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Effects of Sleep Deprivation on Phase Synchronization as Assessed by Wavelet Phase Coherence Analysis of Prefrontal Tissue Oxyhemoglobin Signals
PURPOSE: To reveal the physiological mechanism of the decline in cognitive function after sleep deprivation, a within-subject study was performed to assess sleep deprivation effects on phase synchronization, as revealed by wavelet phase coherence (WPCO) analysis of prefrontal tissue oxyhemoglobin si...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207699/ https://www.ncbi.nlm.nih.gov/pubmed/28046043 http://dx.doi.org/10.1371/journal.pone.0169279 |
Sumario: | PURPOSE: To reveal the physiological mechanism of the decline in cognitive function after sleep deprivation, a within-subject study was performed to assess sleep deprivation effects on phase synchronization, as revealed by wavelet phase coherence (WPCO) analysis of prefrontal tissue oxyhemoglobin signals. MATERIALS AND METHODS: Twenty subjects (10 male and 10 female, 25.5 ± 3.5 years old) were recruited to participate in two tests: one without sleep deprivation (group A) and the other with 24 h of sleep deprivation (group B). Before the test, each subject underwent a subjective evaluation using visual analog scales. A cognitive task was performed by judging three random numbers. Continuous recordings of the near-infrared spectroscopy (NIRS) signals were obtained from both the left and right prefrontal lobes during rest, task, and post-task periods. The WPCO of cerebral Delta [HbO(2)] signals were analyzed for these three periods for both groups A and B. RESULTS: Six frequency intervals were defined: I: 0.6–2 Hz (cardiac activity), II: 0.145–0.6 Hz (respiratory activity), III: 0.052–0.145 Hz (myogenic activity), IV: 0.021–0.052 Hz (neurogenic activity), V: 0.0095–0.021 Hz (nitric oxide related endothelial activity) and VI: 0.005–0.0095 Hz (non-nitric oxide related endothelial activity). WPCO in intervals III (F = 5.955, p = 0.02) and V (F = 4.7, p = 0.037) was significantly lower in group B than in group A at rest. During the task period, WPCO in intervals III (F = 5.175, p = 0.029) and IV (F = 4.585, p = 0.039) was significantly lower in group B compared with group A. In the post-task recovery period, the WPCO in interval III (F = 6.125, p = 0.02) was significantly lower in group B compared with group A. Reaction time was significantly prolonged, and the accuracy rate and F(1) score both declined after sleep deprivation. CONCLUSIONS: The decline in WPCO after sleep deprivation indicates reduced phase synchronization between left and right prefrontal oxyhemoglobin oscillations, which may contribute to the diminished cognitive function. |
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