Chapter 10 375 Sleep Disorders Sleep – Introduction Insomnia A. DSM IV-TR comparison B. Definition C. Epidemiology D. Risk Factors E. Pathophysiology F. Consequences G. Clinical Assessment/Diagnosis H. Differential Diagnosis I. Treatment Hypersomnias of Central Origin J. Hypersomnia K. Narcolepsy Sleep related Breathing Disorders L. Obstructive Sleep Apnea Sleep related Movement Disorders M. Restless Legs Syndrome N. Periodic Limb Movement Disorder Parasomnias Circardian Rhythm Sleep Disorders 376 ANOREXIA NERVOSA (1) Normal sleep—stages and cycles Anorexia nervosa (1) SLEEP INTRODUCTION I. Functions of sleep Sleep and sleep-wake rhythms are found in all higher ani- mals. Among these organisms, some functions of sleep are held in common: 1. Use of a sleeping period as a way to help match ani- mals to their environment. For example, humans are awake during the day when they can rely on their vi- sion while rodents are awake at night when they can rely on smell and touch. 2. Use of sleep and quite wakefulness as a way to phys- ically restore the body. For example, sleep depriva- tion is associated with impaired glucose metabolism and altered immune function. 3. Use of sleep to optimize waking function and cogni- tion. For instance, sleep deprivation may lead to de- creased alertness and decision making capacity. II. Clinical assessment of sleep 1. Sleep history An accurate clinical history is the foundation of the proper diagnosis and treatment of a sleep disorder. a. Current symptoms: nature, severity, duration, frequency, time course, ex- acerbating and reliving factors, effect on daily life and/or impairments b. 24-hour history: the circumstances of sleep and wakefulness. Sleep-related questions may include activities prior to bedtime that may prove incompati- ble with restful sleep, sleep latency (or, the time it takes to fall asleep), number/duration/timing of nighttime awakenings, snoring, limb move- ments, and other behaviors during sleep. Daytime-related questions may in- clude naps, difficulty staying awake, inadvertent sleep episodes, use of alarms clocks, periods of confusion, and amount of time needed to fully awaken. CHAPTER 10 Disorders of behavior 377 c. Regularity and timing of sleep-wake behaviors over time. d. Bed partner history: the reporting of breathing problems (choking, snoring, gasping), limb or muscle movement during sleep as well as complex be- haviors such as sleep walking/talking, changes in mood, substance use. e. Family history of sleep disorders. f. Medication use, including timing and recent changes. g. Substance use, including the timing and use of caffeine, nicotine, alcohol, and illicit substances. h. Previous treatments and their effects on sleep disorders. 2. Actigraphy a. Method to measure motor activity, usually through an activity meter worn on the wrist. Data collected by this device may reveal general patterns of sleep and wakefulness. 3. Sleep diary a. Record created by the patient detail- ing his/her sleep-wake pattern over a period of weeks. Information included in the diary: daily activities, sleep/wake times, naps, exercise, mealtimes, and use of caf- feine/nicotine/alcohol/other substanc- es. 4. Polsomnography (PSG) a. A polysomnogram includes at least one channel of electroencephalog- raphy (EEG) to measure brain activi- ty, electrooculography (EOG) to measure eye movements, and elec- tromyography (EMG) to measure muscle tone, usually in the submentalis muscles. b. Additional channels of PSG may measure nasal-oral airflow or nasal pressure, chest and abdominal movement to measure breathing, oximetry to measure oxygen desatu- ration, and additional EMG channels 378 NORMAL SLEEP—STAGES AND CYCLES of the anterior tibilias muscles to evaluate for movements before or during sleep. c. Polysomnography is indicated for the evaluation of patients with suspected sleep apnea and in some cases of parasomnia. It is not routinely indi- cated for restless legs syndrome, cir- cadian rhythm sleep disorders, and insomnia; in these disorders the diag- nosis relies on the clinical history. 5. Multiple Sleep Latency Test (MSLT) a. MSLT is a variant of polysomnography used to evaluate daytime sleepiness. EEG, EOG, and EMG data is recorded while the pa- tient is allowed to nap 4-5 times at 2- hour intervals throughout the day. The sleep latency and presence or absence of rapid eye movement sleep for each nap is noted. b. Mean sleep latency values > 10 minutes are considered normal, while values < 8 minutes suggest clinically significant sleepiness. The presence of REM sleep in at least 2 naps may indicate the presence of narcolepsy. III. Stages of Normal Sleep 1. Sleep normally cycles through a pattern of stages. The different stages of sleep may be seen in polysomnography, as revealed by EEG. 2. Sleep is divided in Rapid Eye Movement (REM) sleep and Non-rapid eye movement (NREM) sleep. REM and NREM sleep alternate every 90-100 minutes throughout the night. 