Brain injury · 2014
Diffuse brain injury does not affect chronic sleep patterns in the mouse.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Rowe Rachel K, Harrison Jordan L, O'Hara Bruce F, Lifshitz Jonathan
Аннотация
PRIMARY OBJECTIVE: To test if the current model of diffuse brain injury produces chronic sleep disturbances similar to those reported by TBI patients.
METHODS AND PROCEDURES: Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 7; 1.4 atm; 6-10 minutes righting reflex time) or sham injury (n = 5). Sleep-wake activity was measured post-injury using a non-invasive, piezoelectric cage system. Chronic sleep patterns were analysed weekly for increases or decreases in percentage sleep (hypersomnia or insomnia) and changes in bout length (fragmentation).
MAIN OUTCOMES AND RESULTS: During the first week after diffuse TBI, brain-injured mice exhibited increased mean percentage sleep and mean bout length compared to sham-injured mice. Further analysis indicated the increase in mean percentage sleep occurred during the dark cycle. Injury-induced changes in sleep, however, did not extend beyond the first week post-injury and were not present in weeks 2-5 post-injury.
CONCLUSIONS: Previously, it has been shown that the midline fluid percussion model used in this study immediately increased post-traumatic sleep. The current study extended the timeline of investigation to show that sleep disturbances extended into the first week post-injury, but did not develop into chronic sleep disturbances. However, the clinical prevalence of TBI-related sleep-wake disturbances warrants further experimental investigation.
METHODS AND PROCEDURES: Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 7; 1.4 atm; 6-10 minutes righting reflex time) or sham injury (n = 5). Sleep-wake activity was measured post-injury using a non-invasive, piezoelectric cage system. Chronic sleep patterns were analysed weekly for increases or decreases in percentage sleep (hypersomnia or insomnia) and changes in bout length (fragmentation).
MAIN OUTCOMES AND RESULTS: During the first week after diffuse TBI, brain-injured mice exhibited increased mean percentage sleep and mean bout length compared to sham-injured mice. Further analysis indicated the increase in mean percentage sleep occurred during the dark cycle. Injury-induced changes in sleep, however, did not extend beyond the first week post-injury and were not present in weeks 2-5 post-injury.
CONCLUSIONS: Previously, it has been shown that the midline fluid percussion model used in this study immediately increased post-traumatic sleep. The current study extended the timeline of investigation to show that sleep disturbances extended into the first week post-injury, but did not develop into chronic sleep disturbances. However, the clinical prevalence of TBI-related sleep-wake disturbances warrants further experimental investigation.