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 Table of Contents  
REVIEW ARTICLE
Year : 2022  |  Volume : 6  |  Issue : 1  |  Page : 2-5

The complicated simple snoring


Department of Paediatrics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China

Date of Submission10-Dec-2021
Date of Decision20-Feb-2022
Date of Acceptance08-May-2022
Date of Web Publication02-Jan-2023

Correspondence Address:
Ms. Esther Tin Wing Cheng
Department of Paediatrics, Chinese University of Hong Kong, 6/F, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong Special Administrative Region
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/prcm.prcm_22_21

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  Abstract 

Primary snoring, also known as simple snoring, was historically regarded as a benign entity on the sleep-disordered breathing spectrum until recently, when more and more evidence suggested the otherwise. This article aims to provide an overview on the research directions of primary snoring and their relevant clinical significance.

Keywords: Cognition, hypertension, obstructive sleep apnoea, primary snoring


How to cite this article:
Cheng ET. The complicated simple snoring. Pediatr Respirol Crit Care Med 2022;6:2-5

How to cite this URL:
Cheng ET. The complicated simple snoring. Pediatr Respirol Crit Care Med [serial online] 2022 [cited 2023 Feb 8];6:2-5. Available from: https://www.prccm.org/text.asp?2022/6/1/2/366614




  A Continuum of Snoring? Top


Primary snoring (PS), also known as simple or non-apneic snoring, is a relatively common condition characterized by habitual snoring (HS) >3 nights per week and normal conventional polysomnography (PSG). Current estimation reported that 7.2% and 4.8% of children in Hong Kong suffered from HS and obstructive sleep apnoea (OSA) respectively.[1],[2] Positioned at the milder end of sleep-disordered breathing (SDB) spectrum,[3],[4] PS was historically regarded as a benign entity without causing significant medical consequences for the snorer and co-snorer until recently. As accumulating evidence has identified PS as an independent risk factor for complications described originally for OSA, such as poorer neurocognitive-behavioral function[5] and higher cardiovascular risks,[6] an urgent need for a paradigm shift in the current clinical thinking and management strategy of PS is hence required.


  Definition of PS Top


Despite the high prevalence in the general population, currently, we see a lack of consensus regarding the cut-off and occasional requirements of PS. The distinction between PS and other sleep disorders is, conceptually and originally, based on the absence of clinical consequences. Previously, the 2005 American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders (ICSD-2) was amongst the most commonly cited definition of PS.[7] It defined PS as loud upper airway breathing sounds in sleep without episodes of apnoea or hypoventilation.[8] In 2014, the update by ICSD-3 recognized that an absolute absence of apnoea is not essential to delineate the difference in clinical outcomes of PS and other sleep disorders.[9] Since then, <1 apnoea/hypopnoea events per hour of sleep on the Apnoea-Hypopnoea Index (AHI) in the absence of any clinical consequences was commonly used to identify PS in research settings.[7] It is also worth noticing that this working definition is arbitrary, without reliable clinical validation, and varies between studies.

Meanwhile, it is clear that AHI alone may not be sufficient to define PS. In 2016, Kryger redefined PS based on the duration, oxygen saturation, airflow limitation, and the level of anatomical obstruction in the hopes to model the absence of any physical implications due to PS.[10] For the psychological aspect, i.e., to study the disturbance to patients and possibly the co-sleepers, a noise approach that looks into sound patterns and cut-offs of specific acoustic parameters may be appropriate.[11] The limitation of such an approach, however, lies in the subjectivity of individuals’ perception of snoring, making objective quantification of nuisance from PS extremely difficult. Considering the dyadic nature of sleep, recent studies, such as the one by Genlyd et al. on noise exposure, promote the assessment of ‘noise annoyance level’ that include aspects such as ‘daytime sleepiness’ and ‘tiredness’ in the paired comparison.[12]

Currently, to distinguish PS from other sleep disorders, overnight PSG is the only currently available definitive investigation.[5] Diagnosis is made based on clinical history, the number of respiratory events per hour of sleep on PSG, and the corresponding physiological consequences in terms of gas exchange abnormalities and arousals. Some authors choose a composite respiratory disturbance score to diagnose PS based on several factors such as the extent of SpO2 desaturation and respiratory arousals.[13],[14]


