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Published on: December 18, 2016
Potential marker of brain impairment secondary to obstructive sleep apnea: The brain asymmetry
Jianhong Liao1, Yunhan Shi1, Xiaotian Zhu2
1Obstructive Sleep Apnea-Hypopnea Syndrome Clinical Diagnosis and Therapy and Research Centre, Beijing Tongren Hospital, Capital Medical University, Beijing, China; Key Laboratory of Otorhinolaryngology Head and Neck Surgery (Capital Medical University), Ministry of Education, Beijing, China.
Background:
Obstructive sleep apnea (OSA) is one of the leading causes of sleep disorders and often exhibits psychological impairments. Brain asymmetry (BA), a recognized marker of psychological traits, has been found to be significantly elevated in OSA and associated with anxiety and personality traits. However, evidence for a causal relationship between BA and respiratory events remains lacking.
Methods:
Patients undergoing polysomnography at the Sleep Medicine Center were enrolled in this study. Subsequently, sleep apnea or hypopnea with a duration of >15 s and intervals of >20 s were extracted and analyzed for BA changes during peri-respiratory events periods. Differences in power spectrum density in bilateral EEG activity were calculated for the frontal, central, and occipital regions.
Results:
A total of 71 subjects were included in the study and 6445 respiratory events were extracted. We obtained 1265 respiratory events in N1, 3655 in N2, 62 in N3, and 1463 in REM. In frontal, BA was elevated during the event and recovered at the end of the event (P< 0.0001), with a uniform pattern across bands. In central, respiratory events similarly induced BA (P< 0.0001). In the occipital region, a decrease in BA was observed during respiratory events and a sudden rise at the end of the event (P<0.001). Non-severe and severe OSA exhibit similar trends. In addition, subgroup analyses indicated alpha, beta and gamma as the main contributors to BA fluctuations.
Conclusions:
Our findings suggest respiratory events trigger BA across brain regions. These findings, combined with previous studies, suggest BA may be a marker and characteristic phenotype of neurological dysfunction in OSA.
