Parasomnias and dyssomnias are 2 major types of sleep disorders. Parasomnias are disorders characterized by undesirable motor, verbal, or experiential phenomena occurring in association with sleep, specific stages of sleep, or sleep-awake transition phases.[1] They may be broadly categorized as follows:

Unlike dyssomnias, which are characterized by abnormal sleep quality (including initiation, maintenance, duration, timing, and amount of sleep), parasomnias are distinguished by deviant behavioral or physiologic events. These abnormalities or events are reliably associated with either the sleep-wake interface or certain sleep stages. Additionally, parasomnias are manifested by activation of systems (eg, the autonomic nervous system) or programs (eg, cognitive, behavioral, or motor program stimulation).[2, 3, 4]

Classification and definition

The parasomnias have been subdivided according to 2 major classification schemes, the American Psychiatric Association’s Diagnostic Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) and the American Sleep Disorders Association’s International Classification of Sleep Disorders (ICSD).[5, 6, 7, 1]

The DSM-IV-TR lists 4 major types of parasomnias, as follows:

However, it is projected that the fifth edition of the Diagnostic and Statistical Manual,DSM-V, will reclassify parasomnias into disorders of arousal, which will include sleepwalking, sleep terror, and confusional arousals.[8]

The ICSD subdivides the parasomnias into 3 groups according to the sleep state of origin:

This article focuses primarily on the following 6 disorders:

Nightmare disorder (also called dream anxiety attacks) typically occurs during the latter third part of the night, usually during REM sleep, but without any motoric dream enactment. It may be associated with tachycardia, tachypnea, diaphoresis, and arousal. Complete alertness and subsequent recollection of the dreams differentiates nightmares from sleep terrors. Nightmares are another form of dreams, but one with documented emotional and physiologic consequences often invoking anger and embarrassment (most often, fear).[9, 3]

Sleep terror disorder is a disorder of arousal that primarily occurs during stages III and IV of NREM sleep. It is manifested by extreme panic and a loud scream during sleep, followed by motor activities such as hitting objects or moving in and out of the bedroom. Subsequent recollection of these episodes either does not occur or is partial.[3, 10, 11]

Sleepwalking disorder arises from slow-wave stages of NREM sleep. The subject performs complex automatic behaviors, such as wandering aimlessly, carrying objects, going outdoors, and performing other activities of varying complexity and duration.[3, 10, 12]

REM sleep behavior disorder is dream-enacting behavior that includes talking, yelling, punching, kicking, sitting, jumping out of bed, arm flailing, and grabbing. An acute form may occur during withdrawal from ethanol or sedative-hypnotic drugs. The chronic form typically presents for evaluation as a consequence of observations made by bed partners.[3, 13, 14]

RLS and PLMD are common disorders that often coexist. RLS primarily presents as insomnia, whereas PLMD is a well-recognized cause of excessive daytime somnolence. Nearly all patients with RLS have periodic limb movements, but the converse is not the case. RLS and PLMD are not officially classified as parasomnias by the DSM-IV-TR. They can be differentiated from parasomnias by their stereotyped nature.[15, 16, 17, 18, 19]

Two additional parasomnias have been validated and extensively described in the literature:

Somnambulistic sexual behavior is considered a variant of sleepwalking disorder. It was once theorized that sexsomnia occurred in individuals acting out their dreams as a consequence of an underlying psychological condition; however, such theories have been debunked. Sexual behaviors of all types may occur during a sleep automatism, ranging from explicit sexual vocalizations to violent masturbation to complex sexual acts that may include fondling, cunnilingus, fellatio, and even vaginal and anal sex.[20]

Features of sexsomnia are analogous to those of other NREM parasomnias that occur during what is known as a confusional arousal during the deeper stages of sleep. Throughout this time, the brain is in a hybridized state in which cortical areas (which control higher thought processing and reasoning) are deactivated while more primitive functions (eg, eating and sex) remain active. Individuals are typically amnestic for the episode. Those who commit these sexual acts typically have a family or personal history of other parasomnias.

In a small number of sexsomnia cases, medicolegal issues have arisen, though the actual forensic implications remain nebulous. Several of the cases have points in common—namely, the involvement of a male perpetrator younger than 35 years, accusations of sexual assault or rape, claims of amnesia after the event, and a history of prolonged complex somnambulism. This unusual parasomnia behavior is more common than previously thought; many patients with the behavior were identified only after specific questions were asked.[21, 22]

In addition to SRED, the literature describes another disorder involving the consumption of food during the night or at bedtime: night-eating syndrome (NES). A clear distinction should be drawn between SRED and NES: the latter is not categorized as a parasomnia, because full consciousness is maintained during NES episodes.

