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Idiopathic rapid eye movement sleep behavior disorder is a harbinger of dementia with Lewy bodies.

Idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia clinically linked with the alpha-synucleinopathies multiple systems atrophy (MSA), Parkinson's disease (PD), and dementia with Lewy bodies (DLB). Available autopsy information is limited but suggests that the pathologic basis of idiopathic RBD may be neuronal loss and Lewy bodies in pigmented monoaminergic nuclei, including the locus coeruleus and substantia nigra, which project to pontine nuclei mediating atonia during REM sleep. Thus, idiopathic RBD may be an alpha-synucleinopathy per se and a harbinger of impending PD, DLB, or MSA. Inclusion of historical or concurrent idiopathic RBD in the diagnostic criteria for DLB may improve their sensitivity, specificity, and clinical utility.

Aged↗

Evidence for a role of basal ganglia in the regulation of rapid eye movement sleep by electrical and chemical stimulation for the pedunculopontine tegmental nucleus and the substantia nigra pars reticulata in decerebrate cats.

The present study was to determine how afferents from the substantia nigra pars reticulata (SNr) of the basal ganglia to the pedunculopontine tegmental nucleus (PPN) in the brainstem could contribute to the control of behavioral states. We used anesthetized and acutely decerebrated cats (n=22). Repetitive electrical stimulation (10-100 Hz, 20-50 microA, for 4-20 s) to the ventrolateral part of the PPN produced rapid eye movement (REM) associated with a suppression of postural muscle tone (REM with atonia). Although repetitive electrical stimuli (10-200 Hz, 10-60 microA, for 5-20 s) delivered to the dorsolateral part of the SNr did not evoke eye movements or muscular tonus in baseline conditions, it altered the PPN-induced REM with atonia. The following three types of effects were induced: (1) attenuation of the REM with atonia; (2) attenuation of muscular atonia without changes in REM (REM without atonia); and (3) attenuation of only REM. The optimal stimulus sites for these effects were intermingled within the lateral part of the SNr. The PPN-induced REM with atonia was abolished by an injection into the PPN of muscimol (1-15 mM, 0.1-0.25 microl), a GABAA receptor agonist, but not altered by an injection of baclofen (1-10 mM, 0.1-0.25 microl), a GABAB receptor agonist. Moreover, an injection of bicuculline (1-15 mM, 0.1-0.25 microl), a GABAA receptor antagonist, into the PPN, resulted in REM with atonia. On the other hand, an injection of muscimol into the dorsolateral part of the SNr (1-15 mM, 0.1-0.25 microl) induced REM with atonia, which was in turn eliminated by a further injection of muscimol into the PPN (5-10 mM, 0.2-0.25 microl). These results suggest that a GABAergic projection from the SNr to the PPN could be involved in the control of REM with atonia, signs which indicate REM sleep. An excessive GABAergic output from the basal ganglia to the PPN in parkinsonian patients may induce sleep disturbances, including a reduction of REM sleep periods and REM sleep behavioral disorders (REM without atonia).

Animals↗

Sleep disturbances in Parkinsonism.

The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.

Hallucinations↗

Sexual behavior in sleep, sleepwalking and possible REM behavior disorder: a case report.

Seven cases of sexual behavior during sleep (SBS) have been recently reported. The subjects had histories of behavioral parasomnias as well as positive family histories of parasomnia. A 27 year-old man with a history of sexual behavior during sleep was reported. His sleep history disclosed sleepwalking (SW) since 9 years of age. He also developed episodes of highly disruptive and violent nocturnal behavior with dream enactment at age 20 years, which often resulted in physical injuries either to himself or his wife and infant. His wife also reported episodes of amnestic sexual behavior that began 4 years before referral. During the episodes, the patient typically procured his wife, achieving complete sexual intercourse with total amnesia. Physical and neurological diagnostic workups were unremarkable. Family history disclosed sleepwalking in his brother. He was put on 2mg/day of bedtime clonazepam with a remarkable clinical improvement. This case involves either the combination of violent and non-violent sleepwalking with SBS, or the superimposition of presumed REM sleep behavior disorder (RBD) on top of preexisting SW in a man who also developed SBS in adulthood. Thus, this is a case report of probable parasomnia overlap syndrome.

