Clinical Focus

Primary Psychiatry. 2005;12(8):67-74

Rapid Eye Movement and Non-REM Sleep Parasomnias

Carlos H. Schenck, MD, and Mark W. Mahowald, MD
Focus Points Parasomnias comprise the behavioral, experiential, and autonomic nervous system disorders of sleep. Instinctual behaviors, such as locomotion, aggression, feeding, and sex, often emerge with parasomnias. Parasomnias are rarely a direct manifestation of a psychiatric disorder, and can usually be effectively treated. Polysomnography is required for the diagnosis of rapid eye movement sleep behavior disorder. This article details the current clinical knowledge on the parasomnias, focusing on their relevance to psychiatrists. During the past 12 decades, a surprisingly high prevalence and broad range of parasomnias in adults have been identified, along with their interactions with an extensive number of neurologic, medical, psychiatric, and other sleep disorders and their respective treatments. An increasingly detailed understanding of the predisposing and precipitating factors for parasomnias, along with their pathophysiology, has been achieved. The American Academy of Sleep Medicine recently published its revised sleep disorders nosology (The International Classification of Sleep Disorders-2 [ICSD-2]).1

Abstract

Parasomnias comprise the behavioral, experiential, and autonomic nervous system disorders surrounding rapid eye movement (REM) and non-REM sleep and can cause injuries, sleep disruption, and adverse health effects. Parasomnias often involve the abnormal release of instinctual drives, such as locomotion, aggression, feeding, and sex during sleep, and can manifest with dream-enacting behaviors. Parasomnias are relevant to psychiatrists in regards to their misdiagnosis as a psychiatric disorder; their nocturnal extension of a daytime psychiatric disorder; their stress-responsivity; their induction or aggravation by psychotropic drugs; their adverse psychologic consequences; their link to various neurologic and medical disorders; and their forensic implications. Parasomnias can be categorized as primary disorders of sleep, or as secondary organ system disorders emerging during the sleep period. The evaluation of parasomnias includes clinical interviews, review of medical records, screening psychologic tests, neurologic examination, and hospital-based polysomnographic monitoring. This article discusses the six most prominent behavioral parasomnias: REM sleep behavior disorder, sleepwalking, sleep terrors, confusional arousals (including abnormal sleep related sexual behaviors and severe morning sleep inertia), sleep related eating disorder, and sleep related dissociative disorders. Parasomnias can appear at any time in the human life cycle, often demonstrate prominent gender discordances, and can usually be accurately diagnosed and effectively treated.

Relevance of Parasomnias to Psychiatrists

Introduction

Parasomnias are undesirable physical events or experiences that occur during entry into sleep, within sleep, or during arousals from sleep.1 Parasomnias encompass abnormal movements, behaviors, emotions, perceptions, dreams, and autonomic nervous system functioning that can emerge in relation to any sleep stage at any time of the night and during any age in the human life cycle. Parasomnias are clinical disor-

ders because of their resulting injuries, sleep disruption, adverse health effects, and psychological or interpersonal distress. Parasomnias often involve abnormal release of instinctual drives, such as locomotion, aggression, feeding, and sex during sleep that are found clinically with sleepwalking, rapid eye movement (REM) sleep behavior disorder, sleeprelated eating disorder (SRED), sleeprelated abnormal sexual behaviors, and other nocturnal disorders.

There are at least seven reasons why parasomnias should interest psychiatrists. Parasomnias can be misdiagnosed and inappropriately treated as a psychiatric disorder on account of bizarre and violent nocturnal behaviors, especially when they emerge comingled with emotional and perceptual disturbances during sleep. Parasomnias can be a direct manifestation of a psychiatric disorder, eg, a nocturnal dissociative, bulimic, or panic disorder. The emergence and/or recurrence of a parasomnia can be triggered by stress. Psychotropic medications can trigger the initial emergence of a parasomnia, or aggravate a preexisting parasomnia. Parasomnias can cause low self-esteem and other psychological distress, and can induce or reactivate a psychiatric disorder in either the patient or the bed partner, on account of the repeated

Dr. Schenck is associate professor of psychiatry at the University of Minnesota Medical School, and senior staff psychiatrist at the Minnesota Regional Sleep Disorders Center and Hennepin County Medical Center in Minneapolis, MN. Dr. Mahowald is professor of neurology at the University of Minnesota Medical School, and senior staff neurologist and director of the Minnesota Regional Sleep Disorders Center and Hennepin County Medical Center. Disclosure: The authors report no an affiliation with or financial interest in any organization that might pose a conflict of interest. Funding/Support: This work was supported in part by a grant from Hennepin Faculty Associates. Please direct all correspondence to: Carlos H. Schenck, MD, Hennepin County Medical Center, Department of Psychiatry (R7), 701 Park Ave. South, Minneapolis, MN 55415; Tel: 612-873-6201; Fax: 612-904-4207; E-mail: schen010@[Link]; Web sites: [Link] and [Link].