Although NES was first described by Stunkard et al in 1955, no uniform definition of this disorder has yet been adopted. NES is characterized by consumption of excessive amounts of food either before bed or during nocturnal awakenings. It is up to 4 times more common in females and tends to have an onset in late adolescence.[23, 24] According to the most commonly used current definition, NES is present if patients report the following:

Whether NES should be differentiated from nocturnal eating syndrome is not clear in the literature. However, the terms may be usefully distinguished as follows[25] :

SRED, on the other hand, can be conceptualized as a binge eating disorder incorporating disordered arousal, confusional behavior, and amnesia of a non-REM parasomnia. Episodes often occur within the first 2-3 hours of sleep with ingestions of often-high carbohydrate foods in a hurried, uncontrollable manner. In contrast to other non-REM parasomnias, a fluctuation in level of awareness exists between episodes within the same night. There is relatively high comorbidity with RLS.[26]

Illustrative case

Mr A is a 28-year-old veteran of combat in Afghanistan. At one juncture, he was engaged in hand-to-hand combat with guerilla fighters; although he escaped, many members of his unit were killed before his eyes. Since returning home, he has suffered from multiple symptoms of posttraumatic stress disorder (PTSD), particularly nightmares. One night, he had one of his recurring dreams about strangling an enemy combatant. When he awoke, his wife was dead in bed beside him. He had strangled her in his sleep.


Human life encompasses 3 completely different states of existence: wakefulness, REM sleep, and NREM sleep. Sleep is not simply the passive absence of wakefulness; it is an extensive reorganization of central nervous system (CNS) activities occurring during sleep. Each state of being is controlled by its unique neuroanatomic, neurophysiologic, and neurochemical association.[3, 27]

Wakefulness, REM sleep and NREM sleep overlap as transitions occur from one state to another. A large number of neural networks, neurotransmitters, and neurochemicals must be recruited concurrently to assert a given state of existence. Dissociation of these states and the admixture of state-determining variables are the mechanisms that set primary sleep parasomnias in motion.

For example, the intrusion of NREM sleep during wakefulness may produce sleep drunkenness or microsleeps. The occurrence of REM sleep during wakefulness generates cataplexy or wakeful dreaming. The loss of muscle atony during REM sleep sets off the acting out of dreams (ie, REM behavior disorder).[28, 27]

The pathophysiology of parasomnias is undefined, although there has been considerable speculation about the roles of various functional systems. Abnormalities in the normal regulation of different phases of sleep may be present. Disorders of arousal may involve relative deactivation of the frontal lobe and inappropriate activation of the limbic areas. Some disorders (eg, sleep terror and sleepwalking disorders) are primarily disturbances of slow-wave sleep, whereas sleep paralysis and REM behavior disorders are those of REM sleep.

Some studies suggest that sleep deprivation and forced arousals during slow-wave sleep can induce somnambulistic episodes in predisposed adults. Other conditions, such as rhythmic movement disorder (eg, head banging) are those of sleep-wake transition. Because the activation pattern of parasomnias may resemble that of epilepsy (ie, abrupt onset, confusion, disorientation, and amnesia for the event period), parasomnias were once considered a form of epilepsy. However, their nonepileptic nature is now well established.[29, 27, 30]

Rapid eye movement sleep behavior disorder

The physiologic phenomena that occur during REM sleep can be categorized as either tonic or phasic. Tonic phenomena appear throughout an REM period; examples include electromyographic (EMG) suppression and low-voltage electroencephalography (EEG). Phasic phenomena occur intermittently during an REM period; examples include REMs and variability of cardiac cycle and respiratory function.[31]

The tonic and phasic processes are variously dissociated and recombined across different states. Unlike wakefulness, which is characterized by consciousness and muscle tone, REM sleep is associated with dreaming and muscle atony. Generalized atony of REM sleep probably is caused by active inhibition of motor activity by centers identified to be present in the pons.

In cats, REM sleep behavior disorder can be experimentally produced by bilateral pontine tegmental lesions, which are associated with the absence of REM atony. In humans, however, a structural neuropathology is not necessary, because most patients do not have an identifiable neurologic disorder. Therefore, functional dysregulation by depression of brainstem structures is responsible for the atony. The reduced activity of structures responsible for inhibiting phasic activity in the brainstem further contributes to the clinical manifestations of the disorder.

Restless legs syndrome and periodic limb movement disorder

RLS and PLMD may be 2 clinical manifestations of the same CNS dysfunction. The neurophysiologic mechanisms responsible for these disorders are not well described. PLMD occurs with a striking periodicity, which suggests that an underlying CNS pacemaker may be operative. Several observations have suggested that PLMD likely originates in the subcortical region and is regulated by rhythmic fluctuations at the brainstem level.[32]

Both disorders may be behavioral manifestations of CNS processes that become disinhibited. Patients also may have a lower arousal threshold. Polysomnography (PSG) reveals periodic arousing stimuli leading to K complexes, followed by alpha activity and then by leg movements. The neuropharmacologic hypothesis suggests that an impaired CNS dopaminergic mechanism may also be involved. Deficiencies in dopamine binding sites or low concentrations of dopamine and homovanillic acid have been found in several PLMD populations.[33]

The pathology of RLS involves the CNS rather than the peripheral nervous system. CNS involvement in RLS has its basis in the subcortical or brainstem areas of the brain rather than the spinal system. Because clinical evidence clearly indicates that RLS responds to the administration of dopamine or dopamine agonists, abnormality of this system is probably responsible for RLS and PLMD.

