ORIGINAL ARTICLE


https://doi.org/10.4103/ijrc.ijrc_84_20
Indian Journal of Respiratory Care
Volume 10 | Issue 1 | Year 2021

Neurocognitive Profile and Depression in Obstructive Sleep Apnea


Rajasekhar Varma, Narendra Kumar Narahari, Paramjyothi Kruparao Gongati, Afshan Jabeen Shaik1, Bhaskar Kakarla, Padmaja Gaddamanugu1, Ravi Charan Avala2

Departments of Pulmonary Medicine and 1Neurology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, 2Department of Pulmonary Medicine, Apollo Hospitals, Vishakapatnam, Andhra Pradesh, India

Address for correspondence: Dr. Narendra Kumar Narahari, Department of Pulmonary Medicine, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad - 500 082, Telangana, India.

E-mail: drnarendrajipmer@gmail.com

Abstract

Background: Neurocognitive decline and depression are the most common unaddressed but noticeable adverse consequences linked with obstructive sleep apnea (OSA) which can affect work performance, social functioning, and quality of life. It is significant to explore both cognition and mood disorders in OSA, as there is adequate evidence in the literature supporting the efficacy of continuous positive airway pressure (CPAP) in the management. Aims and Objectives: The aim was to assess the neurocognitive profile and depression in patients with OSA in our center. Patients and Methods: This was a cross-sectional observational study conducted in a tertiary care center between January 2017 and January 2018. A total of 92 patients with an established diagnosis of OSA (by polysomnography) were included in the study. All patients were given questionnaires for the assessment of neurocognitive function and depression scoring. Results: Out of 92 OSA patients, 29 (31.5%) had normal cognition, 43 (46.7%) had mild cognitive impairment (CI), and 20 (21.7%) had major CI. Out of twenty patients with major CI, major attention deficit was observed in 17 (85%), memory impairment in 16 (80%), verbal fluency was affected in 13 (65%), deficit in language skills was observed in 7 (35%), and visuospatial abilities were affected in 17 patients (85%). Out of 92 OSA patients, 21 (22.8%) had depression and 71.4% of them were females. Conclusions: OSA is an independent risk factor for both depression and neurocognitive decline. It is highly recommended that patients with OSA should be screened for both, so as to provide better clinical outcomes.

Keywords: Apnea hypopnea index, continuous positive airway pressure, depression, neurocognitive decline, obstructive sleep apnea, sleep disordered breathing

How to cite this article: Varma R, Narahari NK, Gongati PK, Shaik AJ, Kakarla B, Gaddamanugu P, et al. Neurocognitive profile and depression in obstructive sleep apnea. Indian J Respir Care 2021;10:30-4.

Received: 09-08-2020

Revised: 15-08-2020

Accepted: 30-10-2020

Published: 31-01-2021

INTRODUCTION

Obstructive sleep apnea (OSA) is described by repetitive events of partial or complete upper airway collapse during sleep which is highly prevalent condition but still underdiagnosed.[1] Complete airway collapse during sleep is identified as apnea (cessation of airflow for ten or more seconds), and partial airway collapse as hypopneas (when airflow decreases by 30% or more and a drop in oxygen saturation by >3% or an arousal).[2] Untreated OSA may cause fragmentation of sleep, which has many dangerous health consequences, leading to serious morbidity and mortality.[1]

OSA is linked with neurocognitive dysfunction, depression, and mood disorders.[3] Neurocognitive decline is one of the noticeable adverse consequences associated with OSA, which can affect work performance, social functioning, and quality of life.[4] A high prevalence of depression is seen in patients with OSA when compared to those not having OSA.[5] It is still speculative whether depression is a primary consequence of OSA or it is secondary to sleep problems and irritability associated with OSA. In addition, there are many confounding and shared risk factors such as obesity, hypertension (HTN), diabetes, hypothyroidism, and cardiovascular disease which can strongly affect the association of OSA with depression and neurocognitive decline.[5]