  Risk Factors of HS and PS Progression Top


To the best of our knowledge, no studies have evaluated the risk factors of PS thus far. Studies reporting risk factors for HS may provide clues for the predictor of PS development. A large cohort across the Asia Pacific showed a higher prevalence of HS in males and Caucasians,[1] most probably due to their genetically determined craniofacial structure. Nonetheless, prematurely born children may be at a higher risk for snoring and SDB as well.[1] Additionally, the severity can be made significantly lower by breastfeeding for at least 2 months according to one study.[15]

Studies examining the natural history of PS are also scarce. Whether PS is associated with the development of other more severe sleep disorders, for example, OSA remains unclear. In a community-based follow-up study by Li et al, persistent snoring and overweight or obesity were found to be the risk factors for PS progression.[16] Persistent snoring, with its relatively high negative predictive value,[16] can hence be used as a guide for SDB progression. Meanwhile, weight reduction may play an important role in the management of PS. In addition, puberty has no significant effect on PS progression,[16] suggesting that changes in sex hormones were not a primary modulator of upper airway function during puberty. Neither sex nor adenotonsillar hypertrophy was identified as a significant predictor.[16]


  Cardiovascular Impacts of PS Top


Emerging evidence has shown that childhood PS has adverse effects on the cardiovascular system,[17] rendering the need to identify and treat as soon as possible.

A local cross-sectional study by Li et al. published in 2009 was among the very few who first provided evidence on the potential cardiovascular risks in PS children.[18] By demonstrating that PS was an aspect of the dose-response relationship between SDB and blood pressure (BP), it provided a new insight contrary to the universal belief that PS was entirely benign. Nighttime BP particularly was found to be significantly higher in the PS cohort after adjusting for age, sex, and body mass index (BMI). The findings carry prominent significance in the sense that elevated childhood BP is associated with increased carotid intima-media thickness (cIMT) and arterial thickness, which are the preceding markers of atherosclerosis.[19] With a similar elevation in BP level during childhood, it predicts a worse prognosis of future cardiovascular adverse events, adult hypertension, and metabolic syndrome.[20]

The association between PS and endothelial function was first proposed by the same author in 2011, which showed a significantly reduced flow-mediated vasodilation (FMD) among PS children independent of body size and OAHI.[21] Unlike OSA, the mechanism underlying PS and impaired endothelial function is not associated with hypoxia, oxidative stress, and frequent arousals, as reflected by the insignificant differences in all respiratory parameters, arousal indexes, and sleep architecture between PS and controls in the same study. These results, inspiringly, provided grounds on the possibility that PS may not simply be a milder form of OSA, but a part of a more complex phenotype that is yet to be determined.

The causal association between childhood PS and undesirable cardiovascular outcomes is further supported by a recent longitudinal study by Au et al.[22] Predictive markers of cardiovascular disease (CVD), namely reduced FMD, increased cIMT, and elevated BP remained significant at 5-year follow-up of PS subjects aged 6 to 18 irrespective to the change of OSA severity. Strategies to alleviate upper airway narrowing and the resultant CVD burden should, therefore, not be overlooked. Though a proven treatment for childhood snoring is not currently available besides nasal steroids,[23],[24] the study highlighted the clinical importance of regular monitoring for children with PS on their SDB and cardiovascular status.


