RBD, Rapid Eye Movement Sleep Behavior Disoder

Clinic

• RBD is a parasomnia
• It is a sleep disorder in which people act out their dreams. It involves abnormal behavior during REM sleep.
• The major feature of RBD is loss of muscle atonia during otherwise intact REM sleep.
• Loss of motor inhibition leads to sleep behaviors ranging from simple limb twitches to more complex integrated movements
• RBD is a very strong predictor of progression to Parkinson's disease or dementia with Lewy bodies

Characteristics

Main symptoms

• RBD is characterized by the dreamer acting out their dreams, with complex behaviors.
• Dreams often involve Violent / Aggressive actions, Screaming, Shouting, Laughing, Crying, arm flailing, kicking, punching, choking, and jumping
• The sleeping person may be unaware of these movements.

Other symptoms

• Reduced motor abilities
• Posture and gait changes
• Mild cognitive impairment
• Alterations in the sense of smell
• Impairments in color vision
• Autonomic dysfunction (Orthostatic hypotension, Constipation, Urinary problems and Sexual dysfunction)
• Depression

Related disease

• Narcolepsy
• Guillain–Barré syndrome
• Limbic encephalitis
• Morvan's syndrome
• Multiple system atrophy

Causes

• RBD occurs when there is a loss of normal voluntary muscle atonia during REM sleep resulting in motor behavior in response to dream content
• Brainstem circuits that control atonia during REM sleep may be damaged, including those in the pontomedullary brainstem.
• REM sleep circuits are located in caudal brainstem structures—the same structures that are known to lead to be implicated in the synucleinopathies.
• Motor deficits like those seen in RBD are known to result from lesions in those circuits.

Note:

I seems that extrapyramidal tracts are involved actively in RBD

Differential Diagnosis

• Non-REM parasomnias (sleepwalking, sleep terrors)
• Periodic limb movement disorder
• Severe obstructive sleep apnea
• Dissociative disorders

Polysomnography plays an important role in confirming RBD diagnosis.

Entities / Miasms

It belongs to EPS COD. So Its miasms are JE, WNE, GSS, CJD and FFI

The current identification of sleep-related abnormalities and the possible relation to neurodegenerative disorders raises a significant number of research questions. One of the most important issues is that the current studies identifying RBD as a risk factor for later parkinsonian conversion are based on identifying and defining the population at risk. The current studies have identified patients in high-level neurological sleep clinics. It has still not been settled whether this may influence the potential effect on the conversion, eg, if patients identified in broader clinical settings with simpler methods influence the diagnostic pattern and prognosis. The presence of other factors, eg, medication, alcohol, and comorbidities, may also influence the risk association.

Although there are currently no drugs available to prevent or delay the disease process for parkinsonian conversion, any sensitive and specific biological markers would be important in the future for identifying high-risk individuals with the aim of managing the risk. Owing to the complex mechanism of wake–sleep regulation, knowledge of these mechanisms and abnormalities is central to our understanding of the progressive nature of alpha-synucleinopathies. Owing to the early involvement and specific physiological pattern, identification of RBD and probably RSWA is crucial for the development and identification of biomarkers and potential development of disease-modifying medication and interventions.

A number of other symptoms and methods have been identified in RBD/PD, including imaging techniques, testing for olfactory and autonomic abnormalities, molecular techniques, and other sleep measures. It is likely that combinations of such approaches may enable patients to be stratified into specific risk associations that are of use in risk management.

One of the major challenges in defining those at risk is the potential relation between RBD (as defined by video-confirmed evaluation of REM sleep-associated behavior and the presence of simultaneous RSWA) and minor episodes of muscle activity and RSWA. Recently, it was suggested that these minor episodes be identified as REM behavior events.123 Questionnaires’ information may show up intra- and inter-individual variations.124 Current prospective studies and most of the comorbidity studies rely on the classic definition of video-confirmed RBD. The extent to which dream content influences the diagnostic value of RBD is not known, but it may reflect the extent of pathology in the brainstem. Recent studies of day-to-day variation suggest that not only sleep patterns but also motor activity varies between the recorded days. NREM motor phenomena in patients with RBD are not taken into consideration,125 and in many patients with advanced neurodegenerative diseases, the EEG shows major abnormalities, with slowing, pathological microevents (eg, K-complexes, sleep spindles). As a consequence, sleep scoring is often difficult and subject to significant interscorer variability.126

PD, DLB, and MSA are complex neurodegenerative disorders, and their progress, severity, and symptom profile vary greatly between patients. It is not fully established whether iRBD is a precursor of only one PD subgroup. In analyzing iRBD patients with the aim of identifying those at the highest risk of developing PD, it might be unrealistic to expect that a single biomarker will be sufficient. By combining multiple biomarkers, the sensitivity of identifying a person with preclinical PD will increase, due to the fact that more aspects of this complex disease will be revealed. Optimally, a combination of biomarkers expressing alterations in different areas or mechanisms of the brain would indicate the stage of the disease and the pace and direction in which it is progressing. This would not only help identify the patients at the highest risk of developing PD, and thereby possibly facilitate PD treatment before PD diagnosis, but also provide insight into treatment efficiency and thereby help personalized treatment.

We believe that several additional research questions need to be addressed in order to understand brainstem involvement and the associated physiological, imaging, and molecular findings. This is fundamental to our understanding of how to identify high-risk individuals and to the development of risk-reducing agents, including protective medication, for these devastating diseases.