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loss of self-control during sleep, with bizarre behaviors and sleep-related injuries. Familiarity with the parasomnias will allow psychiatrists to be more fully aware of the various medical and neurological disorders that can be associated with disturbed (sleep-related) behavior and disturbed dreaming. Parasomnias carry forensic implications, especially considering that the prevalence of sleeprelated violence is 2%.2 Psychiatrists are often asked to render an expert opinion in medical-legal cases pertaining to violence, including nocturnal violence, and forensic guidelines pertaining to the parasomnias are available.3,4 symptoms); past or current history of abuse (physical, sexual, verbalemotional); and family medical, sleep, and psychiatric history. Screening psychological tests for Axis I and II disorders. With self-administered instruments, such as the Minnesota Multiphasic Personality Inventory, Symptom Checklist-90, Beck Depression/Anxiety Inventories, Dissociative Experiences Scale, etc. Formal psychiatric consultation may also be indicated. Neurologic review of systems and examination. This should include formal consultation at times being indicated. Hospital-based, overnight polysomnographic (PSG) monitoring, with continuous PSG-time-synchronized, audio-visual recording. The PSG montage should include the electrooculogram, electroencephalogram (EEG) with a full conventional seizure montage, chin and four-limb electromyograms, electrocardiogram, and nasal-oral airflow with full respiratory effort monitoring. Fast PSG paper speeds of 1530 mm/second are used during the first night of PSG monitoring in order to detect any epileptiform activity. Urine toxicology screening is performed whenever indicated. Daytime multiple sleep latency testing. If there is a complaint or suspicion of excessive daytime sleepiness, then a scheduled daytime nap study can be conducted in order to objectively confirm excessive daytime sleepiness7 and help identify the specific diagnosis, such as narcolepsy. The most prominent behavioral parasomnias to be covered in this article comprise six of the 12 currently recognized primary parasomnias.1 The table provides a comparison of the salient features of these six behavioral parasomnias. The other six parasomnias that are beyond the space limit of this article include recurrent, isolated sleep paralysis; sleep-related hallucinations; nightmare disorder; nocturnal groaning; sleep enuresis; and exploding head syndrome. Sleep-related movement disorders (eg, restless legs syndrome [RLS] and rhythmic movement disorder) comprise a subset of parasomnias that are classified separately in ICSD-2 and are not covered in this article.

Rapid Eye Movement Sleep Parasomnias

Rapid Eye Movement Sleep Behavior Disorder REM sleep has two major synonyms: active sleep, because of the high level of brain activity during REM sleep, and paradoxical sleep, because of the nearly complete suppression of skeletal muscle tone despite the high level of brain activity. This generalized muscle paralysis (REM-atonia) is one of the three defining features of mammalian REM sleep, along with REMs and an activated EEG pattern virtually identical to that of wakefulness.8,9 The loss of the customary paradox of REM sleep in rapid eye movement sleep behavior disorder (RBD), with reassertion of muscle tone and increased phasic muscle twitching and behavioral release during REM sleep, carries serious clinical consequences, since sleep is no longer safe when the acting-out of dreams becomes possible. A typical clinical presentation of RBD is contained in the description of our index case10:
A 67-year-old dextral man was referred because of violent behavior during sleep...4 years before referral...he experienced the first physically moving dream several hours after sleep onset; he found himself out of bed attempting to carry out a dream. This episode signaled the onset of an increasingly frequent and progressively severe sleep disorder; he would punch and kick his wife, fall out of bed, stagger about the room, crash into objects, and injure himself...his wife began to sleep in another room 2 years before referral. They remain happily married, believing that these nocturnal behaviors are out of his control and discordant with his waking personality.

Classification of Parasomnias: Primary and Secondary Sleep Phenomena

Parasomnias can be categorized as primary parasomnias (disorders of sleep per se) or as secondary parasomnias (disorders of other organ systems that manifest during sleep).5,6 In the ICSD2,1 primary parasomnias comprise 12 diagnostic categories across REM and non-REM sleep. Secondary parasomnias can be subdivided by the organ system involved nocturnally, such as: central nervous system (eg, seizures, headaches); cardiopulmonary (eg, cardiac arrhythmias; angina pectoris, asthma); gastrointestinal (eg, gastroesophageal reflux). Also, various sleep disorders can trigger a secondary parasomnia, such as obstructive sleep apnea (OSA)-induced arousals precipitating an episode of sleepwalking. Finally, medications used in the treatment of various medical, psychiatric, and sleep disorders can cause or aggravate a parasomnia.

