Shared risk factors

OSA and depression share common risk factors, which may partly explain their high comorbidity in the general population. Very frequently in studies of the impact of OSA on cognitive and psychological functioning, a conglomerate of disorders is shown to contribute to the overall neuropsychological outcome. Therefore, the presence of a polypathology often associated with OSA, such as obesity, cardiovascular disease, hypertension and diabetes, should increase the suspicion of an underlying or coexisting OSA in a depressed patient.

Both, depression and OSA, have independently been shown to be associated with metabolic syndrome, and also with the development of cardiovascular disease . The association between depression and metabolic syndrome has been suggested to be reciprocal , and a priori not attributable to genetic factors as twin studies revealed . In particular, insulin resistance (IR) has been suggested to contribute to the pathophysiology of depressive disorder and has been proposed to subserve the association between depression and cardiovascular disease . Similarly, OSA has been observed to be independently associated with the cardiovascular risk factors comprising metabolic syndrome , in particular IR . The magnitude of this association has even led researchers to suggest that metabolic syndrome should encompass OSA .

Although OSA and depression share these common risk factors, there are currently no studies available which have investigated the issue of antecedent or consequence in the relationship between depression, OSA and metabolic syndrome, and if and how these three highly prevalent disorders may interact to exacerbate the risk for cardio – and cerebrovascular morbidity and mortality.

Clinical application

As a consequence of the complex relationship between depression and OSA, the assessment of a patient's individual sleep history should be included in the standard psychiatric clinical interview, and specifically in the assessment of a depressive syndrome. A clinician should suspect OSA particularly in those depressed patients who present with its cardinal symptoms, namely, 1) loud snoring or intermittent pauses in respiration, as witnessed by a bed partner, associated with 2) excessive daytime sleepiness (EDS). Given that patients often deny the latter, standardized questionnaires such as the Epworth Sleepiness Scale (ESS)  or the Functional Outcome Sleep Questionnaire (FOSQ)  are useful tools to assess EDS. The ESS asks the patients to rate their chances to fall asleep during periods of relaxation or inactivity (such as reading, watching television), but also in more active settings (driving a car, sitting and talking to someone). EDS is by far the most frequent daytime symptom of OSA, whereas nocturnal symptoms include restlessness, nocturia, excessive salivation and sweating, gastroesophageal reflux, as well as headache and dry mouth or throat in the morning on awakening. Furthermore, the clinical picture frequently includes obesity and hypertension, and, in those patients who are not obese, special facial abnormalities which narrow the upper airway, such as retrognathia or micrognathia.

However, it should be kept in mind that OSA may not be immediately apparent, but might present in an atypical fashion, with irritability, tiredness, disrupted sleep, difficulty concentrating, difficulties accomplishing tasks and generally decreased psychomotor performance . Women are more likely to present with these symptoms and have been suggested to be particularly underdiagnosed because of their atypical symptoms . The importance of the sleep-wake complaints in a patient's depressive profile, and the onset of those complaints prior to the development of the depressive psychopathology should draw the clinician's attention to a potential underlying or coexisting OSA .

Third, particular attention should be paid to depressive patients who are resistant to treatment. In this case, OSA should be excluded as a major underlying contributing factor , as treatment of OSA could improve not only the compliance to pharmacological antidepressant treatment, but also the treatment response rate for depression . Fourth, comorbid disorders of OSA may also catch the attention of the treating psychiatrist. In addition to the outlined association with the metabolic syndrome, Farney et al. observed that the likelihood of OSA increased significantly when either antihypertensive or antidepressant medications had been prescribed .

Depressed patients with a suspected OSA should be referred to a sleep disorders center for evaluation by nocturnal polysomnography, to confirm the diagnosis of OSA or the presence of other forms of sleep disordered breathing, such as the upper airway resistance syndrome . This is of particular importance, as some of the adjunct treatments to the current pharmacological treatment of depression may actually exacerbate the condition.

If the diagnosis of OSA has been established in a depressed patient, and treatment has been initiated, close follow-up of the improvement of the depressive symptoms might give some indications as to the extent to which the presence of OSA may have contributed to the depressive symptomatology. However, as Baran and Richert point out , the aforementioned diagnostic challenge of a depressive syndrome in the presence of OSA currently remains unresolved.

On the other hand, systematic assessment of depressive symptoms with standardized clinical questionnaires in OSA patients is generally part of the evaluation process in all major sleep disorder centers. However, as these questionnaires have not been specifically designed to assess depression in OSA patients , they might be inappropriate to assess depression in this population, given that it is still unclear if OSA and depression display a true comorbidity or only share similar symptoms . Typically, patients with severe depressive symptoms should be referred to a psychiatrist, particularly if such symptoms do not regress or if fatigue lingers after efficient treatment of OSA .

Conclusion

Recent studies underscore the existence of a complex relationship between depression and OSA in terms of clinical presentation, underlying pathophysiology and treatment. It should incite the treating psychiatrist to be highly aware of a possibly underlying or coexisting OSA in depressed patients. Up to 20% of all patients presenting with a diagnosed depressive syndrome may also have OSA, and vice versa. This relationship might vary widely, depending on age, gender, AHI cut-off and general demographic and health characteristics of the population under investigation. Future clinical research in this area should specifically examine depressed patient populations, taking into account the different sub-type of mood disorders, and investigate a broader range of depressive symptomatology in OSA patients. Basic research should further investigate the causal relationship between depression and OSA, as well as the potential mechanisms by which both disorders may interact.