Rapid Eye Movement Sleep Behavior Disorder: What Is Known and What Should Be Studied

Abstract

Rapid eye movement sleep behavior disorder (RBD), characterized by vivid striking dreams and dream-enacting behaviors, can be classified as both young and old. RBD is young in that it was conceptualized as a distinct clinical disorder by Schenck et al. [1] in 1986, and it is old because it mainly affects older people. In Korea, an RBD case, confirmed by polysom-nography, was reported in 1994. REM sleep without atonia (RWA) on the polysomnography is requisite for RBD diagnosis. Currently, qualitative analysis of RWA is used as RWA quantification is burdensome and time-consuming. Notably, patients complaining of vigorous dreams and violent behaviors are occasionally diagnosed with obstructive sleep apnea or show no definite RWA, which may negate diagnosis based on clinical history or RBD questionnaires. Regarding pathophysiology, dopaminergic degeneration was investigated because of its close relationship with alpha-synucleinopathies. Studies using dopamine transporter (DAT) positron emission tomography (PET) or single photon emission computed tomography (SPECT) showed that dopamine (DA) dysfunction might be implicated in RBD. However, several findings suggest that other pathogenic processes can be involved; 1) in managing RBD symptoms, effectiveness of clonazepam with no influence on DA and little effect of dopaminergic drugs, 2) appearance of RBD in narcoleptic patients, 3) young RBD patients without progression to alpha-synucleinopathies, and 4) RBD symptoms induced by anti-depressants.