Abstract
The symptomatic treatment of REM sleep behaviour disorder (RBD) is very important to prevent sleep-related falls and/or injuries. Though clonazepam and melatonin are usually considered the first-line symptomatic therapy for RBD, their efficiency has not been proven by randomized clinical trials. The role of dopamine agonists in improving RBD symptoms is controversial, and rivastigmine, memantine, 5-hydroxytryptophan, and the herbal medicine yokukansan have shown some degree of efficacy in short- and medium-term randomized clinical trials involving a low number of patients. The development of potential preventive therapies against the phenoconversion of isolated RBD to synucleinopathies should be another important aim of RBD therapy. The design of long-term, multicentre, randomized, placebo-controlled clinical trials involving a large number of patients diagnosed with isolated RBD with polysomnographic confirmation, directed towards both symptomatic and preventive therapy for RBD, is warranted.
Highlights
The first reports of the disorder designated as “rapid eye movement (REM) sleep behaviour disorder” (RBD) were by Schenk et al [1,2] in 1986
The long-term follow-up of patients initially classified as iRBD has shown the development of neurodegenerative diseases, mainly synucleinopathies such as Lewy body dementia (LBD), Parkinson’s disease (PD), or multisystem atrophy (MSA) [9]
While three open-label studies [51,52,54] and a retrospective cohort involving 81 patients with iRBD [55] showed a beneficial effect of pramipexole in 60–80% of patients diagnosed with iRBD, another open-label study showed a lack of improvement of REM sleep behaviour disorder (RBD) symptoms in 11 patients with PD and concomitant RBD treated with low doses of this drug as add-on therapy to levodopa [53]
Summary
The first reports of the disorder designated as “rapid eye movement (REM) sleep behaviour disorder” (RBD) were by Schenk et al [1,2] in 1986. Polysomnography (PSG), which is considered to be necessary for the definitive diagnosis of RBD [3], is characterized by a loss of chin atonia in variable degrees, increased REM ocular activity, increased REM limb-twitch activity, and increased density and duration of stage 3–4 slow-wave sleep. According to their aetiology, RBD can be classified as “idiopathic” or “isolated” (iRBD; this diagnosis requires a lack of evidence of any diagnosed neurological disease) or secondary to narcolepsy, neurodegenerative diseases, drugs, or autoimmune disorders [4,5]. The aim of this narrative review is to provide a description of studies reported to date related to the treatment of this clinical entity
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