Intermittent hypoxia caused by repetitive opening and closure of airways during sleep, systemic inflammation, and endothelial dysfunction altering brain structure and function are most likely pathogenic mechanisms responsible for neurocognitive decline in OSA.[6] It was also observed that severe OSA can be a risk factor for dementia in the elderly.[7] A recent meta-analysis by Leng et al.[6] which included 212,943 patients concluded that adults with OSA are 26% more susceptible to dementia and neurocognitive decline over the period of 3-15 years follow-up. It is important to address and explore both cognition and mood disorders in OSA, as there is adequate evidence in the literature supporting the efficacy of continuous positive airway pressure (CPAP) in the management.[1] It is also relevant to look up for OSA in patients with depression and mood disorders. The current study is aimed to assess the neurocognitive profile and depression in patients with OSA in our center.

MATERIALS AND METHODS

The study was carried out in the department of pulmonary medicine at a tertiary care hospital for both Telangana and Andhra Pradesh states. It was a prospective, observational study conducted between January 2017 and January 2018. Institutional ethics committee approval was obtained. A total of 92 patients with an established diagnosis of OSA (by polysomnography) were included in the study. All patients were given questionnaires for the assessment of neurocognitive function and depression scoring. The following eligibility criteria were observed in the study.

Eligibility criteria

Inclusion criteria

  1. Age >18 years
  2. Diagnosed cases of OSA by polysomnography
  3. Individuals having a minimum of average intelligence
  4. Informed consent.

Exclusion criteria

  1. Persons whose literacy level does not allow administration of neuropsychological tests
  2. Patients with known neuropsychiatric disorders or neurosurgical condition
  3. Patients with sleep disorders other than OSA
  4. Patients who are unable to communicate due to blindness and deafness
  5. Patients with a history of drug abuse (psychoactive medications).

According to 2014 INOSA guidelines, prevalence of OSA is about 2%-4%, so with assumed precision of 10% and 95% confidence level, minimum required sample taken for the study was 92 (n = 92). A detailed history was taken, and all patients were given questionnaires for assessment of neurocognitive function and depression scoring. The questionnaires used in this study were Addenbrook's Cognitive Examination (ACE-III),[8] an authorized questionnaire available in local languages (Hindi and Telugu) for neurocognitive assessment [Supplementary Data 1], and Hamilton Depression rating scale[9] [Supplementary Data 2]. The ACE-III is a brief cognitive test that assesses five cognitive domains, namely, attention (18 points), memory (26 points), verbal fluency (14 points), language (26 points), and visuospatial abilities (16 points). Total score is 100, higher scores indicate better cognitive functioning, and scores <100 indicate worse cognitive functioning.[10]

Statistical analysis

Data were collected and stored in excel sheets with password protection. A copy of collected data was also updated to co-investigators. Thus, collected data were analyzed at the end of the study for descriptive statistics, and Chi-square test was used wherever necessary. P values were calculated with the help of statistician using SPSS software (IBM Corp. Released 2010. IBM SPSS Statistics for Windows, Version 19.0. Armonk, NY: IBM Corp., USA). A P < 0.05 was considered statistically significant.

RESULT

Demographic data

The mean age of the study population was 53.35 ± 11.6. Maximum patients were in the age group of 50-60 years (41%). Out of 92 patients in the present study, 63 were males (68.47%) and 29 were females (31.53%). The comorbidities in the present study were HTN (58.69%), diabetes mellitus (DM) (29.3%), hypothyroidism (17.32%), and coronary artery disease (10.86%).

