0160 Transcranial Direct Current Brain Stimulation During Sleep Deprivation Reduces Performance and Recovery

Abstract Introduction Previous research suggests that transcranial direct current stimulation (tDCS) applied to the prefrontal cortex (PFC) during sleep deprivation (SD) slows the rate of sleep loss-induced performance degradation. However, the effect of tDCS on recovery sleep and subsequent performance has not yet been assessed. The current study was conducted to determine whether, and the extent to which, PFC tDCS enhances performance during sleep loss and recovery. Methods Seventeen healthy adults completed a four-night study with a 2h sleep opportunity at 2300 followed by 46h SD and two 8h recovery sleep opportunities. Four 2mA stimulations were given for 10 min during the SD period (1.5, 2.75, 25.25, and 26.5 hr into SD) for the stim group (N=9). Participants receiving sham stimulation (N=8) experienced a ramp up and down at the beginning and end of the stimulation period. A 10-min PVT was administered every ~75 min, and all sleep periods were investigated using a 13-lead PSG. PVT minor lapses ( 500 ms) and speed change from baseline were analyzed using a 4 (Experimental Day) x 2 (Group) Generalized Linear Model. N3 sleep duration was analyzed for the two recovery nights in a 2 x 2 model. Results Participants in the stimulation group experienced more minor lapses main effect of Group, W(1) = 21.56, p 0.001 and slower speeds main effect of Group, W(1) = 12.65, p 0.001 than the sham group across all experimental days (SD and recovery). Additionally, participants in the stimulation group had more N3 sleep during recovery compared to sham main effect of Group, W(1) = 11.89, p 0.001. Conclusion Contrary to previous findings, PFC tDCS applied during sleep loss did not result in a reduced rate of performance degradation. In fact, it resulted in worse performance throughout both the sleep loss and recovery periods and increased N3 duration during recovery sleep compared to the sham group. These findings may be attributed to the induction of a further increase in the cortical excitatory/inhibitory ratio, already elevated in SD, leading to greater impairment in information processing and accelerating the accrual of homeostatic sleep drive. Support (if any) Military Operational Medicine Research Program/Defense Health Agency