generally more difficult to treat. Early diagnosis and treatment is vital for all hypersomnias to minimize psychosocial sequelae and potentially fatal results (e.g., falling asleep at the wheel of a vehicle).
BREATHING-RELATED SLEEP DISORDER
General Considerations
This disorder is defined as sleep disruption due to abnormal ventilation during sleep, usually presenting as EDS but sometimes as insomnia. This category includes sleep apnea and central alveolar hypoventilation. Obstructive sleep apnea, the most common pathological cause of EDS, is present in 1–2% of the general population.
Because snoring is a common symptom and can cause significant sleep disturbance (with arousals on PSG) even if criteria for sleep apnea are not met, it is described in this section.
Clinical Findings
Sleep apnea is manifested as abnormal breathing during sleep, commonly associated with snoring (often loud enough to disturb bed partners or people in other rooms) and gasping or other evidence of increased respiratory effort. PSG involves apneas (actual cessations of breathing) and hypopneas (shallow, ineffective breaths). The apnea–hypopnea or respiratory disturbance index consists of the total of these events per hour: 10 is abnormal, and 15 almost invariably requires treatment. Based on thoracic and abdominal strain gauges, each period of apnea or hypopnea can be classified as central, obstructive, or mixed, sleep apnea being diagnosed according to the preponderance and pattern of events. PSG often also reveals dysrhythmia and decreased oxygen saturation. Untreated patients are at increased risk of pulmonary hypertension, right-sided heart failure, stroke, myocardial infarction, sudden death, impotence, cognitive problems, and a depressive syndrome that generally remits with treatment.
In central sleep apnea, respiratory drive governed by the brainstem “shuts off” during sleep. This condition may occur in a variety of neurologic and cardiovascular disorders.
Central alveolar hypoventilation, which occurs with “mechanically normal” lungs, produces hypoxia and often hypercarbia even if apneas or hypopneas are not present. It is often encountered in the morbidly obese.
Snoring may be associated with conditions causing airway turbulence (e.g., deviated septum). The upper airway resistance syndrome entails nonocclusive airway collapse associated with negative intrathoracic pressure; PSG confirmation requires the use of an esophageal pressure transducer. Sleep apnea should be ruled out.
Differential Diagnosis (Including Comorbid Conditions)
The differential diagnosis includes other respiratory disorders that can worsen with the physiologic changes of sleep (e.g., asthma), comorbid neurological disorders, and some anxiety disorders. Comorbid PLMs are also common and require disorder-specific treatment if they do not resolve with treatment of apnea.
Treatment
Treatment focuses on achieving and maintaining airway patency. The treatment of choice for obstructive sleep apnea (OSA) is continuous positive airway pressure (CPAP) delivered through a mask. This treatment “props” open the airway with room air delivered at low pressures (typically 5–15 cm H2O). Numerous variations help make this as comfortable as possible for the patient, including a variety of nasal and oral masks, humidifiers, variations on pressure control and timing (e.g., bilevel positive airway pressure [BiPAP]), which provides different pressures for inhalation and exhalation).
A number of dental devices have been developed to hold the tongue forward and the airway open. Surgical procedures have been developed, including the uvulopalatopharyngoplasty, which enlarges the upper airway by removing soft tissue. Bony dysmorphology can be corrected surgically. Obese patients should be encouraged to lose weight; weight loss, even if much less than that required to reach ideal weight, can be very helpful.
If snoring is positional, devices such as pillows to discourage the patient from sleeping in a supine position may be helpful. Laser-assisted uvulopalatoplasty (LAUP), which can be performed under local anesthesia as an outpatient and can be repeated as necessary, may control snoring.
Theophylline, medroxyprogesterone, and some antidepressants have been recommended as respiratory stimulants for central apnea with mixed results.
Complications/Adverse Outcomes of Treatment
The risks of cardiovascular and respiratory sequelae (as well as EDS-related accidents) are obvious. Although CPAP is very effective, noncompliance is common. Many patients, especially those with concomitant anxiety, feel “claustrophobic.” They may benefit from a supportive, behavioral desensitization as well as the correction of faulty beliefs.
When a LAUP is performed without prior PSG, OSA may go undiagnosed when snoring resolves. However, unresolved silent apnea will continue to disrupt sleep and lead to persistent EDS as well as cardiovascular comorbidity.
Prognosis
Early treatment can prevent cardiovascular comorbidity.
