Objectives. Both results of the odor identification and cardiac 123I-metaiodobenzylguanidine accumulation have been investigated for their potential to enhance the detection of pathogenesis resembling that of Lewy body-related α-synucleinopathies in patients clinically diagnosed as having idiopathic REM sleep behavior disorder. Methods. We performed both the Odor Stick Identification Test for Japanese and 123I-metaiodobenzylguanidine scintigraphy in 30 patients with idiopathic REM sleep behavior disorder, 38 patients with Parkinson's disease, and 20 control subjects. Results. In idiopathic REM sleep behavior disorder, reduced odor identification score and an early or delayed heart to mediastinum ratio on 123I-metaiodobenzylguanidine were almost as severe as in Parkinson's disease patients. Delayed cardiac 123I-metaiodobenzylguanidine uptake was even more severe in the idiopathic REM sleep behavior disorder group than in the Parkinson's disease group. Conclusions. Reduced cardiac 123I-metaiodobenzylguanidine uptake, which is independent of parkinsonism, may be more closely associated with idiopathic REM sleep behavior disorder than olfactory impairment. 1. Introduction REM sleep behavior disorder (RBD) is characterized by dream-enacting behaviors and unpleasant dreams and presents a risk for self-injury and harm to others due to abnormal REM sleep during which control of muscle tonus is lacking (REM sleep without atonia) [1, 2]. RBD is a heterogeneous disease entity consisting of a variety of manifestations [1]. Idiopathic RBD (iRBD), which develops in middle age or later and progresses chronically, in particular is a common clinical manifestation of Lewy body-related syndrome and is regarded as a clinical entity from the pathological aspect. For example, it has been elucidated that iRBD is often accompanied by soft motor signs, olfactory and color identification deficits, decreased cardiovascular and respiratory changes between REM and NREM sleep, reduced cardiac 123I-metaiodobenzylguanidine (123I-MIBG) uptake, impairment of visual memory and visuospatial construction on neuropsychological testing, EEG slowing during wakefulness or sleep, and decreased strial dopaminergic innervations, and reduced presynaptic strial dopamine transporter binding on SPECT or positron emission topography (PET) scans, which are considered as nonmotor symptoms of Parkinson’s disease (PD) [3–5]. Furthermore, despite the limited number of pathological reports on iRBD, the characteristics of iRBD have been supported to have a close relationship with Lewy body pathology [6].
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