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(Chest. 2005;128:1304-1309.)
© 2005 American College of Chest Physicians

Symptoms of Depression in Individuals With Obstructive Sleep Apnea May Be Amenable to Treatment With Continuous Positive Airway Pressure*

Daniel J. Schwartz, MD; William C. Kohler, MD and Gillian Karatinos, MD

* From The Sleep Center at University Community Hospital, Tampa, FL.

Correspondence to: Daniel J, Schwartz, MD, The Tampa Sleep Center at University Community Hospital, 3100 E Fletcher Ave, Tampa, FL 33613; e-mail: thetampasleepcenter{at}worldnet.att.net


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 References
 
Objective: To assess the reversibility of symptoms of depression using continuous positive airway pressure (CPAP) in patients with obstructive sleep apnea (OSA).

Patients/methods: Patients referred to our center for evaluation of OSA who had a respiratory disturbance index (RDI) ≥ 15 and who demonstrated a significant response to CPAP (≥ 50% drop in RDI) were evaluated for the symptoms of depression using the Beck Depression Inventory (BDI), and then reassessed after 4 to 6 weeks of treatment with CPAP at home.

Results: In this group of patients, the institution of CPAP therapy resulted in a significant (p < 0.0001) decrease in those symptoms of depression as assessed by the BDI (BDI at baseline, 4.1 ± 3.7; BDI after CPAP, 1.0 ± 2.0). This change in BDI was noted both in those individuals who had received an antidepressant prescription prior to referral, and in those who had not. An analysis of variance failed to reveal any effect on these data related to gender or baseline RDI.

Conclusions: Patients with OSA may present to their primary care physician with symptoms suggesting a diagnosis of depression. In some of these individuals, the symptoms of depression may be ameliorated with CPAP.

Key Words: Beck Depression Inventory • continuous positive airway pressure • depression • obstructive sleep apnea


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusions
 References
 
We noted that a substantive number of the individuals referred to our center for evaluation of obstructive sleep apnea (OSA) had been prescribed antidepressant medication prior to referral. In a preliminary review of 114 consecutive cases referred to our center, 45 patients (39%) were receiving antidepressant medication at the time of referral. When evaluated with the Beck Depression Inventory (BDI) [BDI-Fast Screen for Medical Patients; The Psychological Corporation; San Antonio, TX],1 we found that 41% of these patients had a score suggesting at least mild symptoms of depression, and 12% had a score suggesting moderate-to-severe symptoms of depression.

The prevalence in our patients of symptoms suggesting the diagnosis of depression, and the incidence of their having been prescribed antidepressant medication prior to referral for a suspected diagnosis of OSA seemed disproportionate to the incidence of depression in the general population.234 Therefore, we speculated that the severe fatigue and sleepiness with which individuals with OSA may suffer might be misinterpreted as symptoms of depression, or that the adverse effects of OSA might actually cause clinical depression. Either way, we wondered whether, in patients with OSA syndrome (OSAS), these symptoms of depression might be amenable to treatment with continuous positive airway pressure (CPAP).


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusions
 References
 
Subjects
All patients referred for evaluation of the OSAS were eligible for entry into the study. Each was interviewed and examined by a board-certified sleep specialist, and found to meet standard indications for polysomnographic evaluation for the suspected diagnosis of OSA.45 Our center uses a split-night protocol for those individuals who demonstrate a respiratory disturbance index (RDI) > 15/h, or > 5/h for those who present with excessive daytime somnolence (Epworth sleepiness scale [ESS] > 10). A minimum of 2 h of baseline (before CPAP) recording time is obtained. For these 50 subjects, the average sleep time available at baseline was 179.0 min (95% confidence interval, 157.2 to 200.8 min).

Individuals with a baseline RDI ≥ 15 who demonstrated a ≥ 50% decrease in the RDI with CPAP (using this split-night protocol) were eligible for the study. We chose an RDI ≥ 15 in an effort to establish a defined group with moderate-to-severe OSA, and insisted on a minimum of a 50% improvement in order to define a group with a disorder clearly amenable to CPAP. CPAP was titrated by protocol with the goal to reduce the RDI to < 5 if possible. The optimal CPAP pressure was chosen after review by the board-certified sleep specialist.

