**1. Introduction**

Obstructive sleep apnea (OSA) is a breathing disorder of sleep produced by partial or complete obstruction of the upper airways. This sleep disorder is characterized by breathing cessation and reduction of airflow resulting in temporary decrease, in cerebral oxygenation and sleep disruption [1]. The prevalence of OSA is approximately 10% in men and 3% in women between the ages of 30–49%, but rising to 17% in men older than 50 years and 9% in women post-menopause. It has been reported that prevalence of OSA has increased since 1990 in the United States and other countries. However, 80% of individuals with OSA remain undiagnosed and untreated [2].

The pathophysiology of OSA includes oxygen desaturation, alteration in sleep architecture and abnormal ventilation [3]. Hypoxemia and sleep fragmentation (arousals) cause excessive daytime sleepiness increasing the risk of road and work accidents [4] and reduced quality of life [5]. Additionally, OSA increase the risk of cardiovascular, cerebrovascular and metabolic diseases [6], neurocognitive impairment [7] and death [8]. One at time, cardiovascular diseases and metabolic consequences of OSA increase the risk of cognitive impairment. Cognitive deficits in individuals with OSA include attention and vigilance, episodic memory, delayed long-term visual and verbal memory, visuospatial/constructional abilities and executive functions [9–11]. Some studies reported that psychomotor function and

language do not seem compromised, [12] whereas others demonstrated to psychomotor function is affected by OSA and this domain does not improve with CPAP therapy [13]. Although the cognitive impairment in individuals with OSA is largely recognized as mild cognitive impairment, [14] OSA has also recognized as modifiable risk for dementia, neuropsychiatric disorders and stroke [15, 16]. However, the pathophysiology of cognitive impairment in adults with OSA is complex and the whole mechanisms involved in cognitive deficit have not been clarified yet.
