Action-Monitoring Dysfunction in Obstructive Sleep Apnea - A Pilot Study

Abstract

Obstructive sleep apnea (OSA) is associated with a broad range of frontal lobe dysfunctions. However, no study has investigated action monitoring, a crucial domain of frontal cognitive functions, in patients with OSA. By using the modified Flanker task, we tested the hypothesis that patients with OSA have an impaired action monitoring function. We recruited 25 untreated patients with moderate–severe OSA and 12 control participants who were matched for age, sex, apolipoprotein E4, and education level. Every enrolled participant underwent a standard overnight laboratory-based polysomnography and completed a modified Flanker task. Compared with the controls, the patients with OSA presented a significantly lower correct response rate in all trials (78.9% vs 95.9%, P = .008), congruent trials (84.7% vs 98.3%, P = .016), and incongruent trials (77.4% vs 94.7%, P = .009). The post-error correction rate was significantly lower in the patients with OSA than in the controls (74.9% vs 93.8%, P = .005). Furthermore, strong significant correlations were observed between the arousal index and correct rate in all trials (r = −0.390, P < .05) and in the incongruent trials (r = −0.429, P < .01), as well as between the arousal index and rate of post-error correction (r = −0.435, P < .01). We concluded that the action monitoring function was impaired in the patients with OSA. Sleep fragmentation was a major determinant of impaired action monitoring in these patients.

Compensatory Neural Recruitment for Error-Related Cerebral Activity in Patients with Moderate-To-Severe Obstructive Sleep Apnea

“…Action-monitoring behaviors are mediated by the anterior cingulate cortex (ACC) in the medial frontal lobe [8]. Using the modified Flanker task, action-monitoring dysfunction has been reported in patients with OSA [9]. Despite our previous reports suggesting behavioral action-monitoring dysfunction in patients with OSA, relatively less is known about the associated cerebral substrate underlying this dysfunction in people with different severities of OSA.…”