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22 Allergic Rhinitis andOSA
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threefold increase after 5h of continuous CPAP use, accompanied by up-regulation
of pro-inammatory chemokine MIP-2 [15]. In long term, baseline neutrophilic
local inammation in AR patients signicantly increases after 2 months of continuous CPAP treatment [18]. Thus, CPAP tolerance might be more impaired in patients
with rhinitis, as there would be an added component of CPAP-induced nasal inammation to the preexistent one. This would be troubling, since early CPAP rejection
rates are already high (up to 50%) among OSA patients, even before the initial titration [19]. Therefore, rhinitis patients should be the target of strategies to increase
CPAP acceptance and compliance. CPAP is the rst-line treatment of OSA, and
aside from its benets in reducing apnea events, it also improves subjective nasal
and ocular symptoms in OSA patients with AR [18]. There seems to be a delicate
balance between baseline inammation due to rhinitis, the added inammatory
response due to CPAP, and symptom improvement attributed to this therapy. Thus,
the relationship between rhinitis and OSA is multifactorial and requires consideration during the clinical approach and decision-making. Despite these ndings, rhinitis does not seem to be directly associated with OSA severity as measured by the
apnea/hypopnea index [13].
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22.2.3 Other Allergy-Related Issues Regarding CPAP
Aside from the previously mentioned ndings regarding the relationship between
rhinitis and CPAP therapy, there have also been cases of contact dermatitis attributed to CPAP. Scalf (1999) reported a case of allergic contact dermatitis due to
sensitization to a component of the CPAP mask strap. In this case, eczema developed symmetrically on the patient’s scalp after 1 month of using the mask [20].
Patch testing, the cornerstone of contact allergy diagnosis, yielded positive results
to the neoprene rubber strap, and dialkyl thioureas. The lesions entirely resolved
after replacing the rubber strap with a cloth one. Dialkyl thioureas are used as accelerators in vulcanization and are a known cause of contact allergy to rubber products.
Egesi (2012) reported two cases of facial eczema following CPAP use, welldemarcated and localized on the contact zones with the mask itself [21]. In both
cases, patch testing yielded negative results, and the patients were diagnosed with
irritant contact dermatitis and treated with topical corticosteroids. Despite being a
seemingly rare occurrence, contact dermatitis to CPAP mask components is another
issue that could interfere with tolerance and compliance with this therapy and
should be adequately studied if suspected.
22.2.4 Rhinitis andResponse toSurgery
In OSA patients with anatomical abnormalities, non-invasive treatment might prove
insufcient. These patients may benet from surgical intervention to correct the
identied anatomical anomalies that contribute to sleep apnea. While exible nasal
endoscopy might reveal some treatable pathologies such as a deviated septum,
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turbinate hypertrophy, and tonsillar hypertrophy, others may require further endoscopic studying. Drug-induced sleep endoscopy (DISE) allows for direct evaluation
of the upper airway during sleep and may reveal the specic location and cause of
obstruction. This allows for targeted surgery such as palatopharyngoplasty and
robotic tongue-base resection.
Few studies have evaluated the relationship between rhinitis, its etiology, and
response to corrective surgery in OSA patients. A recent study on 35 patients with
OSA undergoing nasal surgery (septoplasty and inferior turbinate reduction) to correct symptomatic nasal obstruction found that those with AR had higher success
rates (50%) than those without this diagnosis (4%), In contrast, the overall success
rate was 14% [22]. Thus, AR patients with OSA might benet more from nasal
surgery than their non-allergic counterparts, although nasal surgery alone may often
prove insufcient. Therefore, evaluating response to surgery particularly important
in AR patients, given the potential difculties with CPAP compliance in this group.
Further studies are warranted comparing response rates to surgery between AR and
NAR patients in other anatomical levels other than nose.
A. Carvallo and G. Gastaminza
22.3 Allergic Rhinitis andOSA
Although the relation between rhinitis and OSA has been widely studied, the impact
of the specic etiology of rhinitis is not clear. A 2004 study showed that OSA
patients were more likely to be sensitized to perennial allergens (house dust mites
and dog dander) than controls [23]. Atopy was also more prevalent among OSA
patients (32%) than controls (7%). A later study by Zheng (2017) reported that
perennial allergens were the predominant sensitization among OSA patients diagnosed with AR [13]. 49% of these patients were sensitized to perennial allergens
only; 29% to both seasonal and perennial allergens; and 22% were sensitized to
seasonal allergens only.
