Untreated sleep apnea is related to cognitive impairments including speed of information processing, attention and working memory, executive functioning, alertness and sustained attention, visuospatial learning, motor performance, and constructional abilities. Sleep favors the integration of newly acquired memories and promotes permanent storage or consolidation.
While obstructive sleep apnea (OSA) does influence cognitive ability in the ways mentioned above, it largely spares global cognitive functioning and language.
OSA, which has been clearly shown to contribute to dementia, is not only damaging due to hypoxia but also due to disruption of sleep integrity. Sedatives such as benzos or Zolpidem may increase sleep time but impair slow-delta sleep.
Primary areas of brain function affected in OSA is vigilance and executive function, thus working memory may be impaired. Attentional impairments in adult OSA patients are comparable to the effects of alcohol intoxication. Vigilance impairments may be enduring or more momentary, with microsleeps mimicking inattention or lapses in concentration.
OSA markedly impairs the ability to sustain attention for extended periods which has a major adverse effect on driving, occupational functioning and interaction with people. Executive function, defined as the ability to develop, sustain and organize a goal-directed and flexible approach to problem solving is moderately to severely impaired in OSA.
There is inconclusive results in regard to memory function, especially visual and verbal short and long term-memory. There have been findings indicating slow information processing speed and diminished working memory.
Researchers have found that patients using CPAP an average of 6 hours per night were eight times more likely to have memory in the normal range after 3 months of CPAP. This indicates that at least 6 hours per night of CPAP may be needed to produce a reversal of memory impairment in OSA. CPAP adherence is defined as greater than 4 hours of nightly use.
Sleep and Alzheimer’s
Sleep has been shown to have a direct influence on the quantity of beta-amyloid deposition in the brain as measured by PET scanning. Recently, increased neural activity in wakefulness has been shown to correlate with an augmentation of A-beta 42 production, with increased A-beta clearance in sleep. Thus sleep deprivation is a risk for Alzheimer’s disease. Research showed an expansion of the volume of interstitial space during sleep ( a contraction of neuron). There was 60% increase of CSF passage into the venous system, likened to the disposal system for the brain, which allows more effective clearance of toxins, specifically, beta amyloid. Carriers of ApoE4 genotype who are at increased risk of developing AD are even more prone to the disease if they suffer from poor quality sleep.