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eMedicine Specialties > Psychiatry > Adult
Parasomnias
Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Director of Respiratory Medicine, St Boniface General Hospital
Updated: Apr 4, 2007
Introduction
Background
Parasomnias are disorders characterized by undesirable motor, verbal, or experiential phenomenon occurring in association with sleep, specific stages of sleep, or sleep-awake transition phases. Parasomnias may be categorized as (1) primary parasomnias, which are the disorders of sleep states and are further classified according to the sleep state of origin, rapid eye movement (REM), or non–rapid eye movement (NREM) or (2) secondary parasomnias, which are disorders of other organ systems that may manifest during sleep, eg, seizures, respiratory dyskinesias, arrhythmias, and gastroesophageal reflux.
Two major types of primary sleep disorders are described: dyssomnias and parasomnias. Primary sleep disorder is a malady of sleep that does not appear to be secondary to a physical or mental illness and is not substance-induced. Unlike dyssomnias, which are characterized by abnormal sleep quality, including initiation, maintenance, duration, timing, and amount of sleep, parasomnias are distinguished by deviant behavioral and/or physiologic events. These abnormalities/events are reliably associated with either the sleep/wake interface or certain sleep stages. Additionally, parasomnias manifest by activation of systems, such as the autonomic nervous system, or programs, such as cognitive, behavioral, or motor program stimulation.
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). Four major types of parasomnias are included in the DSM-IV-TR. They include (1) nightmare disorder, (2) sleep terror disorder, (3) sleepwalking disorder, and (4) parasomnias not otherwise specified. However, the ICSD subdivides the parasomnias into 3 groups according to the sleep state of origin. They include (1) REM, (2) NREM, and (3) miscellaneous (ie, not respecting the sleep state).
The 5 disorders that are primarily discussed in this article are nightmare disorder, sleep terror disorder, sleepwalking disorder, REM sleep behavior disorder, restless legs syndrome (RLS), and periodic limb movement disorder (PLMD).
Nightmare disorder: Also called dream anxiety attacks, these are frightening dreams that occur during REM sleep and are associated with tachycardia, tachypnea, diaphoresis, and arousal. Complete alertness and subsequent recollection of the dreams differentiates nightmares from sleep terrors. Note that nightmares are another form of dreams except with documented emotional and physiological consequences.
Sleep terror disorder: Sleep terror is a disorder of arousal that primarily occurs during stages III and IV of NREM sleep. Sleep terror manifests as 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.
Sleepwalking disorder: Again, this 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.
REM sleep behavior disorder: 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 presents for evaluation following observations of bed partners.
RLS and PLMD: These are common disorders that often may 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, and only a minority of patients with PLMD also have RLS.
Two parasomnias recently validated and more extensively described in the literature are (1) somnambulistic sexual behavior, or sexsomnia, and (2) night eating disorder.
Sexual behaviors of all types may occur during sleepwalking. Somnambulistic sexual behavior (also called sexsomnia, sleep sex) is considered a variant of sleepwalking disorder. Sexual behavior during a sleep automatism can vary from explicit sexual vocalizations, to violent masturbation, to complex sexual acts including anal, oral, and vaginal penetration. A recent series described 11 patients with distinct behaviors of the sexual nature during sleep. The features are in common with other NREM arousal parasomnias. Medicolegal issues had occurred in a small number of cases. This behavior is more common than previously thought because a significant number of patients with this unusual parasomnia behavior were identified only after specific questions were asked.
The night eating syndrome (NES) was first described by Stunkard et al in 1955. No uniform definition of NES has yet been adopted. Evening hyperphagia originally is the main criterion, which implies that the amount of food consumed is excessive at this time of the day. However, definitions vary in terms of the amount of food consumed, the time frame involved, and whether the evening meal (dinner) is included or not.
The current definition focuses on NES to be present if patients report: (1) skipping breakfast >4 d/wk, interpreted as morning anorexia; (2) consuming more than 50% of total daily calories after 7 pm; and (3) difficulty falling asleep or staying asleep >4 d/wk. Whether NES should be differentiated from nocturnal eating syndrome is not clear in the literature. However, the terms may be defined distinctly as (1) night eating syndrome (defined as morning anorexia, evening hyperphagia, and insomnia) and (2) nocturnal eating syndrome (defined as eating at night after having gone to bed).
Pathophysiology
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 CNS activities occurring during sleep. Each state of being is controlled by its unique neuroanatomic, neurophysiologic, and neurochemical association.
