ABSTRACT
Obstructive sleep apnea (OSA) is characterised by obstruction of the upper airway and the presence of continued respiratory effort with normal central nervous system drive for respiration during sleep. Numerous neurological structures and functions are impacted by OSA and implicated in OSA-related cognitive dysfunction, from brain grey and white matter itself to cortical blood flow, resting metabolism, task related activation, and compensatory activation. The validity of the neurocognitive tasks used in OSA patient studies may be problematic and may not be sensitive enough to detect more subtle impairments seen in patients with sleep disorders. The two main contributors of neurocognitive dysfunction in OSA patients are sleep fragmentation and intermittent hypoxia, or a combination of both factors, and may differ depending on the cognitive domain. While OSA is a treatable disease, some deficits are only partially reversible with treatment, and cognitive function may not be restored to the level of healthy individuals.
