I see two problems with the use of anti-depressants as a way of reducing the AHI. First, a common side effect of anti-depressants is weight gain. For patients whose sleep apnea is largely due to excess fatty tissue around the opening to the upper airway and in the tongue taking this drug could make the apnea by increased crowding.
Second, the value of REM sleep as a part of healthy sleep is now being recognized. Suppressing REM sleep could in fact make the mental illness symptoms worse.
I don't see the value of anti-depressants except to stabilize the patient before other health/environmental issues - including assessing their sleep.
The fact is that REM has a pivotal role in brain function. Apnea management is a long term strategy like controlling the hypertension. You could not even continue antidepressants for more than a year or two for depressed people except than very exceptional cases.
In fact, apneas are longuer during REM sleep but I do not think that they are more apneas in REM sleep than in NREM sleep. This phenomenon is due to lower reactivity to hypercapnia during REM sleep and not to REM sleep muscle atonia.
Moreover the suppression of REM sleep by antidepressants in very effective during the first half of the night, but much of the time there is a rebound during the second half of the night. Put it together the overall reduction is not so important.
CPAP is an efficient treatment without much adverse effects (there are much more with antidepressants), we should concentrate on CPAP acceptation and observance.
An old study, that answer not directly your question, may be helpful to you : colleagues of mine have demonstrated that naltrexone reduces AHI. The supposed mechanism is reduction of REM sleep by naltrexone. Ferber C, Sanchez P, Lemoine P, Mouret J. [Efficacy of the treatment of sleep apnea using naltrexone. A clinical, polygraphic and gasometric study]. C R Acad Sci III. 1988;307(12):695-700. French. PubMed PMID: 3143473. Text in french, summary in English.
the question you pose is intriguing, but it is a matter of evidences that SSRI are potentially as harmful as effective for OSAS patients, and that REM sleep is essential for human wellness !(as other collegues have already underlined).
Here my points for discussion:
1. patients with a SDB can be divided into two main subgroups basing on the presence or the absence of a neurological disorder. I refer only to patients affected also by a neurological disorder
2. any neurological disorder alter " the neurotrasmission" and consequently can unbalance the sleep-wake cycle, the structure, and the microstructure of sleep (CAP).
3. Sleep and breathing are tightly related: any breathing disturb influence both the quality and the quantity of sleep. We have also evidences that sleep disturbs can modify breathing during sleep.
4. AHI per sè is an indicator of the severity of the SDB, therefore is the best outcome measure for trials investigating the effectiveness of pharmacological/non pharmacological treatments of OSA or other breathing disturbs.
5. AHI does not give us any indication on whether the SDB is the cause or the effect of sleep fragmentation.
Therefore we should aim at finding molecules able to balance the sleep network that has been unbalanced by the neurological disease. With this aim we cannot avoid from performing functional MRI and from studying the sleep microstructure (CAP).
Depression is often secondary to OSAS.Using antidepressants reduces REM sleep and impairs strurrura of sleep. I would use medicines that improve the obstruction of the upper airways (theophylline evening) and nasal corticosteroids.
I would not use antidepressants only if you suffer from the disease Psychiatric
OSA is considered as a major cause, if not the most common cause of depression. Some antidepressants are potent REM suppressors, and in theory, could reduce sleep apnea severity, especially OSA that is REM-predominant (REM-related). Of course, antidepressants are not the drug of choice for the treatment of OSA. Anti-depressants can also cause weight gain. Obesity is a well-known risk factor for OSA; however, it is also hypothesized that the effects of OSA itself may predispose patients to weight gain.
That said, REM sleep deprivation in animals vs. humans differ considerably. There is evidence that REM sleep deprivation in animals has more deleterious consequences than in humans. Vast majority of REM deprivation studies in human fail to show that REMD disrupt memory.
I would like to point out this study as well:
http://www.ncbi.nlm.nih.gov/pubmed/6537835
A combination of pharmacotherapy and behavioral therapy might work well!
OSA is a precipitating factor or resistance factor of depression, but it is not a major cause of depression. Most of the publications show that treating OSA alone does not improve depressive symptoms.
I suggests to supress totaly sleep in OSA patients ... without sleep no sleep apneas :)
In depression sleep is usually altered in its aspects of continuity and durability and has its normal quality of recovery and rest. Insomnia depression, most often of central or terminal, often heralds the onset of mood disorder, accompanies the course and its demise heralds the resolution of the crisis.
In the 'OSAS sleep is altered and frammentato.Il antidepressant treatment should be carried out with CPAP; CPAP should restore the architecture of sonno.I antidepressant drugs should be given only after the eventual failure of drug treatment
another point of view is that they might decrease apnea hypopnea index in only REM-related OSA, but in case AHI is about the same during REM and nonREM sleep, reduction of the REM sleep will not be significant. I agree with above statements that REM sleep is important and that the antidepressants have many side effects.