Wakefulness and REM and NREM sleep states overlap as transition occurs 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, intrusion of NREM sleep during wakefulness may produce sleep drunkenness or microsleeps; occurrence of REM sleep during wakefulness generates cataplexy or wakeful dreaming; loss of muscle atonia during REM sleep sets off acting out of dreams, termed REM behavior disorder.
The pathophysiology of parasomnias is unknown, although considerable speculation exists about the role of various functional systems in each disorder. Abnormalities in the normal regulation of different phases of sleep may be present. Some disorders, such as sleep terror and sleepwalking disorders, primarily are disturbances of slow-wave sleep, whereas sleep paralysis and REM behavior disorders are those of REM sleep. Others, such as rhythmic movement disorder (eg, head banging) are those of sleep-wake transition. Because the pattern of activation of parasomnias may resemble epilepsy (abrupt onset, confusion, disorientation, and amnesia for the event period), parasomnias originally were considered a form of epilepsy. Gastaut and Broughton's elegant work in 1965 and Broughton's work published in 1968 established the nonepileptic nature of parasomnias.
Rapid eye movement sleep behavior disorder
The physiologic phenomena that occur during REM sleep can be categorized as tonic and phasic. Tonic phenomena appear throughout an REM period. Examples include electromyographic (EMG) suppression and low-voltage electroencephalography (EEG). The phasic phenomena occur intermittently during an REM period. Examples include rapid eye movements and variability of cardiac cycle and respiratory function.
The tonic and phasic processes have been observed to be variously dissociated and recombined across different states. In contrast to wakefulness, which is characterized by consciousness and muscle tone, REM sleep is associated with dreaming and muscle atonia. Generalized atonia of REM sleep probably is caused by active inhibition of motor activity by centers identified to be present in the pons. REM sleep behavior can be experimentally produced in cats by bilateral pontine tegmental lesions, which are associated with the absence of REM atonia. However, in humans, a structural neuropathology is not necessary for REM behavior disorder because most patients do not have an identifiable neurological disorder. Therefore, functional dysregulation by depression of brainstem structures is responsible for atonia. The reduced activity of structures responsible for inhibiting phasic activity in the brain stem further contributes to the clinical manifestations of REM sleep behavior disorder.
Restless legs syndrome and periodic limb movement disorder
RLS and PLMD may be 2 clinical manifestations of the same CNS dysfunction. The neurophysiological mechanisms responsible for these disorders are not well described. PLMD occurs with a striking periodicity, suggesting 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.
Both of these disorders may be the behavioral manifestation of CNS processes that become disinhibited. Patients with these disorders also may have a lower arousal threshold. Polysomnographic recordings exhibit periodic arousing stimuli leading to K complexes, followed by alpha activity, and then leg movements. The neuropharmacological hypothesis supports that an impaired CNS dopaminergic mechanism also may be involved. The deficiency of dopamine binding sites or low concentrations of dopamine and homovanillic acid have been found in several populations who have PLMD.
RLS pathology involves the CNS rather than the peripheral nervous system. CNS involvement in RLS is based in the subcortical or brainstem areas of the brain rather than the spinal system. Since clinical evidence clearly points to the responsiveness of RLS to administration of dopamine or dopamine agonists, abnormality of this system likely is responsible for RLS and PLMD.
Various conditions commonly associated with secondary RLS such as end-stage renal disease, pregnancy, and gastric surgery are associated with iron insufficiency. These conditions make it difficult for the brain to access iron sufficiently 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 correlated with RLS severity. Furthermore, a connection may exist between iron insufficiency and dopamine pathology in RLS.
Single-photon emission computed tomography (SPECT) studies of the brain have identified defects in striatal dopamine D2 receptors. Other studies have pointed out an abnormality of the endogenous opioid system and abnormalities in iron metabolism with ferritin deficiency. Recent studies have reported low tissue iron content in substantia nigra and red nuclei on brain MRI scans of RLS patients. Consequently, interactions between the opioid and dopamine systems that occur in the basal ganglia, brainstem, and spinal cord contribute to the genesis of RLS and PLMD.
Frequency
United States
Nightmare disorder: Of children aged 3-5 years, 10-50% may have this disorder. The prevalence in adults is unknown, although up to 50% of adults report occasional nightmares.
Sleep terror disorder: Information regarding frequency is limited at best. The DSM-IV estimates the prevalence rate to be 1-6% in children and less than 1% in adults.
Sleepwalking disorder: The criterion-based 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 and 7% of clinical samples of adults.