3. NREM sleep is further subdivided into 4 stages of de- creasing arousability. a. Stage 1 is viewed as a transitional sleep stage. b. Stage 2 occupies the majority of NREM sleep. c. Stages 3 and 4 are “deep” sleep. 4. Normal sleep stages, as characterized on PSG: CHAPTER 10 Disorders of behavior 379 a. Wakefulness: low-voltage, fast fre- quency EEG pattern (alpha pattern), voluntary eye movements, tonic mus- cle tone. b. Stage 1 NREM sleep: small increase in EEG amplitude with slowing of EEG frequency, slow rolling eye movements in EOG channels c. Stage 2 NREM sleep: increase in amplitude and further slowing of EEG frequencies, presence of “K complex- es” (isolated large-amplitude slow waves) and “sleep spindles” (episodic bursts of fast EEG activity), reduction in muscle tone d. Stage 3 NREM sleep: large ampli- tude, slow EEG activity also known as “delta” or “slow-wave sleep” the com- prises 20-50% of a 30 second epoch, low muscle tone, EOG pattern mirrors EEG activity e. Stage 4 NREM sleep: same as stage 3 sleep, except delta activity consti- tutes >50% of an epoch f. REM sleep: return of fast-frequency, mixed voltage EEG activity similar to Stage 1 NREM sleep. Phasic rapid eye movements are characteristically seen. Muscle tone is essentially ab- sent aside from muscle twitches. 380 NORMAL SLEEP—STAGES AND CYCLES Disorders of Sleep N.B. The International Classification of Sleep Disorders Second Edition (ICSD-2) is commonly used by sleep medicine practition- ers as a diagnostic manual. As the sleep medicine field encom- passes practitioners from various fields, including psychiatry, pulmnology, and neurology, this manual allows medical personnel to use a standardized manual from which to draw information. However, in deference to the use of the DSM IV-TR by psychia- trists reference has been made to both ICSD and DSM definitions when applicable. While the information contained in these two manuals is generally consistent, some differences in sleep disor- der classification are present. Thus, naming by Classifications will be denoted as follows: Inter- national Classification of Sleep Disorders Second Edition (ICSD- 2) in italics, and [DSM IV-TR] in brackets ICSD-2 classification will be referred to in italics while DSM IV-TR coding will be referred to in brackets . Insomnia [Primary Insomnia] DSM IV-TR contains two diagnoses that fall under this category: Prima- ry Insomnia and Insomnia Related to Axis I or II. DSM critieria state that the predominant complaint of difficulty initiating/maintaining sleep, or nonrestorative sleep, must be present for at least 1 month and be asso- ciated with impairment of functioning. Under the ICSD, insomnia is defined as: 1. Insomnia symptoms may consist of difficulty falling asleep, nighttime awakenings, inadequate sleep quality or sleep duration. 2. Insomnia causes significant distress or impairment in function- ing. 3. Adequate opportunity for sleep exists. Epidemiology Prevalence of insomnia symptoms is 30-40% in the general population. Prevalence of insomnia disorder is 5-10%. Risk Factors Risk factors include female sex, advanced age, unemployment, comorbid illnesses, genetics, psychosocial stressors, and counterproductive sleep habits. Pathophysiology Physiological model proposes that insomnia is a disorder of in- creased arousal. Cognitive-behavioral model propose that insomnia arises from the interaction of predisposing factors, external precipitating factors, and cognitive-behavioral perpetuating factors. CHAPTER 10 Disorders of behavior 381 Consequences Insomnia is a risk factor for developing depressive, anxiety, and substance abuse disorders. Insomnia is associated with motor vehicle accidents, work absenteeism, and reduced quality of life. Clinical Assessment and Diagnosis The clinical assessment relies on careful history taking. Review of the insomnia history, including a 24-hour perspective. Symptoms, chronology, alleviating and exacerbating factors, and previous treatments should be assessed. In addition, sleep/wake times, regularity of these hours, and daytime activities should also be questioned. Evaluation of underlying psychiatric, medical, comorbid sleep disorders should be performed. Medication and substance use history must also be ascer- tained. Sleep-wake diaries, actigraphy, and polysomnography may also play a role in making the diagnosis. Differential Diagnosis The differential diagnosis list is broad. Primary insomnia refers to a disorder in which the