REMSleep Behavior Disorder in Parkinson's Disease and Other Synucleinopathies

Abstract

Rapid eye movement sleep behavior disorder is characterized by dream enactment and complex motor behaviors during rapid eye movement sleep and rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia) during polysomnography. Rapid eye movement sleep behavior disorder may be idiopathic or symptomatic and in both settings is highly associated with synucleinopathy neurodegeneration, especially Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. Rapid eye movement sleep behavior disorder frequently manifests years to decades prior to overt motor, cognitive, or autonomic impairments as the presenting manifestation of synucleinopathy, along with other subtler prodromal "soft" signs of hyposmia, constipation, and orthostatic hypotension. Between 35% and 91.9% of patients initially diagnosed with idiopathic rapid eye movement sleep behavior disorder at a sleep center later develop a defined neurodegenerative disease. Less is known about the long-term prognosis of community-dwelling younger patients, especially women, and rapid eye movement sleep behavior disorder associated with antidepressant medications. Patients with rapid eye movement sleep behavior disorder are frequently prone to sleep-related injuries and should be treated to prevent injury with either melatonin 3-12 mg or clonazepam 0.5-2.0 mg to limit injury potential. Further evidence-based studies about rapid eye movement sleep behavior disorder are greatly needed, both to enable accurate prognostic prediction of end synucleinopathy phenotypes for individual patients and to support the application of symptomatic and neuroprotective therapies. Rapid eye movement sleep behavior disorder as a prodromal synucleinopathy represents a defined time point at which neuroprotective therapies could potentially be applied for the prevention of Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. © 2017 International Parkinson and Movement Disorder Society.

Neuroscience: A Distributed Neural Network Controls REM Sleep

“…But, the most alarming aspect of RBD is that the majority of patients develop a neurodegenerative disease within 6–15 years of initial RBD diagnosis [129]. RBD is currently the strongest known predictor of a class of neurodegenerative disorders known as synucleinopathies with 80–90% of patients developing Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy [130–132]. …”

“…Because 80% of RBD patients ultimately develop a synucleinopathy, it seems reasonable to assume that RBD is the earliest symptom in these disorders, that is, RBD is itself a synucleinopathy [132]. But, why does neurodegeneration affect REM sleep circuitry years before the onset of synpucleinopathies such as Parkinson's disease?…”

Evidence-Based Review of Therapeutic Approaches in Dementia with Lewy Bodies

“…The hallmark of the diagnosis of REM sleep behavior disorder is the absence of atonia during REM sleep and "dream enactment" [35][36][37][38][39][40]. Reliable history has to be obtained from caregivers in order to give such diagnosis because not all patients are aware of themselves having this disorder.…”

“…3-12 mg Melatonin dosing is effective in enhancing the physiologic REM sleep phase. It decreases periods without atonia during REM sleep [36,42]. Clonazepam is also a first-line therapy for RBD [42].…”

“…It decreases periods without atonia during REM sleep [36,42]. Clonazepam is also a first-line therapy for RBD [42]. It seems to alter dream content and consequently ameliorate the vigorous verbal and physical activity [37,42].…”