Prevalence of neurocognitive impairment in obstructive sleep apnea

Out of 92 OSA patients in the present study, 29 patients (31.5%) had normal cognition, 43 (46.7%) had mild cognitive impairment (CI), and 20 (21.7%) had major CI. Of the 20 OSA patients with major CI, 13 (65%) were females and 7 (35%) were males and most of the patients, 14 (70%), were in the age group of 50-70 years. Out of the twenty patients with major CI, 18 patients were known hypertensive, 10 of them were diabetic, and 5 were hypothyroid. In the present study based on the Chi-square test, we conclude that there was a statistically significant association between HTN and neurocognitive impairment with a P = 0.0001. However, there was no significant association between DM or hypothyroidism and neurocognitive impairment with a P = 0.55.

Profile of neurocognitive decline in cases of obstructive sleep apnea

Out of twenty patients with major CI in our study, major attention deficit was observed in 17 patients (85%), memory impairment in 16 (80%), verbal fluency was affected in 13 (65%), deficit in language skills was observed in 7 (35%), and visuospatial abilities were affected in 17 patients (85%). Out of the twenty patients with major CI, 15 patients had education of <12 years and 5 patients had more than 12 years of education. In the present study based on the Chi-square test, we conclude that there was a significant statistical association between education years and neurocognitive impairment indicating that patients with a lesser number of years of education had more chances of having major CI with a P = 0.0007.

Association between neurocognitive impairment and severity of obstructive sleep apnea

Out of the 92 OSA patients in the study, 13 patients (14.1%) had mild OSA, of these three patients had normal cognition and ten patients had mild CI. Thirty-two patients (34.8%) had moderate OSA, of these seven patients had normal cognition, 16 patients had mild CI, and nine patients had major CI. Forty-seven patients (51.1%) had severe OSA, of these 19 patients had normal cognition, 17 patients had mild CI, and 11 patients had major CI. There was a significant statistical association between the severity of apnea hypopnea index (AHI) and neurocognitive impairment with a P = 0.047.

Prevalence of depression in cases of obstructive sleep apnea

Out of 92 OSA patients in the present study, 21 patients (22.8%) had depression, of which nine patients (9.7%) had mild depression, seven (7.6%) had moderate depression, and five (5.4%) had severe depression. Of the 21 OSA patients with depression in our study, 14 (71.4%) were females and 6 (28.5%) were males, and most of the patients 13 (61.9%) were in the age group of 50-70 years.

Association between depression and severity of obstructive sleep apnea

Out of the 92 OSA patients in the study, 13 patients (14.1%) had mild OSA, of these one patient had severe depression. 32 patients (34.8%) had moderate OSA, of these eight patients had depression (1 - mild depression, 4 - moderate depression, and 3 - severe depression). Forty-seven patients (51.1%) had severe OSA, of these 12 patients had depression (mild - 8, moderate - 3, and severe - 1). We conclude that there was no significant association between the severity of AHI and severity of depression with a P = 0.13. In the present study, there was a significant statistical association between the severity of body mass index and severity of depression with a P = 0.0017. Furthermore, there was a significant statistical association between the severity of depression and education levels, indicating that patients with a less number of education years had more chances of having major depression with a P = 0.04.

DISCUSSION

The present study assessed the neurocognitive profile and depression in patients with OSA in our center. Out of 92 patients in the present study, 63 were males (68.47%) and 29 were females (31.53%). Out of 92 OSA patients, 29 (31.5%) had normal cognition, 43 (46.7%) had mild CI, 20 (21.7%) had major CI, and 21 patients (22.8%) had depression. The present study shows 21.7% prevalence of major neurocognitive impairment in patients with OSA. This is in concordance with a recent meta-analysis which showed that patients with sleep-disordered breathing (SDB) are 26% more prone to develop CI.[6] A multicenter cohort study by Yaffe et al.[11] in 228 elderly women showed that OSA patients had high rate of mild degree of CI (44.8%) with odds ratio of 1.85, when compared to those not having OSA, whereas our study reported that 46.7% of patients had mild degree of neurocognitive impairment. The prevalence of depression in majority of studies ranged from 7% to 63%;[12] however, in our study, it was 22.8%. There was no association between severity of OSA and severity of depression in our study.