Clinical Evaluation of Parasomnias

Patients with complex and violent nocturnal behaviors should be referred to an accredited sleep disorders center where the evaluation should consist of the following points.7 Clinical sleep-wake interview and examinations. The bed partner is urged to attend the interview. Past and current medical records are reviewed, along with a patient-completed questionnaire that covers: sleep-wake, medical, and psychiatric history, and caffeine/alcohol/chemical use and abuse history; review of systems (ie, review of any current physical and mental-emotional 68

Clinical Findings There is a distinct clinical profile in the chronic form of RBD.8,9 There is a striking older male predominance, although females and virtually any age group can develop RBD. All published series on RBD from numerous centers across many countries in various continents have documented a male predominance, ranging from 66% to 88% of reported subjects.8,11-13 Although the reason(s) for the male predominance has not been determined, hormonal factors and/or male and age-related vulnerability in the brain regions subserving motor function in REM sleep are currently the most likely explanations. Approximately 90% of patients with RBD act out distinctly altered dreams

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that have become intensely vivid, actionpacked, confrontational, and violent. Patients with RBD do not act out their customary dreams, but rather act out dreams that are altered in a stereotypical, abnormal fashion. The typical RBD dream scenario involves being threatened or attacked by unfamiliar people, animals, or insects, and then fighting the attacker to protect oneself or a loved one from being harmed. (Of note is that sexual dreams or psychologically meaningful dreams rarely or never occur with RBD). Therefore, RBD is a dream disorder almost as much as it is a behavioral disorder arising from REM sleep. Dream-enacting behaviors observed by the bed partners and documented during sleep lab monitoring, include talking, yelling, swearing, gesturing, grabbing, arm flailing, punching, kicking, sitting, jumping out of bed, crawling, and running. Patients with RBD often have had to resort to using a sleeping bag, padded waterbed, a barricade of pillows, a mattress placed on the floor, or tying themselves to their beds or bedposts with belts, ropes, or dog leashes in order to protect themselves while they sleep. The wives of men with RBD are often battered by their husbands violent dream-enacting behaviors. Not uncommonly, physicians and nurses question whether willful domestic abuse has taken
Table

place. It is evident to these wives that their husbands are asleep and dreaming while they engage in their aggressive and violent nocturnal behavior. No case of marital separation or divorce has been reported with RBD, probably because most couples affected by RBD had been married for decades before the onset of RBD, and the wives knew that their husbands were mild-mannered and lacked a propensity for aggression or violence during their waking lives. In contrast, marital discord directly related to RBD has been reported in a recently married young adult couple, which resolved when the RBD was eventually controlled with appropriate treatment.14 Greater than 50% of RBD cases are closely associated with a broad variety of brain disorders, but predominantly neurodegenerative conditions (especially parkinsonism), narcolepsy, and stroke.8 RBD may be the first sign of a neurologic disorder whose other (classic) manifestations may not emerge until several years or decades after the onset of RBD. For example, we now know, from our sleep centers ongoing research, that two-thirds of men >50 years of age with RBD, who were initially diagnosed with idiopathic RBD, will eventually develop Parkinsons disease or a related condition, such as multiple system atrophy or dementia with Lewy

bodiesat a mean interval of 13 years (range=229 years).15,16 Thus, routine neurologic evaluations are indicated in the long-term management of RBD. The prevalence of RBD is unknown; the course is usually progressive. (There is also an acute-onset, usually self-limited, form of RBD that emerges during withdrawal from alcohol or drug abuse and with various medication intoxication states).9 There is no evidence to date that handedness plays a role in RBD. Association with Psychiatric Disorders and Stress Psychiatric disorders are rarely associated with RBD.17 However, psychotropic medications used to treat psychiatric disorders can induce or aggravate RBD, particularly selective serotonin reuptake inhibitors (fluoxetine, sertraline, citalopram, etc), venlafaxine, mirtazapine, tricyclic antidepressants, and monoamine oxidase inhibitors.9 Also, a precursor of RBDREM sleep with increased electromyographic tonecan be associated with serotonergic antidepressant therapy.18 In contrast, no case of RBD presumably caused or aggravated by bupropion has been reported, and it could be speculated that bupropion may actually protect against RBD because of its dopaminergic activity. Acute major stress and posttraumatic stress disorder (PTSD) at times can be

Comparisons Among the Behavioral Parasomnias

Parasomnia Categories REM Sleep Behavior Disorder Main Symptoms Dream-enactment (complex, vigorous, violent, injurious), >1.5 hours after sleep onset, with subsequent recall of the enacted dream. Disorders of Arousal (CA, SW, ST) CA, SW, ST, with screaming, running, agitation, 15 minutes2 hours after sleep onset, with partial or no recall. Sleep-Related Eating Disorder High caloric, sloppy binge-eating after arousals from sleep at any time of the night, with partial or no recall. Sleep-Related DD Elaborate behaviors, including reenactment of sexual and/or physical abuse, emerging at any time in the night, with no recall.