REM sleep behavior disorder: The 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. It is diagnosed most often in the sixth or seventh decade of life. This disorder often is familial. As many as 60% of patients presenting to sleep clinics may have a positive family history. Men and women are affected equally. Although not proven, autosomal dominant transmission is expected. A telephone survey has shown an overall prevalence rate of violent behaviors during sleep of 2%, approximately one quarter of these likely were REM sleep behavior disorder, indicating REM sleep behavior disorder has an overall prevalence rate of 0.5%.
RLS and PLMD: The prevalence rate 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 to 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 hypersomnia in 11% of patients evaluated at sleep disorder clinics.
International
The prevalence rates are not known to be any different from US rates.
Mortality/Morbidity
The death rate of these 3 parasomnias is quite low; few, if any, reliable statistics exist regarding mortality. Similarly, the morbidity associated with the parasomnias mostly is secondary, such as 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.
Of note is the inclusion of 2 parasomnias in the ICSD, the hallmark of which is death. The first is sudden unexplained nocturnal death syndrome, which is most common in otherwise healthy young adults of Southeast Asian descent, such as Laotian, Kampuchean, and Vietnamese people. The other is the better-known sudden infant death syndrome.
Race
Information regarding the racial distribution of parasomnias is not available.
Sex
Women report nightmares more frequently, in a ratio of 2-4:1.
Among children, sleep terror disorder is more prevalent in males than in females, 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 is similar between men and women.
Age
See Frequency for the differences in age distributions of the parasomnias.
Clinical
History
The history associated with each subtype of the parasomnias follows:
Nightmare disorder (dream anxiety disorder)
The history is that of a frightening dream.
Arousal during the dream is common.
The presence of a dream is the essential feature that differentiates nightmare disorder from sleep terror disorder.
History of traumatic experiences (This is a key symptom of PTSD.)
Sleep terror disorder (pavor nocturnus)
A sleep terror is characterized by a sudden arousal from NREM sleep (usually from slow-wave sleep) and associated autonomic and behavioral manifestations of fear.
Commonly, patients cry out or scream as they are aroused.
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.
Incoherent vocalizations or micturition have been reported to accompany the event.
Sleepwalking (somnambulism)
Episodes of sleepwalking 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 most often is confused and amnestic regarding the event.
The 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 if this 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, although 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.
Following awakening, the patient's behavior and interactions are normal.
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.
Despite nocturnal behavior, few patients develop excessive daytime sleepiness or fatigue.
Restless legs syndrome and periodic limb movement disorder
Patients with 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 patients 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.
PLMD primarily occurs during sleep. This disorder is described as rhythmic extension of the great toe, associated with dorsiflexion of the ankle and light flexion of the knee and hip. Because PLMD occurs during sleep, these symptoms often are not appreciated by the patient. Patients often present with symptoms of excessive daytime sleepiness, initially during passive activities such as watching TV, 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 disorder with hyperactivity or as growing pains.
RLS and PLMD are present in a significant proportion of pregnant woman, and exacerbations are observed during menstruation and menopause.
These disorders are associated with numerous neurological conditions such as peripheral neuropathy, postpolio syndrome, spinal cord pathology, and various causes of myelitis.
RLS and PLMD affect 20-40% of patients with chronic renal failure who are on dialysis.
A history of iron-deficiency anemia also is quite common in these patients.
RLS and PLMD should be considered if a patient complains of insomnia or excessive daytime sleepiness.
Physical
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, such as falling for a sleepwalker.
Patients with RLS and PLMD may have physical signs of peripheral neuropathies and other neurological disorders, such as radiculopathy and spinal cord pathology. Thus, a detailed neurological and musculoskeletal examination must be performed.
For diagnosis of REM sleep behavior disorder following a complaint from the patient or bed partner, a complete neurological and psychiatric examination should be conducted.
Diagnostic guidelines for primary restless legs syndrome
Discomfort is present in both legs (tingling, prickling, tension, aching), accompanied by irresistible movements of the limbs.
Symptoms appear at rest, show a circadian pattern by occurring mainly in the evening, and can interfere with sleep onset.
The severity may vary from week to week and may occur in upper limbs.
Partial or complete relief is obtained by physical maneuvers such as rubbing, shaking, stomping, or walking.
Neurological symptoms or neurological signs are absent.
DSM-IV-TR diagnostic criteria for nightmare disorder
Repeated awakenings from the major sleep period or naps occur, with detailed recall of extended and extremely frightening dreams, usually involving threats to survival, security, or self-esteem. The awakenings generally occur during the second half of the sleep period.