It is a known fact that neurocognitive deficits occur in OSA, but the exact prevalence in adult patients with OSA is still unknown.[3] This could be explained by variability in study design, various shared risk factors, and comorbidities independently affecting cognitive decline irrespective of severity of OSA.[3,13] It was observed that increasing age, male sex, current cigarette smoking, obesity, HTN, DM, metabolic syndrome, hypothyroidism, and alcohol consumption are the common shared risk factors for both OSA and cognitive decline.[13] Our study had twenty OSA patients with major neurocognitive deficit, of which 70% were in the age group of 50-70 years. This supports the fact that middle and elderly aged are at a higher risk for developing cognitive deficits when compared to the younger age with the same severity of OSA.[14] The comorbidities observed in the present study were HTN (58.69%), DM (29.3%), hypothyroidism (17.32%), and coronary artery disease (10.86%).

OSA leads to intermittent hypoxia and systemic inflammation. This along with changes in sleep micro- and macroarchitecture causing micro infarcts, stroke, reduced neurogenesis, changes in brain gray, and white matter and abnormal levels of Alzheimer's disease biomarkers can lead to progressive cognitive decline and dementia.[15] Thus, OSA through intermittent hypoxia can predispose and further amplify the pathologic mechanisms, resulting in the progression and worsening of depressive symptoms and cognitive deficits.[1,6]

The domains of the neurocognition such as attention, memory, verbal fluency, and visuospatial abilities were affected in most of the patients with major neurocognitive deficit.[1618] However, language skills were preserved.[19] In our study, twenty patients with OSA had major neurocognitive deficit, and in these patients, attention (85%), memory (80%), verbal fluency (65%), and visuospatial abilities (85%) were affected sparing language skills (35%) which was intact in most of the affected patients. A meta-analysis by Bucks et al.[20] including 33 studies concluded that deficits of attention, memory, and executive functions are the most affected cognitive domains in OSA. A systematic review and meta-analysis by Leng et al.[6] concluded that SDB is linked with a higher risk of CI and a small worsening in executive function.

Results of our study showed that an increase in severity of OSA can aggravate the neuropsychological deficit (P < 0.047). A study by Bedard et al.[18] showed that OSA not only worsens the neuropsychological deficits present in moderately affected patients but also produces new deficits. Several studies examined the strength of association between OSA severity as measured by AHI and the cognitive deficits. A few studies reported that more severe the OSA (AHI >30), more likely the cognitive deficits when compared to mild or moderate OSA,[4] while there was no association seen in some studies.[2123] Heterogeneous studies with different study designs and methods of assessing SDB are limiting factors to make firm conclusions on the strength of association.

Various studies[5,12] reported a much higher prevalence of depression among patients with OSA than the current study. In a study conducted by Mosko et al.,[24] 58% of patients with OSA met the Diagnostic and Statistical Manual criteria for depression and a study by Millman et al.[25] revealed that 45% of patients with OSA had depressive symptoms. A study by Aloia et al.[26] in 2005 which included 93 patients showed that 24% of the patients had mild depression, 5% moderate depression, and 4% had severe depression. In the present study, 21 patients (22.8%) had depression, out of which 9.7% had mild depression, 7.6% had moderate depression, and 5.4% had severe depression. Diverse definitions and instruments used in assessing depression in these studies can partially explain the variances in the prevalence of depression among patients with OSA. The present study did not show any significant association between severity of depression and AHI severity, which was concurrent with the available literature[27,28] but that does not prove the fact that there is no link between the two conditions.

OSA can be a risk factor for depression and both commonly share risk factors such as obesity, increasing age, and adverse lifestyles and symptoms such as daytime sleepiness, insomnia, fatigue, and poor quality of life.[29] Similar to previous studies,[29,30] our study showed that depression was more common among women (71.4%). In a study by Smith et al.[31] in 2002 which included 773 participants, 14% of patients had diagnosis of depression. Female patients with OSA were twice as likely as male to have depression.

