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Results for “REM Sleep Behavior Disorder”

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At least 19 recordsLinked to original sources

PubMed2000

Decreased striatal dopaminergic innervation in REM sleep behavior disorder.

REM sleep behavior disorder (RBD) is a possible herald of neurodegenerative disorders with parkinsonism. The authors determined the density of striatal dopaminergic terminals with [11C]dihydrotetrabenazine PET in six elderly subjects with chronic idiopathic RBD and 19 age-appropriate controls. In subjects with RBD, there were significant reductions in striatal [11C]dihydrotetrabenazine binding, particularly in the posterior putamen.

Aged↗

PubMed1988

REM sleep behavioral disorders.

REM sleep behaviors were recently described as wild, dream-enacting behaviors during REM sleep with loss of usual atonia on submental muscles. We examined 6 patients (5 M, 1F) with characteristic episodes of behavioral manifestations during REM sleep. Polysomnographic data indicate a decrease in first REM latency, an absence of stage 4 NREM, altered phasic motor activity and behavioral episodes during REM sleep even with normal chin muscle atonia. Three patients had Shy-Drager syndrome, 1 olivopontocerebellar atrophy and 2 patients had no neurological disease. The crucial importance of a disinhibited locomotor system during sleep appears to be responsible for this REM parasomnia.

Adult↗

PubMed2000

REM sleep behavior disorder.

REM sleep is the stage associated with vivid dream mentation, desynchronous cortical EEG, and atonia of antigravitary muscles. REM sleep behavior disorder (RBD) is characterized by the intermittent loss of REM sleep atonia and by the appearance of elaborate motor activity associated with dream mentation. The animal model of REM sleep without atonia indicates that lesions to the perilocus coeruleus disrupt the excitatory connection to the nucleus reticularis magnocellularis in the descending medullary reticular formation and disable the hyperpolarization of the alpha spinal motoneurons. Extensive neurologic evaluations in humans suffering from both idiopathic and symptomatic forms have not identified specific lesions; however, findings in some patients suggest that diffuse lesions of the hemispheres, bilateral thalamic abnormalities, or primary brain-stem lesions may result in the RBD. Symptomatic RBD cases are associated with several neurologic disorders such as dementia, cerebrovascular diseases, multiple sclerosis, brain-stem neoplasm. RBD has been often documented to precede or to co-occur with neurodegenerative disorders, such as dementia, Parkinson's disease and multiple system atrophy. Most importantly, RBD is readily diagnosable and treatable. Patients and their bed partners usually report immediate improvement in sleep-related motor behavior with small doses of clonazepam.

Brain↗

PubMed2002

REM sleep behavior disorder and REM sleep without atonia in Parkinson's disease.

OBJECTIVE: To determine the frequency of REM sleep behavior disorder (RBD) among patients with PD using both history and polysomnography (PSG) recordings and to further study REM sleep muscle atonia in PD. BACKGROUND: The reported occurrence of RBD in PD varies from 15 to 47%. However, no study has estimated the frequency of RBD using PSG recordings or analyzed in detail the characteristics of REM sleep muscle atonia in a large group of unselected patients with PD. METHODS: Consecutive patients with PD (n = 33) and healthy control subjects (n = 16) were studied. Each subject underwent a structured clinical interview and PSG recording. REM sleep was scored using a method that allows the scoring of REM sleep without atonia. RESULTS: One third of patients with PD met the diagnostic criteria of RBD based on PSG recordings. Only one half of these cases would have been detected by history. Nineteen (58%) of 33 patients with PD but only 1 of 16 control subjects had REM sleep without atonia. Of these 19 patients with PD, 8 (42%) did not present with behavioral manifestations of RBD, and their cases may represent preclinical forms of RBD associated with PD. Moreover, the percentage of time spent with muscle atonia during REM sleep was lower among patients with PD than among healthy control subjects (60.1% vs 93.2%; p = 0.003). CONCLUSIONS: RBD and REM sleep without atonia are frequent in PD as shown by PSG recordings.

Aged↗

PubMed1996

Cardiac autonomic activity during wakefulness and sleep in REM sleep behavior disorder.

