Altered Sleep Mechanisms following Traumatic Brain Injury and Relation to Waking Function

Sleep difficulties are commonly reported following traumatic brain injury (TBI), but few studies have systematically examined the neurophysiological characteristics of sleep. Sleep EEG was quantified over multiple nights to examine mechanisms underlying sleep disruption in individuals who had sustained a TBI and to explore the relationship between sleep disruption and waking function. Sleep was recorded from 20 individuals with a TBI (18-64 years) and 20 age-matched controls over two uninterrupted nights, as well as during a night where auditory stimuli were delivered. All participants underwent neuropsychological testing and waking performance assessment. Compared to controls, the TBI group had subjective complaints of falling asleep, delayed sleep onset on polysomnography (PSG), less Slow Wave (< 1 Hz) and delta (1-4 Hz) EEG power in non-REM sleep, fewer spontaneous and evoked k-complexes, reduced periodicity of spontaneous k-complexes, and lower amplitude of evoked k-complexes. While for controls, the density, duration and periodicity of sleep spindles diminished with deepening of non-REM as typically observed, this pattern was disrupted in the TBI group with peak spindle presentation occurring in Stage 3 sleep. Night-to-night-stability of Stage 2 spindles was high for controls but absent for the TBI group. Greater injury severity was related to fewer evoked k-complexes and lower spindle density. Greater spindle production predicted better waking function in the TBI group. Taken together, these data demonstrate impairment in sleep regulatory and inhibitory mechanisms as factors underlying sleep complaints following a TBI. Spindle generation may be adaptive or a marker of resiliency following TBI.