Various conditions commonly associated with secondary RLS (eg, end-stage renal disease, pregnancy, and gastric surgery) are associated with iron insufficiency. These conditions make it difficult for the brain to access sufficient iron for proper functioning.

Iron is stored and transported in the form of ferritin; transferrin transports iron into the cells through the transferrin receptor. When iron is low, ferritin is decreased, but transferrin levels are increased. Cerebrospinal fluid (CSF) and serum from patients with RLS have lower CSF ferritin levels and higher CSF transferrin levels. Low ferritin levels correlate with the severity of RLS. Furthermore, a connection may exist between iron insufficiency and dopamine pathology in RLS.

Single-photon emission computed tomography (SPECT) of the brain has identified defects in striatal dopamine D2 receptors. Other studies have identified abnormalities of the endogenous opioid system and impaired iron metabolism with ferritin deficiency. Low tissue iron content has been reported in substantia nigra and red nuclei on brain magnetic resonance imaging (MRI) in RLS patients. Thus, interactions between opioid and dopamine systems in the basal ganglia, brainstem, and spinal cord contribute to the genesis of RLS and PLMD.[31]


Few if any specific etiologies exist for these parasomnias, but each is associated with a number of predisposing factors.

For nightmare disorder, predisposing factors include the following:

For sleep terror disorder, predisposing factors include the following:

For sleepwalking disorder, predisposing factors include the following[34] :

REM sleep behavior disorder is mostly idiopathic but has been associated with the following:

RLS and PLMD also are mostly idiopathic, but predisposing factors may include the following:


In the United States, 10-50% of children aged 3-5 years may have nightmare disorder. The prevalence in adults is unknown, though as many as 50% of adults report occasional nightmares, and perhaps 5-8% experience recurring nightmares.[36]

Information regarding the frequency of sleep terror disorder is limited at best. The DSM-IV-TR estimates the prevalence rate to be 1-6% in children and less than 1% in adults.[36]

Sleepwalking disorder is estimated to occur in 5% of children, but episodes of the disorder have been documented in as many as 30% of clinical samples of children. The highest prevalence of this condition is between the ages of 3 and 10. Some clinical samples have shown prevalence rates exceeding 7% in adults, though approximately 80% of these cases are a continuation of childhood behavior.[36] Lifetime prevalence of nocturnal wandering with altered consciousness (including sleepwalking) may be as high as 30%, with a one-year prevalence of more than 3%.[37]

REM sleep behavior disorder may be rare; however, because many other sleep disorders, in particular the other parasomnias, may be misdiagnosed as REM sleep behavior disorder, the true prevalence is not known. This disorder is diagnosed most often in the sixth or seventh decade of life. It is frequently familial. As many as 60% of patients presenting to sleep clinics may have a positive family history.[5]

REM sleep behavior disorder affects men and women equally. Autosomal dominant transmission is expected, though not proved. In a telephone survey, the overall prevalence of violent behaviors during sleep was 2%, and approximately one quarter of these likely were REM sleep behavior disorder, indicating that REM sleep behavior disorder has an overall prevalence rate of 0.5%.[38, 39, 40]

The prevalence of RLS is estimated to be as high as 10% in the general population and increases with age. The prevalence of PLMD also increases with age: 5% of the population aged 30-50 years has PLMD, compared with 30% of the population older than 50 years and 40% of the population older than 65 years. PLMD has been reported to be responsible for insomnia in 17% of patients and for hypersomnia in 11% of patients evaluated at sleep disorder clinics.[41, 40]

The international prevalence of parasomnias is not known to be any different from their prevalence in the United States.

Sex- and race-related demographics

Women report nightmares more frequently, in a ratio of 2-4:1. Among children, sleep terror disorder is more prevalent in boys than in girls, but in adults, the ratio is even. Sleepwalking disorder occurs with equal frequency in both sexes. REM sleep behavior disorder is more prevalent in males, but the exact ratio is not known. The prevalence of RLS and PLMD in men is similar to that in women.

Information regarding the racial distribution of parasomnias is not available.


Although there are few, if any, reliable statistics regarding mortality from parasomnias, death rates appear to be quite low, on the whole. Similarly, the morbidity associated with the parasomnias is mostly secondary (eg, the consequences of sleepwalking, assaulting others while asleep, and sleep deprivation in caretakers). One specific morbidity issue is eating behavior associated with sleepwalking. The associated morbidity primarily relates to excessive food intake.

It is worth noting, however, that the ICSD classification includes 2 parasomnias whose hallmark is death. The first is sudden unexplained nocturnal death syndrome, which is most common in otherwise healthy young adults of Southeast Asian (eg, Laotian, Cambodian, or Vietnamese) descent. The other—a considerably better known condition—is sudden infant death syndrome (SIDS).

Most children outgrow nightmare disorder. In a small number of patients (the exact percentage is unknown), the disorder persists into adulthood and becomes a lifelong problem. Some patients may experience an attenuation of the symptoms later in life.

