Le trouble comportemental en sommeil paradoxal (SP) correspond à des cauchemars agités la nuit chez des personnes d’âge moyen, et chez la moitié des Parkinsoniens, par perte de l’atonie normale en SP (probable lésion pontique). Au-delà du risque de blessure nocturne, ce trouble aide à comprendre le contrôle moteur et cognitif en SP. Ainsi, le syndrome parkinsonien disparaît transitoirement pendant ces comportements nocturnes, pour laisser place à des mouvements rapides mais saccadés, suggérant que le message délétère des ganglions de la base est amoindri ou court-circuité. L’observation de comportements appris, du répertoire gestuel des métiers et de phrases syntaxiquement correctes en SP suggère que ces comportements sont générés par les mêmes structures corticales qu’en éveil. Ce modèle nous permet d’observer que les mouvements rapides des yeux en SP sont codés dans la même direction que l’action des mains et des bras, comme si le dormeur « regardait » les paupières fermées ce qu’il faisait en rêve. Ainsi, l’accès immédiat au scénario moteur et verbal du rêve (vidéo/audio), aux données neurophysiologiques (polysomnographie), puis au contenu mental (récit du rêve) en différé, détaille une triangulation qui permet, en recherche, de valider plusieurs hypothèses sur le SP et les rêves.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by violent, or potentially violent, movements during REM sleep, corresponding to enacted dreams. During sleep monitoring, there is a partial or total loss of the normal muscle atonia during REM sleep. REM sleep behavior disorder predominantly affects elderly subjects without any other disease (idiopathic RBD, a precursor of Parkinson disease and Lewy body dementia) or suffering from various neurological and neurodegenerative diseases, mainly synucleinopathies. In addition to being a treatable cause of nocturnal injury of the patients or their bed-partners, RBD is a fantastic window into motor and cognitive control during REM sleep. Notably, parkinsonism transiently disappears during RBD. The patient’s voice is louder and better articulated than when awake, and movements are rapid (but jerky) suggesting that the deleterious message from the basal ganglia to the primary motor cortex is reduced or bypassed. As we observed culturally-acquired behaviors, retired patients practicing their former work with mastered gestures, as well as sentences pronounced with appropriate prosody, gesturing, fluency, and syntax during the RBD, we suggest that these behaviors are generated by the same cortical areas as during wakefulness. This model also enables the demonstration that REM during REM sleep are coded in the same direction as the arm and hand movements, as if the dreamer were scanning the dream images. This online access to the motor and verbal dream scenario (through the video and audio monitoring), and the physiological measures (via the EEG, eye movements, muscle tone, respiration, heart rate), together with the offline access to the mental content (dream report after the awakening) constitute a triangulation for validating new hypotheses about REM sleep and dreams.