Four to six weeks after successful use of CPAP at home, the patients returned for follow-up evaluation. Those attesting to the nightly use of CPAP (at least 6 h/night, 7 nights/wk), are the focus of this report. Any individual who indicated that their use of CPAP was sporadic or < 6 h/night was excluded from the study.

All patients completed an ESS6 and the BDI1 before polysomnography and again at follow-up, having consistently used CPAP at home for 4 to 6 weeks. This study was reviewed and approved by the Research Ethics Review Board of University Community Hospital.

The ESS
The ESS67 asks the individual to rate the likelihood of dozing in eight specific situations, answered on a scale of 0 to 3, with 0 being little or no chance of dozing, and 3 representing a high chance of dozing. Therefore, the scale goes from 0 to 24. There is no fixed scoring recommendation, but a score ≥ 10 is probably abnormal, and a score > 14 might suggest a more significant degree of daytime hypersomnolence.89

The BDI
The BDI asks seven questions pertaining to feelings of sadness, discouragement about the future (pessimism), personal failures, perceived decreases in self-confidence, a sense of being overly self-critical, the ability to derive pleasure from things (anhedonism), and suicidal ideation.1 Each question is answered on a scale of 0 to 3 (0 being little or none, and 3 representing a high level of the characteristic in question). Therefore, the scale for the sum of the seven questions goes from 0 to 21. The suggested scoring is 0 to 3 = minimal symptoms of depression, 4 to 6 = mild symptoms of depression, 7 to 9 = moderate symptoms of depression, and 10 to 21 = severe symptoms of depression.

Polysomnography
Standard polysomnography in our laboratory uses the following protocol. After the patient is acclimated to the facility, he/she is fitted with EEG (C3/A2,C4/A1,O2/A1,O1/A2), electro-oculographic (right outer canthus/A1, left outer canthus/A2), and chin electromyogram electrodes for sleep staging, according to the criteria outlined by Rechtschaffen and Kales.10 Electrodes are placed on both legs, as described in the American Sleep Disorders Association Atlas Task Force report,11 to monitor myoclonic activity. Uncalibrated inductive plethysmography bands are used to monitor chest and abdominal movement, and impedance devices are placed to monitor intercostal muscle activity. A nasal pressure transducer (Pro-Tech Services; Mukilteo, WA) is used to monitor airflow. Pulse oximetry (Nonin Medical; Plymouth, MN) is assessed at the finger to evaluate oxygen saturation. ECG leads are placed to monitor cardiac rhythm (modified lead 2). Concurrent monitoring of audio, video, and body position supplement the other measured parameters.

Definition of Polysomnography Scoring Parameters
Sleep staging was scored according to the criteria of Rechtschaffen and Kales.10 Arousals were scored as defined in the American Sleep Disorders Association Atlas Task Force report on EEG arousals.12 The arousal index is defined as the number of cortical arousals per hour of sleep (each ≥ 3 s). The awakening index is defined as the number of cortical awakenings per hour of sleep (each ≥ 15 s). The sleep disturbance index is defined as the sum of the arousal index plus the awakening index.

Respiratory Event Staging
An apnea was defined as a reduction of the measured parameter of airflow to ≤ 10% of baseline, with a duration of at least 10 s. A hypopnea was defined as any reduction of the measured parameter of airflow with a duration of at least 10 s, which was accompanied by a ≥ 4% decrease in measured oxygen saturation, or a contiguous arousal. The RDI is defined as the total number of apneas and hypopneas per hour of sleep. The desaturation index is defined as the total number of desaturation events, each ≥ 4%, per hour of sleep.

Statistical Analysis
These data were analyzed using statistical software (SPSS version 12.0; SPSS; Chicago, IL). Data presented are mean ± 1 SD. A paired-sample t test was used for scalar data, and the Wilcoxon signed-rank test or Mann-Whitney U test were used for ordinal data as indicated. An analysis of variance was used to evaluate the effect of covariants on the identified change of the BDI after CPAP.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusions
 References
 
Demographics
Our sample of 50 patients included 33 men and 17 women (average age, 48.4 ± 9.3 years; body mass index, 37.0 ± 8.6); of these, 19 patients were receiving antidepressant medication at the time of referral (38%). All were receiving a stable dose of antidepressant medication for at least 2 months prior to evaluation, and no adjustment in medication was made during the course of this study.

