This guest article discusses the need for screening of depressed patients for sleep apnea. This is the third page of this report. Sleep Apnea and Depression, Part 1, begins here.
Compared to the large number of studies investigating depressive symptomatology in OSA patients, far fewer studies have focused on the screening for OSA in a primarily depressed study population.
In one of the few investigations of the prevalence of OSA in a depressed cohort, Reynolds et al. found, in a small sample of 17 older patients with major depression, that 17.6% also had an OSA syndrome, compared to 4.3% of 23 healthy elderly controls .
This suggests that OSA might be an important confounding factor for studies on mood disorders in general, as its presence is not routinely determined in either research studies examining mood or clinical settings. However, many more studies are required to assess the prevalence of OSA in primarily depressed patients, particularly as it can be suspected from existing studies that OSA is greatly underdiagnosed in this patient population.
Clinically, this is of particular concern, as sedative antidepressants and adjunct treatments for depression may actually exacerbate OSA.
Notably hypnotics prescribed to treat depression-related insomnia might further decrease the muscle tone in the already functionally impaired upper airway dilatator muscles, blunt the arousal response to hypoxia and hypercapnia as well as increase the arousal threshold for the apneic event, therefore increasing the number and duration of apneas .
These effects might differ depending on the patient population and the severity of OSA. Older depressive subjects are of primary concern: both, frequency of OSA and depressive symptoms increase with age, as do prescription and consumption of sedative psychotropic medication. Pharmacologic treatment of depression and depression-related insomnia in this age group should therefore routinely consider the potential presence of a concomitant OSA.
Finally, as Baran and Richert point out, the diagnosis of a mood disorder in the presence of OSA has its very own challenges . Considering the DSM-IV definitions , it could either be viewed as a mood disorder due to a general medical condition, or classified as an adjustment disorder with depressed mood, due in particular to EDS and its debilitating consequences on the patients’ daytime functioning. The identification of pathophysiological features that allow distinction between OSA and depression might assist with such diagnostic issues.
Neurobiology of depression and upper airway control in OSA: the role of serotonin
The high comorbidity of OSA and depression suggests that both disorders may share a common neurobiological risk factor. On the neurotransmitter level, the serotoninergic system has a central role as a neurobiological substrate underlying impairments in the regulations of mood, sleep-wakefulness cycle, and upper airway muscle tone control during sleep. Depression is associated with a functional decrease of serotoninergic neurotransmission, and is mostly responsible for the alterations in sleep as outlined above .
The physiopathology of OSA involves numerous factors, among whose the abnormal pharyngeal collapsibility during sleep is one of the most compelling. Serotonin delivery to upper airway dilatator motor neurons has been shown to be reduced in dependency of the vigilance state .
This leads to reductions in dilator muscle activity specifically during sleep, which may contribute to sleep apnea. However, whereas the role of serotonin in mood disorders has been largely documented, its involvement in the pathophysiology of sleep apnea remains to be clarified. Interestingly, molecules increasing 5-HT neurotransmission such as the Serotonin reuptake inhibitors (SSRI) are widely prescribed antidepressant molecules that are suggested to similarly improve the apnea hypopnea index in OSA.
Serotoninergic drugs such as fluoxetine, protryptiline and paroxetine have already been tested for OSA, with limited success and numerous adverse effects . Several 5-HT receptor ligands and bi-functional molecules are under development, which may in the future be able to target both, the depressive syndrome and OSA.
Continued on page 4 – Depression and Sleep Apnea – Shared Risk Factors
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