chief complaint is insom- nia in the absence of another disorder as a possible cause. Secondary insomnia arises from other causes, including many psychiatric illnesses. Medical diseases such as congestive heart failure, COPD, stroke, Parkinson’s disease, chronic renal failure, diabetes, hyperthyroidism, arthritis, and fibromylagia may cause insomnia. Substance use including alcohol, caffeine, nicotine, and stimulants must be considered. Medications such as antidepressants, decongestants, corticosteroids, and statins may also cause insomnia. Treatment of Insomnia Pharmacological management should focus on short-term use (2-4 weeks), followed by a gradual taper and discontinuation of medication. For primary insomnia, the first-line choice is a short-acting benzodiazepine receptor agonist, such as zoplidem, eszopliclone, or zaleplon. A sedating antidepressant such as doxepin or amitriptyline may be used adjunctively. A third-line choice is gabapentin or tiagabine. Psychological and behavioral treatments may be used alongside medica- tions. Sleep restriction therapy maximizes sleep efficiency by restrict- ing time spent in bed with strict bedtime and waking hours. Stimulus control therapy reinforces connections between sleep and the sleep environment; the patient is told to use the bed/bedroom for sleep and sex only and to enter the bedroom only when sleepy. If still awake after 20 minutes, the patient must leave the bedroom until sleepy once more. Cognitive therapy uses psychological methods to both chal- lenge and change misconceptions about sleep and insomnia. A combination of behavioral and cognitive techniques may also be utilized. 382 NORMAL SLEEP—STAGES AND CYCLES Hypersomnias of central origin ICSD-2 names three types of hypersomnia of central origin: Narcolepsy, Idiopathic Hypersomnia, and Recurrent Hypersomnia. DSM IV-TR contains three diagnoses that fall under this category: Narcolepsy, Primary Hyper- somnia, and Hypersomnia Related to an Axis I or II disorder. In ICSD-2 narcolepsy is further defined as occurring with cata- plexy, without cataplexy, due to a medical condition, or unspeci- fied; these distinctions are not made in the DSM IV-TR, which simply lists the diagnosis as narcolepsy. Narcolepsy Definition The DSM criteria for narcolepsy include: irresistible attacks of refreshing sleep that occur daily over at least 3 months; and the presence of cataplexy and/or recurrent rapid eye movement intrusions in the transition between sleep and wakefulness, as manifested by sleep paralysis and hypno- pompic or hypangogic hallucinations. In ICSD narcolepsy is defined as a complaint of irresistible attacks of refresh- ing sleep occurring on a daily basis for at least 3 months in addition to the following: On the multiple sleep latency test (MSLT), mean sleep latency is ≤ 8 minutes and 2 or more sleep onset rapid eye movement periods are found in patients who have had at least 6 hours of sleep the night before the test. CSF hypocretin-1 levels ≤110 pg/mL or one-third of mean control values are also considered to be diagnostic. Cataplexy, which is defined as a transient loss of muscle tone that occurs suddenly in response to strong emotion. Epidemiology Narcolepsy with cataplexy occurs in 0.02% to 0.18% of the U.S. population. Males and females are equally affected. Prevalence of narcolepsy without cataplexy, narcolepsy due to a medical condition, and unspecified narcolepsy are unknown. Risk Factors Narcolepsy with cataplexy is associated with human leukocyte antigen (HLA) subtypes DR2/DRB1*1501 and DQB1*0602. First-degree relatives of patients with these subtypes have a 10 to 40 fold increased risk for narcolepsy with cataplexy. Pathophysiology Narcolepsy with cataplexy is linked to a loss of hypotha- lamic neurons that contain hypocretin. An underlying autoimmune process may lead to elimination of the hypocretin cells. Consequences Significant impact on psychosocial functioning with negative effects on social interactions and work. Clinical Assessment and Diagnosis Patients commonly present with excessive daytime sleepiness. This symptom may manifest as nodding off or falling asleep in CHAPTER 10 Disorders of behavior 383 low-stimulation environments. Urges to sleep, known as sleep at- tacks, irritability, poor concentration or memory, and automatic behavior, characterized by nonsensical behavior performed while sleepy, may also characterize the disorder. Cataplexy may range from total body collapse to more localized muscular involvement such as ptosis or slurred speech. While any strong emotional stimuli can trigger an event, laughter is a common trigger. Hypnagogic (occur as patient transitions from wakefulness to sleep) or hypnopompic (occur as