The prognosis for sleep terror disorder is excellent if the onset is in childhood. If the onset is in adulthood, the prognosis is poorer because the disorder tends to be chronic, with a waxing and waning course.

The prognosis for sleepwalking disorder is also excellent if the onset is in childhood. If the onset is in adulthood and there is no evidence of an underlying neurologic or substance abuse problem, the prognosis is poorer because the disorder tends to be chronic, following a waxing and waning course.

The prognosis for RLS and PLMD is quite variable.[42] Many patients develop long-term remissions, whereas others continue to experience the symptoms throughout life. Generally, severity increases as patients become older.

Patient Education

When parasomnias present during childhood, the most important aspect of patient education is support of the parents and providing tips on how to respond to episodes of the disorder. When these disorders present during adulthood, educating the patient regarding the chronicity and recurrence of these episodes is important.

Advising patients and caretakers about the risks of injury to self and others during sleepwalking, along with emphasizing avoidance of such damage, is critical; failure to provide such advice could even be construed as actionable in some situations, depending on the extent of the damage sustained. Sleepwalkers’ homes should be redesigned to avoid injuries.[43]

The following good sleep hygiene measures should be used in all these disorders:

Cohabitants—in particular, bed partners—should be advised on how to recognize and handle relatives suffering from a sleep disorder. The following are some brief suggestions, but consultation with a physician is always recommended.[44]

For patient education resources, see the Sleep Disorders Center, as well as Disorders That Disrupt Sleep (Parasomnias), REM Sleep Behavior Disorder, Sleepwalking, Periodic Limb Movement Disorder, Night Terrors, and Sleep Disorders and Aging.

In addition, the following Web sites provide useful resources for patient education:


The history can help differentiate among the various parasomnia subtypes.

Nightmare disorder

In nightmare disorder, patients complain of a frightening dream (in addition to fear, patients can also experience anger, embarrassment, sorrow). Nightmares typically occur in the latter third portion of the night. Arousal during the dream is common. The presence of a dream is the essential feature that differentiates nightmare disorder from sleep terror disorder.

Nightmares can lead to either sleep onset or sleep maintenance insomnia, which may be a presenting complaint. There is often a history of traumatic experiences (this is a key symptom of posttraumatic stress disorder [PTSD]).

Sleep terror disorder

Sleep terror disorder (pavor nocturnus) is characterized by a sudden arousal from non–rapid eye movement (NREM) sleep (usually from slow-wave sleep) and associated autonomic and behavioral manifestations of fear. Commonly, patients let out a piercing scream, followed by fear, crying and inconsolability. In adults, agitation is often seen. Significant autonomic hyperactivity is present, with tachycardia, tachypnea, flushing, diaphoresis, and increased muscle tone.

The patient is routinely unresponsive to external stimuli and, when awakened, is confused, disoriented, and amnestic regarding the event. It should be cautioned that confrontation of an individual during an episode may be dangerous, in that the individual may become violent. Incoherent vocalizations or micturition have been reported to accompany the event.


Episodes of sleepwalking (somnambulism) are associated with behaviors that range from simply sitting up in bed to walking, possibly with associated complex behaviors such as eating. Talking behavior also has been noted during these episodes. Upon awakening, the patient is most often confused and amnestic regarding the event; however, patients may be able to recall simple motivations (such as the desire to urinate) if awakened during an episode. Individuals typically have their eyes open during an event.

The sleepwalking event occurs during NREM sleep (usually slow-wave sleep) and may be more common after sleep deprivation. The event may spontaneously terminate, or the patient may return to bed or lie down somewhere else and return to sleep without ever awakening.

Rapid eye movement sleep behavior disorder

The hallmark of rapid eye movement (REM) sleep behavior disorder is the acting out of dreams. The behavior can include punching, kicking, leaping, and running from the bed. The most common reason for medical consultation is injury to the bed partner, though the effects of sleep disruption also can precipitate such consultation. The event occurs during REM sleep (the dreams), hence the name.

In patients with REM sleep behavior disorder, arousals from sleep to alertness and orientation occur rapidly, and patients usually have a vivid recall of their dreams. After awakening, the patient exhibits normal behavior and interactions. Despite nocturnal behavior, few patients develop excessive daytime sleepiness or fatigue.

Acute and chronic forms exist. The acute form can emerge during withdrawal from ethanol or sedative-hypnotic abuse and with anticholinergic and other drug intoxication states.

Restless legs syndrome and periodic limb movement disorder

Patients with restless legs syndrome (RLS) describe discomfort in lower extremities, using terms such as “pulling, searing, crawling, creeping, and boring” to describe sensations. The symptoms usually occur at bedtime or during other periods of inactivity. These distressing symptoms are relieved by moving the legs, walking about, rubbing the legs, squeezing or stroking the legs, and by taking hot showers or baths. The symptoms may wax or wane over the patient’s lifetime.

Patients with RLS commonly present with complaints of insomnia (difficulty initiating sleep), and, in severe cases, the disorder may cause depression and suicidal thoughts.