Upon awakening from the frightening dreams, the person rapidly becomes oriented and alert (in contrast to the confusion and disorientation observed in patients with sleep terror disorder and some forms of epilepsy).
The dream experience, or the sleep disturbance resulting from the awakening, causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
The nightmares do not occur exclusively during the course of another mental disorder (eg, a delirium, posttraumatic stress disorder) and are not due to the direct physiological effects of a substance (eg, a drug of abuse, a medication) or a general medical condition.
DSM-IV-TR diagnostic criteria for sleep terror disorder
Recurrent episodes of abrupt awakening from sleep occur, usually during the first third of the major sleep episode, and begin with a panicky scream.
Intense fear and signs of autonomic arousal, such as tachycardia, rapid breathing, and sweating, occur during each episode.
Patients demonstrate relative unresponsiveness to efforts by others to comfort the person during the episode.
No detailed dream is recalled, and amnesia develops regarding the episode.
The episodes cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
The disturbance is not due to the direct physiological effects of a substance (eg, a drug of abuse, a medication) or a general medical condition.
DSM-IV-TR diagnostic criteria for sleepwalking disorder
Repeated episodes of rising from bed during sleep and walking about occur, usually during the first third of the major sleep episode.
While sleepwalking, the person has a blank staring face, is relatively unresponsive to the efforts of others to communicate with him or her, and can be awakened only with great difficulty.
Upon awakening (either from the sleepwalking episode or the next morning), the person has amnesia regarding the episode.
Within several minutes after awakening from the sleepwalking episode, mental activity or behavior is not impaired, although a short period of confusion or disorientation may be present.
The sleepwalking causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
The disturbances are not due to the direct physiological effects of a substance (eg, a drug of abuse, a medication) or a general medical condition.
Causes
Few if any specific etiologies exist for these parasomnias, but each has a number of predisposing factors, described as follows:
Nightmare disorder
Personality disorders (most frequently schizotypal)
Relationship difficulties
Other stressors
Levodopa, beta-adrenergic agents, and withdrawal of REM-suppressing medications
Sleep terror disorder
Fever
Sleep deprivation
CNS depressant medications
Sleepwalking disorder
Possible hereditary/familial trend
Thioridazine, fluphenazine, perphenazine, desipramine, chloral hydrate, and lithium
Fever
Sleep deprivation and obstructive sleep apnea
Other disorders that disrupt slow-wave sleep
Internal stimuli such as a distended bladder
External stimuli such as noises
Rapid eye movement sleep behavior disorder
Mostly idiopathic
Has been associated with dementia, subarachnoid hemorrhage, ischemic cerebrovascular disease, olivopontocerebellar degeneration, multiple sclerosis, and brain stem neoplasms
Restless legs syndrome and periodic limb movement disorders
Mostly idiopathic
Iron-deficiency anemia
Pregnancy, menstruation, and menopause
Chronic renal failure
Osteoarthritis of the hips and knees
Drugs
Caffeine
Tricyclic antidepressants
Selective serotonin reuptake inhibitors
Dopamine receptor-blocking drugs
Neurological disorders
Peripheral neuropathies (diabetes, idiopathic or toxic)
Various causes of myelitis
Postpolio syndrome
Spinal cord pathology (syringomyelia, radiation-induced myelopathy)
Lumbar/sacral radiculopathy
Differential Diagnoses
Anxiety Disorders
Obstructive Sleep Apnea-Hypopnea Syndrome
Panic Disorder
Posttraumatic Stress Disorder
Sleep Disorder, Geriatric
Other Problems to Be Considered
Dissociative fugue
Epilepsy
Hypnagogic hallucinations
Sundowning
Workup
Laboratory Studies
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.
For RLS and PLMD, a CBC count 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.
Imaging Studies
Imaging studies generally are of little utility in diagnosing a parasomnia. Their usefulness is only in determining the presence of a source for the medical illness that may be causing the parasomnia.
Other Tests
Polysomnography 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 NREM sleep. Postarousal EEG may show the persistence of sleep, the admixture of sleep and wakefulness, or complete wakefulness.
Polysomnogram of patients with REM sleep behavior disorder exhibits loss of REM atonia on submental EMG findings. Limb twitching also may be present on EMG findings. One must exclude epileptiform EEG activity during REM sleep.
When the differential diagnosis includes sleep-related epilepsy, polysomnography 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 using a polysomnographic study.
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.