In REM sleep behavior disorder (RBD) it has been reported that tachycardia may not accompany the impressive movements associated with dream mentation. Up to now there are no data concerning the cardiac autonomic activity during wakefulness as well as during sleep out of nocturnal dream-enacting behaviors, in RBD. We evaluated 14 RBD patients. Our study shows that only 36% of patients had normal results in all traditional autonomic tests during wakefulness. Moreover, RBD patients had a reduced tonic and phasic heart rate variability during sleep. Autonomic evaluation during sleep may show impairment earlier than the traditional tests during wakefulness. No difference was found between idiopathic RBD patients and symptomatic ones.

Aged↗

PubMed1998

[REM sleep behavior disorder (RBD) and dissociated REM sleep].

REM sleep behavior disorder (RBD) is characterized by the appearance of somnambulism-like behavior associated with dream mentation, and the intermittent loss of muscle atonia during REM sleep (stage 1-REM with tonic EMG; stage 1-REM). RBD is caused symptomatically or idiopathically, and its manifestation of symptoms sometimes associated with psychosocial stress. Muscle tone is often augmented during impared REM sleep observed in RBD patients. Animal experimental studies suggest that dysfunction or lesions of muscle inhibitory system in brain stem is rerated with pathogenesis of RBD. Clonazepam is effective for organic behavior and nightmare, but not remarkable for dissociated REM sleep. Other benzodiazepines and tricyclic antidepressants can be one of the choices of medications. Directions for safe-bedroom and psychotherapy is sometimes necessary.

Animals↗

PubMed1989

Magnetic resonance findings in REM sleep behavior disorder.

Rapid eye movement (REM) sleep behavior disorder is characterized by bizarre acts during nocturnal sleep that may lead to physical injuries. Dream content suggests that motor overactivity is an attempted dream enactment and polygraphic studies reveal REM stage without atonia, an alteration of REM sleep generation that facilitates excessive motor activity. In 6 patients with REM sleep behavior disorder. MRI of the brain showed multifocal signal intensity lesions suggestive of lacunar infarcts in periventricular regions (5 patients) and in dorsal pontomesencephalic areas (3 patients). REM sleep behavior disorder may be the result of injury to the midrostral tegmentum nuclei, the tegmentoreticular tracts, or both. This condition is easily controlled with clonazepam.

Aged↗

PubMed1999

Juvenile Parkinson's disease with REM sleep behavior disorder, sleepiness, and daytime REM onset.

We describe an unmedicated patient with juvenile PD with difficulties maintaining wakefulness and the atonia of REM sleep. Laboratory testing showed enhanced muscle activity in REM sleep consistent with a history of dream enactment behavior (i.e., REM sleep behavior disorder) and daytime sleepiness, and REM-sleep onsets on multiple sleep latency testing. The results emphasize the potential role of dopamine and basal ganglia circuits in the modulation of activated behavioral states (e.g., wakefulness and REM sleep).

Adolescent↗

PubMed2002

[REM Sleep behavioral disorder].

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia which occurs only during REM sleep. RBD is characterized by the loss of skeletal muscle atonia, which is the principal feature of REM sleep, and by abnormal behavior representing the attempted enactment of dreaming. Clinically, it consists of abnormal behavior, frequently violent, that may lead to injuries. A polysomnographic study is necessary to assess the diagnosis showing the absence of REM sleep atonia and related abnormal behavior. RBD usually affects older men. Its exact etiological factors remain unknown. However, RBD is sometimes linked with drug use or exposure to toxic conditions. Moreover, the association with neurological disorders is frequently reported, particularly cerebrovascular, tumoral or neurodegenerative disease. Neurodegenerative disorders with parkinsonism are frequently involved. In Lewy body dementia, RBD is particularly frequent. In many cases, RBD may have a predictive value, preceding other symptoms of neurodegenerative disorders with parkinsonism. The biochemical mechanisms underlying RBD still remain unclear but could involve the dopamino-cholinergic balance and the serotoninergic pathway.