Periodic limb movement disorder (PLMD) primarily occurs during the first half of the night and progressively declines as the night goes on; episodes typically take place while the individual is asleep. PLMD is described as rhythmic extension of the great toe, associated with dorsiflexion of the ankle and light flexion of the knee and hip. The upper extremity may be involved, as manifested by intermittent flexion of the elbow.

Because PLMD occurs during sleep, these symptoms are often not appreciated by the patient. Patients often present with symptoms of excessive daytime sleepiness, initially during passive activities such as watching television, being a passenger in a car, or reading. In later stages, patients may have excessive daytime sleepiness during activities requiring alertness, such as driving, operating machinery, or talking with people.

RLS and PLMD may occur even during childhood and present as attention deficit hyperactivity disorder (ADHD) or as growing pains. These disorders are present in a significant proportion of pregnant women, and exacerbations are observed during menstruation and menopause.

RLS and PLMD are associated with numerous neurologic conditions, such as peripheral neuropathy, postpolio syndrome, spinal cord pathology, and various causes of myelitis. They affect 20-40% of patients with chronic renal failure who are on dialysis. A history of iron-deficiency anemia is also quite common in these patients.[35] RLS and PLMD should be considered if a patient complains of insomnia or excessive daytime sleepiness.

A related phenomenon is sleep-related leg cramps, which can occur while awake or asleep. These are characterized by involuntary, nonperiodic, and painful contractions in the calf or foot. Although RLS can mimic the painful sensations experienced in this condition, a useful distinction can be made. Because leg cramps involve actual spasms, they are usually isolated to specific muscle groups; accordingly, they are alleviated only by stretching, not just by simple movement (as in RLS).

Physical Examination

In patients with parasomnias that are not attributable to a general medical condition, physical findings are either absent or nonspecific. The only physical findings that can be specific to one of these parasomnias would be those findings associated with complications of the sleep disorder (eg, falling, for a sleepwalker).

Patients with RLS and PLMD may have physical signs of peripheral neuropathies and other neurologic disorders, such as radiculopathy and spinal cord pathology. Thus, a detailed neurologic and musculoskeletal examination must be performed. For diagnosis of REM sleep behavior disorder after a complaint from the patient or bed partner, a complete neurologic and psychiatric examination should be conducted.

Diagnostic guidelines for primary RLS include the following:

Diagnostic Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) diagnostic criteria for nightmare disorder include the following:

DSM-IV-TR diagnostic criteria for sleep terror disorder include the following:

DSM-IV-TR diagnostic criteria for sleepwalking disorder include the following:

A Mental Status Examination of patients suffering from parasomnias is useful because medical disorders, psychiatric disorders, and stress may precipitate or aggravate parasomnias. A careful assessment for alcohol or drug use, anxiety disorders, depression, and delirium should be performed. Relevant mental status findings are those associated with the following conditions:

Patients found to have an underlying psychological or psychiatric disorder should be seen by a psychologist or psychiatrist, and appropriate therapy should be offered. Depression or atypical affective disorders may well be masked and not apparent to a casual observer. Furthermore, the Mental Status Examination of Sleep provides a framework for assessing a broad range of consequences of parasomnias and facilitating the formulation of target symptoms to be controlled with treatment.


Accidental injury to self or others can occur, particularly in patients with sleepwalking disorder (injury to self), sleep terror disorder (injury to self or others because the patient sometimes moves violently while trying to escape the terror), and REM sleep behavior disorder (the patient may act out a complex series of dream-related violent behaviors).

Reports exist of patients eating during episodes of sleepwalking, with partial or complete amnesia for the event. Excessive intake of food can be considered a complication of this disorder.

Parasomnias can adversely affect obstructive sleep apnea by interfering with nasal continuous positive-pressure therapy.

Approach Considerations

No specific lab studies are necessary for parasomnias. The only studies that could be helpful are those related to the differential diagnosis, such as studies for substance abuse or evidence of medical illnesses that could mimic a parasomnia.

Imaging studies generally are of little utility in diagnosing a parasomnia. Their usefulness lies solely in determining the presence of a source for the medical illness that may be causing the parasomnia.

Laboratory Studies

Although, as a rule, no specific laboratory studies are required for diagnosis, in cases of restless legs syndrome (RLS) or periodic limb movement disorder (PLMD), a complete blood count (CBC) should be performed to exclude anemia as an underlying cause. Even in the absence of microcytic anemia, serum ferritin and serum iron levels should be measured to estimate iron stores. These tests should be followed by appropriate investigations to elicit the cause of the iron-deficiency anemia.

Polysomnography and Other Tests for Sleep Disorders

Polysomnography (PSG; see the image below) may be indicated for some of the parasomnias but not all of them. Episodes of sleepwalking and sleep terrors arise abruptly during arousals from stage III and IV of non–rapid eye movement (NREM) sleep. Postarousal electroencephalography (EEG) may show the persistence of sleep, the admixture of sleep and wakefulness, or complete wakefulness.

View Image

Polysomnographic study demonstrates apnea (absence of carbon dioxide fluctuation indicating no flow), chest wall paradox, abrupt increase in tidal vol....

