Patients suffering from RBD enact their dreams and nightmares during periods of REM sleep devoid of the physiological muscle atonia. They show purposeful hand and arm movements which are sometimes violent and may lead to injuries of the patient or their bed companion. They talk, shout, fall out of bed, but only rarely do they walk like sleepwalkers do when emerging from slow wave sleep. Such RBD can be observed in all types of parkinsonism, whether they result from synucleinopathies (affecting one third of PD patients and almost all patients with Lewy body dementia or multisystemic atrophy), tauopathy, as in supranuclear palsy (Arnulf et al., 2005), or Parkin gene mutation (Kumru et al., 2004). In one quarter of the patients, this behavior disorder has heralded other symptoms of PD by 5 to 10 years. The lesion responsible for RBD is unknown, but lesions of the locus subcoeruleus in the pontine teg-mentum led to typical RBD (initially named ''oneiric behavior'') in animal models of RBD and was observed in single human RBD cases (Arnulf et al., 2000b). In addition, PD patients with RBD have slower EEG rhythms when awake, suggesting they have concomitant cortical, thalamic or brainstem lesions (Gagnon et al., 2004). Finally, an intriguing aspect of patients during RBD is their clinically normal motor behavior and speech, together with the almost total absence of tremor and dystonia. This suggests a transient functional normalization of the basal ganglia motor loop during REM sleep. Understanding how this ''sleep benefit'' occurs during REM sleep could help to find new treatments in Parkinson's disease.
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