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Abstract

Objectives: Sleep wake disturbances have often been described in patients after traumatic brain injury (TBI), but so far no adequate animal model has been developed to elucidate the cause of these symptoms, and to evaluate its functional significance in the context of the trauma. This study aimed at developing a closed diffuse TBI model in rats in order to examine posttraumatic sleep–wake behavior and its correlation to the histological outcome of sleep–wake regu- lating neuronal populations. Methods: For this purpose, 24 h electroencephalographic record- ings were obtained prior and at different time points after the injury in a novel model of rodent TBI. Results: The recording analysis showed an increased proportion of slow wave sleep in costs of wakefulness 28 days after the trauma. This hypersomnia-like effect in high severity TBI was linked to long term tissue damage evidenced by loss of histaminergic cells, a wake- promoting cell population. Conclusions: This study provides a new insight into the cause of hypersomnia after TBI and could serve as a rationale for the development of appropriate treatment methods.