Gender/Age Preference

Males: Middle-aged/ No gender preference, Females: Adolescent, Females: Adolescent, older adult. apart from male pre- young, middle-aged young, middle-aged dominance in injurious adult. adult. adult SW, ST. Tonic and phasic electromyographic and behavioral abnormalities in REM sleep. Abrupt partial arousals from stage 3/4 (delta, slow-wave) Non-REM sleep. Admixture of sleep and nocturnal eating disorders emerging from any sleep stage. Same as daytime DD, but emerging during awakenings from REM and stages 1/2 sleep.

Pathophysiology

Primary Treatment(s)

Clonazepam 0.51.0 Sleep hygiene, hypnosis, Control of any under- Specialized psychiatric mg, up to 4 mg at HS. stress reduction therapy, lying sleep disorder; treatment(s) of DD. benzodiazepines at HS. topiramate 50150 mg, up to 300 mg at HS.

REM=rapid eye movement; CA=confusional arousals; SW=sleepwalking; ST=sleep terrors; DD=dissociative disorders. Schenck CH, Mahowald MW. Primary Psychiatry. Vol 12, No 8. 2005.

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associated with RBD,19,20 but the extent of increased propensity for RBD with stress and stress disorders remains an open question, and hospital-based PSG must be performed to confirm the diagnosis of RBD in relation to dream-enacting behaviors and stress-related disorders.8 Diagnosis The diagnostic criteria include1: increased muscle tone and/or increased muscle twitching during REM sleep; abnormal behaviors documented during REM sleep and/or a history of injurious or disruptive sleep behaviors (usually with dream-enactment); and absence of epileptic brain-wave activity or frank seizures during REM sleep. Treatment Clonazepam controls the behavioral and the dream-disordered components of RBD in approximately 90% of treated patients, at a typical bedtime dose of 0.5 1.0 mg or as high as 4 mg.8 The long-term efficacy and safety of chronic, nightly clonazepam treatment of RBD has been established.17,21 Clonazepam appears to preferentially suppress excessive phasic motor activity and behavioral release during REM sleep rather than help restore REM-atonia.8 Other benzodiazepines or benzodiazepine receptor agonists do not seem to be effective in controlling RBD compared to clonazepam, but systematic studies have not been conducted. In fact, a list of reported alternative therapies to clonazepam (eg, carbamazepine, clonidine, levodopa, pramipexole) does not contain another benzodiazepine.9 Melatonin (dosage range=315 mg HS) can be effective in controlling RBD,8,22 especially when combined with reduced doses of clonazepam in the treatment of RBD in patients with neurodegenerative disorders who may be at increased risk for developing morning sedation from bedtime administration of clonazepam.22 The mechanism of action of melatonin efficacy in RBD is unknown, but may involve partial restoration of REM atonia.8 Maximizing the safety of the sleeping environment should always be encouraged. after sleep onset, but can occur throughout most of the sleep period in adults. There is an abrupt and inappropriate activation of locomotion, eating, sexual behavior, aggression, and urination immediately upon arousing from (delta) sleep. The duration of each episode can vary widely, ranging from <1 minute to >1 hour. Episodes of SW and ST in children are usually benign, but episodes in adults can result in injuries and embarrassment from aggressive, violent, sexual, and other abnormal behaviors.7,23,24 SW is characterized by wandering about aimlessly or semi-purposely, carrying objects nonsensically from one place to another, rearranging furniture, engaging in inappropriate eating or sexual activity, urinating in closets or into waste baskets, running around, going outdoors, jumping into a lake or a river, or driving an automobile. The eyes are usually wide open and have a glassy or peculiar stare, and there may be some mumbling or talking, including prolonged talking that may be punctuated by shouting or loud swearing. Clumsiness can be observed. Communication with a sleepwalker is usually limited or impossible. Frenzied or aggressive behavior, the wielding of weapons (knives, guns, baseball bats), or the calm suspension of judgment (eg, going out a bedroom window, wandering far outdoors on a winters night, driving an automobile) can result in inadvertent injury or death to oneself or others. Homicidal SW has been reported.25 The following is a wifes description of her husbands agitated SW7:
He seems to have the strength of 10 men and shoots straight up from bed onto his feet in one motion. Hes landed clear across the room on many occasions and has pulled down curtains (bending the rods), upset lamps, and so forth. Hes grabbed me and pulled on me, hurting my arms, because hes usually dreaming that hes getting me out of danger...Hes landed on the floor so hard that hes injured his own body... There are low windows right beside our bed and Im afraid hell go through them some night.

Non-Rapid Eye Movement Sleep Parasomnias

Sleepwalking, Night [Sleep] Terrors, and Confusional ArousalsDisorders of Arousal Sleepwalking (SW) and sleep terrors (ST) typically arise abruptly from slowwave, non-REM sleep 15120 minutes 70

ST are characterized by sudden, loud, terrified screaming, with wide dilation of the pupils, rapid heart rate and breathing, and profuse sweating. The person may sit up rapidly while shouting or screaming, and engage in frenzied activity and become injured. Some patients have run through glass doors or jumped off balconies. Childhood SW and ST are characterized by complete amnesia for the events.