Polysomnographic Data
The polysomnographic data delineated in Table 1 confirm that this group of individuals had fairly severe OSA and demonstrated a significant improvement with CPAP.


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  		Table 1.. Polysomnographic Data Before and After CPAP*

 
Analysis of BDI Before and After CPAP
At follow-up, after use of CPAP at home consistently for 4 to 6 weeks, the BDI demonstrated a significant decrease (Table 2 ). Of those patients for whom a decrease in the BDI was possible (initial BDI > 0), 98% (40 of 41 patients) were found to have experienced a fall in the BDI. Of those patients who had an abnormal BDI (> 3) before CPAP, 100% (25 of 25 patients) were noted to have had a fall in the BDI, and the average decrease was 5.4 (from a significantly elevated initial value of 7.2 to a normal value of 1.8 after CPAP).


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  		Table 2.. BDI Before and After CPAP*

 
Segregating these data into those who had or had not been prescribed antidepressant medication prior to referral (Table 3 ), it is noted that the patients receiving antidepressants had a higher initial BDI than those for whom an antidepressant had not been prescribed, although both groups showed a significant decrease in BDI after CPAP therapy. Although more women than men were prescribed antidepressant medication prior to referral (11 of 17 women vs 8 of 33 men, p = 0.0057), the initial BDI at baseline was not different (men, 4.3 ± 3.7; women, 3.8 ± 3.7; p = 0.627), and analysis of variance failed to identify gender as a cofactor in the noted change in BDI (p = 0.552).


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  		Table 3.. BDI Delineated by Prior Prescription of Antidepressant Medication*

 
The overall RDI failed to demonstrate a significant correlation with the baseline BDI; however, if one looks at those with an abnormal BDI (> 3), the correlation with the RDI is statistically significant (r = 0.451, p = 0.024). Again, however, analysis of variance failed to identify the baseline RDI as a cofactor for the noted change in BDI after CPAP either for the group as a whole (p = 0.590), or for those with a baseline BDI > 3 (p = 0.465).

The ESS score improved from a baseline of 14.6 ± 5.0 before CPAP, falling to 6.5 ± 4.1 after CPAP (p < 0.0001). Whether the improvement in the patient’s perceived sleepiness may have had an effect on the BDI responses cannot be determined on the basis of this study, but the possibility thereof should be acknowledged.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusions
 References
 
Patients with OSAS will frequently report feeling tired, fatigued, sleepy, and poorly motivated.1314 These symptoms may affect the individual’s ability to perform their job, can undermine the individual’s relationship with their family, and may ultimately limit their ability to enjoy life.151617 Patients with OSAS may have difficulty concentrating, difficulty remembering factual data, may become irritable or withdrawn, and may find themselves losing interest in, or deriving little pleasure from activities that should be an integral part of their lives.181920 These symptoms bear striking similarity to some of those ascribed to depression, and may potentially fulfill the criteria for a major depressive episode using Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria.21

Whether the diagnostic problem is that the presenting symptoms in both syndromes (OSA and depression) are similar enough to result in the potential for the practitioner to confuse one with the other, leading to a misdiagnosis, or whether one disorder might increase the likelihood of the other occurring, is unknown. Previous studies2223 have identified the increased incidence of the symptoms of depression in patients with OSA and the increased incidence of OSA in patients with depression. However, other reports24252627282930313233 on the effectiveness of various measures to treat OSA on the symptoms of depression have provided mixed results.

Borak et al24 reported on 20 men with OSA, noting no significant change in the BDI after CPAP. There are, however, no data with regard to the frequency (days per week) and length (hours per night) of use of CPAP in these patients. Thus, it is unclear whether the failure to identify a change was due to the fact that no change occurred, whether there simply were not enough cases to identify a change, or whether the lack of consistent use of CPAP could have obviated any change that might have occurred.

