Their occurrence in an independent narcolepsy mouse model, the orexin/ataxin 3 transgenic mouse, undergoing loss of orexin neurons, was confirmed. Although not exclusive to overt cataplexy, cataplexy-associated state and hypersynchronous paroxysmal theta activities are highly enriched during cataplexy in hypocretin/orexin knockout mice. Altogether, these data contradict the hypothesis that cataplexy is a state similar to paradoxical sleep, even if long cataplexies may evolve into paradoxical sleep. In contrast to cataplexy onset, exit from cataplexy did not show a predictable sequence of activities. Cataplexy almost invariably started with a brief phase of wake-like electroencephalogram, followed by a phase featuring high-amplitude irregular theta oscillations, defining an activity profile distinct from paradoxical sleep, referred to as cataplexy-associated state and in the course of which 1.5-2 s high-amplitude, highly regular, hypersynchronous paroxysmal theta bursts (∼7 Hz) occurred. A knockout-specific state and a stereotypical paroxysmal event were introduced to account for signals and electroencephalogram spectral characteristics not seen in wild-type littermates. Using a novel video/electroencephalogram double-blind scoring method, we show that cataplexy is not a state per se, as believed previously, but a dynamic, multi-phased process involving a reproducible progression of states. Here we reassess cataplexy in hypocretin (Hcrt, also known as orexin) gene knockout mice. The neural mechanisms underlying cataplexy are unknown, but commonly thought to involve those of rapid eye movement-sleep atonia, and cataplexy typically is considered as a rapid eye movement sleep disorder. Narcolepsy with cataplexy is characterized by irresistible bouts of sleep during the day, sleep fragmentation during the night and episodes of cataplexy, a sudden loss of muscle tone while awake and experiencing emotions. This control is profoundly impaired in narcolepsy with cataplexy, a disease resulting from the loss of orexin/hypocretin neurotransmitter signalling in the brain. In mammals and birds, electroencephalographic recordings reveal alternating states of wakefulness, slow wave sleep and paradoxical sleep (or rapid eye movement sleep). Six episodes out of 11 were associated with bradycardia, that was maximal during the atonic phase.Īnalysis of the muscular phenomena that characterize cataplectic attacks in a standing patient suggests that the cataplectic fall occurs with a pattern that might result from the interaction between neuronal networks mediating muscular atonia of REM sleep and neural structures subserving postural control.Īstute control of brain activity states is critical for adaptive behaviours and survival. We identified, based on the video-polygraphic analysis of the episodes, 3 phases: initial phase, characterized essentially by arrest of eye movements and phasic, massive, inhibitory muscular events falling phase, characterized by a rhythmic pattern of suppressions and enhancements of muscular activity, leading to the fall atonic phase, characterized by complete muscle atonia. Polygraphic recordings monitored EEG, EMG activity from several cranial, trunk, upper and lower limbs muscles, eye movements, EKG, thoracic respiration.Įleven attacks were recorded, all of them lasting less than 1 min and ending with the fall of the patient to the ground. To perform a video-polygraphic analysis of 11 cataplectic attacks in a 39-year-old narcoleptic patient, correlating clinical manifestations with polygraphic findings.
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