In a systematic review and meta-analysis by Gupta et al.,[32] it was concluded that CPAP improves depressive symptoms in patients with OSA, and the positive effect is more in patients with severe depression. Another systematic review by Zheng et al.,[33] which included twenty randomized trials and 4255 participants, confirmed the same benefit of CPAP. The ADIPOSA study (anxiety and depression in patients with OSA before and after CPAP) concluded that 12-week CPAP therapy was highly favorable at improving the lack of positive affect, and stresses to use more precise depression and anxiety scales.[34] Similarly, a study by Edwards et al.[35] reported the beneficial effect of 3 months of CPAP in 228 subjects with OSA and depression. In this study, 3 months of CPAP treatment resulted in decrease in percentage of depression at baseline from 74.6 to 3.9 stressing the fact that prolonged treatment with CPAP may be beneficial.

Research also showed that long-term CPAP adherence can improve the cognition and slow the 1-year cognitive decline in older OSA patients.[36] The PROOF Study (protective effect of long-term CPAP therapy on cognitive performance in elderly patients with severe OSA) concluded that CPAP therapy may protect and maintain cognitive performance and functions in patients with OSA.[37] In a multicenter, double-blind, randomized study, Apnea Positive Pressure Long-term Efficacy Study, which studied the effects of CPAP versus SHAM concluded that cognitive function in severe OSA improved better than milder OSA patients. However, long-term follow-up did not show any improvement in attention/psychomotor and learning/memory functions.[38]

Clinical studies have demonstrated that successful treatment of OSA with CPAP improves cerebral microvascular perfusion and oxygenation, reduces vascular inflammatory responses, and thus may further inhibit cerebral and neurovascular damage.[1,6] As symptoms of cognition and depression overlap with that of OSA, there is a tendency to overlook these factors which may hinder the diagnosis and management of these conditions.[1]

Limitations

In the present study, a relatively small number of patients were evaluated (n = 92). The number of patients required to evaluate the prevalence of neurocognitive impairment and depression has to be prospectively determined by larger studies. The response to the treatment was not checked in these patients. The questionnaires that were administered were unblinded. The other risk factors such as smoking and alcoholism were not considered in present study.

CONCLUSIONS

OSA is identified as an independent risk factor for both depression and neurocognitive decline. It is highly recommended that OSA patients should be screened for neurocognition and depression. CPAP therapy is shown to have a positive effect on improving and maintaining cognitive performance and depressive symptoms. However, long-term prospective studies, randomized controlled trials, standardized methodology with uniform assessment scores, and definitions can overcome the hurdles and address the limitations in making firm future recommendations. This may better help to augment the diagnostic accuracy as well as to provide better clinical outcomes. Clinicians should closely monitor patients with OSA for cognitive dysfunction and depression as effective treatment of both the conditions can improve the overall quality of life.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Access this article online

Quick Response Code:

QC code

Website:
www.ijrc.in

DOI:
10.4103/ijrc.ijrc_84_20

REFERENCES

1. Kerner NA, Roose SP. Obstructive sleep apnea is linked to depression and cognitive impairment: Evidence and potential mechanisms. Am J Geriatr Psychiatry 2016;24:496-508.

2. Berry RB, Budhiraja R, Gottlieb DJ, Gozal D, Iber C, Kapur VK, et al. Rules for scoring respiratory events in sleep: Update of the 2007 AASM Manual for the scoring of sleep and associated events. Deliberations of the sleep apnea definitions task force of the American academy of sleep medicine. J Clin Sleep Med 2012;8:597-619.

3. Krysta K, Bratek A, Zawada K, Stepańczak R. Cognitive deficits in adults with obstructive sleep apnea compared to children and adolescents. J Neural Transm (Vienna) 2017;124:187-201.

4. Kielb SA, Ancoli-Israel S, Rebok GW, Spira AP. Cognition in obstructive sleep apnea-hypopnea syndrome (OSAS): Current clinical knowledge and the impact of treatment. Neuromolecular Med 2012;14:180-93.

