Effect of Treatment of Sleep Apnea on Depression

The belief that depression is an actual phenomenon seen increasingly in patients with sleep apnea is well documented by numerous studies showing significant improvement in depression, daytime sleepiness, and quality of life following treatment of sleep apnea with CPAP (58-63). Schwartz et al. (62) demonstrated this effect in patients with RDI > 15 and in patients with and without antidepressant pharmacotherapy. Hilleret et al. (64) reported an interesting case of a 50-year-old man with no previous history of bipolar disorder, diagnosed with severe depression and resistant to seven weeks of treatment with venlafaxine and trazodone. A diagnosis of OSA and use of CPAP was followed a few days later by a mood switch to first hypomania and then a mixed disorder. Thus OSA might not only be associated with a depressive syndrome but its presence may also be responsible for failure to respond to appropriate pharmacological treatment. Furthermore, undiagnosed OSA might be exacerbated by adjunct treatments to antidepressant medications, such as benzodiazepines. Also, high anxiety and/or depression scores can lead to CPAP nonadherence (65). Conversely, a few other studies have questioned the relation of mood improvement with sleep apnea treatment. Li et al. (66) reported moderate improvement in mood postoperatively after extended uvulopalatal flap surgery on 84 patients with sleep apnea. However, this improvement in mood was not significantly associated with changes in RDI, maximum arterial oxygen saturation, or the ESS scores. Yu et al. (67) conducted a randomized, placebo-controlled trial of CPAP treatment on patients with sleep apnea and compared mood improvement in the two groups seven days after starting CPAP. Both the CPAP treatment and placebo CPAP groups showed significant improvement in mood states, raising the possibility of placebo effect. A longer trial of CPAP versus placebo is suggested to truly evaluate and differentiate real differences from the placebo effect.

However, as suggested by O'Hara and Schröder (68), OSA and MDD do share some common pathophysiological mechanisms, for example, the serotonergic system central to depressive disorders is implicated in the regulation of mood as well as the sleep-wake cycle and upper airway muscle tone control during sleep. Further, the common risk factors and covariables (e.g., obesity, diabetes, hypertension, and cardiovascular disease) shared by OSA and MDD also suggest the presence of common pathophysiological mechanisms. This may be supported by imaging studies showing increased subcortical white matter hyperintensities in patients with severe compared to minimal OSA and also a trend for increased subcortical hyperintensities with an elevated level of depression (69).

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