Both types of rhinitis-AR and NAR-seem to affect sleep quality, but to which
extent one might be more impactful than the other is not yet clear. Few studies that
compare OSA parameters directly between AR and NAR patients. Zheng (2017)
conducted a study of 240 OSA patients, of which 27% were diagnosed with AR and
29% with NAR.They found that OSA patients with AR suffered lower sleep efciency than those diagnosed with NAR and those without rhinitis [13]. On the other
hand, NAR patients had lower oxygen saturation than those without rhinitis.
Kalpaklioğlu (2009) compared patients with AR and NAR and performed polysomnography evaluations. They found lower sleep efciency and shorter sleep duration
in the NAR group than in AR patients [24]. The proportion of subjects diagnosed
with OSA was signicantly higher in the NAR group (83%) than in the AR group
(36%), and NAR correlated with OSA diagnosis and apneas. A recent meta-analysis
of 27 observational studies reported that OSA patients with AR presented more
sleep disturbances and daytime dysfunction than the control groups. However, the
quality of evidence was reportedly low [25]. Thus, which rhinitis subtype has more
inuence on OSA still lacks a clear answer.
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401
The mechanisms involved in allergenic inammation are complex and dynamic,
several elements might explain the effects of the etiology of rhinitis on OSA parameters. As previously mentioned, IL-4 is an integral part of the inammatory response
in allergic rhinitis. IL-4 also seems also related to sleep quality, as it positively correlates with time to onset of REM sleep and negatively correlates with REM sleep
time [26]. Thus, sleep in AR patients would be less restorative, contributing to more
daytime dysfunction and other observed sleep-related disturbances. It is worth noting that IL-4 expression in atopic individuals seems to be independent of the presence and intensity of rhinitis symptoms, while other cytokines such as IL-5 are more
expressed in symptomatic individuals during pollen season [27]. This would mean
that sleep efciency, related to IL-4, might be more impaired in allergic individuals
independently of symptomatic seasonal variations. Thus, the relationship between
AR and OSA may go well beyond the presence of nasal congestion. Further investigation is warranted to determine whether the effect on sleep parameters is due to
allergenic inammation, the persistence or seasonality of nasal symptoms, a combination of both, or some other factor.
Take-Home Message
• Allergic rhinitis and OSA seem interwoven, although the specic physiological
mechanisms that explain the observed differences in OSA characteristics
between AR and NAR patients require further study. The available evidence
points to an association between baseline allergenic inammation and lower
sleep quality and efciency in these patients. There is also a link between AR and
compliance and response to non-invasive and invasive OSA treatment. Thus,
evaluation by an allergy specialist is recommended when approaching a patient
with a suspicion of sleep apnea and nasal symptoms. Further investigation is
warranted regarding the relationship between these two frequently coexisting
pathologies.
References
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rhinitis and its impact on asthma (ARIA) guidelines-2016 revision. J Allergy Clin Immunol.
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2. Ojeda P. Alergológica 2015: a National Survey on allergic diseases in the Adult Spanish
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Population. J Investig Allergol Clin Immunol. 2018;28(5):321–9.
4. Bousquet J, Anto JM, Bachert C, Baiardini I, Bosnic-Anticevich S, Walter Canonica G, etal.
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5. Lebman DA, Coffman RL.Interleukin 4 causes isotype switching to IgE in T cell-stimulated
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6. Harb H.Mechanisms of dupilumab. Clin Exp Allergy. 2020;50(1):5–14.
7. Corren J.Anti-interleukin-5 antibody therapy in asthma and allergies. Curr Opin Allergy Clin
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8. Miyahara S.IL-13 is essential to the late-phase response in allergic rhinitis. J Allergy Clin
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9. Rondon C.Prevalence and clinical relevance of local allergic rhinitis. Allergy. 2012;67:1282–8.
10. Ogulur I. Advances and highlights in biomarkers of allergic diseases. Allergy.
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11. Zidarn M.Clinical and immunological differences between asymptomatic HDM-sensitized
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12. Lofaso F, Coste A, d'Ortho MP, Zerah-Lancner F, Delclaux C, Goldenberg F, Harf A.Nasal
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13. Zheng M, Wang X, Ge S, Gu Y, Ding X, Zhang Y, Ye J, Zhang L.Allergic and non-allergic
rhinitis are common in obstructive sleep apnea but not associated with disease severity. J Clin
Sleep Med. 2017;13(8):959–66.