patient transitions from sleep to wakefulness) hallucinations, especially of a visual nature, may oc- cur. Auditory and tactile hallucinations may also occur. Sleep paralysis, or the inability to move, during the the transition from sleep to wakefulness may occur. Polysomnography is performed to rule out other sleep disorders such as sleep apnea, periodic limb movement disorder, and REM sleep disorder. Multiple Sleep Latency Test (MSLT), in which a patient is pre- sented with four or five 20 minute nap opportunities every 2 hours in the morning and afternoon, will show a sleep latency of 8 minutes or less. Differential Diagnosis For excessive daytime sleepiness: sleep apnea, idiopathic hypersomnia, periodic limb movement disorder, insufficient sleep, depression, neurodegen- erative disorder. For cataplexy: transient ischemic attack, seizure, vestibular disorder. Treatment Pharmacologic treatment for daytime sleepiness includes: modafanil (Provigil), sodium oxybate/GHB (Xyrem), and traditional stimulants including methylphenidate, dextroamphetamine, and methamphetamine. Note: use of traditional stimulants may be accompanied by side effects such as rebound hypersomnia and tachyphylaxis. Sodium oxybate, tricyclic antidepressants, selective serotonin reuptake inhibitors may be used in the treatment of catplexy. Behavioral treatments include: regular sleep schedule, scheduled daytime naps, and elimination of shift work. 384 NORMAL SLEEP—STAGES AND CYCLES Idiopathic Hypersomnia Definition Idiopathic Hypersomnia is defined by the following: excessive daytime sleepiness occurring for at least 3 months on an almost daily basis; Multiple Sleep Latency Test showing mean sleep latency < 8 minutes and < 2 sleep onset REM periods; polysomnography results exclude other causes sleepiness. Epidemiology Prevalence is unknown. Risk Factors A possible familial link may exist. Pathophysiology Etiology is unknown, but daytime sleepiness may be preceded in some patients by a viral illness such as Guillain-Barre syndrome or mononucleosis. Consequences Significant impact on psychosocial functioning with negative effects on social interactions and work. Clinical Assessment and Diagnosis As in narcolepsy, the main complaint of this disorder is excessive daytime sleepiness. Unlike patients with narcolepsy, idiopathic hypersomnia patients do not present with cataplexy, reduced CSF hypocretin levels, or nocturnal sleep disruption. Furthermore, if these patients take naps, they are characterized as unrefreshing. Polysomnography reveals normal to increased total sleep time without the sleep fragmentation commonly seen in patients with narcolepsy. The MLST shows a short sleep latency but no evi- dence of sleep onset REM periods. Differential Diagnosis Narcolepsy, sleep-related breathing disorders, insuffi- cient sleep, periodic limb movement disorder, depression. Treatment Treatment of excessive daytime sleepiness in idiopathic hyper- somnia follows that of narcolepsy. Recurrent Hypersomnia This category includes both Kleine-Levin Syndrome and menstrual-related hypersomnia. Kleine-Levin Syndrome is an idiopathic disorder primarily seen in adolescent males. Patients present with periods of daytime sleepiness in conjunction with hyperphagia, hypersexuality, and aggression. While not sleeping patients may also manifest confusion, stupor, and irritability. They then have periods in which they are asymptomatic. Polysomnography shows long total sleep time, high sleep efficiency, and decreased slow-wave sleep. The disorder is usually self-limited. Menstrual-related hypersomnia is characterized by daytime sleepiness in the days preceding menstruation. Etiology and prevalence are not known. Treatment with medication that blocks ovulation, such as oral contraceptives, may be beneficial. CHAPTER 10 Disorders of behavior 385 Sleep related breathing disorder [Breathing related sleep disorder] Definition DSM IV-TR defines the sleep disorders that fall under this catego- ry as sleep-related breathing conditions that lead to disruption in sleep, as manifested by excessive sleepiness or insomnia. Specific examples include obstructive and central sleep apneas as well as central alveolar hypoventila- tion syndrome. This diagnosis should be coded on both Axis I and Axis III. Obstructive Sleep Apnea (OSA) Definition OSA is defined as repetitive episodes of obstruction in the upper airway that occur during sleep, resulting in snoring, apneic periods, gasping, and choking, and ultimately sleep disruption. The disruption in sleep results in daytime symptoms including sleepiness and fatigue. An obstructive apnea is defined as a significantly decreased or lack of air- flow (less than 25% of a normal breath) for