The muscle twitches are associated with electroencephalographic 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) of more than 5 per hour 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 then wanes.
Actigraphy may be useful in quantifying PLMD but lacks reliable validation data for widespread clinical use.
A suggested immobilization test (SIT) can be performed in the awake state. The patient lies in bed motionless, and repetitive leg movements are counted to assess severity of RLS. This test needs further validation before it can be considered a reliable diagnostic tool.
Procedures
No procedures are indicated.
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The treatment of parasomnias is aimed at lessening the frequency and/or intensity of the events.
Whether any of the disorders responds better to one of the commonly used agents than another remains unclear.
The treatment of rapid eye movement behavior disorder is as follows:
Treatment for REM behavior disorder is initiated with clonazepam at 0.5-1.5 mg taken at bedtime. This medication has been shown to be beneficial in the long-term. Drug discontinuation 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 levodopa/carbidopa, gabapentin, and clonidine have been published, but the benefit of these drugs has not been systemically evaluated.
Restless leg syndrome and periodic limb movement disorder are treated with 3 classes of medications. Treatment guidelines are as follows:
Anti-Parkinson medications, such as levodopa/carbidopa, bromocriptine, and pramipexole (Mirapex), have been used.
Benzodiazepines, such as diazepam, clonazepam, temazepam, and lorazepam, also have been used.
Opiates, such as codeine, oxycodone, methadone, and propoxyphene, are other drugs that have been used.
Several studies have reported efficacy of different medications belonging to the aforementioned groups, but comparative studies between various classes of drugs or even individual drugs do not exist. Therefore, patients should receive one agent, and, if no response is noted, they should be placed on another agent of the same or a different class.
A combination of drugs may be required in more severe cases. 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 doses 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.
Effect of levodopa (L-dopa) in the treatment of RLS has been confirmed by a large number of studies. However, most patients on levodopa, after some time, develop a consequence called augmentation. Augmentation is 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 with less risk for augmentation.
The American Academy of Sleep Medicine made recommendations for the treatment of RLS and PLMD with dopaminergic drugs as follows: levodopa with decarboxylase inhibitor, and the dopaminergic agonists pergolide (withdrawn from US market March 29, 2007), pramipexole, and ropinirole are effective in the treatment of RLS and PLMD. Other dopamine agonists (talipexole, cabergoline, piribidel, and alpha-dihydroergocryptine) and the dopaminergic agents amantadine and selegiline may be effective in the treatment of RLS and PLMD, but the level of effectiveness of these medications is not currently established. No specific recommendations can be made regarding dopaminergic treatment of children or pregnant women with RLS or PLMD.
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 of less than 50 mcg/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).
Behavioral treatments, such as relaxation therapy, biofeedback, and stress reduction, may be helpful, although they are not universally effective.
Several studies have reported that levodopa is effective in treating RLS and PLMD.
An oral dose of 50-100 mg, 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 completely suppress RLS and PLMD.
The major adverse effects of levodopa therapy are (1) rebound of symptoms during the daytime and (2) tardive dyskinesia, which is extremely uncommon.
For rebound symptoms during the daytime, or for augmentation, patients can be treated with dopamine agonists (eg, pramipexole), anticonvulsants (eg, gabapentin, carbamazepine), or benzodiazepines (diazepam, lorazepam).
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 compared with levodopa 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.
Oral repletion with ferrous sulfate at 640–960 mg per day in patients who have reduced iron stores.
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.
In general, no reason exists to restrict or change the patient's activity when a parasomnia has been diagnosed; however, certain precautions are valuable in the treatment of sleepwalking.
Remove potentially dangerous items.
Locate the bedroom on the ground floor if possible.
Lock the doors and windows.
Cover glass windows with heavy drapes.
Place an alarm or bell on the bedroom door.
Inpatient care is not indicated for parasomnias.
If the patient is violent during these episodes, consider hospitalization.
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.
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.
No Information is available regarding deterrence and prevention.
Accidental injury to self or others can occur, particularly in patients with sleepwalking disorder (to self), sleep terror disorder (self or others because the patient sometimes moves violently while trying to escape the terror), and REM sleep behavior disorder (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.
Nightmare disorder
Most children outgrow this disorder.
A small number (percentage unknown) of patients report this disorder persisting into adulthood and becoming a lifelong problem.
Some patients may experience an attenuation of the symptoms later in life.
Sleep terror disorder
If the onset is in childhood, the prognosis is excellent.
If the onset is in adulthood, the prognosis is poorer because the disorder tends to be chronic, with a waxing and waning course.