14. Parikh NG, Junaid I, Sheinkopf L, Randhawa I, Santiago SM, Klaustermeyer WB.Clinical
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15. Almendros I, Acerbi I, Vilaseca I, Montserrat JM, Navajas D, Farré R.Continuous positive
airway pressure (CPAP) induces early nasal inammation. Sleep. 2008;31(1):127–31. https://
doi.org/10.1093/sleep/31.1.127.
16. Pépin JL, Leger P, Veale D, Langevin B, Robert D, Lévy P.Side effects of nasal continuous
positive airway pressure in sleep apnea syndrome. Study of 193 patients in two French sleep
centers. Chest. 1995;107(2):375–81. https://doi.org/10.1378/chest.107.2.375.
17. Brander PE, Soirinsuo M, Lohela P. Nasopharyngeal symptoms in patients with obstructive
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I.Effects of CPAP in patients with obstructive apnoea: is the presence of allergic rhinitis relevant? Sleep Breath. 2017;21(4):893–900.
19. Engleman HM, Wild MR.Improving CPAP use by patients with the sleep apnoea/hypopnoea
syndrome (SAHS). Sleep Med Rev. 2003;7(1):81–99.
20. Scalf LA, Fowler JF Jr. Allergic contact dermatitis caused by dialkyl thioureas in a patient with
sleep apnea. Am J Contact Dermat. 1999;10(3):169–71.
21. Egesi A, Davis MD.Irritant contact dermatitis due to the use of a continuous positive airway
pressure nasal mask: 2 case reports and review of the literature. Cutis. 2012;90(3):125–8.
22. Kim SD, Jung DW, Lee JW, Park JH, Mun SJ, Cho KS.Relationship between allergic rhinitis and nasal surgery success in patients with obstructive sleep apnea. Am J Otolaryngol.
2021;42(6):103079.
23. Canova CR, Downs SH, Knoblauch A, Andersson M, Tamm M, Leuppi JD.Increased prevalence of perennial allergic rhinitis in patients with obstructive sleep apnea. Respiration.
2004;71(2):138–43.
24. Kalpaklioğlu AF, Kavut AB, Ekici M.Allergic and non-allergic rhinitis: the threat for obstructive sleep apnea. Ann Allergy Asthma Immunol. 2009;103:20–5.
25. Liu J, Zhang X, Zhao Y, Wang Y.The association between allergic rhinitis and sleep: a systematic review and meta-analysis of observational studies. PLoS One. 2020;15(2):e0228533.
26. Krouse HJ, Davis JE, Krouse JH.Immune mediators in allergic rhinitis and sleep. Otolaryngol
Head Neck Surg. 2002;126(6):607–13.
27. Nakai Y, Ohashi Y, Kakinoki Y, Tanaka A, Washio Y, Nasako Y, Masamoto T, Sakamoto H,
Ohmoto Y.Allergen-induced mRNA expression of IL-5, but not of IL-4 and IFN-gamma, in
peripheral blood mononuclear cells is a key feature of clinical manifestation of seasonal allergic rhinitis. Arch Otolaryngol Head Neck Surg. 2000;126(8):992–6.
A. Carvallo and G. Gastaminza
Psychiatric Illness andObstructive Sleep
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Apnea
HectorOlivaresRodriguez
23.1 Introduction
Despite multiple meta-analyses and articles that have addressed the issue of psychiatric illness and obstructive sleep apnea for decades, there is an inconsistent correlation between these medical conditions that persists, causing signicant bias handling
guidelines of both, not only in clinical practice but more signicantly in the information that students receive in medical schools worldwide.
The purpose of this chapter is to emphasize that the chronic presence of undiagnosed sleep apnea in the presence of certain mental illness can increase the severity
of the condition and provide poor pharmacological treatment that worsens both
medical conditions. Thus, I will address the most related psychiatric conditions, like
depression, attention-decit disorder and hyperactivity, eating disorders, and
insomnia.
23
23.2 Depression
The WHO denes depression as a disorder characterized by persistent sadness and
a lack of interest or pleasure in previously rewarding activities. In addition, it can
alter sleep and appetite, often accompanied by tiredness and lack of concentration.
It is a signicant cause of disability worldwide and signicantly impacts morbidity.