Adult↗

[Behavior disorders during REM sleep. Two clinical cases].

INTRODUCTION: The behavior disorder occurring during REM (Rapid Eye Movement) sleep is a parasomnia characterized by absence of atonia typical of this phase of sleep, although the other characteristics are maintained, namely rapid eye movements and desynchronization of cortical electrical activity. Clinically it is accompanied by abrupt, often violent movements, which may involve a limb or the trunk in relation to dreams typical of this phase of sleep, and which may interrupt sleep. Many pathological processes have been described, including: the Shy-Dragger syndrome, Parkinson's disease, olivopontocerebellar atrophy, multisystemic atrophy, in relation to certain antidepressant drugs, and most frequently the idiopathic form. CLINICAL CASES: We present two cases, one diagnosed as olivopontocerebellar atrophy and another in which there were no pathological findings. Both were referred to our department for the study of possible sleep disorders. In both cases neurophysiological studies, basically polysomnography with monitorization of various muscle groups and video, led to the diagnosis. CONCLUSIONS: We discuss the diagnostic and physiological criteria, and physiopathological explanations of each case, with special reference to N-Methyl-D-Aspartate (NMDA) and non-N-Methyl-D-Aspartate (non-NMDA) receptors. Finally we consider the pharmacological treatment of this disorder.

Adult↗

[Behavior disorder of the REM sleep in 2 documented cases with polysomnography].

We report a 69 years old male with a parkinsonian syndrome and a 50 years old female without neurological problems who showed violent behavior during REM sleep. Polysomnography showed that both bad tonic or phasic muscular activity during REM sleep and a REM sleep behavior disorder was diagnosed. Clonazepam was used in both, with good clinical response. This condition is frequently unrecognized and confused with nightmares, nocturnal delirium or other parasomnias.

Aged↗

Rapid eye movement sleep behavior disorder in children with autism.

We performed nocturnal polysomnography on 11 children with autism who had symptoms of disrupted sleep and nocturnal awakenings. We identified rapid eye movement (REM) sleep behavior disorder in 5 of these 11 patients. Since REM sleep behavior disorder typically affects elderly males with neurodegenerative diseases, the identification of this phenomenon in autistic children could have profound implications for our understanding of the neurochemical and neurophysiologic bases of autism. Further, accurate diagnosis of REM sleep behavior disorder would enable specific treatment with clonazepam and help the family and the child consolidate sleep and improve daytime performance.

Anticonvulsants↗

Stages 1-2 non-rapid eye movement sleep behavior disorder associated with dementia: a new parasomnia?

A 55-year-old woman with a progressive dementia and frontal syndrome was hospitalized because she was agitated every night after falling asleep (spoke, laughed, cried, tapped, kicked, walked, and fell down). She slept 5.5 hours during video polysomnography, but the theta rhythm electroencephalograph recording typical of sleep stages 1 to 2 and the spindles and K-complexes typical of sleep stage 2 contrasted with continuous muscular twitching, prominent rapid eye movements, vocalizations, and continuous, complex, purposeful movements typical of rapid eye movement (REM) sleep behavior disorder. This newly described stages 1--2 non-REM sleep behavior disorder suggests that central motor pattern generators were disinhibited during non-REM sleep.

Dementia↗

Rem sleep without atonia--from cats to humans.

Basic science research observations often lead to unexpected surprises. It is likely that in 1965 when Dr. Michel Jouvet placed bilateral peri-locus coeruleus lesions in cats and observed REM sleep without atonia (RWA) and "oneiric" behavior that could only be explained by "acting out dreams" (or "dreaming out acts"), he recognized that it was an important observation, but had little inkling of its true significance. Nor could he even imagine that it would lead to such greater understanding of wake/sleep phenomena in humans. Likely also, the first observation of REM sleep behavior disorder (RBD) in humans was felt to be interesting and novel - again with no true appreciation of what this seemingly simple observation would lead to important clinical relationships with numerous neurodegenerative disorders. The identification of RBD in humans also buttressed the concept of state dissociation, which has served to explain many previously unexplainable human behavioral phenomena.

