**3. Primary rapid eye movement sleep behavior disorder (synucleinopathies)**

Once diagnosed, RBD can be classified as primary (idiopathic) or secondary. *Idiopathic RBD* can be considered an early symptom of alpha synucleinopathies which include: Parkinson's disease, Lewy Body Dementia and Multiple System Atrophy. The diagnosis of RBD can be made years before any other neurologic symptoms are identified. In 80% of cases RBD preceded the diagnosis of neurodegenerative disease (more easily recognized motor features), by a mean of 14 years [11]. There is evidence to suggest that patients with RBD and mild cognitive impairment will develop dementia in an interval of 5 years or less [9]. Other subtle potentially predictive biomarkers of RBD (see **Table 4**) include: olfactory loss/anosmia, autonomic dysfunction (ranging from sexual dysfunction to cardiovascular symptoms), color vision deficit, cognitive impairment, excessive daytime sleepiness, psychiatric disorders (such as anxiety, depression, psychosis, impulse control disorders), personality changes, dopamine dysfunction, and excessive EMG activity [11]. The pathophysiology and temporal relation between these symptoms and motor symptom onset is highly variable. Subsequent neurological examination may show subtle signs of Parkinsonism such as mild bradykinesia, while neurocognitive testing can show evidence of memory and executive dysfunction. Neuroimaging is useful if dopamine transporter scan shows evidence of decreased dopamine uptake in the putamen. Electroencephalogram can show cortical slowing as well [9]. Biopsy of the colon and submandibular gland in patients with idiopathic RBD has shown evidence of phosphorylated alpha synuclein deposits.

**81**

*REM-Behavior Disorder*

**5. Treatment**

*DOI: http://dx.doi.org/10.5772/intechopen.86277*

beta blockers have also been identified as culprits.

**(non-synucleinopathy)**

time injuries associated with RBD.

reported by bed partners.

**6. Ethical considerations**

patients' quality of life.

**4. Secondary rapid eye movement sleep behavior disorder** 

Other causes of RBD include neurologic disorders stemming from structural lesions such as pontine stroke or multiple sclerosis plaques. This can also rarely occur in the setting of progressive supranuclear palsy, Alzheimer's disease, and Huntington disease among others. RBD can coexist with narcolepsy in 50% of patients. Medications that can precipitate RBD include antidepressants such as selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), tricyclics, and monoamine oxidase inhibitors (MAOi). Some

Symptomatic management of RBD should be approached from multiple angles. First, maintaining a safe sleep environment for the patient by removing objects that can inflict harm or lowering the bed closer to the floor. Bed partners may also opt for sleeping in separate bed for their own safety. Co-sleeping is an important part of intimacy, however, and this can continue by advising the patient to sleep in a sleeping bag on top of the bed shared with their loved one. Bed alarms to warn loved ones about the patient exiting the bed can also be helpful in reducing night

Medical management with melatonin or low dose benzodiazepines such as clonazepam has been shown to reduce the dream enacting behaviors.

Benzodiazepines are thought to work by suppressing REM sleep. Theoretically, other REM suppressant medications (including SSRIs, TCAs, selective SNRIs) may also help, given their mechanism of action. However there are no trials supporting or refuting their efficacy and some may precipitate RBD as previously mentioned. These medications do, however, have lower tolerance and abuse potential than benzodiazepines. These treatments do not modify the risk of progression to PD, MSA, or LBD. Dopaminergic agents have not been shown to reduce dream enactment behaviors but may help comorbid periodic limb movements if present. In RBD cases refractory to conventional treatment, cholinesterase inhibitors such as rivastigmine (studied in one trial) and donepezil (several cases) have been noted to reduce the number of dream enactment episodes as

As stated previously, development of RBD can herald a diagnosis of potentially disabling neurological disorders by over a decade. While not every patient with primary RBD will go on to develop one of these conditions, we believe that patients should be informed of the association between RBD and the alpha synucleinopathies and therefore their risk of developing one of these disorders. The discussion should be geared towards ensuring periodic follow up and reducing anxiety by answering any questions the patient may have on the subject. Serial neurologic exams, either comprehensive or focused on Parkinsonian features like tremor, rigidity, and bradykinesia should be performed. This can ensure early, effective treatment of motor and other non-motor symptoms that can positively impact

Anosmia Autonomic dysfunction Color vision deficit Cognitive impairment Excessive daytime sleepiness Psychiatric disorders Personality changes Dopamine dysfunction Excessive EMG activity

**Table 4.** *Potential biomarkers of RBD.*
