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PubMed2007

Testosterone not associated with violent dreams or REM sleep behavior disorder in men with Parkinson's.

We examined the relationship between testosterone levels, violent dreams, and REM sleep behavior disorder (RBD) in 31 men with Parkinson's disease (PD): 12 with clinical RBD and 19 without. All PD patients with clinical RBD experienced violent dreams, but none of the 19 non-RBD patients reported violent dreams. While dream content appears to be more aggressive in PD patients with clinical RBD, the presence of violent dreams or clinical RBD is not associated with testosterone levels in men with PD.

Aged↗
PubMed2004

Longitudinal change in REM sleep components in a patient with multiple system atrophy associated with REM sleep behavior disorder: paradoxical improvement of nocturnal behaviors in a progressive neurodegenerative disease.

A 60-year-old patient with multiple system atrophy (MSA) who presented with rapid eye movement (REM) sleep behavior disorder was investigated longitudinally by all-night polysomnography. REM sleep components, i.e. rapid eye movements and chin muscle activity, were analyzed together with the frequency of behaviors/movements on the videorecording. Decreased frequency of elaborate motor activity during REM sleep with time in this patient was compatible with the observation by his wife, and this change seemed to correlate with predominant tonic chin electromyogram with relatively suppressed phasic chin muscle activity, but the reduction of the REM sleep behavior disorder (RBD) episodes could be interpreted as being due to the increased rigidity along with MSA progression. The chronological change in REM sleep components in RBD with neurological disorders is worth studying in large follow-up series to enlarge our knowledge about the mechanism of behavioral manifestation of RBD in humans.

Brain Stem↗
PubMed2005

Idiopathic REM sleep behavior disorder: toward a better nosologic definition.

REM sleep behavior disorder (RBD) is a parasomnia characterized by a lack of motor inhibition during REM sleep leading to potentially harmful dream-enacting behaviors. RBD affects mainly older men and its prevalence in the general population is estimated to be around 0.5%. RBD may be idiopathic or associated with other neurologic disorders. A strong association between RBD and alpha-synucleinopathies has been recently observed, with the parasomnia often heralding the clinical onset of the neurodegenerative disease. The idiopathic form accounts for up to 60% of the cases reported in the three largest series of patients with RBD. Small clinical follow-up studies revealed that a proportion of these patients will eventually develop a parkinsonian syndrome or a dementia of Lewy bodies type in the years following the RBD diagnosis, while some patients will never show other neurologic signs within several decades from the RBD onset. Recent studies have looked at neurophysiologic and neuropsychological functions in idiopathic RBD and have found evidences of CNS dysfunction during both wakefulness and sleep. An impairment of the cortical activity, specific neuropsychological deficits, and signs of autonomic dysfunction have been observed in a variable proportion of these patients, challenging the concept of idiopathic RBD. Identifying subjects with a high risk of developing a neurodegenerative process may be crucial in order to develop early intervention strategies.

Brain↗
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↗
PubMed2005

Validation of a polysomnographic score for REM sleep behavior disorder.

STUDY OBJECTIVES: Rapid eye movement (REM) sleep behavior disorder (RBD) was described more than 2 decades ago, but only 1 report on 5 patients and 5 normal subjects has tested the effectiveness of a method by which relevant polysomnographic findings can be quantified. We sought to validate this method in a larger sample of patients and control subjects. DESIGN: Cross-sectional. SETTING: Academic hospital. INTERVENTIONS: A clinician interviewed 17 patients at risk for RBD secondary to neurodegenerative disorders and 6 controls to assess whether RBD was present by history. Bed partners completed a questionnaire that quantified RBD symptom severity. From 2 consecutive nocturnal studies in each patient, 2 different polysomnographic RBD scores were generated: the percentage of 30-second REM epochs with at least 15 seconds of tonically maintained electromyographic activity, and the percentage of 3-second REM mini-epochs that contained phasic electromyographic bursts. MEASUREMENTS AND RESULTS: The tonic and phasic measures, combined together, were higher in patients with clinical determinations of probable or possible RBD (n=9) than in patients judged unlikely to have RBD (n=4, P = .023). The overall polysomnographic measure correlated with the symptom scores (rho = 0.42, P = .048). Specific polysomnographic RBD measures on night 1 correlated highly with those on night 2 (rho > 0.70, P < .0001). CONCLUSIONS: This quantitative method to assess the severity of RBD polysomnographic features appears to be both valid and reliable in patients at risk for RBD because of neurodegenerative disorders.

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↗
PubMed2006

A unique episode of REM sleep behavior disorder triggered during surgery for Parkinson's disease.

REM sleep behavior disorder (RBD) is characterized by vigorous movements during REM sleep. Here, the authors report the case of a patient who presented such a disorder immediately after the implantation of the definitive electrode for left subthalamic stimulation. Interestingly, this was and has remained a unique episode in his medical history. It was found that a microlesion in or near the upper part of the pars compacta of the substantia nigra was very likely responsible for this phenomenon.

Deep Brain Stimulation↗
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↗
PubMed2005

REM sleep behavior disorder in patients with Parkinson's disease.