In patients with rapid eye movement (REM) sleep behavior disorder, PSG reveals loss of REM atony on submental electromyography (EMG). Limb twitching also may be present on EMG. One must exclude epileptiform EEG activity during REM sleep. When the differential diagnosis includes sleep-related epilepsy, PSG with an extended montage should be performed. Otherwise, the hallmark of the various parasomnias is whether they occur during REM sleep, at the sleep-wake transition, or during slow-wave sleep.

Formal sleep studies are not indicated in most cases of RLS. However, PLMD is diagnosed primarily by means of PSG (see the image below). PLMDs are recognized by EMG findings; both of the anterior tibialis muscles are recorded. The EMG findings may show a single contraction or a cluster of several contractions. A sequence of at least 4 muscle contractions that last 0.5-5 seconds and occur at 4- to 90-second intervals establishes the diagnosis.

View Image

Periodic limb movements on polysomnographic study show intermittent leg electromyographic activity accompanied by electroencephalographic arousals.

The muscle twitches are associated with EEG signs of arousal, such as K complex followed by alpha activity, which may either precede or follow muscular contractions. A PLMD index (ie, number of periodic limb movements per hour of sleep) higher than 5/h is considered abnormal. The PLMD primarily occurs during stages I and II of NREM sleep and generally varies from night to night. The frequency of PLMD is greatly increased in the first half of the night and wanes thereafter.

Other tests

Actigraphy may be useful in quantifying PLMD, but there are not sufficient reliable validation data to justify its widespread clinical use.

A suggested immobilization test (SIT) can be performed in awake patients. The patient lies in bed motionless, and repetitive leg movements are counted to assess the severity of RLS. This test must be further validated before it can be considered a reliable diagnostic tool.

Approach Considerations

Medical disorders, psychiatric disorders, and stress may precipitate or aggravate parasomnias. A careful history of psychosocial stresses, alcohol or drug use, and symptoms of depression should be obtained. Also, a detailed Mental Status Examination should be performed. Patients found to have an underlying psychological or psychiatric disorder should be seen by a psychologist or psychiatrist, and appropriate therapy should be offered.[45, 17, 3, 46, 47]

Pharmacologic treatment of parasomnias is aimed at lessening the frequency or intensity of the events. Whether any of the disorders respond better to one of the commonly used agents than to another remains unclear. Currently, no medications are available that are specifically indicated for these disorders; all medications used for these disorders are used off label.

For restless legs syndrome (RLS) and periodic limb movement disorder (PLMD), behavioral treatments (eg, relaxation therapy, biofeedback, and stress reduction) may be helpful, though they are not universally effective.

Surgical therapy is not indicated in the treatment of parasomnias.

Inpatient care is not indicated for parasomnias. If the patient is violent during these episodes, consider hospitalization. Should the patient need inpatient treatment for any other reason, outpatient medications should be continued unless contraindicated by the condition for which the patient is hospitalized.

Frequent contact and encouragement is critical for patients undergoing treatment for one of the parasomnias. When these disorders occur in children, parents must be encouraging and comforting.

Pharmacologic Therapy

Rapid eye movement sleep behavior disorder

Treatment for rapid eye movement (REM) sleep behavior disorder is initiated with clonazepam 0.5-1.5 mg taken at bedtime. This medication has been shown to be beneficial in the long term. Drug discontinuance often results in prompt relapse. The exact mechanism of action of clonazepam in patients with REM behavior disorder is not known, but its serotonergic properties may inhibit nocturnal motor activity in the brainstem and thus prevent arousals.

Tricyclic antidepressants occasionally are used in the treatment of REM behavior disorder. Imipramine, which has serotonergic effects, has been used in the treatment of REM behavior disorder, but the effects are unpredictable. Anecdotal reports of the use of levodopa-carbidopa, gabapentin, and clonidine have been published, but the benefit of these drugs has not been systemically evaluated.

Restless legs syndrome and periodic limb movement disorder

RLS and PLMD are treated with 3 classes of medications.[48, 49, 50, 51, 52] Antiparkinsonian medications (eg, levodopa-carbidopa, bromocriptine, and pramipexole), have been used, as have benzodiazepines (eg, diazepam, clonazepam, temazepam, and lorazepam). Opiates (eg, codeine, oxycodone, methadone, and propoxyphene [now withdrawn from the US market]) have also been employed.

Several studies have reported efficacy of different medications belonging to these groups, but comparative studies between various classes of drugs or even individual drugs do not exist. Therefore, patients should receive a single agent, and, if no response is noted, they should be placed on another agent of the same or a different class. In more severe cases, a combination of drugs may be required. Some patients who do not respond to benzodiazepines alone, levodopa alone, or a combination of both may be treated with opiates.

Patients should receive the smallest possible dose and should be closely observed for the development of dependency. Accumulated experience dictates that the incidence of abuse, tolerance, or addiction to opiates or benzodiazepines in patients with severe RLS appears to be insignificant. The disabling condition of severe RLS must be treated aggressively.