5. Ejaz SM, Khawaja IS, Bhatia S, Hurwitz TD. Obstructive sleep apnea and depression: a review. Innov Clin Neurosci 2011;8:17-25.

6. Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of sleep-disordered breathing with cognitive function and risk of cognitive impairment: A systematic review and meta-analysis. JAMA Neurol 2017;74:1237-45.

7. Kim SJ, Lee JH, Lee DY, Jhoo JH, Woo JI. Neurocognitive dysfunction associated with sleep quality and sleep apnea in patients with mild cognitive impairment. Am J Geriatr Psychiatry 2011;19:374-81.

8. Hodges JR, Larner AJ. Addenbrooke's cognitive examinations: ACE, ACE-R, ACE-III, ACEapp, and M-ACE. In: Cognitive Screening Instruments: A Practical Approach. 2nd ed. Berlin, Alemania: Springer; 2017. p. 109-37.

9. Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry 1960;23:56-62.

10. Bruno D, Schurmann Vignaga S. Addenbrooke's cognitive examination III in the diagnosis of dementia: A critical review. Neuropsychiatr Dis Treat 2019;15:441-7.

11. Yaffe K, Laffan AM, Harrison SL, Redline S, Spira AP, Ensrud KE, et al. Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women. JAMA 2011;306:613-9.

12. Bjornsdottir E, Benediktsdóttir B, Pack AI, Arnardottir ES, Kuna ST, Gíslason T, et al. The prevalence of depression among untreated obstructive sleep apnea patients using a standardized psychiatric interview. J Clin Sleep Med 2016;12:105-12.

13. Lal C, Strange C, Bachman D. Neurocognitive impairment in obstructive sleep apnea. Chest 2012;141:1601-10.

14. Alchanatis M, Zias N, Deligiorgis N, Liappas I, Chroneou A, Soldatos C, et al. Comparison of cognitive performance among different age groups in patients with obstructive sleep apnea. Sleep Breath 2008;12:17-24.

15. Gosselin N, Baril AA, Osorio RS, Kaminska M, Carrier J. Obstructive sleep apnea and the risk of cognitive decline in older adults. Am J Respir Crit Care Med 2019;199:142-8.

16. Mazza S, Pépin JL, Naëgelé B, Plante J, Deschaux C, Lévy P. Most obstructive sleep apnoea patients exhibit vigilance and attention deficits on an extended battery of tests. Eur Respir J 2005;25:75-80.

17. Archbold KH, Borghesani PR, Mahurin RK, Kapur VK, Landis CA. Neural activation patterns during working memory tasks and OSA disease severity: Preliminary findings. J Clin Sleep Med 2009;5:21-7.

18. Bédard MA, Montplaisir J, Richer F, Rouleau I, Malo J. Obstructive sleep apnea syndrome: Pathogenesis of neuropsychological deficits. J Clin Exp Neuropsychol 1991;13:950-64.

19. Aloia MS, Arnedt JT, Davis JD, Riggs RL, Byrd D. Neuropsychological sequelae of obstructive sleep apnea-hypopnea syndrome: A critical review. J Int Neuropsychol Soc 2004;10:772-85.

20. Bucks RS, Olaithe M, Eastwood P. Neurocognitive function in obstructive sleep apnoea: A meta-review. Respirology 2013;18:61-70.

21. Olaithe M, Bucks RS. Executive dysfunction in OSA before and after treatment: A meta-analysis. Sleep 2013;36:1297-305.

22. Sforza E, Haba-Rubio J, De Bilbao F, Rochat T, Ibanez V. Performance vigilance task and sleepiness in patients with sleep-disordered breathing. Eur Respir J 2004;24:279-85.

23. Shpirer I, Elizur A, Shorer R, Peretz RB, Rabey JM, Khaigrekht M. Hypoxemia correlates with attentional dysfunction in patients with obstructive sleep apnea. Sleep Breath 2012;16:821-7.