Sleep disorders have a high prevalence in patients with Parkinson's disease--some authors report it to be in the range of 60% - 98%. Together with the underlying motor symptoms, sleep disorders are the main causes of disability and have a substantial impact on the quality of life of these patients. Of particular interest are the behavior disorders of REM sleep (RBD) which are reported in many cases to precede the development of Parkinson's disease. In cases of diagnosing a REM sleep behavior disorder, it is absolutely necessary to exclude any underlying neurodegenerative process. Unlike the diagnosis of idiopathic RBD which can easily be made by conducting only a structured clinical interview, more than half of the RBD cases in patients with Parkinson's disease would be omitted using this technique. Patients with Parkinson's disease should be examined by polysomnography as the clinical interview's sensitivity alone can hardly reach 33%. This is so because there are mild forms of RBD in Parkinson's disease while the idiopathic forms always present with markedly severe clinical manifestations. Pathogenetically, Parkinson's disease share many similar features with RBD. Both conditions are characterized by a reduced striatal dopaminergic mediation. And yet there is no definitive answer to the question why RBD does not develop in all patients with Parkinson's disease. Clonazepam is highly effective in the treatment of RBD. Early diagnosis is thus critical for the prevention of injuries to the patient or to the patient's bed partner.

Anticonvulsants↗
PubMed2002

Exacerbation of REM sleep behavior disorder by chocolate ingestion: a case report.

REM sleep behavior disorder (RBD) is manifest by loss of normal rapid eye movement sleep atonia and the acting out of dreams of often violent content. Both idiopathic and secondary forms of RBD exist. We report on chocolate as a possible new precipitating agent for RBD and comment on a possible mechanism of action in this disorder.

Journal Article↗
PubMed1996

HLA class II genes associated with REM sleep behavior disorder.

Twenty-five white men with rapid eye movements (REM) sleep behavior disorder, but without narcolepsy, underwent HLA class II antigen typing: 84% (N=21) were DQwl (DQB1*05,06) positive (28% [N=7] were DR2 positive); DQB1*0501 (N=9) and DQB1*0602 (N=7) were the most common phenotypes. The 84% DQwl rate in men with REM sleep behavior disorder was significantly greater (p=0.015) than the 56% DQwl rate found in a local white comparison group (N=66), and was greater than the 39 to 66% DQwl rates published for 12 white groups (N=40-418/group). Thus, another disorder of REM sleep dysregulation (besides narcolepsy) appears to be strongly associated with specific HLA class II genes.

Electromyography↗
PubMed2003

REM sleep behavior disorder and vocal cord paralysis in Machado-Joseph disease.

We evaluated the occurrence of REM sleep behaviour disorder (RBD) and vocal cord abductor paralysis (VCAP) in a group of 9 Machado-Joseph disease (MJD) patients. RBD was diagnosed by clinical history plus audiovisual polysomnography in 4 men and 1 woman (55%). While dreaming, 4 fell out of the bed and the other injured his arms. Laryngoscopy detected bilateral VCAP in 1 patient with stridor who required emergency tracheotomy, and partial vocal cord abductor restriction in 2. RBD and VCAP are two potentially injurious conditions that should be considered part of the clinical spectrum of MJD.

Adult↗
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↗
PubMed1997

REM sleep behavior disorder: clinical and physiopathological findings.

Abnormalities of REM sleep i.e. absence of atonia and abnormal motor control which are described in patients with REM sleep behavior disorder, have induced clinical and physiopathological interest. Initial hypothesis of a simple dysfunction of REM sleep generators has not been confirmed. The prevalence in older subjects and in patients with parkinsonian syndromes suggest that the appearance of the parasomnia is related to alteration in the neurons of pontine area i.e. nucleus peduncolopontine, in which there is an integration of sleep-wake mechanisms and locomotor systems. Controversy surrounds the specificity of absence of atonia in the diagnosis of the parasomnia. Since this polygraphic finding may be present in subjects without any sleep complaint and in patients with initial neurological impairment, diagnosis of the sleep disorders might be allowed only when the polygraphic characteristic of persistent tonus and complex motor behavior are recorded.

Journal Article↗
PubMed2002

Rapid Eye Movement (REM) sleep behavior disorder: a sleep disturbance affecting mainly older men.

Rapid Eye Movement (REM) sleep behavior disorder is characterized by the intermittent loss of REM-related muscle atonia and the appearance of elaborated motor behaviors (sometimes violent behavior) and vocalizations associated with dream mentation. Nine patients were diagnosed in our Sleep Disorders Unit with this syndrome during the period August 1997-April 2000. All were male, average age 67.9 +/- 6.9 years. The complaint of all our patients was the occurrence of violent or injurious sleep behavior mainly during the dream stage. Jumping or falling out of bed and slapping or beating their wives were more common. None had history or showed signs of dementia, Parkinson or other neurodegenerative diseases. A relative high amount of SWS (20.9%) was found. Seven showed an intermittent increase in chin EMG tonus while the other two had an almost continuous high chin EMG tonus during REM sleep. We did not observe any violent motor behavior during the polysomnographic recordings. Phasic activities during REM sleep were high but density quantification was not performed. Six patients had also Periodic Limb Movement (PLM) Disorders, four had also Obstructive Sleep Apnea (OSA) Syndrome. The treatment recommended to all patients was Clonazepam beginning with a 0.5-mg dose. Four patients reported a decrease or disappearance of sleep agitation and nightmares and were very happy with the treatment and without side effects. The others decided not to try Clonazepam or stopped after a few days of using it. RBD appears to be a sleep disturbance affecting mainly aged men. Its violent expression may frighten the patients and their bed-partners and may cause injury to both. In some cases this sleep disorder seems to be an early manifestation of a neurodegenerative disorder while in others it may represent only an idiopathic form. Clonazepam at lower doses is a good agent for the treatment of this condition.

Adult↗