RLS and PLMD are chronic conditions that require long-term pharmacologic therapy. Some patients may develop symptoms of restless legs during the daytime, and this may be treated with controlled release of levodopa-carbidopa administered in the evening and morning.

The effectiveness of levodopa (L-dopa) in the treatment of RLS has been confirmed by numerous studies. However, most patients on levodopa eventually develop a consequence called augmentation, in which when RLS symptoms appear earlier during the day and involve new parts of the body with increasing severity. Several studies have now confirmed that dopamine agonists can also be effective in RLS and PLMD while carrying a lesser risk of augmentation.

The American Academy of Sleep Medicine made the following recommendations for the treatment of RLS and PLMD with dopaminergic drugs[17] :

Avoidance of certain drugs, such as tricyclic antidepressants, fluoxetine, or lithium, may be helpful because these generally worsen the symptoms of RLS and PLMD.

A decrease in body iron stores, as indicated by serum ferritin levels lower than 50 µg/L, should be corrected with iron supplementation. Oral iron is preferred but takes a long time because gastrointestinal absorption is low. However, replenishment is an effective treatment strategy for iron-deficiency anemia and may also relieve RLS and PLMD symptoms (if present). Oral repletion may be done with ferrous sulfate at a dosage of 640-960 mg/day in patients who have reduced iron stores.

An oral dose of 50-100 mg of levodopa in a controlled-release formulation is prescribed as initial therapy for RLS. For PLMD, a controlled-release preparation of levodopa combined with a decarboxylase inhibitor (carbidopa) at a dose of 50-100 mg is begun. A dose increase, not to exceed 200 mg, may be required to suppress RLS and PLMD completely. The major adverse effects of levodopa therapy are as follows:

For rebound symptoms during the daytime or for augmentation, patients can be treated with dopamine agonists (eg, pramipexole), anticonvulsants (eg, gabapentin or carbamazepine), or benzodiazepines (diazepam or lorazepam).[53] Tardive dyskinesia with use of levodopa is uncommon but may occur. The probable mechanism is denervation supersensitivity, which usually occurs in patients with Parkinson disease.

Dopamine agonists (eg, pramipexole) cause fewer problems than levodopa does and have become first-line drugs in the treatment of RLS and PLMD. In RLS patients refractory to therapy, opioids have been effective; however, such patients must be monitored for addictive behavior.


In general, there is no reason to restrict or change the patient’s activity when a parasomnia has been diagnosed. However, the following precautions are valuable in the treatment of sleepwalking:


Consultation with a medical specialist or psychiatrist is indicated for the treatment of underlying conditions that may precipitate the symptoms of the parasomnias.

Consultation with a hypnotherapist may be of use for patients with sleep disorders. Hypnotherapy has been found to be a cost-effective and noninvasive treatment in adults with sleepwalking and sleep terrors.

Medication Summary

The drugs most commonly used to treat parasomnias are benzodiazepines and anticonvulsants. The general aim of medication treatment is to prevent arousal out of sleep or to suppress rapid eye movement (REM) sleep. Currently, no medications are available that are specifically indicated for these disorders; all medications used for these disorders are used off label.

Diazepam (Valium, Diastat)

Clinical Context:  Diazepam is the medication most frequently used in children, especially those with night terrors; it is the drug of choice for parasomnias. Other benzodiazepines also may be used.

Alprazolam (Xanax, Niravam)

Clinical Context:  Alprazolam is the second choice for parasomnias in this category. Its advantages are the brief duration of action and the decreased likelihood of morning effects (eg, grogginess). Its disadvantages include the potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.

Clonazepam (Klonopin)

Clinical Context:  Like alprazolam, clonazepam is a good alternative to diazepam. Its main advantage is the presumed specificity for central nervous system (CNS) gamma-aminobutyric acid (GABA) receptors. Its disadvantages include the potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.

Class Summary

Benzodiazepines help suppress REM sleep and limit arousal.

Carbamazepine (Tegretol, Carbatrol, Equetro)

Clinical Context:  Carbamazepine is the most commonly used anticonvulsant for these disorders, but anecdotal evidence supports the possible use of GABA-enhancing agents such as valproate or gabapentin. With respect to all of these agents, both a bedtime dose alone and titration (as for epilepsy) have been reported.

Valproate (Depakene, Depakote, Stavzor, Depacon)

Clinical Context:  With valproate, as with other drugs in this category, both bedtime and standard doses have been reported to be useful in treating parasomnias.

Gabapentin (Neurontin, Gralise)

Clinical Context:  Gabapentin has not been used as frequently as the other 2 anticonvulsants, and less information is available. As with the other 2 agents in this category, no information is available, nor has a consensus been reached, regarding the use of bedtime dosing as opposed to standard antiepileptic dosing.

Gabapentin Enacarbil (Horizant)

Clinical Context:  A prodrug of gabapentin, gabapentin enacarbil has been approved by the FDA. In a randomized, placebo-controlled study, 1200 mg taken orally once daily provided sustained gabapentin exposure and maintained improvements in restless legs syndrome symptoms compared with placebo.

