Psychomotor Vigilance Impairment During Total Sleep Deprivation Is Exacerbated in Sleep-Onset Insomnia
Received 25 July 2019
Accepted for publication 18 November 2019
Published 11 December 2019 Volume 2019:11 Pages 401—410
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Sutapa Mukherjee
Devon A Hansen,1,2 Matthew E Layton,1–3 Samantha M Riedy,1,2 Hans PA Van Dongen1,2
1Sleep and Performance Research Center, Washington State University, Spokane, WA, USA; 2Department of Medical Education and Clinical Sciences, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA, USA; 3Program of Excellence in Addictions Research, College of Nursing, Washington State University, Spokane, WA, USA
Correspondence: Devon A Hansen
Sleep and Performance Research Center, Washington State University Spokane, 412 E. Spokane Falls Blvd., Spokane, WA 99202, USA
Purpose: Individuals with primary insomnia frequently report cognitive impairment as a next-day consequence of disrupted sleep. Studies attempting to quantify daytime impairment objectively in individuals with insomnia have yielded mixed results, with evidence suggesting impairments in aspects of executive functioning but not psychomotor vigilance. It has been suggested that persons with insomnia may have latent performance deficits for which they would be able to compensate effectively under normal daytime circumstances – suggesting that any such deficits may be exposed through perturbation. In this context, we used a laboratory-based total sleep deprivation (TSD) paradigm to investigate psychomotor vigilance performance in individuals with chronic sleep-onset insomnia as compared to healthy normal controls.
Participants and methods: Fourteen participants, seven individuals with chronic sleep-onset insomnia (ages 24–40y) and seven age-matched, healthy normal sleepers completed a highly controlled in-laboratory study involving 38 h of TSD. A 10 min and a 3 min version of the psychomotor vigilance test (PVT) were administered every 3 h during TSD.
Results: In both the individuals with sleep-onset insomnia and the age-matched normal sleepers, lapses of attention and false starts on the PVT were relatively infrequent during the first 16 h of the TSD period, but increased significantly when wakefulness was extended beyond 16 h. However, the effects of TSD on PVT performance were considerably exacerbated in the sleep-onset insomnia group, which showed about twice as many lapses of attention, more than twice as many false starts, and approximately twice as big a time-on-task effect on the 10 min PVT as the age-matched normal sleepers group, with similar findings on the 3 min PVT.
Conclusion: These findings indicate that daytime impairment reported by individuals with sleep-onset insomnia has an objective performance component that is exposed during TSD. Thus, persons with sleep-onset insomnia could be at increased risk of performance impairment in settings that involve extended wakefulness. This underscores the importance of treating insomnia and suggests that laboratory sleep deprivation studies could serve to document the effectiveness of treatment approaches.
Keywords: bedtime-specific hyperarousal, chronic insomnia, cognitive performance, extended wakefulness, primary insomnia, vulnerability to sleep loss
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