Sleepwalking disorder
If the onset is in childhood, the prognosis is excellent.
If the onset is in adulthood and no evidence of an underlying neurological or substance abuse problem is present, the prognosis is poorer because the disorder tends to be chronic, following a waxing and waning course.
Restless legs syndrome and periodic limb movement disorder
The prognosis of these disorders is quite variable.
Many patients develop long-term remissions, whereas others continue to experience the symptoms throughout life.
Generally, the severity increases as patients become older.
When these disorders 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/or caretakers about the risks of injury to self and others during sleepwalking, and emphasizing avoiding such damage, is critical. Sleepwalkers' homes should be redesigned to avoid injuries.
The following good sleep hygiene measures should be used in all these disorders:
Patients should go to bed at the same time each night, use the bed only for sleeping and intimacy, and avoid napping.
Patients should avoid stress, fatigue, and sleep deprivation. Vigorous activity prior to bedtime should also be avoided, though a brief period of aerobic activity 4 hours before bedtime may be helpful.
Patients should avoid cigarettes, alcohol, and excessive caffeine.
For excellent patient education resources, visit eMedicine's Sleep Disorders Center. Also, see eMedicine's patient education articles Disorders That Disrupt Sleep (Parasomnias), REM Sleep Behavior Disorder, Sleepwalking, Periodic Limb Movement Disorder, Night Terrors, and Sleep Disorders and Aging.
Parasomnias cover a wide variety of peculiar, distressing, and potentially dangerous sleep behaviors. These bizarre and frightening nocturnal experiences are not a manifestation of psychologic or psychiatric disorders and are scientifically explainable
Wakefulness, REM sleep, and NREM sleep may occur simultaneously or in dissociated or incomplete forms to produce primary sleep parasomnias. Dysfunction of other organ systems may manifest during the sleep state, resulting in secondary parasomnias.
Parasomnias often are misdiagnosed and inappropriately treated as psychiatric disorders.
Experienced sleep professionals should evaluate patients with these disorders.
Parasomnias also may have forensic implications. Accidents, homicides, and suicides have occurred during these bizarre nocturnal experiences.
Parasomnias can adversely affect obstructive sleep apnea by interfering with nasal continuous positive-pressure therapy.
Failing to advise patients and/or their caretakers about the risks of injury to self or others could be construed as actionable, depending on the extent of the damage sustained.
Failure to look for an underlying cause for one of the parasomnias, especially when the onset is in adulthood, also could be actionable.
RLS had been misunderstood for several hundred years until the twentieth century. It is a neurologic disorder caused by dopaminergic dysfunction and is strongly associated with iron insufficiency.
Pediatric - Consequences of falls and other injuries to self or others
Geriatric - Consequences of sleep deprivation, falls, and other injuries to self or others
Treatment
Medical Care
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.
Surgical Care
It is not indicated in the treatment of parasomnias.
Consultations
Activity
Medication
The most common drugs used to treat these disorders are benzodiazepines and anticonvulsants. The general aim of medication treatment is to prevent arousal out of sleep or to suppress REM sleep. Currently, no medications are available that are indicated for these disorders; all medications used for these disorders are used off-label.
Benzodiazepines
Help suppress REM sleep and limit arousal.
Diazepam (Valium)
Medication most frequently used in children, especially with night terrors; DOC for parasomnias. Other benzodiazepines also can be used, most commonly, alprazolam or clonazepam.
Dosing
Adult
Not established; titration of benefits vs adverse effects recommended
Pediatric
Administer as in adults
Interactions
Other CNS depressing agents may exacerbate depressant effects; some SSRI agents, such as fluoxetine, can prolong half-life
Contraindications
Documented hypersensitivity; narrow-angle glaucoma
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)
Alprazolam (Xanax)
Second choice in this category for parasomnias. Advantages are its brief duration of action and decreased likelihood of morning effects (eg, grogginess). Disadvantages include potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
Dosing
Adult
Not established; titration of benefits vs adverse effects recommended
Pediatric
Administer as in adults
Interactions
Carbamazepine and disulfiram decrease effects; toxicity increases with cimetidine, lithium, contraceptives, and CNS depressants (including alcohol)
Contraindications
Documented hypersensitivity; severe respiratory depression, narrow-angle glaucoma, preexisting hypotension
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Withdrawal symptoms, including seizures, may occur upon abrupt discontinuation
Clonazepam (Klonopin)
Similar to alprazolam, it is a good alternative option to diazepam. Advantages are the presumed specificity for CNS GABA receptors. Disadvantages include potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
Dosing
Adult
Not established; titration of benefits vs side effects recommended
Pediatric
Not established
Interactions
Phenytoin and barbiturates may reduce effects; coadministration of CNS depressants increase toxicity
Contraindications
Documented hypersensitivity; severe liver disease and acute narrow-angle glaucoma
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation of the medication
Anticonvulsants
Agents in this drug category inhibit arousal.