Class Summary

Anticonvulsants inhibit arousal.

Levodopa-carbidopa (Sinemet CR, Parcopa)

Clinical Context:  Levodopa is a large neutral amino acid that is absorbed in the proximal small intestine by a saturable carrier-mediated transport system. Absorption is decreased by meals that include other large neutral amino acids. Only patients with meaningful motor fluctuations need to consider a low-protein or protein-redistributed diet.

Greater consistency of absorption is achieved when levodopa taken 1 hour or more after a meal. Nausea often is reduced if levodopa taken immediately after meals. Some patients with nausea benefit from additional carbidopa in dosages not to exceed 200 mg/day. The half-life of levodopa-carbidopa is approximately 2 hours. The most common acute adverse effects are nausea, hypotension, and hallucinations. Long-term adverse effects include motor fluctuations and dyskinesia (chorea).

Provide at least 70-100 mg/day of carbidopa. When more carbidopa is required, substitute one 25/100 tablet for each 10/100 tablet. When more levodopa is required, substitute a 25/250 tablet for the 25/100 or 10/100 tablet.

The controlled-release (CR) formulation of levodopa-carbidopa is absorbed more slowly and provides more sustained levodopa levels than the immediate-release (IR) form. It is as effective as the IR formulation when levodopa is initially required and may be more convenient when fewer intakes are desired.

Patients with dissipating motor fluctuations (and no dyskinesia) often benefit from prolongation of short-duration response when switched from IR to CR levodopa-carbidopa. However, patients with meaningful fluctuations and dyskinesia often experience an increase in dyskinesia when switched to the CR formulation.

Pramipexole (Mirapex)

Clinical Context:  Although pramipexole is used for Parkinson disease, it has also been found to be beneficial in RLS and PLMD. Pramipexole is a nonergot dopamine agonist with specificity for the D2 dopamine receptor; it also has been shown to bind to D3 and D4 receptors and possibly may stimulate dopamine activity on the nerves of striatum and substantia nigra.

Ropinirole (Requip)

Clinical Context:  Ropinirole is a dopamine D2-receptor agonist that has been approved by the FDA for the treatment of Parkinson disease. It has also has been used in patients with restless legs syndrome.

Class Summary

Antiparkinsonian agents are very effective for treating restless legs syndrome (RLS) and periodic limb movement disorder (PLMD). Levodopa-carbidopa is the most commonly used agent, but ropinirole, pergolide, and pramipexole also are effective.

Pergolide was withdrawn from the US marketonMarch 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. It is important not to stop pergolide abruptly. Health care professionals should assess patients’ need for dopamine agonist therapy and consider alternative treatment. If continued treatment with such an agent is needed, another dopamine agonist should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

Hydromorphone (Dilaudid)

Clinical Context:  Hydromorphone is a potent semisynthetic opiate agonist similar in structure to morphine. It is approximately 7-8 times as potent as morphine on mg-to-mg basis, with a shorter or similar duration of action. It has been used in patients with severe restless legs syndrome who do not benefit from other therapy.


Clinical Context:  This and other opioids can be helpful in decreasing the symptoms of restless legs syndrome, serving as a treatment of second choice when other treatments have failed or caused augmentation problems.

Propoxyphene (Darvon)

Clinical Context:  Withdrawn from the US market. Propoxyphene has been used for severe restless legs syndrome. It binds to opiate receptors in the CNS, causing inhibition of ascending pain pathways and altering perception of and response to pain.

Class Summary

Opiates such as codeine, propoxyphene, and dihydromorphone have been used in patients with severe RLS who do not benefit from other therapy. Patients should be closely observed for development of tolerance and dependency.

Propoxyphene products were withdrawn from the United States market on November 19, 2010. The withdrawal was based on new data showing QT prolongation at therapeutic doses. For more information, see the FDA MedWatch safety information.


David Bienenfeld, MD, Professor of Psychiatry, Vice-Chair and Director of Residency Training, Department of Psychiatry, Wright State University, Boonshoft School of Medicine

Disclosure: Lippincott Williams Wilkins Royalty Author


Ariz Anklesaria, DO, Resident Physician, Department of Psychiatry, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych (UK), Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of Health Sciences: Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Mohammed A Memon, MD Chairman and Attending Geriatric Psychiatrist, Department of Psychiatry, Spartanburg Regional Medical Center

Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


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Polysomnographic study demonstrates apnea (absence of carbon dioxide fluctuation indicating no flow), chest wall paradox, abrupt increase in tidal volume at end of apnea, and oxygen desaturation. All of these features are consistent with obstructive sleep apnea.

Periodic limb movements on polysomnographic study show intermittent leg electromyographic activity accompanied by electroencephalographic arousals.

Polysomnographic study demonstrates apnea (absence of carbon dioxide fluctuation indicating no flow), chest wall paradox, abrupt increase in tidal volume at end of apnea, and oxygen desaturation. All of these features are consistent with obstructive sleep apnea.

Periodic limb movements on polysomnographic study show intermittent leg electromyographic activity accompanied by electroencephalographic arousals.