Cognitive Impairment and Dementia

There is evidence that SDB affects patients' cognitive functioning. Several studies have reported the negative effect of severe SDB (AHI > 30) on cognitive dysfunction, with specific impairments in attentional tasks, immediate and delayed recall of verbal and visual material, executive tasks, planning and sequential thinking, and manual dexterity (26,43,44). Studies examining the relationship between milder SDB and cognition are less clear-cut, and have found that mild SDB (AHI 10-20) does not cause cognitive dysfunction in the absence of sleepiness (43). However, it is important to note that SDB might not affect all areas of cognitive functioning equally, and therefore, it is possible that in a study that only examined a small number of cognitive tasks, the findings could be (falsely) negative.

Researchers have proposed two explanatory theories for the cognitive deficits found in patients with SDB. The first is that the hypoxia caused by the SDB results in the cognitive impairments. Evidence for this theory comes from studies, which found that in patients with continuous hypoxia, there is an association between the severity of cognitive dysfunction and nocturnal oxygen saturation (45,46). In particular, as the oxygen saturation decreases, the performance on various neuropsychological testing worsens. Whether this relationship holds when the hypoxia is intermittent is unclear. An important consideration to make is that the patient's performance on cognitive tasks might vary depending on the severity of SDB and hypoxia experienced the night before the testing. This variability may in fact partially explain some of the inconsistencies reported in the literature with regards to the effects of SDB on cognitive functioning. It remains unclear whether these hypoxia-related cognitive deficits are reversible with treatment.

The second theory is that the EDS contributes to the cognitive impairment found in patients with SDB. It is well known that one of the primary symptoms of SDB is EDS, and that EDS can impair cognitive functioning including auditory verbal learning (47), executive functioning, and working memory (48). It is also possible that the cognitive deficits found in SDB patients are a product of multiple factors, which may include both hypoxia and EDS. In addition, there is evidence that many of the progressive dementias involve degenerative pathologies in brainstem regions, areas that are responsible for regulating respiration and other autonomic functions relevant to sleep maintenance (49). Therefore, because many older adults suffer from dementia, it is possible that sleep disorders such as SDB may be more likely to occur in this group of patients.

There are studies showing that the severity of the dementia is associated with the severity of the SDB (14,18). In institutionalized elderly, those patients with severe dementia [based on the Dementia Rating Scale (DRS)] had more severe SDB compared to those with mild-moderate or no dementia (14). Furthermore, there was a positive relationship between severity of the SDB and dementia, and patients with more severe SDB performing worse on the DRS. A study by Kim et al. (50) estimated that an AHI = 15 is equivalent to the decrement of psychomotor efficiency associated with an additional five years of age.

There is some speculation that SDB could actually be a cause of vascular dementia (51). Studies have shown that the hypertension, arrhythmias, decreased cardiac output, stroke volume, and cerebral perfusion associated with SDB may lead to an increased likelihood of cerebral ischemia and/or localized infarcts (52).

In our own laboratory, we have studied the relationship between SDB and cognitive impairment in patients with AD that were both institutionalized and community-dwelling (3,14,15,53). We found that SDB was highly prevalent in both populations. In addition, in the institutionalized AD patients, as AHI increased, cognitive functioning worsened, even when controlling for age (14). There is also evidence to suggest that the severity of sleep disruptions in AD parallels the decline in cognitive functioning. We are currently completing a study that examines whether treatment of SDB in patients with AD results in improvement in cognitive abilities (54,55).

The prevalence of SDB is also higher in patients with Parkinson's disease (PD) compared to age-matched controls (56,57). It is known that the majority of PD patients experience subtle changes in cognition, and that approximately 40% will progress to PD dementia (58). PD patients also commonly experience alterations in respiratory function while awake; hence, there are compelling reasons to think that patients with PD may be at risk of nocturnal hypoxemia and SDB. There is evidence that in PD patients there is a degeneration of the neurons in the reticular activating system as well as a degeneration of the pathways arising from the dorsal raphe and locus coeruleus, all of which are likely to contribute to sleep disturbances and daytime sleepiness in these patients (59). The role that SDB plays in the cognitive dysfunction and eventual development of dementia experienced by the majority of PD patients is a question that still needs to be explored.

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