at least 10 seconds at the nose and mouth despite efforts to breathe. An obstructive hypopnea is defined as a decrease in airflow, usually at least 30% of baseline. Both apneas and hy- popneas are associated with a 4% or greater decrease in blood oxygen satu- ration. The Apnea Hypopnea Index (AHI) is a measure of syndrome severity and is defined as the total number of apneas and hypopneas per hour of sleep. An AHI with fewer than 5 events per hour of sleep is normal. An AHI of 5-15 events per hour of sleep is defined as mild OSA, 16-30 events per hour as moderate OSA, and greater than 30 events per hour as severe OSA. Epidemiology Estimates of prevalence vary based on the criteria used to define the disorder. In one study in which the disorder was defined as having an AHI > 5 in addition to excessive daytime sleepiness, prevalence was esti- mated at 24% of men and 9% of women. The ratio of men to women with OSA is 2:1. Risk Factors The major risk factor is obesity. Other risk factors include head and neck structural abnormalities, such as enlarged tonsils or adenoids, increased neck circumference, menopause, hypothyroidism, smoking (causes inflammation, swelling, and narrowing of the upper airway), sedative or alcohol use (causes relaxation of the musculature of the upper airway), and Marfan syndrome, and Down syndrome. Pathophysiology Upper airway narrowing during sleep causes OSA. In turn, this narrowing may be secondary to a variety of factors such as bulky soft tissue in the oropharynx, craniofacial abnormalities, and decreased pharynge- al muscle tone. Consequences Increased risk of hypertension secondary to repeated triggering of the sym- pathetic nervous system. Increased risk of motor vehicle accidents. 386 NORMAL SLEEP—STAGES AND CYCLES Decreased neurocognitive function with negative effects on vigilance, coor- dination, and executive functioning. A possible relationship between OSA and depression may exist. Up to 20% of patients presenting with depressive symptoms may have OSA and vice versa. Clinical Assessment and Diagnosis Patients may complain of snoring, choking, snorting, or breathing cessation at night (noted by their bed partner) as well as sleepiness, fatigue, and insom- nia. Physically patients may present with obesity, retro/micrognathia, enlarged tonsils, elongated soft palate, or right heart failure. On polysomnography breathing disordered events are usually marked by an arousal on EEG and by a drop in oxyhemoglobin saturation. Paradoxical movement of the chest and abdomen and bradytachycardia may also be seen. Differential Diagnosis Depression, chronic sleep deprivation, narcolepsy, insomnia. Treatment Lifestyle interventions such as weight loss, avoidance of sleep deprivation, supine sleeping position, alcohol, or sedatives, as well as smoking cessation Pharmacologic interventions include treating any medical conditions that may be contributing to OSA, such as hypothyroidism and allergic rhinitis. Positive pressure delivered through a nasal or nasal-oral mask pneumatical- ly splints open the airway during sleep. Options include Continuous Positive Airway Pressure (CPAP) and Bilevel Positive Airway Pressure (BiPAP). CPAP and BiPAP are considered first line therapy. Second line therapies,include oral appliances to change the position of the tongue and mandible in order to maximize the airway opening and surgery, such as uvulopalatopharyngoplasty. CHAPTER 10 Disorders of behavior 387 Sleep related movement disorder [Dyssomnia Not Otherwise Specified] DSM IV-TR includes both Restless Legs Syndrome and Periodic Limb Movements in this category. They fall under an NOS label because they do not fit under defined categories of dyssomnias, such as insomnia, hyper- somnia, narcolepsy, and circardian rhythm disorders. Restless Legs Syndrome (RLS) Definition Four criteria are required for diagnosis: a) an urge to move the legs commonly accompanied with unpleasant sensation in the legs; b) exac- erbation of sensations during rest or inactivity; c) relief of sensations with movement; and d) increased sensations in the evening or night. Epidemiology Three to five percent of adults of Northern European descent. Female to male ratio 1.5-2:1. Risk Factors Secondary RLS may be associated with iron deficiency anemia, rheumatoid arthritis, end-stage renal disease, or pregnancy. Medication use including sedating antihistamines, dopamine-receptor an- tagonists, and antidepressants (especially serotonergic). Pathophysiology Possible mechanisms include: impaired transport and intracellular use of iron in the central nervous system; an autosomal dominant inheritance pattern; hypodopaminergic state. Consequences Increased risk of insomnia and daytime