H. O. Rodriguez (*)
Faculty of Medicine of the Universidad Autonoma de San Luis Potosi,
San Luis Potosi, Mexico
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_23
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H. O. Rodriguez
It is estimated that at least 322 million people worldwide suffer from depression,
up 18% from a decade ago. Depression and anxiety increased by more than 25%
only during the rst year of the pandemic [1, 2].
1
In the DSM V, the term depression is used primarily to refer to any depressive
disorder.
For the diagnosis of major depression, ≥5 of the following symptoms must have
been present almost every day for a given period of 2weeks, and one of them should
be depressed mood or loss of interest or pleasure:
Depressed mood most of the day.
A marked decrease in interest or pleasure in all or almost all activities most of
the day.
Signicant increase or loss (>5%) of weight, or decrease or increase in appetite.
Insomnia (often sleep-maintaining insomnia) or hypersomnia.
Agitation or psychomotor delay observed by others (not reported by the same
patient).
Fatigue or loss of energy.
Feelings of worthlessness or excessive or inappropriate guilt.
Decreased ability to think or concentrate, or indecision.
Recurrent thoughts of death or suicide, attempted suicide, or a specic plan to
commit suicide [3].
The ICD currently denes obstructive sleep apnea (OSA), when one of these
two criteria is met
1. The presence of an apnea–hypopnea index (AHI) ≥15 h, predominantly
obstructive.
2. The presence of an AHI 5 and 15 accompanied by one or more of the following
factors: excessive daytime sleepiness, nonrestorative sleep, excessive tiredness,
and/or sleep-related deterioration of quality of life, not justiable by other
causes [4].
OSA is a disease characterized by total or partial occlusion of the upper airway
of patients during sleep. Because of this, breathing stops until a microarousal occurs
that reactivates the muscles and reopens the airways. Apnea occurs when the elements that tend to close the airway cannot be compensated by the ability of the
dilator muscles of the pharynx and/or respiratory centers to keep it open.
Due to these apneas, which produce hypoxia and sleep fragmentation, patients
cannot sleep and rest properly and, during the day, they usually suffer from daytime
sleepiness or tiredness [4].
In physiological terms, several symptoms of a depressed mood are the consequence of sleep apnea, and the impact of hypoxemia and hypoxia at the cellular
level is considered a result of a neuro inammatory process [5] (Fig.23.1).
1
American Psychiatric Association, DSM V Diagnostic Criteria Consultation Guide, Arlington,
VA, American Psychiatric Association, 2013.
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23 Psychiatric Illness andObstructive Sleep Apnea
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23.3 Neuroinflammation Theory
Neuroinammation is dened as the brain’s response to injury, infection, or disease.
In general, the purpose of inammation is to remove or inactivate potentially harmful agents or damaged tissue. This response is mainly mediated through two cellular
systems: the central nervous system glia and the hematopoietic system’s lymphocytes, monocytes, and macrophages.
The results of studies suggest that patients with a major depressive disorder show
changes in immunological markers, including an increase in proinammatory cytokines activity [6].
In addition, chronic low-grade inammation can lead to changes in brain structure and synaptic plasticity that led to neurodegeneration. Therefore, it should be
added that neuronal repair due to increased glucocorticoid levels may be the initial
markers of depression and a prelude to dementia in older people [7].
Signicantly, chronic stress can exacerbate the release of proinammatory cytokines and thus precipitate depressive episodes. It has been shown that stress, through
its interaction with the immune system, can increase levels of proinammatory
cytokines such as tumor necrosis factor TNF-α, interleukin IL-1β, IL-6, and
IL-2R [8, 9].
Inammatory markers, such as IL-6, IL-1β, CRP, and TNF-α, are increased in
inammatory diseases and otherwise healthy people with MDD.
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H. O. Rodriguez
23.3.1 Relation Between Inflammatory Process andDepression
Cytokines make changes to the central nervous system through four pathways
[10, 11]
1. Cytokines can activate primary afferent neurons.
2. Cytokines, released by macrophage-like cells in response to disease-causing
agents, diffuse through the cerebral circumventricular organs.
3. Cytokine transporters saturate the blood–brain barrier.
4. Cytokine IL-1 activates receptors on perivascular macrophages and endothelial
cells of brain venules and generates the local release of prostaglandin E2.