Carbamazepine (Tegretol, Carbatrol)
Most commonly used agent for these disorders, but anecdotal evidence supports the possible use of GABA-enhancing agents such as valproate (Depakene, Depakote) or gabapentin (Neurontin). With respect to all of these agents, both hs dose alone and titration (as for epilepsy) has been reported.
Dosing
Adult
Not to exceed 400 mg PO hs; titrate according to monotherapy levels of this agent
Pediatric
Not established; 10-20 mg/kg/d PO in divided doses suggested; titrate by levels to monotherapy doses
Interactions
Do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; may decrease blood levels of a number of other drugs, including valproic acid and phenytoin, through its effect on the cytochrome P-450 enzyme system; however, also can increase effects of other CNS depressant agents through its CNS effects
Contraindications
Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain CBCs and serum iron baseline prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness
Valproate (Depakene, Depakote)
As with other drugs in this category, both hs and standard doses have been reported to be useful in treating parasomnias.
Dosing
Adult
No standard information available; doses not to exceed 1000 mg PO hs may be given
For standard titration, administer 10-15 mg/kg/d, not to exceed 60 mg/kg/d as initial dose
Pediatric
Not established; base dosing on epilepsy and migraine, similar limits of mg/kg/d dosing advised
For single hs dosing, likewise, no information available
Interactions
Coadministration with cimetidine, felbamate, and erythromycin may increase toxicity by increasing valproate levels; rifampin may significantly reduce levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations, with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely)
May increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in HIV seropositivity; because of its effects on platelets, should be used with caution with aspirin and other antiplatelet agents
Coadministration with lamotrigine may result in an increased risk of Stevens-Johnson syndrome when standard dose titration of lamotrigine is used
Contraindications
Documented hypersensitivity; hepatic disease/dysfunction
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Thrombocytopenia and abnormal coagulation parameters have occurred; the risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations of >110 mcg/mL in females and 135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis/coagulation disorder occurs; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness; should abdominal/GI symptoms develop, consideration also should be given to the possibility of pancreatitis
Gabapentin (Neurontin)
Has not been used as frequently as the other 2 anticonvulsants, and information is less available. As with the other 2 agents in this category, no information is available nor consensus reached regarding the use of hs dosing vs standard antiepileptic dosing.
Dosing
Adult
Not established; 300 mg PO tid suggested; titrate to 3600 mg/d in divided doses; not to exceed 1200 mg/dose
Pediatric
Not established
Interactions
Antacids may significantly reduce bioavailability (administer > 2 h following antacids)
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in severe renal disease
Antiparkinsonian drugs
Very effective for RLS and PLMD. Sinemet CR is the most commonly used drug, but pergolide and pramipexole also are effective. Pergolide was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. It is important not to abruptly stop pergolide. Health care professionals should assess patients' need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.
Levodopa and carbidopa (Sinemet CR)
Large neutral amino acid absorbed in proximal small intestine by 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 achieved when levodopa taken 1 h or more pc. Nausea often is reduced if levodopa taken immediately following meals. Some patients with nausea benefit from additional carbidopa in doses not to exceed 200 mg/d. Half-life of levodopa/carbidopa is approximately 2 h.
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/d carbidopa. When more carbidopa is required, substitute one 25/100-tab for each 10/100-tab. When more levodopa is required, substitute 25/250-tab for the 25/100-tab or 10/100-tab.
The SR formulation of levodopa/carbidopa is absorbed more slowly and provides more sustained levodopa levels than the IR form. It is as effective as 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.