NARCOLEPSY
Clinical Findings
Narcolepsy is associated with uncontrollable sleep attacks in inappropriate, embarrassing, and even dangerous situations (e.g., while driving). Although sleep attacks have been described as brief (e.g., lasting 15–20 minutes) and refreshing, this is not always true. Most narcoleptics experience related symptoms, particularly cataplexy (a sudden loss of muscle tone), hypnagogic hallucinations (dreamlike experiences while falling asleep), and sleep paralysis (brief paralysis associated with the onset of sleep or wakefulness). However, only 10–15% of narcoleptic patients have all four major symptoms. Many narcoleptic patients report having performed complex behavior (such as walking from one place to another or writing) without recalling it.
Even in the absence of serious consequences, these symptoms can be frightening and frustrating for patients and vexing for family members, coworkers, and others. Cataplexy (which can involve the whole body but at times is confined to one area, such as the hand) is often associated with emotions such as surprise or anger. The symptoms can be misinterpreted or misidentified by lay people and unwary clinicians. For example, mild episodes of cataplexy (dropping a cup upon hearing a joke) may be attributed to carelessness or clumsiness. A patient may be misdiagnosed as psychotic if the doctor mistakenly assumes the hypnagogic hallucinations have occurred during full wakefulness or have the same significance as waking hallucinations.
Narcolepsy is associated with defective REM sleep regulation. Cataplexy and sleep paralysis can be thought of as atonia without REM, whereas hypnagogic hallucinations and sleep attacks have been likened to REM intrusion. Though the absolute risk of developing narcolepsy is only 1–2% in first-degree relatives of accurately diagnosed probands, an increased prevalence of certain histocompatibility locus antigen subtypes has been reported. Recently, animal models of narcolepsy have shown hypocretin neuron deficiencies. Decreased cerebrospinal fluid hypocretin levels have been reported in human narcolepsy.
The diagnosis of narcolepsy is confirmed by a positive Multiple Sleep Latency Test (MSLT) (with the finding of REM onset during two daytime nap opportunities) following a night of PSG ruling out other causes for abnormal MSLT. Sleep-onset REM periods are often present on nocturnal PSG.
Differential Diagnosis (Including Comorbid Conditions)
Sleep attacks and cataplexy-like episodes have been reported in neurological disorders such as traumatic brain injury (e.g., Harriet Tubman). Experts believe that narcolepsy-like syndromes without cataplexy are almost always produced by comorbid neurologic disorder. When no such neurologic disorder is found, such a syndrome would be referred to as Primary Hypersomnia.
Narcolepsy patients are not exempt from other causes of hypersomnia. If narcolepsy worsens in a patient with previously well-controlled symptoms, careful questioning should be conducted about other possible causes of hypersomnia (medications, sleep apnea, and PLMs). Some patients fabricate a history of narcolepsy to obtain stimulants. Obtaining PSG confirmation or previous medical records will protect against this.
Treatment
Although some patients with narcolepsy achieve reasonable control of sleep attacks with scheduled naps, many require medication. Modafinil is the treatment of choice for EDS and may be helpful for EDS related to neurologic comorbidity, medications (e.g., sedating antipsychotics such as clozapine), and OSA in which EDS persists despite optimization of all disorder-specific treatments. Armodafinil is also used. The exact mechanisms by which modafinil is effective are unknown. It is not related to the amphetamines and appears to have less risk of side effects (e.g., insomnia, psychosis) and misuse than “scheduled” stimulants, (e.g., methylphenidate, amphetamines), which are still used. Sodium oxybate (gamma-hydroxybutyrate [GHB]), an endogenous GABA metabolite, is the only medication for cataplexy approved by the FDA. Its exact anticataplectic mechanisms are unknown, although other anticataplectic medications (tricyclic antidepressants [TCAs], monoamine oxidase inhibitors [MAOIs], selective serotonin reuptake inhibitors [SSRIs]) may act via serotonergic mechanisms or by increasing norepinephrine through decreased reuptake or increased release. GHB also alleviates sleep attacks somewhat, perhaps indirectly by alleviating disturbed nocturnal sleep by inducing SWS and consolidating sleep. Because of frequent use as a “club drug” with catastrophic consequences (neurological sequelae and death from intoxication and life-threatening withdrawal not treatable with BZDs), GHB is scheduled and available only through a tightly regulated distribution program. A longer acting version was in trials at the time of the latest revision.