Likewise, Klonoff et al25 reported on 11 patients, noting no significant change in BDI after uvulopalatopharyngoplasty (UPPP) surgery. In similar fashion, one might question whether 11 patients are an adequate sample from which to draw this conclusion.

In contrast, a number of authors have documented significant improvement in a variety of measure of quality of life parameters after CPAP and surgery. D’Ambrosio et al26 and Sin et al,27 using a health-related quality of life questionnaire (Short Form-36), reported a significant improvement in "vitality." Derderian et al,28 using the Profile in Moods State Assessment, reported on a significant improvement in mood after CPAP, and Li et al29 noted a significant improvement in mood using a mental health scale for patients with OSA after surgery (extended UPPP). None of these authors, however, specifically addressed the symptoms of depression.

Englemann et al,30 using the Hospital Anxiety and Depression Scale, reported on 32 patients with OSA, and found that their depression index fell significantly after CPAP; and Dahlof et al31 reported on 49 patients after treatment of OSA with surgery (tonsillectomy and UPPP), noting an improvement in the Comprehensive Psychopathologic Rating Scale and a significant decrease in the number of individuals with a diagnosis of depression by direct psychiatric examination. This study,31 however, used an unusual format to identify individuals with OSA (respiratory events were defined by the changes noted from analysis of a static charge sensitive bed, correlated to the changes in oxygen saturation).

The two studies most relevant to ours are the reports of Sanchez et al,32 and that of Means and colleagues.33 Sanchez et al32 reported on 51 patients with OSA diagnosed using a cardiorespiratory polygraph limited to flow, respiratory movement, ECG, and oxygen saturation. The definition of a respiratory event was essentially limited to airflow and time constraints, without imposing either concurrent desaturation or arousal criteria. Moreover, there is no data with regard to the frequency (days per week) or length (hours per night) of CPAP use. Nonetheless, a significant improvement in the BDI was noted at 1 month and 3 months after CPAP initiation.

The findings presented by Means et al33 correlate best with our findings. They reported on 39 patients, noting a significant improvement in the BDI after CPAP treatment. Their design and compliance definition is different than ours. Some of their patients underwent split-night studies; others underwent two full-night studies. Some were titrated for CPAP in the laboratory; others received auto-CPAP at home. Compliance in their study was defined as an average usage of 4.5 h/night, without definition of the number of nights used or the consistency of usage (compliance in their study was documented for 27 of 39 patients using computer chip analysis, and for 12 of 37 patients by testimony). Moreover, the severity of the measured symptoms of depression was less in their patients than in ours. In the study by Means et al,33 only 10% (4 of 39 patients) had a moderate-to-severely abnormal BDI score, whereas in our patient population 22% (11 of 50 patients) had moderate-to-severely abnormal BDI scores. Despite these differences, their study, like ours, noted a significant correlation between the use of CPAP and the improvement in the BDI. Thus, despite the differences in our studies, the findings are remarkably similar.

Our study provides a distinct database in which a group of individuals with a well-defined syndrome, with documented reversibility, and affirmed use of CPAP have been followed up and reassessed with a quantifiable measure of the symptoms of depression. Our data strongly support the potential for CPAP to produce a highly significant degree of improvement in the measured symptoms of depression.

One criticism of our methods might be that we did not monitor actual CPAP use (we did not have access to computerized internal monitors for each and every user); therefore, the attestations of CPAP use might be inaccurate. We would suggest that even if inaccurate the results of our study would likely be unchanged because it is unlikely for an individual to underestimate their CPAP use (that is, it is very unlikely that someone would tell the physician that they were using CPAP for fewer hours per night than their actual use). It is possible, perhaps even likely, that some individuals overestimated their CPAP use (telling the physician that they used CPAP more hours per night than they actually did). If so, it would make the findings of this study even more significant, suggesting that CPAP use of fewer hours per night than the minimum on which we insisted might cause a similar improvement in the symptoms of depression we measured.

A second concern is with regard to the applicability of our results to other populations. The potential for a selection bias in our population based on either enrollment criteria or the inherent bias attendant to those factors that determine which patients choose to use CPAP and return for follow-up, and which do not, is acknowledged. Nor can we rule out the possibility of a placebo effect (patients expecting to feel better with CPAP). However, the consistency with which this effect was seen (40 of 41 patients for whom a decrease in BDI was possible), and the size of the change (from significantly elevated at 7.2 to normal at 1.8) would seem to make the possibility of a placebo effect unlikely.