Anticonvulsants↗

PubMed2003

Increased muscle activity during rapid eye movement sleep correlates with decrease of striatal presynaptic dopamine transporters. IPT and IBZM SPECT imaging in subclinical and clinically manifest idiopathic REM sleep behavior disorder, Parkinson's disease, and controls.

STUDY OBJECTIVES: Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by complex behavior during REM sleep. The etiology of this disorder is still unknown, but a recent study showed that RBD precedes symptoms of Parkinson disease (PD) by several years, and in a previous study, we found reduced striatal dopamine transporters in idiopathic clinically manifest RBD. DESIGN: Hypothesizing that subclinical RBD shows a less severe reduction of striatal dopamine transporters than clinically manifest RBD, we studied striatal postsynaptic dopamine D2-receptors with (S)-2hydroxy-3iodo-6-methoxy-([1-ethyl-2-pyrrolidinyl]methyl) benzamide labeled with iodine 123 (IBZM) and the striatal presynaptic dopamine transporters with (N)-(3-iodopropene-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl) tropane labeled with iodine 123 (IPT) using single-photon emission computed tomography (SPECT) in the following groups: 8 patients with idiopathic subclinical RBD, 8 patients with idiopathic clinically manifest RBD, 11 controls, and 8 patients with PD stage Hoehn & Yahr I. RESULTS: The IPT uptake was highest in controls. There was a significant decrease in IPT uptake from controls to patients with subclinical RBD, from patients with subclinical RBD to clinically manifest RBD, and from patients with clinically manifest RBD to patients with PD (controls: right = 4.07 +/- 0.29, left = 4.07 +/- 0.30; subclinical RBD: right = 3.56 +/- 0.21, left = 3.55 +/- 0.25; clinically manifest RBD: right = 3.18 +/- 0.43, left = 3.2 +/- 0.43; PD: ipsilateral to the clinically affected body side = 3.25 +/- 0.35, contralateral to the clinically affected body side = 2.51 +/- 0.28). Muscle activity during REM sleep lasting persistently longer than 0.5 seconds was independently associated with reduction of striatal dopamine transporters (P = 0.001). The IBZM uptake was not significantly different between the groups. CONCLUSIONS: This study suggests that there is a continuum of reduced striatal dopamine transporters involved in the pathophysiologic mechanisms causing increased muscle activity during REM sleep in patients with subclinical RBD.

Adult↗

PubMed1992

Motor dyscontrol in narcolepsy: rapid-eye-movement (REM) sleep without atonia and REM sleep behavior disorder.

Narcolepsy involves abnormalities of rapid-eye-movement (REM) sleep, including a short latency to the onset of REM sleep, hypnagogic hallucinations, and sleep paralysis. In addition, persistence of muscle tone by electromyographic criteria or excessive muscle twitching during REM sleep or both have been reported in treated and untreated narcoleptic patients. We report that another previously described abnormality of REM sleep, REM sleep behavior disorder, may also be a symptom of narcolepsy. This disorder was found in 10 narcoleptic patients during routine clinical evaluations involving polysomnography and multiple sleep latency tests. During REM sleep, 7 additional narcoleptic patients displayed persistent muscle tone and/or excessive twitching, which we believe to be subclinical components of REM sleep behavior disorder. These 17 patients, diagnosed by established criteria for narcolepsy and for REM sleep behavior disorder, ranged in age from 8 to 74 years. Seventy-one percent were male. Narcolepsy and REM sleep behavior disorder most commonly emerged in tandem. In 3 patients, treatment of narcolepsy-cataplexy with stimulants and tricyclics either induced or exacerbated REM sleep behavior disorder.

Adolescent↗

PubMed2002

Brainstem proton magnetic resonance spectroscopy in idopathic REM sleep behavior disorder.