23.3.2 Analysis
After reviewing the contexts of global nomenclature of both medical conditions and
the physiology of the inammatory processes that occur in OSA, the correlation
between the two can be appreciated, which must be included in every patient’s clinical history. Both in people with depressive symptoms and respiratory alterations
should be intentionally explored. In people with the already assigned diagnosis of
OSA, the presence of depression or depressive symptoms should be explored since
this causes depression that ends up being classied as resistant or poorly addressed.
On the other hand, the results in the approaches to OSA will not be those expected
by the health professional due to the omission of the condition of depression in the
patient’s medical history [12].
The most common symptoms shared by both medical conditions are shown in
Table23.1.
23.3.3 Conclusions
It is essential that the curricula of medical schools are updated and devote more
hours/class, in sleep medicine, since the panorama reported by the WHO is worrying in the issue of the incidence and prevalence of depression in the last year, and if
the problem continues to be addressed as before, the numbers will only continue to
be exposed (Fig.23.2).
Table 23.1 Most common symptoms shared by both medical conditions
Cognitive and emotional symptoms Physical symptoms
Difculty in the ability to acquire Excessive daytime sleepiness
Decreased memory capacity Hypersomnia
Decreased attention span Fragmented sleep
Loss of interest in conducting activities Alterations in appetite
Labile mood Low libido
Apathy Impotence
23 Psychiatric Illness andObstructive Sleep Apnea
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Fig. 23.2 Common consequences of fragmented sleep
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Multidisciplinary work is needed in the treatment of major depressive disorder, a
medical condition of multifactorial origin, ranging from the molecular, the genetic,
the cellular, the systemic, including to the environment, and is not reduced only to
“a neurochemical imbalance of certain substances in the brain”.
It is key to prove solid foundations of physiology and understand the concept of
general systems theory, taking it to clinical practice, to be able to see the real picture
and not just a part of it.
Returning to the term “allostasis” would help a lot to understand that many conditions that we classify as “diseases” are simply the way in which the body, after
being subjected to situations of stress, makes physiological changes to readapt and
maintain its viability.
23.4 Insomnia
Most people are not adequately informed about what it is to sleep well and therefore
do not know how to distinguish between sleeping well and poor sleeping or sleeping
poorly and the consequences of not doing so.
Sleeping well is one of the healthiest and most fruitful habits, but unfortunately
one of the least practiced and is treated as a “great luxury.”
The WHO considers insomnia the difculty in falling asleep or maintaining
sleep; or the complaint feeling of nonrestorative sleep that generates a signicant
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H. O. Rodriguez
discomfort or interference with social and work activities and occurs on at least
three nights a week [1].
Excessive daytime sleepiness is a condition that makes the person feel very sleepy
during the day and is considered a continuum of insomnia or sleep disturbances.
Without the presence of insomnia or any disorder that affects the quantity and
quality of sleep, there is no presence of excessive daytime sleepiness [13].
According to the World Health Organization, lack of sleep represents one of the
most common problems in people: 40% of the world’s population has insomnia [1].
23.4.1 Statistical Impact
In the United States, according to the Sleep Foundation [14], with data updated to
May 2022, between 10 and 30% of adults struggle with chronic insomnia. Women
have a lifetime risk of insomnia that is up to 40% higher than men. As many as
15–30% of men and 10–30% of women meet a broad denition of obstructive sleep
apnea. The second sleep disorder with the highest incidence and prevalence is
obstructive sleep apnea. It has a prevalence of 10–30%, which together with insomnia represent 80% of the causes of poor sleep (Fig.23.3).
The impact of insomnia on during the pandemic was that the incidence and prevalence rate increased more than any other mental health condition [15].
The body takes insomnia as an inammatory process, which will have repercussions at the genetic, cellular, systemic, and environmental levels.
23.4.2 Aftermath ofCOVID-19
Insomnia is the most common sequelae of persistent COVID-19. U.S. researchers
have found that moderate to severe sleep disturbances are prevalent among the postacute sequelae of SARS-CoV-2 infection.
As per a team of researchers from the Cleveland Clinic (USA) who presented at
the SLEEP 2022 meeting, almost 40% of people with persistent COVID-19 suffer
from a sleep-related problems.
They analyzed data collected from 962 patients with long COVID-19 or persistent COVID-19 between February 2021 and April 2022. Patients recovered from
COVID-19 and completed sleep disturbance and fatigue questionnaires.
Fig. 23.3 Sleep disorders
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