24. Mosko S, Zetin M, Glen S, Garber D, DeAntonio M, Sassin J, et al. Self-reported depressive symptomatology, mood ratings, and treatment outcome in sleep disorders patients. J Clin Psychol 1989;45:51-60.

25. Millman RP, Fogel BS, McNamara ME, Carlisle CC. Depression as a manifestation of obstructive sleep apnea: Reversal with nasal continuous positive airway pressure. J Clin Psychiatry 1989;50:348-51.

26. Aloia MS, Arnedt JT, Smith L, Skrekas J, Stanchina M, Millman RP. Examining the construct of depression in obstructive sleep apnea syndrome. Sleep Med 2005;6:115-21.

27. Kripke DF, Ancoli-Israel S, Klauber MR, Wingard DL, Mason WJ, Mullaney DJ. Prevalence of sleep-disordered breathing in ages 40-64 years: A population-based survey. Sleep 1997;20:65-76.

28. Pillar G, Lavie P. Psychiatric symptoms in sleep apnea syndrome: Effects of gender and respiratory disturbance index. Chest 1998;114:697-703.

29. Harris M, Glozier N, Ratnavadivel R, Grunstein RR. Obstructive sleep apnea and depression. Sleep Med Rev 2009;13:437-44.

30. Asghari A, Mohammadi F, Kamrava SK, Tavakoli S, Farhadi M. Severity of depression and anxiety in obstructive sleep apnea syndrome. Eur Arch Otorhinolaryngol 2012;269:2549-53.

31. Smith R, Ronald J, Delaive K, Walld R, Manfreda J, Kryger MH. What are obstructive sleep apnea patients being treated for prior to this diagnosis? Chest 2002;121:164-72.

32. Gupta MA, Simpson FC, Lyons DC. The effect of treating obstructive sleep apnea with positive airway pressure on depression and other subjective symptoms: A systematic review and meta-analysis. Sleep Med Rev 2016;28:55-68.

33. Zheng D, Xu Y, You S, Hackett ML, Woodman RJ, Li Q, et al. Effects of continuous positive airway pressure on depression and anxiety symptoms in patients with obstructive sleep apnoea: Results from the sleep apnoea cardiovascular endpoint randomised trial and meta-analysis. E Clinical Medicine 2019;11:89-96.

34. Carneiro-Barrera A, Amaro-Gahete FJ, Saez-Roca G, Martin-Carrasco C, Ruiz JR, Buela-Casal G. Anxiety and depression in patients with obstructive sleep apnoea before and after continuous positive airway pressure: The ADIPOSA study. J Clin Med 2019;8:2099.

35. Edwards C, Mukherjee S, Simpson L, Palmer LJ, Almeida OP, Hillman DR. Depressive Symptoms before and after Treatment of Obstructive Sleep Apnea in Men and Women. J Clin Sleep Med 2015;11:1029-38.

36. Richards KC, Gooneratne N, Dicicco B, Hanlon A, Moelter S, Onen F, et al. CPAP adherence may slow 1-year cognitive decline in older adults with mild cognitive impairment and apnea. J Am Geriatr Soc 2019;67:558-64.

37. Crawford-Achour E, Dauphinot V, Martin MS, Tardy M, Gonthier R, Barthelemy JC, et al. Protective effect of long-term CPAP therapy on cognitive performance in elderly patients with severe OSA: The proof Study. J Clin Sleep Med 2015;11:519-24.

38. Kushida CA, Nichols DA, Holmes TH, Quan SF, Walsh JK, Gottlieb DJ, et al. Effects of continuous positive airway pressure on neurocognitive function in obstructive sleep apnea patients: The apnea positive pressure long-term efficacy study (APPLES). Sleep 2012;35:1593-602.

images

images

images

images

images

images

images

images

________________________
© 2021 Indian Journal of Respiratory Care. This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.