Pitolisant is a histamine 3 inverse agonist effective against EDS in narcolepsy and idiopathic and symptomatic hypersomnia. Solriamfetol, a DA and norepinephrine reuptake inhibitor, is used for EDS in narcolepsy and OSA, although the underlying cause of the OSA should definitely be treated as well as possible.
The treatment of cataplexy and the other cardinal symptoms of narcolepsy was previously based on REM sleep inhibition, which is still useful.
Complications/Adverse Outcomes of Treatment
Although the misuse of stimulants is rare in the absence of a comorbid substance abuse history, withdrawal symptoms, physiological tolerance, and, occasionally, psychosis can develop, particularly with amphetamines and sometimes with methylphenidate. Dramatic cataplexy rebound is to be expected if any anticataplectic agent is stopped, with TCAs being generally more dangerous than SSRIs in this regard.
PARASOMNIAS
See Table 36–6.
Table 36–6 A Comparison of Parasomnias by Symptoms and Findings
Characteristic | Nightmare Disorder | Sleep Terror Disorder | REM Behavior Disorder | Sleepwalking Disorder |
|---|---|---|---|---|
Sleep stage | REM | NREM | REM | NREM |
Dream recall | Yes | No | Yes | No |
Motor activity | No | Screaming, motoric agitation | Yes | Yes |
On awakening | Alert | Confused, disoriented | Alert | Confused, disoriented |
Time of night | Last third | First third | Second half | First half |
Prevalence | Children 20%, adults 5–10% | Children 5%, adults <1% | Unknown | Children 1–20%, adults <1% |
Autonomic activation | Slight, secondary to fear | Extreme, with sweating and vocalizations | Associated with REM and motor activity | Not present |
Danger to self | No | No | Patient acts out dream, may accidentally injure bed partner | Patient walks anywhere |
Treatment | Monitor; symptoms usually decrease with age; if severe consider psychotherapy and/or suppress REM (MAOIs or other antidepressants) | Monitor; symptoms usually decrease with age; if severe consider low dose tricyclic or BZD | Safe environment for all; clonazepam; consider if triggered by antidepressants; treat neurological comorbidity (common) or watch for future development; not uncommon in narcolepsy | Maintain a safe environment and monitor symptoms; if severe consider suppression of SWS (BZDs, TCAs) |
Data from Salzman C. Clinical Geriatric Psychopharmacology, 2nd ed. Baltimore: Williams & Wilkins; 1992.
General Considerations/Clinical Findings
Parasomnias are sleep-related disorders characterized by unusual events or behavior occurring either during sleep or during sleep–wake transitions. Parasomnias occurring during non-REM sleep are more often associated with being difficult to arouse, confusion upon awakening, and a lack of memory for the event. REM parasomnias generally involve waking clearly and rapidly, with recall for the event. These features are important in obtaining a proper diagnosis.
Differential Diagnosis (Including Comorbid Conditions)
Frequent nightmares should always raise the possibility of psychiatric comorbidity (particularly mood or anxiety disorder). REM sleep behavior disorder can present as a reversible complication of several antidepressants; otherwise, it is generally associated with current or future neurologic comorbidity, such as narcolepsy and PD. Criminal defendants may allege REM behavior disorder as a defense, particularly for violent or egregious actions; however, it is believed that REM behavior disorder cannot be simulated on PSG.
Treatment
Treatment depends on the particular disorder. The reassurance that children do not suffer during sleep terrors or recall them afterward can be very helpful for families. It is especially important in sleepwalking and REM behavior disorder to maintain a safe environment for the patient and others. Lock balcony doors. Use special precautions when sleeping in unfamiliar surroundings such as hotels. Move the bedmate into a separate room if needed. Careful instruction in sleep hygiene is important in all parasomnias. Bruxism (tooth grinding) can be treated with dental devices.
Some authorities believe that sudden infant death syndrome is a parasomnia. Parents should be aware that the risks of sudden infant deaths are reduced when infants are put to bed supine (e.g., the “Back to Sleep” campaign).
Complications/Adverse Outcomes of Treatment
These are often the result of inadequate treatment but may result from medication side effects.
Prognosis
Prognosis depends on the underlying disorder and the prevention of accidents.
CIRCADIAN RHYTHM DISORDERS
See Table 36–3.
