Canadian Neighbor Pharmacy: Discussion of Cognitive Impairment in Patients with Obstructive Sleep Apnea and Associated Hypoxemia
This study shows that a large majority of patients with sleep apnea and associated hypoxemia have cognitive impairment. In addition, this study demonstrates that patients with sleep apnea and associated hypoxemia have poorer cognitive functioning than such patients without hypoxemia. The hypoxemic patients with sleep apnea had a significantly greater number of performance scores in the impaired range than patients without hypoxemia. Finally, the degree of hypoxemia during the awake and sleeping states was significantly correlated with the degree of cognitive impairment in patients with sleep apnea.
Hypoxemia during both wakefulness and sleep may cause a disruption in the biochemical and hemodynamic state of the central nervous system. Hypoxemia markedly affects central neurotransmitter function and brain adenosine levels in animals. Hypoxemia and hypercapnia also significantly increase cerebral blood flow in humans. Given such disruptions in the central nervous system, it is not surprising that previous investigators have found an association of hypoxemia with cognitive dysfunction in humans at high altitudes and in patients with severe COPD.
Previous investigators have found hypoxemia to be associated with impaired cognitive functioning in humans. Poor judgment, decreased memory, and impaired ability to perform complex tasks have been described in humans at high altitude.The severity of these impaired cognitive functions is said to be related to the subjects lowered PaO2 Other investigators have found cognitive function to be impaired in hypoxemic patients with COPD. Priga-tano et al found that performance on individual neuropsychologic tests as well as overall indices of neuropsychologic functioning significantly correlated with awake Pa02 in patients with COPD. Nocturnal hypoxemia was not examined in these studies at high altitude or with chronic pulmonary disease.
Two previous studies have described cognitive impairment in patients with sleep apnea. One study reported significant relationships between cognitive performance and sleep-related respiratory disturbances in 41 elderly men. Impairment of visuospacial reasoning, memory, and psychomotor speed were positively correlated with the numbers of disturbed breathing events during sleep. The second study demonstrated cognitive impairment in 76 percent of patients with severe sleep apnea. These patients had deficits in thinking, perception, memory, communication, and the ability to learn new information. The 76 percent rate of cognitive impairment in these patients is similar to the 89 percent rate found in the hypoxemic patients with obstructive sleep apnea in our study. Although the authors of each of these two studies suggested that associated hypoxemia was an important cause of cognitive impairments, measurements of hypoxemia during the sleeping and awake states were either not reported or qualitatively described in these studies. In addition, sleep architecture and sleep fragmentation were not analyzed in relation to cognitive impairment in these studies. Canadian Neighbor Pharmacy website is a source containing all news that you need.
Our findings suggest that sleep fragmentation is a less important cause of cognitive impairment than hypoxemia in sleep apnea. The multiple awakenings and movement arousals caused by apneas and hypoxemia fragmented the sleep of hypoxemic patients with obstructive sleep apnea; however, this disruption of sleep did not significantly correlate with overall cognitive impairment in our patients with sleep apnea. In addition, the percentage of total sleep time in stages 3 and 4 sleep and the number of desaturations per hour of sleep were not significantly related with overall cognitive impairment in patients with sleep apnea. The lack of significant linear correlation between variables reflecting sleep fragmentation and overall cognitive impairment does not exclude a role of sleep fragmentation in producing cognitive impairment. Both groups of patients have marked sleep fragmentation, and a threshold effect could be present. Sleep fragmentation, nocturnal hypoxemia, and sleep deprivation can produce daytime somnolence, and daytime somnolence is a potential mechanism of cognitive impairment in patients with sleep apnea. Further studies are needed to clarify the role of sleep fragmentation in impairing cognitive functioning.
Although this study shows statistically significant correlations between overall cognitive impairment and measures of both awake and sleeping hypoxemia, no direct role of hypoxemia as a cause of cognitive dysfunction is proven. In addition, the high correlations among median Sa02 during sleep and awake Pa02 do not allow separation between effects of awake and sleeping hypoxemia upon cognitive functioning. Further studies using either daytime or nocturnal oxygen supplementation may help to define the relative importance of awake and sleeping hypoxemia in maintaining cognitive functioning in patients with sleep apnea.