Abstract
Sleep apnea–hypopnea syndrome is a common breathing disorder that can lead to organic brain injury, prevent memory consolidation, and cause other adverse mental-related complications. Brain activity while sleeping during respiratory events is related to these dysfunctions. In this study, we analyzed variations in electroencephalography (EEG) signals before, during, and after such events. Absolute and relative powers, as well as symbolic transfer entropy (STE) of scalp EEG signals, were calculated to unveil the activity of brain regions and information interactions between them, respectively. During the respiratory events, only low-frequency power increased during rapid eye movement (REM) stage (δ-band absolute and relative power) and N1 (δ- and θ-band absolute power, δ-band relative power) sleep. But absolute power increased in low- and medium-frequency bands (δ, θ, α, and σ bands), and relative power increased mainly in the medium-frequency band (α and σ bands) during stage N2 sleep. After the respiratory events, absolute power increased in all frequency bands and sleep stages, but relative power increased in medium and high frequencies. Regarding information interactions, the β-band STE decreased during and after events. In the γ band, the intrahemispheric STE increased during events and decreased afterward. Moreover, the interhemisphere STE increased after events during REM and stage N1 sleep. The EEG changes throughout respiratory events are supporting evidence for previous EEG knowledge of the impact of sleep apnea on the brain. These findings may provide insights into the influence of the sleep apnea–hypopnea syndrome on cognitive function and neuropsychiatric defects.
Highlights
Sleep apnea–hypopnea syndrome (SAHS) is a breathing disorder characterized by partial or complete closure of the upper airways during sleep (Torabi-Nami et al, 2015; Liu et al, 2018)
Sleep EEG Response to Respiratory Events imaging study revealed that the gray matter volume of patients with obstructive sleep apnea (OSA) increased in the insula, primary motor cortices, brainstem, left premotor cortex, cerebellum, and left hippocampus, whereas it decreased in the prefrontal cortex, right posterior cingulate cortex, occipital lobe, amygdala, and left cerebellar cortex (Fatouleh et al, 2014)
We found that the EEG spectral power during apnea–hypopnea is related to secondary respiratory events (Huang et al, 2018) and end-apneic cortical arousal (Yan et al, 2016), and sleep stages influence cortical responses
Summary
Sleep apnea–hypopnea syndrome (SAHS) is a breathing disorder characterized by partial or complete closure of the upper airways during sleep (Torabi-Nami et al, 2015; Liu et al, 2018). In addition to suffering from fatigue, fragmented sleep, and cardiovascular diseases, extensive evidence shows that major brain changes occur in SAHS patients. Recurrent hypoxia, and cortical arousal induced by apnea events have been associated with these EEG variations (Carvalho et al, 2014; Fatouleh et al, 2014; Chen et al, 2015; Sun et al, 2018) and may interrupt the removal of metabolic waste products from the brain by cerebrospinal fluid, which affects cognitive function (Fultz et al, 2019). The study of brain activity during apnea can provide insights on brain dysfunction due to SAHS and related complications
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