Abstract

Sleep deprivation (SD) is a common condition and an important health concern. In addition to metabolic and cardiovascular risks, SD associates with decreases in cognitive performance. Neurovascular coupling (NVC, "functional hyperemia") is a critical homeostatic mechanism, which maintains adequate blood supply to the brain during periods of intensive neuronal activity. To determine whether SD alters NVC responses and cognitive performance, cognitive and hemodynamic NVC assessments were conducted prior to and 24 h post-SD in healthy young male individuals (n = 10, 27 ± 3 years old). Cognition was evaluated with a battery of tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB). Hemodynamic components of NVC were measured by transcranial Doppler sonography (TCD) during cognitive stimulation, dynamic retinal vessel analysis (DVA) during flicker light stimulation, and functional near infrared spectroscopy (fNIRS) during finger tapping motor task. Cognitive assessments revealed impairments in reaction time and sustained attention after 24 h of SD. Functional NIRS analysis revealed that SD significantly altered hemodynamic responses in the prefrontal cortex and somatosensory cortex during a motor task. NVC-related vascular responses measured by DVA and TCD did not change significantly. Interestingly, TCD detected decreased task-associated cerebral blood flow (CBF) in the right middle cerebral artery in sleep deprived participants. Our results demonstrate that 24 h of SD lead to impairments in cognitive performance together with altered CBF and hemodynamic components of cortical NVC responses.

Highlights

  • Sleep deprivation (SD) is a common condition and an important health concern

  • No other cognitive domain examined by the Cambridge Neuropsychological Test Automated Battery (CANTAB) tests was affected by the short-term sleep deprivation applied in current study

  • N-back test found no significant difference in the percentage of correct responses (1-back: 98.33 [98.33 to 100]% pre-SD vs. 98.33 [96.67 to 100]% post-SD, p = 0.66; 2-back: 98.33 [95.83 to 100]% pre-SD vs. 96.67 [90.83 to 100]% post-SD p = 0.09), and reaction time was significantly different during the 1-back condition (502 ± 140 ms pre-SD vs. 542 ± 146 ms post-SD, p < 0.01), but not the 2-back condition (657 ± 184 ms pre-SD vs. 665 ± 201 ms post-SD, p = 0.83)

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Summary

Introduction

Sleep deprivation (SD) is a common condition and an important health concern. In addition to metabolic and cardiovascular risks, SD associates with decreases in cognitive performance. In addition to elevated risks of chronic somatic ­diseases[5], short sleep duration is strongly associated with decreases in cognitive p­ erformance[6], which may have a significant implication on work productivity and incidence of accidental injuries in a working class of adults. G. in the posterior or middle cerebral artery)[16,17], and its ability to sensitively detect changes in NVC in response to interventions has been recently d­ emonstrated[18] Both TCD and fNIRS are capable of measuring the hemodynamic components of NVC at different levels of the vasculature. This response, compared to responses recorded with TCD or fNIRS, is a form of NVC with fewer confounders, as the stimulus (flicker light) can be standardized, and the evoked activation of a neuronal population is more localized

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