In adult SW and ST, there can be subsequent recall of the events, and also recall of dreaming during the events7,26 that usually involve being threatened by an imminent danger, such as a menacing intruder, a fire, or the ceiling caving in. The prevalence of SW can reach 17% in childhood (peaking at 48 years of age), and 4% in adults. The prevalence of ST ranges from 1% to 6.5% in children and 2.3% to 2.6% in those 1564 years of age, before dropping to 1% for those >65 years of age. A familial-genetic basis for SW and ST is well established, with sleep deprivation, stress, alcohol use or abuse, fever (in children), menstruation, pregnancy, medical and psychiatric disorders, and various medications (eg, anticholinergics, lithium, zolpidem) being recognized precipitating factors. Injurious SW and ST are male-predominant; otherwise there is no gender preference for SW or ST. Confusional arousals (CAs) comprise the third category of disorder of arousal, and represent partial manifestations of SW and ST. CAs can last for variable intervals of time, including prolonged episodes with irritability and anger. CAs are especially prevalent among children and adults <35 years-old. Prevalence rates in children 313 years of age can reach 17%. The prevalence among adults >15 years of age is 2.9% to 4.2%. Genetic factors are the most important predisposing factors, with rotating shift work, night shift work, other sleep disorders (hypersomnia, insomnia, circadian), sleep insuffiency (and recovery sleep), stress, and anxiety, bipolar and depressive disorders, alcohol consumption, psychotropic medication use, drug abuse, and forced awakenings being recognized precipitating factors. Sleep inertiathe inability to promptly and appropriately transition oneself both physically and mentally from sleep to wakefulnessis commonly present with CAs, and a distinct variant consists of severe morning sleep inertia, in which the affected individual is unable to exit sleep and enter wakefulness in a timely fashion, resulting in adverse consequences at school, work, and with interpersonal relationships.1 Also, sleep-related abnormal sexual behaviors is another variant of CAs and of SW, with reported behaviors including loud sexual vocalizations, prolonged and/or violent masturbation, sexual molestation and assaults of minors or

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adults (including spouses), initiation of sexual intercourse irrespective of the menstrual status of the bed partner (unlike during wakefulness), and kinky or altered sexual repertoire and affect.1,24,27,28 The presence of snoring during nocturnal sexual activity has clearly indicated that the person was asleep (ie, sleepsex.)27,28 Polysomnographic Findings Episodes of SW, ST, and CAs arise abruptly during arousals from delta non-REM sleep, and at times from stage 2 sleep. During an episode, the EEG can show either the persistence of sleep, the admixture of sleep and wakefulness, or else complete wakefulness. There can be an impressive dissociation between a fully awake EEG and the spacey appearance and confused behavior of the affected person. It most cases, however, the postarousal EEG during a SW episode shows the persistence of sleep (namely, rhythmic delta activity; delta and theta waves), which demonstrates that the disorders of arousal are physiologic disorders of non-REM sleep.29 Association with Psychiatric Disorders The relationship between SW, ST, and psychopathology in adults remains open to debate. The early literature indicated a likely association, but PSG monitoring was not conducted, and selection biases may have been influential in reaching these conclusions. In contrast, the recent literature involving PSG-confirmed cases has indicated that most adult cases are not closely associated with psychiatric disorders.7,30,31 In a consecutive series of 54 adults with PSG-confirmed injurious SW/ST,2 35% had a current Axis I Diagnostic and Statistical Manual of Mental Disorders, Third Edition, disorder (usually nonpsychotic depression) at the time of evaluation, but none had concurrent onsets of SW and ST and their psychiatric disorder(s). Furthermore, treatment of any current Axis I disorder, or past treatment of a prior Axis I disorder, did not usually improve the SW and ST. In contrast, treatment with bedtime clonazepam was quite effective in nearly 90% of these patients. In England, a psychological profile of normality has been reported in adults with PSG-confirmed SW/ST.32 Further research with PSG monitoring is needed in this area.31 Treatment Treatment of SW, ST, and CAs is often not necessary (especially in childhood cases), other than identifying and minimizing any precipitating factor, and maximizing the safety of the bedroom. Obtaining sufficient nocturnal sleep and maintaining a regular sleep-wake schedule should be considered priorities, since sleep deprivation has been identified as the most potent risk factor for SW and ST. If a child or an adult has left the bed, he or she should be calmly redirected back to bed, avoiding any intervention which could agitate the individual. Use of night lights, motion sensors, door alarms, and other safety devices should always be considered. Teaching a patient to practice self-hypnosis33 or other relaxation techniques at bedtime can be effective in milder cases of childhood or adult SW and ST. For some patients with stress-related SW and ST or with other forms of psychologically-mediated SW and ST, psychotherapy may be of benefit in helping control the parasomnia. Also, in cases involving non-injurious SW and ST associated with an Axis I disorder, it may be reasonable to first control the Axis I disorder and then determine whether the SW and ST are also controlled; if not, then separate treatment of the SW and ST can be initiated. In cases involving sleep-related injury (usually in adults), treatment with bedtime medication is usually necessary and can be life-saving. A benzodiazepine taken 3075 minutes before bedtime is usually effective. Long-term, nightly benzodiazepine treatment of adults with SW and ST has been found to be safe and effective.7,21 Other medications, such as imipramine or paroxetine, can also be used. Finally, if sleep-disordered breathing (eg, OSA) is diagnosed in a patient with SW or ST, then control of the former problem (that could serve as a stimulus for disordered arousals) may also control the associated parasomnia, but this needs to be carefully assessed. Successful treatment of severe morning sleep inertia consists of administration of methyphenidate sustainedrelease (SR) and/or bupropion SR taken immediately before falling asleep.34 Treatment of abnormal sleep-related sexual behaviors primarily consists of treating the underlying disorder23,28; eg, with CAs and SW, bedtime administration of clonazepam is effective, and with OSApromoting CA and/or SW with abnormal sexual behaviors, nasal continuous positive airway pressure therapy is effective. Also, the physician should consider referral of the patient and spouse or significant other to a psychologist or psychiatrist to explore the marital/interpersonal relationship as a contributing factor to the sexual parasomnia, and/or to deal with the adverse consequences (personal and interpersonal) of the sexual parasomnia.23 Treatment of a related parasomnianocturnal panic attacks (characterized by awakenings from stages 2/3 non-REM sleep with full consciousness and immediate awareness of experiencing a typical panic attack) consists of cognitive-behavioral therapy and/or medications, such as imipramine or benzodiazepines.35