Another criticism of this study might be with regard to the use of the BDI. The BDI is used mainly as a screening tool for the symptoms of depression. Its applicability as a tool with which to follow any changes in these symptoms is less clear, but we would point out that others have used the BDI and similar tools for ongoing evaluation of symptoms.24252627282930313233

The BDI has the advantage of providing a numerical value that can be used for statistical analysis. It asks the pertinent questions pertaining to mood and anhedonism but, in addition, asks specifically about pessimism and suicidal ideation. Although perhaps imperfect, this tool permits some insight into the symptoms of depression, and we would note that none of the questions on the BDI ask about fatigue, tiredness, sleepiness, or any of the more traditional symptoms usually attributable to OSAS.

This distinction is important because we would suggest that it is exactly this perception on the part of the physician (that the presenting chief complaint of patients with the OSAS is exclusively that of excessive daytime somnolence) that leads to a failure to consider OSA in patients presenting with symptoms of depression. Moreover, we believe that these data strongly support the fact that for some individuals with OSA, symptoms of depression may well be their presenting complaint (it was pervasive enough to have led to almost 40% of our patients having been prescribed antidepressants prior to referral).

As stated previously, our primary goal was to evaluate, in a group of individuals with well-defined OSA, the potential role of CPAP in ameliorating those symptoms that might be attributable to depression. These data clearly show an unequivocal improvement in an objective measure of these symptoms. The potential explanation for this improvement is, however, undefined.

One possible explanation is that these individuals were not depressed but were misdiagnosed as being depressed based on the similarity of the presenting symptoms. In this case, relief of the presumed causative factor (the respiratory events and subsequent sleep fragmentation) with CPAP alleviated the symptoms.

A second potential explanation would be that the obstructive respiratory events and the subsequent sleep fragmentation might cause neurochemical alterations in the brain that result in depression. In this case, the diagnosis of depression is accurate, with the cause of the depression being attributed to a medical condition (OSA). One might posit that treatment of the underlying cause (the medical condition, OSA) could result in an improvement of the secondary syndrome (depression).

A third possibility is that the two entities have a similar underlying mechanism; that is, whatever the neurochemical aberration in the brain is that increases the likelihood of depression might also be associated with the neuromuscular abnormality, which is presumably a factor contributing the occurrence of OSA. Whether treatment with CPAP might affect these neurochemical alterations is unknown, but changes in some neurotransmitters or receptors have been posited.434

We have no doubt that there may well be any number of explanations for the findings of this study, but whatever the pathophysiology is, it is clear that individuals who present to their physicians with symptoms of depression might well be best served if the physician knew to ask questions pertinent to the identification of the OSAS. For those individuals so identified, a polysomnographic evaluation and, if indicated, a trial of CPAP might be worthwhile. If CPAP produces a salutary response, it might, for at least some of these individuals, obviate the need for an antidepressant medication.

We therefore suggest that despite the unanswered questions this study might raise, the findings of this study strongly suggest that the symptoms of depression be acknowledged as a part of OSAS; and not only should patients suspected of having OSAS be queried with regard to the symptoms of depression, but patients presenting primarily with symptoms of depression should be queried with regard to the possible presence of the OSAS. An analysis of these parameters may substantively affect the treatment of these patients.


   Conclusions
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
References
 
We conclude that individuals with OSAS may manifest symptoms of depression, and for at least some of these individuals, the symptoms of depression may be ameliorated by treatment with CPAP.


   Footnotes
 
Abbreviations: BDI = Beck Depression Inventory; CPAP = continuous positive airway pressure; ESS = Epworth sleepiness scale; OSA = obstructive sleep apnea; OSAS = obstructive sleep apnea syndrome; RDI = respiratory disturbance index; UPPP = uvulopalatopharyngoplasty

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestjournal.org/misc/reprints.shtml).

Received for publication November 19, 2004. Accepted for publication February 2, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 References
 

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