Animals↗

The association between narcolepsy and REM behavior disorder (RBD).

BACKGROUND AND PURPOSE: Rapid eye movement (REM) sleep Behavior Disorder (RBD) is a movement disorder associated with loss of REM-related muscle atonia and is characterized by complex, vigorous and frequently violent dream-enacting behavior during REM sleep. RBD is usually idiopathic or secondary to neurological problems such as Parkinson's disease. This study looked at the association of RBD with another sleep disorder, narcolepsy. PATIENTS AND METHODS: Seventy-eight questionnaires were sent to known narcoleptics chosen at random from those with contact details available at the center. The questionnaire addressed current narcolepsy symptoms, medication use and symptoms of RBD. Positive questionnaire results were followed up with a telephone interview. Limited polysomnography (PSG) data was also analyzed. RESULTS: Fifty-five patients responded (response rate 71%). Of these, 20 (36%) had symptoms suggestive of RBD. The typical RBD patient is an older male (mean age of onset 60.9 years, 87% male); however, in this study, females were as likely to have RBD as males, and the mean age was 41 years. Sixty-eight percent of patients who regularly experienced cataplexy and the associated symptoms of narcolepsy (sleep paralysis, hypnogogic hallucinations and automatic behavior) had RBD, compared to 14% of those who never or rarely experienced these symptoms. CONCLUSION: This study implies a stronger relationship between these disorders than a previously published figure of 7-12% This is clinically significant as RBD is a potentially distressing but readily treatable disorder. It follows that narcoleptics, especially those with cataplexy and other associated symptoms, should be questioned about symptoms of RBD and treated accordingly. Similarly, anyone presenting with RBD should be assessed for symptoms of narcolepsy, particularly if female or of a younger age group than would otherwise be expected.

Adolescent↗

Brainstem function in rapid eye movement sleep behavior disorder: the evaluation of brainstem function by proton MR spectroscopy (1H-MRS).

Brainstem function was evaluated by proton magnetic resonance (MR) spectroscopy (1H-MRS) in a 69-year-old man with idiopathic rapid eye movement (REM) sleep behavior disorder. An analysis of spectral peak area ratios revealed an increase in the choline/creatine ratio. This change suggests that brainstem neurons have functional impairment at the cell membrane level. Further, our results suggest that 1H-MRS may provide for non-invasive, metabolic evaluation of brainstem neuronal function in REM sleep behavior disorder and find application in the differentiation of secondary REM sleep behavior disorders with neurodegenerative disorders from idiopathic disorders.

Aged↗

Rapid eye movement sleep behavior disorder. A treatable parasomnia affecting older adults.

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia defined by intermittent loss of electromyographic atonia during REM sleep with emergence of complex and vigorous behaviors. Punching, kicking, and leaping from bed during attempted dream enactment caused repeated injury in nine of our first ten adult patients. Mean age at onset was 62 years; nine of the patients were male. All patients underwent standard polysomnographic studies with videotaping of behaviors and extensive neurologic and psychiatric evaluations. The RBD was unrelated to psychopathologic conditions but in five cases was closely linked with major neuropathologic disorders: dementia (two), olivopontocerebellar degeneration, subarachnoid hemorrhage, and the Guillain-Barré syndrome. Other common polysomnographic abnormalities were high REM density, increased stage 3/4 (slow-wave) sleep, and both periodic and aperiodic limb twitching in non-REM sleep. Eight patients had dream changes involving motor overactivity and violent confrontations of dream characters. Clonazepam induced rapid and sustained improvement of dream and sleep behavior problems in seven patients, as did desipramine hydrochloride in one patient.