Sleep-Related Eating Disorder

Clinical Findings Whyte and Kavey36 first reported on abnormal nocturnal eating that utilized PSG monitoring, which called attention to somnambulistic eating in three patients. Although SW remains the most commonly identified predisposing condition for SRED, other conditions and precipitating factors have been identified, such that in 1991 our center reported37 on sleep-related eating disorders in 19 patients, with a subsequent report38 in 1993 on 38 patients. The following comments were made by the index patient:
I have buttered pop cans and then tried to eat them...I will take the big container of salt--not the salt shakerand Ill pour it in my hand and Ill eat it just like that. Why do I eat salt sandwiches? Thats a biggie...I have sat at the kitchen table eating pancakes at 2 oclock in the morning with no clothes on...How primitive can one get? Leftover casserolesits awful.

The hallmark of SRED is involuntary eating and drinking during sleep that usually occurs during partial arousals from sleep, with limited or no recall the next morning. However, a broad range of consciousness and of subsequent recall can be present.36-39 Problems associated with recurrent episodes of SRED include the sloppy consumption of peculiar forms or odd combinations of food, or of inedible or toxic substances; insomnia from sleep disruption; sleeprelated injury; morning anorexia (lack 71

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of hunger) and abdominal distention; and adverse health consequences (eg, weight gain/obesity). Most affected people report a nightly frequency of eating, including multiple times nightly. These episodes of eating can occur during any time of the night. High caloric foods are eaten with preference, such as chocolate, sweets, pasta, peanut butter, and milkshakes; fruits and vegetables are ignored. Alcohol is rarely consumed at night, even in those who enjoy drinking alcohol or former alcoholics. There is typically a lack of hunger or thirst during episodes of SRED. If an individual is interfered with during an episode, then the usual response is irritability and agitation. Simple foods or entire meals can be prepared, cooked, and consumed. Food is often brought back to bed, often to the consternation of the bed partner. A preliminary study utilizing a selfreport questionnaire found a nearly 5% prevalence of SRED, defined as eating during partial awakenings from sleep at least once weekly.40 This included a prevalence of 4.6% in an unselected university student group. This study suggests that SRED may be a common and considerably under recognized [Link] is female predominant, with approximately 66% to 75% of published cases being female. The age of onset is usually the late teens or early twenties, however, a very broad range exists. The onset can be insidious and sporadic, or it can be precipitous and fulminant with rapid development of nightly episodes of eating. SRED is often a relentless, longstanding disorder. Although it can be an idiopathic disorder, it is often associated with a primary, underlying sleep disorder or other clinical condition. For example, SW is the most commonly associated sleep disorder, although once eating becomes part of the behavioral repertoire of SW, it quickly becomes the predominant, if not the exclusive SW behavior. Other sleep disorders that can be closely associated with SRED include RLS, OSA, and circadian rhythm disorders (such as irregular sleep/wake pattern). Medication-induced (amnestic) SRED has been reported with zolpidem in patients with RLS and insomnia,41,42 and sporadically with other psychotropics. At least two, if not four, groups of patients should avoid taking zolpidem as a hypnotic agent (apart from hypersensitivity reactions): patients with SRED 72 (and perhaps patients with daytime eating disorders, such as bulimia nervosa, and also patients with nocturnal eating syndrome, a disorder of wakeful eating after intervals of sleep); patients (especially females) with complex medical, psychiatric, or sleep disorder histories who may be on multiple medications and who take moderate-to-high doses of zolpidem (1020 