Original ArticleNeurobehavioral and autonomic alterations in adults with obstructive sleep apnea

•Frontal cognitive decline and sympathetic hyperactivity occur in OSA patients.•Cognitive and sympathetic dysfunctions were related to oxygen desaturation.•Frontal cognitive decline and sympathetic hyperactivity were not associated.•Cognitive decline and sympathetic dysfunction occur independently from each other.

ObjectiveObstructive sleep apnea (OSA) is associated with sympathetic hyperactivity, excessive nocturnal sweating, sleepiness, and neurobehavioral cognitive alterations. However, it is not well known if cognitive consequences of OSA are independent from autonomic alterations. Thus, we assessed the association between polysomnographic, autonomic, and cognitive tests performance in OSA patients.MethodsFifty eight OSA patients (53 male) were administered with questionnaires assessing demographic, Epworth, Beck Depression Inventory, Syndrom Kurz test (SKT), Trail Making part B (TMT-B), and Frontal Assessment Battery (FAB) tests. Spectral analysis of heart rate variability (HRV) and night sweating symptoms (NSwS) score were used to assess autonomic function.ResultsGlobal cognitive function (SKT) was normal in mild-moderate (M-OSA) and severe (S-OSA) patients. In S-OSA patients AHI was correlated with TMT-B (r = 0.30 P < 0.05) and with FAB (r = −0.31 P < 0.05). Oxygen desaturation was correlated with TMT-B (r = −0.45 P = < 0.001) and FAB (r = 0.29 P = < 0.05). Sympathetic overactivity was correlated with oxygen desaturation: HRV (r = −0.39 P < 0.05) and NSwS score (r = −0.49 P < 0.01), but HRV and NSwS score were not correlated with TMT-B and FAB.ConclusionFrontal cognitive dysfunction and predominance of sympathetic drive occur in OSA patients. Abnormal frontal cognitive function and sympathetic hyperactivity were related to oxygen desaturation, but not between each other. We conclude that neurobehavioral changes and autonomic imbalance in OSA patients take place independently from each other, suggesting different pathophysiological pathways.