sleepiness. Increased risk of depression (13 times higher in men with RLS versus men without RLS). Eighty percent of RLS patients also have periodic limb movement disorder. Clinical Assessment and Diagnosis RLS is a clinical diagnosis. Common descriptions of sensory symptoms include achy, itchy, or “creepy-crawly” sensations in the legs. Symptoms tend to worsen in the evening, particularly when patient is trying to go to sleep. Complaints of sleep disturbance, especially sleep onset insomnia, are there- fore common. Relief may occur with movement and stimulation of the legs by rubbing or hot baths. Suggested Immobilization Test (SIT) may be helpful in assessing the severi- ty of RLS. The patient lies supine for one hour and does not move legs unless necessary. Meanwhile, he/she rates sensory complaints every 5 minutes while an EMG of anterior tibialis is taken. Differential Diagnosis To consider with motor restlessness: akathisia, anxiety disorder, attention deficit hyperactivity disorder, periodic limb movement disorder To consider with sensory symptoms: peripheral neuropathy, opiate with- drawal. Treatment 388 NORMAL SLEEP—STAGES AND CYCLES Treat reversible causes of RLS such as iron deficiency, medication-related symptoms, and opiate withdrawal. Lifestyle modifications include limited caffeine and alcohol intake 12 hours prior to bedtime and preventing sleep deprivation. First-line therapy for RLS includes long-acting dopaminergic agonists such as pramipexole, ropinirole, and pergolide. Of note, these medications must be used in caution with psychotic patients as they may exacerbate psychosis. Adjunctive medications include gabapentin, opiates, and benzodiazepines. Periodic Limb Movement Disorder (PLMD) Definition PLMD is defined by sleep disturbance or daytime fatigue in the setting of polysomnographic findings of stereotyped, repetitive limb move- ments. Limb movements must be 0.5-5 seconds in duration, occur in a se- quence of at least 4 movements, and be separated by intervals of 5 to 90 seconds. A periodic limb movement arousal index of greater than 15 events per hour is also required. Epidemiology Prevalence is not known, although up to 34% of people over the age of 60 may be affected. Risk Factors Increased risk with advancing age. Increased risk of periodic limb movements during sleep with restless legs syndrome (80-90% of patients), REM sleep behavior disorder (70%), and narcolepsy (45-65%). Medication use, including selective serotonin reuptake inhibitors, lithium, tricyclic antidepressants, and dopamine-receptor antagonists, may lead to or aggravate periodic limb movements. Low level of iron in the central nervous system may exacerbate periodic limb movements. Pathophysiology Etiology is not known, although a connection with dopa- minergic impairment has been hypothesized. Consequences Insomnia or hypersomnia secondary to non-restful sleep. Disturbance of bed partner’s sleep. Increased risk of depression, memory and attention deficits. Clinical Assessment and Diagnosis Periodic limb movements usually occur in the lower extremities, commonly involving extension of the big toe with partial flexion of ankle, knee, or hip. Movements can also occur in the upper extremities. The patient is usually unaware of movement. Patients may complain of difficulty with sleep onset or sleep maintenance. Fatigue and excessive daytime sleepiness may also accompany the condition. In addition to the clinical presentation, polysomnographic evidence of limb movements as set by the definition of the disorder is necessary for diagnosis. Differential Diagnosis Sleep starts, fragmentary myoclonus, seizure disorder. Treatment Medication options include benzodiazepines, dopaminergic agents, and gabapentin. CHAPTER 10 Disorders of behavior 389 Parasomnias Classification of Parasomnias: DSM IV-TR divides parasomnias into the 4 categories listed above. Another approach to understanding parasomnias, as used in the ICSD-2, is to distinguish between parasomnias associated with NREM sleep versus REM sleep. Disorders that arise in NREM sleep include Confusional Arousals, Sleepwalking and Sleep Terrors. Disorders that arise in REM sleep include Nightmare Disorder, Recurrent Isolated Sleep Paralysis, and REM Sleep Behavior Disorder. The latter two disorders are classified in DSM IV-TR as Parasomnia Not Otherwise Specified. Confusional Arousals Definition Mental confusion occurring upon arousal or awakening from sleep. Epidemiology Prevalence is 17% in children up to 13 years of age and ranges from 2.9 to 4.2% in those over 15 years of age. Risk Factors Genetic factors, shift work, insomnia, hypersomnia, circadian rhythm disorder, mood disorder, substance abuse, sleep