mg).42 Onset of SRED can also occur with cessation of cigarette smoking, cessation of alcohol and substance abuse (especially cocaine and amphetamine), acute stress (usually involving major separation reactions), after daytime dieting, and with onset of narcolepsy, migraine headaches, and other conditions. SRED at times can be associated with daytime eating disorders (such as bulimia nervosa), and with a nocturnal dissociative disorder (eg, multiple personality disorder, with one of the alter personalities being a nocturnal eater). Serious complications can occur on account of recurrent nocturnal eating. Eating peculiar forms or combinations of food (eg, frozen pizzas; raw bacon; peanut butter, salt and sugar sandwiches; cat food sandwiches), or inedible or toxic substances (eg, cigarettes, coffee grounds, glue, nail polish; ammoniacontaining cleaning compounds) can be hazardous. Insomnia related to sleep disruption from repeated episodes of eating can also occur, with daytime sleep-deprivation symptoms: tiredness, fatigue, irritability, moodiness, interpersonal problems, reduced attention span, diminished memory, and sub-par work or school performance. Sleep-related injury can occur (ie, cutting oneself from carelessly cutting food or opening cans; internal/external burns from consuming or spilling hot or scalding foods or beverages; and poisoning and internal injuries from ingesting toxic substances). Dangerous behaviors can be performed while seeking food (eg, driving a car while half-asleep, or starting a fire in the kitchen while engaged in sleeprelated cooking prior to eating). Morning anorexia can occur, often with bloating and no desire to eat breakfast. Adverse health consequences from recurrent binge-eating excessive quantities of high-caloric foods include: excessive weight gain/obesity; destabilization (or precipitation) of diabetes mellitus (type II and I), hypertriglyceridemia, hypercholesterolemia; dental caries and periodontal disease; consuming foods to which one is allergic; consuming foods that are contraindicated with monoamine oxidase therapy; eating the night when one is supposed to be fasting can compromise next-day surgery. Secondary depressive disorders may emerge from a longstanding personal dejection and a sense of failure over the inability to control the nocturnal eating. Differential Diagnosis There are two main differential diagnostic considerations for abnormal nocturnal eating, besides SRED. These are nocturnal bulimia nervosa or bingeeating disorder (ie, extensions of a daytime eating disorder) and nocturnal eating syndrome.43 If inappropriate compensatory behavior in order to prevent weight gain from the nocturnal eating is present, such as self-induced vomiting, enemas, misuse of laxatives, diuretics or other medications, or if there is body image distortion, then an eating disorder should be diagnosed (bulimia nervosa, bingeeating disorder, anorexia nervosa). However, patients with longstanding SRED and excessive weight gain may eventually fast during the daytime and/ or engage in excessive exercise to prevent further weight gain and obesity. If a history of excessive eating between dinner and sleep onset, and/or excessive eating after a complete awakening from sleep is present, then the diagnosis would probably be nocturnal (night) eating syndrome,43 which is not a parasomnia, but rather a disorder of wakefulness. Sometimes patients with SRED will eat dinner, or have a substantial second dinner, shortly before going to bed at night in futile attempts to suppress the compulsion to eat after subsequently arousing from sleep. Treatment Treatment is at first directed at controlling any underlying sleep disorder, or to discontinue any medication that is suspected to be causing or promoting the SRED. For example, in patients with SRED presumably induced by OSA, treatment of the OSA with CPAP may also control the abnormal nocturnal eating. In patients with SRED associated with RLS (or SW), treatment with a dopaminergic medication, at times combined with codeine and/or a

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Rapid Eye Movement and Non-REM Sleep Parasomnias

