Excessive Daytime Sleepiness in Obstructive Sleep Apnea. Mechanisms and Clinical Management

Abstract

Many patients with obstructive sleep apnea (OSA) experience excessive daytime sleepiness (EDS), which can negatively affect daily functioning, cognition, mood, and other aspects of well-being. Although EDS can be reduced with primary OSA treatment, such as continuous positive airway pressure (CPAP) therapy, a significant proportion of patients continue to experience EDS despite receiving optimized therapy for OSA. This article reviews the pathophysiology and clinical evaluation and management of EDS in patients with OSA. The mechanisms underlying EDS in CPAP-treated patients remain unclear. Experimental risk factors include chronic intermittent hypoxia and sleep fragmentation, which lead to oxidative injury and changes in neurons and brain circuit connectedness involving noradrenergic and dopaminergic neurotransmission in wake-promoting regions of the brain. In addition, neuroimaging studies have shown alterations in the brain’s white matter and gray matter in patients with OSA and EDS. Clinical management of EDS begins with ruling out other potential causes of EDS and evaluating its severity. Tools to evaluate EDS include objective and self-reported assessments of sleepiness, as well as cognitive assessments. Patients who experience residual EDS despite primary OSA therapy may benefit from wake-promoting pharmacotherapy. Agents that inhibit reuptake of dopamine or of dopamine and norepinephrine (modafinil/armodafinil and solriamfetol, respectively) have demonstrated efficacy in reducing EDS and improving quality of life in patients with OSA. Additional research is needed on the effects of wake-promoting treatments on cognition in these patients and to identify individual or disorder-specific responses.

Deep Learning–Based Assessment of Brain Connectivity Related to Obstructive Sleep Apnea and Daytime Sleepiness

“…Hippocampus damage caused by OSA may lead to worsening daytime sleepiness as well as cognitive impairments. 46 The present study has several limitations. The DTI data had a limited number of isotropic gradient directions (n = 15) and were measured at a relatively low diffusion weight (b = 1000 s/mm 2 ).…”

“…Hippocampus damage caused by OSA may lead to worsening daytime sleepiness as well as cognitive impairments. 46 …”

Risk of obstructive sleep apnea and traffic accidents among male bus drivers in Ecuador: Is there a significant relationship?

“…Around 25–50% of patients with OSA will experience EDS, and it can negatively affect daily functioning, cognition, mood, and other aspects of well-being [ 22 ]. Its pathophysiology involves chronic intermittent hypoxia and sleep fragmentation causing oxidative injury and changes in neurons and neurotransmitters that regulate wake-promoting regions of the brain [ 23 ]. Such is the link between EDS and OSA that in our study we found a weak positive correlation between STOP-Bang and ESS scores, and a statistically significant association between OSA risk and daytime sleepiness categories.…”

Residual excessive daytime sleepiness in patients treated for obstructive sleep apnea: guidance for assessment, diagnosis, and management

“…Among those who do report EDS, studies have shown that the severity of EDS does not correlate with the severity of OSA (as determined by apnea hypopnea index [AHI]), suggesting that factors other than respiratory events and arousal (eg, hypoxia-and/or sleep fragmentation-related brain injury [8]) contribute to EDS in this population [9][10][11]. Indeed, EDS has been shown to persist in some patients despite the normalization of breathing, oxygenation, and sleep quality with continuous positive airway pressure (CPAP) (the gold standard treatment for OSA), known as residual EDS [12,13].…”