deprivation. Pathophysiology Etiology is unknown, although a familial component may exist. Consequences Children with this disorder may develop sleepwalking as adolescents. Significant social, school, and work impairment may result. Clinical Assessment and Diagnosis Confusional arousals commonly arise in the earlier part of the sleep cycle. On EEG, arousal episodes may correlate with delta waves, theta or alpha activity. Three variants found in adults include excessive sleep inertia, abnormal sleep-related sexual behavior, and sleep-related violence. Differential Diagnosis Seizure disorder, sleepwalking, sleep terrors. Treatment The decision to treat is based on impairment or distress as well as the de- gree of danger to individual or others. A regular sleep schedule, avoidance of sleep deprivation, safe sleep and home environment (e.g., locking of windows, sleeping on the ground floor) may be beneficial. 390 NORMAL SLEEP—STAGES AND CYCLES Sleepwalking Definition Ambulation that occurs during sleep and is associated with at least one of the following: difficulty arousing the individual, mental confusion upon awakening, amnesia of the episode, routine behaviors occurring at inappropri- ate times, inappropriate or dangerous behaviors. Epidemiology Prevalence peaks between ages of 5-10 years old. 10-20% of children and 1-4% of adults are affected. Risk Factors A significant genetic component exists. Precipitating factors include sleep deprivation, central nervous system insult such as stroke or trauma, hyperthyroidism, migraines, stress, irregular sleep schedules, and the use of lithium, anticholinergics, and phenothiazines. Pathophysiology Etiology is unknown. Consequences Possible injury to the individual or co-habitors, disruption of bed partner’s sleep. Clinical Assessment and Diagnosis Sleepwalking usually arises during slow-wave sleep and thus commonly starts in the first few hours of sleep. Goal-directed activity such as attempts to use bathroom may occur. The individual’s eyes may be open. On EEG, arousal from slow-wave sleep followed by an increase in autonom- ic activity may be seen. Polysomnography can help to determine if precipi- tants such as seizure disorder, periodic limb movements, or a breathing disor- der may be triggering arousal. Differential Diagnosis Sleep terrors, REM sleep behavior disorder, sleep related epilepsy, malingering. Treatment The decision to treat is based on impairment or distress as well as the de- gree of danger to the individual or others. A regular sleep schedule, avoidance of sleep deprivation, safe sleep and home environment (e.g., locking of windows, sleeping on the ground floor) may be beneficial. Clonazepam and other benzodiazepine receptor agonists can be used without tolerance developing in the individual. CHAPTER 10 Disorders of behavior 391 Sleep Terrors Definition An episode of terror commonly associated with a loud cry which occurs and is seen with autonomic or behavioral arousal. In addition, at least one of the following must also be present: difficulty arousing individual, mental confusion upon awakening, amnesia of episode, or dangerous behaviors. Epidemiology Prevalence is 5% of children and 1-2% of adults. Risk Factors A genetic component exists. Precipitants may include a breathing disorder such as OSA. Pathophysiology Etiology is unknown. Consequences Social impairment, possible injury to individual or co-habitors. Clinical Assessment and Diagnosis Sleep terrors usually arise during slow-wave sleep and thus commonly start in the first few hours of sleep. Episodes usually start with arousal followed by a loud cry or scream. In- creased autonomic activity, such as elevated heart or respiratory rate, diapho- resis, and increased muscle tone may follow. Confusion during the event and amnesia of the event are common. On EEG, arousal from slow-wave sleep followed by an increase in autonom- ic activity may be seen. Polysomnography can help to determine if precipi- tants such as periodic limb movements or a breathing disorder may be trigger- ing arousal. It may also help to exclude REM sleep behavior disorder. Differential Diagnosis Sleepwalking, confusional arousals, REM sleep, behavior disorder, seizure disorder, nocturnal panic attack, malingering. Treatment The decision to treat is based on impairment or distress as well as the de- gree of danger to the individual or others. A regular sleep schedule, avoidance of sleep deprivation, safe sleep and home environment (e.g., locking of windows, sleeping on the ground floor) may be beneficial. Clonazepam and other benzodiazepine receptor agonists can be used without tolerance developing in the individual. 