Medications — Approximately half of all RBD patients develop dream enactment after initiating a serotonergic antidepressant medication, typically a selective serotonin reuptake inhibitor (SSRI), serotonin-norepinephrine reuptake inhibitor (SNRI), or serotonin modulating agent [66,67].
RBD has been associated with antidepressant medications such as tricyclic antidepressants, fluoxetine, venlafaxine, and MAO inhibitors. Although REM behavior disorder has been associated with the use of serotonergic reuptake inhibitors, there are actually very few documented cases in the literature.
REM sleep behavior disorder may be associated with other neurological conditions, such as Lewy body dementia (also called dementia with Lewy bodies), Parkinson's disease or multiple system atrophy.
In 45 percent of cases, RBD is associated with alcohol or sedative-hypnotic withdrawal, tricyclic antidepressant (medications, such as imipramine) or serotonin reuptake inhibitor use (medications, such as fluoxetine, sertraline or paroxetine) or other types of antidepressants (for example, mirtazapine).
Diagnostic criteria
You have repeated times of arousal during sleep where you talk, make noises or perform complex motor behaviors, such as punching, kicking or running movements that often relate to the content of your dreams. You recall dreams associated with these movements or sounds.
More than 80 percent of people with rapid eye movement sleep behavior disorder (RBD), as the condition is known, go on to develop certain neurodegenerative maladies such as Parkinson's disease, multiple system atrophy or dementia with Lewy bodies, studies have found.
Other medications, such as tricyclic antidepressants, may be effective in some patients with RBD. However, tricyclics are also known to actually precipitate RBD. The newer generations of antidepressants, particularly venlafaxine and mirtazapine, are frequent precipitators or aggravators of RBD.
RBD is strongly associated with certain neurodegenerative disorders. About 97% of people who have isolated (idiopathic) RBD will have Parkinson's disease, Lewy body dementia or multiple system atrophy within 14 years of diagnosis. Up to 36% of people with Type 1 narcolepsy have secondary (symptomatic) RBD.
Rapid eye movement sleep behavior disorder (RBD) has rarely been associated with a psychiatric condition. We report a series of cases of RBD presenting as psychiatric disorders.
RBD is an attractive target for future neuroprotective treatment trials to prevent evolution of overt parkinsonism or memory decline, but currently, there are no known effective treatments and future trials will be necessary to determine if RBD is an actionable time point in the evolution of overt synucleinopathy.
The prognosis of RBD depends on its etiology. In idiopathic cases, the symptoms are controlled with medications. In secondary cases, the prognosis depends on the underlying primary disease. No deaths have been reported in idiopathic cases of RBD; however, patients and bed partners may experience serious injury.
REM sleep is characterized by relaxed muscles, quick eye movement, irregular breathing, elevated heart rate, and increased brain activity. Most adults need about two hours of REM sleep each night.
While REM sleep behavior disorder may occur in conjunction with, or as a predecessor to, certain neurological disorders such as Parkinson's disease, it can also result from medication usage.
Symptoms of RBD may be gradual or sudden. Episodes may occur from time to time, or several times in one night. Symptoms usually worsen over time.
RBD is also caused by antidepressant medications (table 1), narcolepsy, and pontine lesions such as those from stroke or multiple sclerosis. (See 'Etiology' above.) Diagnosis – The diagnosis of RBD is based upon a history of dream-enactment behavior and REM sleep without atonia (RSWA), as documented by polysomnography.
RBD mimics include arousalrelated motor manifestations in severe obstructive sleep apnea, disorders of arousal from NREM sleep, sleep-related movement disorders, temporal and frontal nocturnal epileptic seizures, insulinoma-related hypoglycemia and psychogenic disorders.
Clonazepam (Klonopin) is highly effective in the treatment of REM sleep behavior disorder (RBD), relieving symptoms in nearly 90% of patients with little evidence of tolerance or abuse. The response usually begins within the first week, often on the first night.
Medication. A number of medications have proven effective in cases of RBD depending on which symptoms present. Low doses of clonazepam, from the benzodiazepine class of drugs, can help in about 90 percent of people with RBD. These drugs suppress muscle activity and relax the body during sleep.
Discovered in 1982, RBD is a "parasomnia," loosely described as abnormal behavior during sleep, like sleepwalking and sleep terrors. As Poma would learn, RBD is often a warning sign of other serious brain troubles to come. About half of people diagnosed with RBD will develop Parkinson's disease within a decade.
Idiopathic REM sleep behaviour disorder (iRBD) is a powerful early sign of Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. This provides an unprecedented opportunity to directly observe prodromal neurodegenerative states, and potentially intervene with neuroprotective therapy.
RBD can have a genetic origin. The results of the exome study in this kindred suggest that gabaergic circuits may be altered in patients with RBD. Further studies in this family or in other pedigrees with familial RBD may clear the role of this gene in this disorder.
We suggest melatonin as initial therapy rather than clonazepam (Grade 2C). A typical starting dose of melatonin for RBD is 3 mg at bedtime, increased in 3 mg increments until behaviors subside (table 2). Most patients find relief with doses between 6 and 18 mg.
Some studies reported specific anatomical regions related with RBD, including the dysfunction of a network among the midbrain and pontine tegmentum, the locus subcoeruleus, the medullary magnocellular reticular formation, and focal lesions of the pontine or mesencephalic tegmentum [4, 5].