Abstract
Sir, We have read with great interest the article entitled 'Ictal SPECT in patients with rapid eye movement sleep behaviour disorder' published March 2015 by Mayer et al. (2015) in Brain. In this article, the authors evidence brain regions activated during an episode of rapid eye movement (REM) sleep behaviour disorder (RBD) using ictal single photon emission tomography (SPECT).Four patients were included in this study: one with idiopathic RBD, one with RBD and Parkinson's disease, and two with RBD and nar-colepsy. Ictal SPECT in an RBD episode as compared to wakefulness revealed RBD-related activations in the bilateral premotor areas, the interhemispheric cleft, the peria-queductal area, the dorsal and ventral pons and the anterior lobe of the cerebellum in all patients, thus bypassing the basal ganglia. The authors also claim this to be the first study to report results with ictal SPECT in patients with idiopathic RBD, or associated with Parkinson's disease or narcolepsy.We here dispute this claim. Indeed, in 2011 we published the first SPECT recording during a well-documented and controlled RBD episode associated with multiple system atrophy, in which we demonstrated a selectively increased perfusion in the supplementary motor area (Dauvilliers et al., 2011). We used the same technique as Mayer et al. (2015), i.e. ictal SPECT immediately (14 s) after the onset of a long (2-min duration) and complex RBD episode in a 54-year-old right-handed man with a 3-year history of probable multiple system atrophy-cerebellar (predominance of cere-bellar ataxia) (Dauvilliers et al., 2011). Dream-enacting behaviours were particularly frequent and violent in this patient, and confirmed by video-polysomnography that documented profound REM sleep disturbances with only 8% of REM sleep with atonia. Additionally, and at variance with the study of Mayer et al., we scanned in similar conditions two healthy control subjects matched for age and gender in both normal REM sleep (i.e. without RBD) and during wakefulness. In these controls, we found no perfusion changes in the supplementary motor area in REM sleep as compared to wakefulness. However, a higher perfusion was found in the anterior cingulate cortex both in the RBD and normal REM sleep states, a finding mostly related to the decreased perfusion in this area during wakefulness time. No perfusion changes were found in the brainstem. To sum up, both our own and the recent Mayer et al. studies have underlined a neuralfinger-print (i.e. the activation of the cortical premotor supplementary area) associated with the generation of movements during an RBD episode, whether idiopathic or comorbid with Parkinson's disease, multiple system atrophy or narcolepsy (Dauvilliers et al., 2011; Mayer et al., 2015).