STUDY OBJECTIVES: Rapid-eye-movement (REM) sleep behavior disorder (RBD) is thought to result from a dysfunction of the brainstem structures that regulate physiologic REM sleep muscle atonia. Proton magnetic resonance spectroscopy (1H-MRS) is a noninvasive method that allows detection of in vivo neuronal dysfunction in localized brain areas. The aim of our study was to investigate whether 1H-MRS can detect brainstem abnormalities in patients with idiopathic RBD. DESIGN: 1H-MRS centered on the midbrain and the pontine tegmentum was acquired in 15 patients with idiopathic RBD and 15 control subjects matched for age and sex. SETTING: University hospital sleep laboratory center. PARTICIPANTS: Fifteen untreated patients with chronic RBD diagnosed by history and video-polysomnography, normal neurologic examination, and normal cranial MRI. Fifteen healthy controls with no sleep complaints and normal polysomnography and brain MRI. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The metabolic peaks detectable with 1H-MRS, N-acetylaspartate (NAA), creatine-phosphocreatine (Cr), choline-containing compounds (Cho) and myoinositol (mI), and the ratios of NAA, Cho and ml to Cr were evaluated both in the midbrain and pontine tegmentum. No significant differences in N-acetylaspartate/creatine, choline/creatine and myoinosito/creatine ratios were found between patients and controls. CONCLUSIONS: The results do not suggest that marked mesopontine neuronal loss or 1H-MRS detectable metabolic disturbances occur in idiopathic RBD.

Aged↗

PubMed1992

Polysomnographic features of REM sleep behavior disorder: development of a scoring method.

REM sleep behavior disorder (RBD) is characterized by the intermittent absence of REM sleep EMG atonia and the appearance of elaborate motor activity associated with dream mentation. There are no specific diagnostic criteria for RBD based upon polysomnographic findings. We describe a new scoring method and show its sensitivity to treatment with clonazepam. An increased phasic submental EMG density occurs in RBD patients, but REM density is similar to that of controls. Clonazepam selectively decreases REM sleep phasic activity but exerts no effect on REM sleep atonia. Periodic limb movements in sleep (PLMS) occur equally in both REM and NREM sleep in RBD patients, suggesting that normal suppression of PLMS in REM sleep is due to motor inhibition.

Adult↗

PubMed2003

Physiological and anatomical link between Parkinson-like disease and REM sleep behavior disorder.

Parkinson's disease (PD) is a progressive neurodegenerative disease that is caused by a loss of neurons in the ventral midbrain. Parkinsonian patients often experience insomnia, parasomnias, and daytime somnolence. REM sleep behavior disorder (RBD) is characterized by vigorous movements during REM sleep, and may also be caused by neuronal degeneration in the central nervous system (CNS); however, the site of degeneration remains unclear. Both Parkinsonism and RBD become more prevalent with aging, with onset usually occurring in the sixties. Recent findings show that many individuals with RBD eventually develop Parkinsonism. Conversely, it is also true that certain patients diagnosed with Parkinsonism subsequently develop RBD. Postmortem examination reveals that Lewy bodies, Lewy neurites, and alpha-synuclein are found in brainstem nuclei in both Parkinsonism and RBD patients. In this article, we will discuss evidence that Parkinsonism and RBD are physiologically and anatomically linked, based on our animal experiments and other studies on human patients.

Animals↗

PubMed1997

Melatonin effects in a patient with severe REM sleep behavior disorder: case report and theoretical considerations.

REM sleep behavior disorder (RBD) is so far a possibly underestimated yet well-described sleep disorder. Its major impact is the vigorous sleep behavior that often results in injuries to the patient himself or to people sleeping nearby. We treated a 64-year-old male with a clinically and polysomnographically confirmed diagnosis of RBD with 3 mg melatonin, which led to a significant reduction of motor activity during sleep, as measured by actigraphy (p < 0.0001 in all analyzed movement parameters), and a full clinical recovery over a 5-month treatment period. RBD phenomena gradually returned after melatonin administration was stopped. After 2 months' treatment, polysomnography showed no major changes except an increase of REM sleep (13 vs. 17% of sleep period time) and a better preservation of REM-sleep-associated muscle atonia. Our results suggest that melatonin might be able to reinforce REM sleep in RBD patients by enhancing its active inhibition of motor activity.

Humans↗

PubMed2000

Presumed REM sleep behavior disorder arising from cataplexy and wakeful dreaming.