General Considerations/Clinical Findings
In disturbances of circadian rhythm, there is a misalignment between the timing of sleep–wake patterns and the desired or normal pattern. These patients may complain of either insomnia or hypersomnia (or both at different times of the 24-hour day). Two processes appear to mediate the propensity to sleep: a homeostatic process by which the propensity to sleep is related directly to the duration of prior wakefulness, and a circadian process that regulates the propensity across a 24-hour day. In persons living on a normal sleep schedule, the circadian sleep propensity is greatest at night and mid-afternoon.
DELAYED SLEEP PHASE TYPE
The major symptoms are prolonged sleep latency and difficulty waking up at the desired time. Most common in adolescence, it can also be encountered with “jet lag” and shift work.
THE JET LAG TYPE
This type is characterized by sleepiness and alertness out of synchrony with the “new” time zone. It may be encountered with delayed or advanced sleep phase. Eastward travel (entailing a phase advance of the biological clock) usually takes longer to adjust to than does westward travel (which entails a phase delay).
THE SHIFT WORK TYPE
This type involves insomnia, hypersomnia, or both, at inappropriate times, in relationship to work schedules (e.g., rotating or permanent shift work, or irregular work hours). Complications include gastrointestinal or cardiovascular symptoms, increased use of alcohol, disruption of family and social life, low morale and productivity, and high absenteeism. Many individuals never adjust completely to the work schedule because they try to revert back to a normal sleep–wake schedule on weekends and holidays in order to participate in family and social activities.
UNSPECIFIED TYPE
Unspecified type includes advanced sleep phase syndrome and non-24-hour sleep–wake syndrome. Common in older persons, advanced sleep phase syndrome is characterized by early evening sleepiness, early sleep onset, and early morning awakening. In non-24-hour sleep–wake syndrome, patients live on a free-running rest–activity cycle continuously shifting in and out of phase with real-world time. This disorder can complicate chronic poor sleep–wake hygiene. It is usually found in the blind, probably because light does not properly synchronize the SCN with the environment.
Differential Diagnosis
Includes other disorders involving circadian disruption (e.g., depression) but is usually not difficult given the history.
Treatment
Involves patient education, the promotion of sleep hygiene, and an attempt to synchronize sleep and wakefulness with the underlying phase position of the circadian clock. Because the natural cycle length of the circadian clock is longer than 24 hours, it is usually easier to phase-delay the clock than to phase-advance it. Shift workers, for example, tend to do better when shifting in a “clockwise direction” (i.e., from day to evening to night work schedules) than when shifting in a counterclockwise direction. This kind of schedule shift should be implemented in personnel planning for shift workers as much as possible. Many schools are starting later in the morning to minimize tardiness, accidents driving to school, and suboptimal performance related to the near-ubiquitous delayed sleep phase in teenagers.
Appropriate time cues (zeitgebers and timed exposure to bright light) can be very helpful in readjusting and synchronizing the sleep–wake rhythm and the internal clock.
Bright light in the evening produces a phase delay (e.g., retiring later and arising later) and can be very helpful for advanced sleep phase syndrome. In contrast, early-morning bright light phase advances the sleep–wake cycle and is helpful in delayed sleep phase syndrome. It is important to maintain darkness during the desired sleep period: blackout curtains and sunglasses may be helpful. Light administration using sunlight and additional indoor lighting is very useful even if a proper light box is not available. In addition, it is important to maintain the desired sleep–wake schedule and prevent a rapid “relapse” to the previous pattern.
MEL is more effective as a “resynchronizing” agent than as a soporific per se. It can be administered in carefully timed doses to ameliorate jet lag, but unforeseen changes in travel plans can bring severe discomfort. Treatment with both bright light and MEL must be carefully timed, because the sensitivity of the biological clock undergoes a circadian variation.
Treatment of Shift Work Sleep Disorder depends on the individual’s symptoms and timing. It may involve judicious use of bright light, MEL, hypnotics, caffeine, and modafinil in any combination. In general, bright light promotes alertness and should be utilized in shift work environments where possible.
Complications/Adverse Outcomes of Treatment
Include the potential “overcorrection” of the circadian phase, “overtreatment” of a given symptom (e.g., if the patient drinks coffee at the end of the shift in order to stay awake long enough to drive home, sleep latency is prolonged), and maladaptive behaviors (e.g., using alcohol as a hypnotic) arising from attempts to self-treat. Excessive doses of MEL have been reported to trigger free running, which is very difficult to treat.
Prognosis
Depends on the underlying disorder and the minimization of safety risks (e.g., preventing drowsy driving during jet lag).