Morvan’s syndrome and the sustained absence of all sleep rhythms for months or years: An hypothesisReport as inadecuate




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* Corresponding author 1 LNIA - Laboratoire de Neurosciences intégratives et adaptatives

Abstract : Despite the predation costs, sleep is ubiquitous in the animal realm. Humans spend a third of their life sleeping, and the quality of sleep has been related to co-morbidity, Alzheimer disease, etc. Excessive wakefulness induces rapid changes in cognitive performances, and it is claimed that one could die of sleep deprivation as quickly as by absence of water. In this context, the fact that a few people are able to go without sleep for months, even years, without displaying any cognitive troubles requires explana- tions. Theories ascribing sleep to memory consolidation are unable to explain such observations. It is not the case of the theory of sleep as the hebbian reinforcement of the inhibitory synapses ToS-HRIS. Hebbian learning Long Term Depression – LTD guarantees that an efficient inhibitory synapse will lose its efficiency just because it is efficient at avoiding the activation of the post-synaptic neuron. This erosion of the inhibition is replenished by hebbian learning Long Term Potentiation – LTP when pre and post- synaptic neurons are active together – which is exactly what happens with the travelling depolarization waves of the slow-wave sleep SWS. The best documented cases of months-long insomnia are reports of patients with Morvan’s syndrome. This syndrome has an autoimmune cause that impedes – among many things – the potassium channels of the post-synaptic neurons, increasing LTP and decreasing LTD. We hypothesize that the absence of inhibitory efficiency erosion during wakefulness thanks to a decrease of inhibitory LTD is the cause for an absence of slow-wave sleep SWS, which results also in the absence of REM sleep.





Author: Claude Touzet -

Source: https://hal.archives-ouvertes.fr/



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