REM sleep behavior disorder (RBD) is an injurious parasomnia occasionally associated with narcolepsy. RBD usually occurs within REM sleep. We report a case of RBD in a narcoleptic patient arising from cataplexy and wakeful dreaming. The problem of state boundary control inherent in narcolepsy together with the pharmacological effects of tricyclic antidepressants used to treat cataplexy are usually the reason of RBD in narcoleptics. By similar mechanism our patient has presumed RBD out of REM intrusions into wakefulness.

Journal Article↗

PubMed1997

A parasomnia overlap disorder involving sleepwalking, sleep terrors, and REM sleep behavior disorder in 33 polysomnographically confirmed cases.

A series of 33 patients with combined (injurious) sleepwalking, sleep terrors, and rapid eye movement (REM) sleep behavior disorder (viz. "parasomnia overlap disorder") was gathered over an 8-year period. Patients underwent clinical and polysomnographic evaluations. Mean age was 34 +/- 14 (SD) years; mean age of parasomnia onset was 15 +/- 16 years (range 1-66); 70% (n = 23) were males. An idiopathic subgroup (n = 22) had a significantly earlier mean age of parasomnia onset (9 +/- 7 years) than a symptomatic subgroup (n = 11) (27 +/- 23 years, p = 0.002), whose parasomnia began with either of the following: neurologic disorders, n = 6 [congenital Mobius syndrome, narcolepsy, multiple sclerosis, brain tumor (and treatment), brain trauma, indeterminate disorder (exaggerated startle response/atypical cataplexy)]; nocturnal paroxysmal atrial fibrillation, n = 1; posttraumatic stress disorder/major depression, n = 1; chronic ethanol/amphetamine abuse and withdrawal, n = 1; or mixed disorders (schizophrenia, brain trauma, substance abuse), n = 2. The rate of DSM-III-R (Diagnostic and Statistical Manual, 3rd edition, revised) Axis 1 psychiatric disorders was not elevated; group scores on various psychometric tests were not elevated. Forty-five percent (n = 15) had previously received psychologic or psychiatric therapy for their parasomnia, without benefit. Treatment outcome was available for n = 20 patients; 90% (n = 18) had substantial parasomnia control with bedtime clonazepam (n = 13), alprazolam and/or carbamazepine (n = 4), or self-hypnosis (n = 1). Thus, "parasomnia overlap disorder" is a treatable condition that emerges in various clinical settings and can be understood within the context of current knowledge on parasomnias and motor control/dyscontrol during sleep.

Adult↗

PubMed2025

Post-traumatic stress disorder and REM-sleep behavior disorder: exploring genetic associations and causal links.

OBJECTIVE: To explore potential genetic and/or causal associations between Post-Traumatic Stress Disorder and neurodegeneration-related isolated/idiopathic rapid-eye-movement sleep behavior disorder. METHODS: We conducted polygenic risk score, genetic correlation, and Mendelian randomization analyses using the latest genome-wide association studies summary statistics and individual genotyping data. Next, a blinded observer examined dopamine transporter imaging binding status-a marker of neurodegeneration-in patients with isolated/idiopathic rapid-eye movement sleep behavior disorder, with (N = 6) and without Post-Traumatic Stress Disorder (N = 32). RESULTS: Polygenic risk scores for Post-Traumatic Stress Disorder were associated with isolated/idiopathic rapid-eye-movement sleep behavior disorder, with each standard deviation increase linked to 14.7% higher odds (odds ratio = 1.15, 95% confidence interval: 1.04 to 1.26, p = 0.005). However, genetic correlation was weak, and Mendelian randomization did not support a potential causal relationship. The proportion of individuals with abnormal dopamine transporter imaging binding status was significantly higher in the Post-Traumatic Stress Disorder group compared to those without the disorder (p=0.01, X2 = 6.62). INTERPRETATION: Polygenic risk scores analysis identified an association between Post-Traumatic Stress Disorder and neurodegeneration-related isolated/idiopathic rapid-eye-movement sleep behavior disorder, consistent with the result from the small exploratory substudy. The lack of strong genetic correlation or causation may reflect limited sample size. Further research with larger and more diverse cohorts is crucial to clarify the genetic, biological and physiological mechanisms underlying this association.

Journal Article↗