Dosing
Adult
Slow-release preparation: 100/25 mg PO 1 h before hs; may be doubled if indicated
Pediatric
Not established
Interactions
Hydantoins, pyridoxine, phenothiazine, and hypotensive agents may decrease effects of levodopa; levodopa toxicity increases with antacids and MAOIs
Contraindications
Documented hypersensitivity; narrow-angle glaucoma, malignant melanoma, or undiagnosed skin lesions
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Certain adverse CNS effects (eg, dyskinesias) may occur at lower dosages and earlier in therapy with SR form; caution in patients with history of myocardial infarction, arrhythmias, asthma, and peptic ulcer disease; sudden discontinuation of levodopa may cause worsening of Parkinson disease; high-protein diets should be distributed throughout the day to avoid fluctuations in levodopa absorption
Pergolide (Permax)
Pergolide was withdrawn from the US market. Believed to exert therapeutic effect by directly stimulating postsynaptic dopamine receptors in nigrostriatal system. Usually administered in divided doses tid. During dosage titration, dosage of concurrent levodopa/carbidopa may be cautiously decreased.
Dosing
Adult
0.05 mg PO hs for first 2 d initially; gradually increase by 0.05 mg/d q3d over next 12 d, followed by increments of 0.25 mg/d q3d until optimal therapeutic dosage is achieved, generally 0.25-0.5 mg is effective
Pediatric
Not established
Interactions
Dopamine antagonists (eg, neuroleptic phenothiazines, butyrophenones, thioxanthenes, or metoclopramide) may diminish effectiveness of pergolide, a dopamine agonist; because pergolide mesylate is >90% bound to plasma proteins, exercise caution if coadministered with other drugs known to affect protein binding
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in cardiac dysrhythmias; may cause or exacerbate preexisting states of confusion and hallucinations or dyskinesia
Pramipexole (Mirapex)
Although used for Parkinson disease, has been found to be beneficial in RLS and PLMD.
Nonergot dopamine agonist with specificity of the D2 dopamine receptor, but 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.
Dosing
Adult
Week 1: 0.125 PO mg hs
Week 2: 0.25 mg PO hs
Week 3: 0.5 mg PO hs
Pediatric
Not established
Interactions
Cimetidine may increase toxicity; levodopa levels are increased with concurrent use
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in renal insufficiency and preexisting dyskinesias
Opiates
Opiates such as codeine, propoxyphene, and dihydromorphone have been used in patients who have severe RLS who do not benefit from other therapy. Patients should be closely observed for development of tolerance and dependency.
Propoxyphene (Darvon)
Drug combination indicated for severe RLS. Binds to opiate receptors in CNS, causing inhibition of ascending pain pathways, altering perception and response to pain
Dosing
Adult
1-2 tab (15-30 mg) PO hs
Pediatric
Not established
Interactions
Toxicity increases with concurrent administration of tricyclic antidepressants, MAOIs, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics; may increase serum concentrations of MAOIs, tricyclic antidepressants, carbamazepine, phenobarbital, and warfarin
Contraindications
Documented hypersensitivity; HACE diagnosis; elevated ICP
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Use to treat cough in patients with HAPE only if absolutely necessary; may depress hypoxic ventilatory rate and respiratory drive during sleep; caution in patients dependent on opiates, substitution may result in acute opiate withdrawal symptoms; caution in severe renal or hepatic dysfunction
Follow-up
Further Inpatient Care
Further Outpatient Care
Inpatient & Outpatient Medications
Deterrence/Prevention
Complications
Prognosis
Patient Education
Miscellaneous
Medicolegal Pitfalls
Special Concerns
Multimedia
Media file 1: The polysomnographic study in this picture demonstrates apnea (absence of carbon dioxide fluctuation indicating no flow), chest wall paradox, abrupt increase in tidal volume at the end of apnea, and oxygen desaturation. All of these features are consistent with obstructive sleep apnea.
Media file 2: Periodic limb movements on this polysomnographic study show intermittent leg electromyographic activity accompanied by electroencephalographic arousals.
References
Keywords
nightmare disorder, sleep terror disorder, sleepwalking disorder, rapid eye movement sleep behavior disorder, REM sleep behavior disorder, non–rapid eye movement, NREM, restless legs syndrome, RLS, periodic limb movement disorder, PLMD, dyssomnias, sleep drunkenness, microsleeps
Contributor Information and Disclosures
Author
Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Director of Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.
Medical Editor
Mohammed Memon, MD, Medical Director of Geriatric Psychiatry, Department of Psychiatry, Spartanburg Regional Hospital System
Mohammed 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.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
Iqbal Ahmed, MD, Program Director, General and Geriatric Psychiatry Residency Programs, Department of Psychiatry, Vice Chair for Education, Professor, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, and American Psychiatric Association
Disclosure: Nothing to disclose.
CME Editor
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry, Assistant Professor, Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; BMS Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Other; Northstar Grant/research funds Other; Novartis Other
Chief Editor
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration
Disclosure: Nothing to disclose.
Further Reading
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