benzodiazepine, can control both sleep problems.37,38 Interestingly, benzodiazepine monotherapy is rarely effective in controlling somnambulistic eating. Topiramate taken at bedtime is a promising new treatment of SRED.44 Cognitivebehavioral therapies and hypnosis are not usually effective in SRED. ture in the home had imprints of his teeth. The episode documented in the sleep laboratory occurred during wellestablished EEG wakefulness after an interval of sleep. Episodes of nocturnal dissociation can be elaborate and last several minutes to >1 hour, and often involve behaviors that represent reenactments of previous physical or sexual abuse scenarios. This activity may occur with perceived dreaming, which is actually a dissociated wakeful memory of past abuse. Sexualized behavior (eg, pelvic thrusting) can occur and be paired with defensive behavior (eg, warding off or hitting an attacker) and with congruent verbalization (eg, telling the attacker to stop or go away). Other dissociative episodes may occur as confusional states, with or without elaborate behaviors, that are not associated with perceived dreaming. A post-assault headache can be reexperienced during nocturnal dissociation. One patient has been reported with at least two episodes of nocturnal fugues, in which she awakened from sleep, drove her car to an airport, purchased a ticket and then flew to a distant city, where shortly upon arrival she came to and realized she had just finished another dissociative episode. Sleep-related DD are highly femalepredominant. Age of onset ranges from childhood to early-mid adulthood. Onset can be abrupt and fulminant, or it can be gradual and sporadic. The course is usually chronic and severe, with episodes often occurring several times weekly or multiple-times nightly. Complications include repeated injuries to oneself and/or ones bed partner while the person is in a dissociative state, including bruises, fractures, lacerations, and burn wounds. Skin and genital infections from self-mutilation can also occur. A past and/or current history of physical, sexual or verbalemotional abuse, along with a severe and chronic history of psychiatric disorders, are the major predisposing and precipitating factors. Specialized outpatient or inpatient treatment of DD should be recommended to patients with sleep related DD, who generally also have daytime DD. Treatment is multimodal, and often includes individual psychotherapy, group therapy, and pharmacotherapy. Clonidine, (at bedtime doses ranging from 0.10.3 mg or higher) a centrallyacting -adrenergic agonist that reduces sympathetic outflow from the brain, can be beneficial in the treatment of sleep DD by blunting hyperarousal states that interfere with sleep onset and sleep maintenance and that also may promote episodes of DD. Bedtime administration of periactin 416 mg46,47 and prazosin 510 mg48 are used in the treatment of nightmares in PTSD, may be helpful in controlling nightmares, or the perception of nightmares during dissociated wake-sleep states, associated with sleep-related DD.

Sleep Related Dissociative Disorders

Clinical Findings This category of parasomnia emerges during well-established wakefulness after periods of sleep.7,45 Sleep related dissociative disorders (DD) can emerge any time during the night from wellestablished EEG wakefulness, either at the transition from wakefulness to sleep or several minutes after an awakening from any stage of sleep. This is distinctly different from SW or ST that emerge rapidly during precipitous arousals from slow-wave, non-REM sleep. Sleep related DD comprise a sleep-related variant of dissociative disorders, which are defined in Diagnostic Statistical and Manual of Mental Disorders, Fourth Edition as: The essential featureis a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment. Most patients with sleep-related DD also have corresponding daytime DD, and also have past and/or current histories of physical and/or sexual abuse. PTSD, major mood disorders, severe anxiety disorders, multiple suicide attempts, self-mutilating behaviors, and repeated psychiatric hospitalizations are also common. Nevertheless, sleep-related DD at times can seemingly occur in isolation, without a daytime component. During the sleep period, patients with DD can scream, walk or run around in a frenzied manner, engage in selfmutilating behaviors (including genital and body slashing with a knife, burning oneself with a lit cigarette, head banging, hair pulling); and potentially becoming homicidally violent toward the bed partner. Animalistic behavior has been documented during PSG monitoring in a 19-year-old male, who for several years would twice weekly during the night act like a large jungle cat with prominent growling and dragging a mattress or other furniture around the house with his jaws.45 Many pieces of furni-

Differential Diagnosis of Dream-Enacting Behaviors and Other Parasomnias

RBD is not the only parasomnia associated with dream-enacting behaviors.8 This is one of the main reasons why patients with dream enactment should have extensive overnight PSG monitoring at an accredited sleep lab with a sleep technologist in continuous attendance. Various parasomnias other than RBD can manifest with attempted dream enactment, such as SW, ST, SRED, OSA,49 sleep-related DD, and nocturnal seizures (particularly complex partial seizures). Some patients with severe OSA/hypopnea can present with pseudo-RBD that closely mimics RBD on account of problematic dreamenacting behaviors in middle aged and older males. These patients experience recurrent apnea/hypopnea-induced arousals or awakenings from REM sleep manifesting with complex, vigorous, and violent dream-enacting behaviors. The state of consciousness immediately post-awakening is the persistence of dreaming with simultaneous physical dream enactment. These patients have a disorder of arousal from REM-sleep (sleep-disordered breathing subtype), and not RBD which is a within-REM sleep motor and dream disorder.

Conclusion

Parasomnias can have prominent gender discordances, with SRED and sleep-related DD being female predominant; and RBD, injurious SW/ST, and abnormal sleep-related sexual behaviors being male predominant. Educational resources are now available for the parasomnias in adults. The first DVD documentary on the parasomnias has recently been released, in which patients and their families describe coping with 73

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C.H. Schenck, M.W. Mahowald

ST, SW, RBD, SRED and RLS for years before being referred to a sleep center and having their conditions diagnosed and effectively treated.50 Sleep laboratory footage of parasomnia behaviors and scientific explanations by sleep physicians experienced with parasomnias are contained in this documentary. Also, a book51 containing over 60 personal accounts by patients with parasomnias and their families, along with pertinent clinical information, complemented by the forensic aspects of the parasomnias, will soon be published. PP
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