Aged↗

Rapid eye movement sleep behavior disorder preceding Parkinson's disease with therapeutic response to levodopa.

Rapid eye movement (REM) sleep behavior disorder (RBD) involves complex behavior and a loss of muscle atonia occurring during REM sleep. Half of these patients with RBD have an underlying neurologic disorder including dementia, olivopontocerebellar atrophy, subarachnoid hemorrhage, and cerebrovascular disease. Clonazepam is the drug of choice for RBD. RBD has been rarely reported to precede the onset of Parkinson's disease (PD). Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment. It is postulated that levodopa ameliorates RBD by suppressing REM sleep, and it remains to be seen whether levodopa can be an alternative to clonazepam in idiopathic RBD without PD.

Aged↗

Sleep bruxism as a manifestation of subclinical rapid eye movement sleep behavior disorder.

A 59-year-old man with temporomandibular joint pain/dysfunction syndrome presented with a long history of nocturnal bruxism. All-night polysomnographic recordings with video monitoring showed episodes of teeth grinding or clenching occurring exclusively during rapid eye movement (REM) sleep, which were often associated with movements of the hands and fingers and/or brief vocalization. Throughout REM sleep, there was excessive phasic chin electromyographic twitching, without increased tone, and also excessive phasic electromyographic twitching in multiple muscle sites. The patient maintained a normal nonrapid eye movement-REM cycle, but showed increased REM density. Polysomnographic characteristics suggested that there may be a common pathophysiology in a certain type of sleep bruxism and the REM sleep behavior disorder. Sleep bruxism seen in this case is concluded to be a manifestation of subclinical REM sleep behavior disorder.

Bruxism↗

A polysomnographic and clinical report on sleep-related injury in 100 adult patients.

In 100 consecutive adults who came to a sleep disorders center complaining of repeated nocturnal injury, polysomnographic study identified five disorders: night terrors/sleepwalking (N = 54), REM sleep behavior disorder (N = 36), dissociative disorders (N = 7), nocturnal seizures (N = 2), and sleep apnea (N = 1). Ninety-five patients sustained ecchymoses, 30 had lacerations, and nine had fractures. DSM-III axis I disorders (past or current) were found in 48.1% of the group with night terrors/sleepwalking and in 30.6% of the group with REM sleep behavior disorder; these were mainly affective disorders. In these two groups, clonazepam controlled the symptoms of 51 of the 61 patients to whom it was given.

Adolescent↗

Sleep and wakefulness disturbances in Parkinson's disease.

Patients with Parkinson's disease experience prominent difficulties in maintaining sleep, painful night-time abnormal movements, and daytime sleepiness, sometimes culminating in sleep attacks. Recent insights into the pathophysiology of sleep disorders in PD points to a complex interaction between movement disorders, side-effects of dopamine agents and lesions in sleep-wake regulating systems. Treatment with dopamine agonists provides a twice higher risk of daytime sudden sleep episodes than levodopa, with no difference between ergotic and non ergotic compounds. Insomnia can be improved by a better control of night-time disability, restless legs syndrome and dystonia using subthalamic nucleus stimulation or night-time levodopa. A specific REM sleep disorder contributes to REM sleep behavior disorder and also to hallucinations (suggesting they could be awake dreams) and excessive daytime sleepiness. The management of sleep and alertness problems requires to analyze their potential causes, to monitor night-time and daytime sleep, and to subtly adjust psychotropic and dopaminergic treatment.

Hallucinations↗

REM-sleep motor disorder in children.

In 1986, Schenck and coworkers described REM-sleep behavior disorder as a treatable parasomnia affecting older males. This disorder is characterized by intermittent loss of the muscle atonia, which normally characterizes the rapid eye movement (REM) sleep state. Complex motor behaviors occur that are often injurious and are associated with dreaming. We have identified five children who meet the criteria for REM-sleep behavior disorder and describe the clinical and polysomnographic characteristics of these patients, along with corresponding polysomnographic characteristics of matched comparison subjects.

Child↗