  Neurocognitive and Behavioral Impacts of PS Top


There is growing evidence that children with PS exhibit cognitive and behavioral deficits equivalent to children with OSA when compared to non-snoring controls.[25],[26]

In a pioneer study by Blunden et al. published in 2000, a significant difference in cognitive functioning was accidentally found between snoring children and controls.[27] The unexpected finding sparked much intrigue surrounding the morbidity of PS. Subsequently, cognitive outcomes, such as IQ score, memory, attention, executive function, organization ability, motor coordination, verbal ability, and fluency, were investigated by various studies.[25],[28],[29],[30] The observation of deficit in PS children is not universal. It is noted that in the majority of studies, results of cognitive assessment in PS subjects, even if found to be significantly lower than controls, still fall within normative limits. This highlights that whether snoring is associated with cognitive impairment later in life still requires further investigation. However, the adverse effect of PS on cognitive functioning is still undeniable if we compare the percentage of PS children labelled with impaired cognition and those who are carefully matched to control.[31]

Studies have consistently shown behavioral impairment in children with PS.[13],[27] Most commonly reported deficits include hyperactivity, inattention, and somatic complaints. A surprising finding was found in the Jackman et al. study in which the PS group exhibited the greatest deficit in a majority of the behavioral domains, followed by the mild OSA group.[32] Another cross-sectional study by Brockman et al. also reported that children with PS had a higher risk of inattentive behavior than those with OSA.[33] A 10-fold increase in sleepiness was observed as well in PS children compared to a 5-fold increase in the OSA group.[33] All evidence seems to be hinting that PS may not simply be a milder form of OSA at the SDB spectrum.


  Proposed Mechanistic Pathways Top


Currently, the clinical outcomes of OSA are explained by the hypoxic insult to the developing brain and sleep disruption due to repeated arousals.[34] There has been an endeavor to evaluate if those physiological stresses also account for the deficit in PS. However, current data cannot depict the association.[31] It is possible that the subtle differences in oxygen level and sleep parameters could be missed using the conventional protocol. Measures of cerebral oxygenation in response to a respiratory event may be inaccurately reflected at the periphery and that excessive daytime sleepiness may not be a fit measurement for arousals. More objective assessments, such as differences in cerebral blood flow velocity[35] and sleep latency test,[36] may hence be required for further investigation.

Some of the neurocognitive and cardiovascular impacts of PS, nonetheless, can be explained by a large community-based study by Zhu et al. in 2014 consisting of 619 subjects.[37] Compared to non-snoring children, the percentage of slow-wave sleep (SWS) decreased significantly in the prepubertal PS group. SWS is associated with better neurocognitive functioning.[38] Meanwhile, the percentage of non-rapid eye movement stage 1 (N1) sleep as well as wake after sleep onset (WASO), a representation of sleep deficiency, were both significantly elevated in the pubertal sub-group. With less N1 sleep, impacted learning and memory are explained. Along with a study by Zhang et al. which showed the direct correlation between lower sleep efficiency (i.e. higher WASO) and increased sympathetic activity as reflected by a higher 24-hour urinary catecholamine level,[39] the critical role of PS in mediating cardiovascular complications is also conjointly manifested.


  Treatment of PS Top


PS management can be conservative or non-conservative, depending on the associated underlying conditions. For snorers with obesity and orofacial myofunctional disorders (OMDs), for instance, weight loss and myofunctional therapy would be the first-line treatment respectively.[40] The AASM also recommends oral appliance (OA) therapy for PS in general.[41] There is currently no consensus on the optimal design of OAs but the therapeutic outcome in term of AHI and oxygen desaturation index (ODI) appear to be better if the device is custom-made.[42] It is worth noted that OAs, though effective, are associated with low compliance.[43] Meanwhile, surgical approaches like uvulopalatopharyngoplasty (UPPP) and adenotonsillectomy, though radical, are also available for patients with associated obstructed upper airway due to craniofacial anomalies as well as adenotonsillar hypertrophy. Till date, there are no drugs available for treating the primary pathology of PS.[44]


  Conclusion Top


PS is a relatively common sleep disorder amongst the paediatric population. Although the original definition aims to delineate PS from OSA based on the absence of clinical consequences, increasing evidence revealed that snoring, even without associated changes in respiratory markers, may be associated with extensive cardiovascular and neurocognitive outcomes. More studies are required to elucidate the effects of PS on various disease development and appropriate action may be required to prevent these adverse outcomes.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Abstract
A Continuum of S...
Definition of PS
Risk Factors of ...
Cardiovascular I...
Neurocognitive a...
Proposed Mechani...
Treatment of PS
Conclusion
References

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