392 NORMAL SLEEP—STAGES AND CYCLES Nightmare Disorder Definition Recurrent awakenings with recollection of disturbing dreams. No confusion or disorientation upon awakening and clear recollection of dream content are present. Disorder is also marked by either delayed return to sleep following episode or occurrence of episode in latter half of sleep. Epidemiology Prevalence is 5% in adults and is higher in women. Seventy-five percent of children report having at least one nightmare during childhood. Generally, nightmares decrease in frequency and intensity with age. Of note, nightmares are seen in at least 50% of individuals with PTSD. Risk Factors PTSD or acute stress disorder, female sex, low socioeconomic status, antidepressants, dopamine-receptor agonists. Pathophysiology Etiology is unknown. Consequences Sleep avoidance, insomnia, depression, daytime sleepiness. Clinical Assessment and Diagnosis Clinical history, including evaluation for a traumatic event. Differential Diagnosis Sleep terrors, sleep paralysis, REM sleep behavior disorder. Treatment Medication: prazosin Imagery rehearsal, in which new versions of a nightmare are rescripted during the day. CHAPTER 10 Disorders of behavior 393 Circadian Rhythm Sleep Disorders Classification DSM IV-TR divides circadian rhythm sleep disorders into four subtypes: delayed sleep phase, jet lag, shift work, and unspecified types. ICSD-2 makes similar divisions, but also includes other subdivisions, including advanced sleep phase. Background Circadian, or 24-hour, rhythms underlie physiology. The sleep-wake cycle is one example of a circadian rhythm. In mammals the suprachiasmatic nucleus (SCN) acts as a pacemaker to maintain a self-sustaining rhythm. The SCN also synchronizes the endogenous rhythm to the 24-hour day. Light, the strongest synchronizing agent, can delay circadian rhythms if expo- sure occurs in the first half of the night. Similarly, light exposure in the second half of the night may advance the rhythm. In addition, melatonin exposure in the early evening can phase advance, while exposure in the early morning can phase delay. Delayed Sleep Phase Type Definition Habitual sleep-wake times are delayed, usually by more than 2 hours, relative to socially accepted times. Typically the patient may have difficulty falling asleep and prefer later wake-up times; however, once asleep sleep is normal. When allowed to choose a preferred schedule, the patient will demonstrate a delayed but stable circadian phase. Epidemiology More common in adolescents and young adults, with a preva- lence of 7-16%. Mean age of onset is 20 years. Prevalence in the general population is <1%. Risk Factors Genetic factors, bright light exposure in the evening, minimal light exposure in the morning, caffeine or stimulant use, shift work, travel across time zones. Pathophysiology Etiology is unknown. Consequences Difficulty conforming to required school and work schedules. Clinical Assessment and Diagnosis A stable delay of the sleep period coupled with an inability to fall asleep and awaken at socially accepted times forms the diagnosis. Patients may fit the description of extreme “night owls.” Sleep log or actigraphy for at least 7 days will show a stable delay in the sleep period. Differential Diagnosis Normal sleep, insomnia, depression. Treatment Chronotherapy: bedtime is delayed by 3 hours every 2 days until the desired sleep time is achieved. Exposure to bright light in the early morning and dark in the evening. Melatonin administered in the evening can phase advance sleep-wake times. 394 NORMAL SLEEP—STAGES AND CYCLES Advanced Sleep Phase Type Definition Advance in the sleep period relative to desired sleep/wake times, resulting in early morning awakenings and the inability to stay awake until a desired bedtime. When allowed to choose a schedule, patients will demon- strate advanced, but stable, sleep-wake patterns. Epidemiology Prevalence increases with age. Prevalence in the general population is unknown. Risk Factors Genetic factors, environmental factors. Pathophysiology Etiology is unknown. Consequences Difficulty conforming to conventionally accepted times for social interaction. Clinical Assessment and Diagnosis A stable advancement of the sleep period coupled with an inability to fall asleep and awaken at socially accepted times forms the diagnosis. Patients may fit the description of extreme “morning larks.” Sleep log or actigraphy for at least 7 days will show a stable advance in the sleep period. Differential Diagnosis Normal sleep, insomnia, depression. Treatment Chronotherapy: bedtime is advanced by 2 hours every 2 days until the de- sired sleep time is achieved. Exposure to bright light in the early evening.
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