Can snoring induce or worsen obstructive sleep apnea?

Medical Hypotheses (1998) 50, 125-129

© HarcourtBrace & Co. Ltd 1998

Can snoring induce or worsen obstructive sleep apnea? D. TECULESCU INSERM Unit6 420. Facult6 de M~decine, B.P. 184, 54505 Vandoeuvre, France (Tel: +33 383592595; Fax: +33 383592596)

Abstract - - Snoring and sleep apneas are breathing disorders intimately associated during sleep. Most snorers are 'simple' or 'nonapneic', as the prevalence of snoring is much higher than that of sleep apneas. The vibrations transmitted to the pharyngeal structures by snoring span a large range of frequencies, while the energy transmitted may reach high values. A deleterious effect of these vibrations can therefore be considered. In 1983 a group of investigators from Bologna described five cases of heavy snorers of increasing severity, suggesting that they correspond to the natural history of 'heavy snorers' disease'. The present article reviews the data published since 1983 in favor of this hypothesis: anatomic lesions of the upper airway mucosa, pharyngeal muscles and nerves, and clinical observations in snorers. The conclusion stresses the absence of ultimate proof in favor of this attractive hypothesis: we lack the demonstration of a significant increase of the incidence of sleep apnea in a group of nonapneic snorers in a longitudinal follow-up study.

Introduction Breathing irregularities during sleep were noticed more than one hundred years ago in healthy subjects (1). Using complex polygraphic recording Gastaut and coworkers documented cessation of breathing during sleep, and described central, obstructive and mixed apneas in 1965 (2). Guilleminault et al stressed the clinical significance of sleep apneas and proposed the criterion of 10 s as a limit of normal (3). Subsequently, arterial desaturation and other symptoms were described in patients in whom breathing does not stop; Gould et al proposed the term 'sleep Based on a lecture deliveredat the 4th NationalUpdatein Pulmonology,Coimbatore,TamilNadu, India, May 12, 1996.

hypopnea syndrome' as these patients were found to hypoventilate (4). There is no consensus to date on the definition of sleep hypopnea (5): some authors accept a reduction of at least 50% of airflow and thoracoabdominal movements, lasting more than 10 s; other authors also require an associated desaturation. The severity of breathing disturbance is expressed by indices computed from the number of events per hour of sleep: 'apnea index' (AI) or 'apnea-hypopnea index' (AHI). The upper limits of normal, proposed originally by Guilleminault et al on clinical bases (6) are 5 and 15 per hour, respectively. The term 'sleep apnea syndrome' was coined for patients with recurrent sleep apneas/hypopneas associated with clinical impairment: e.g. daytime excess sleepiness, impaired cardiopulmonary function, etc.

Received 12 September1996 Accepted 17 December1996 125

126 (7). A novel entity, the 'upper airways resistance syndrome' has been described recently by Guilleminault et al (in patients with a clinical complaint (excess daytime sleepiness) and flow limitation during sleep (evidenced by increase in peak inspiratory pressure and decrease in tidal volume) related to repeat transient micro-arousals (8). The latter lead to sleep fragmentation, explaining the daytime sleepiness; no desaturation is observed. Out of the 15 patients decribed by the authors, only l0 were snorers (9). Robin (10) was the first to attempt to define snoring and decribe its generation. 'Simple snoring' is defined currently by the American Thoracic Society Board of Directors as 'fricative upper airways noise not associated with apneas or hypopneas' (7). Snoring is usually an inspiratory sound, expiratory snores being infrequent (11). Liistro et al have demonstrated differences between nasal (= vibration of the uvula) and mouth (= vibration of whole soft palate) simulated snores (12). Several authors have proposed various classifications based on duration, intensity or frequency of snores. For example, Guilleminault et al speak of 'continuous snores' if these are present more than 75% of the night and of 'intermittent snores' if less than this threshold (8). Lugaresi et al describe 'continuous' and 'discontinuous' snores (13); according to the frequency, they distinguish 'simple' snores generated by the soft palate vibrating at a frequency of 40 to 60 Hz, while in patients with obstruction sleep apnea (OSA) the pharynx may vibrate at 1000 to 3000 Hz. The severity of snoring may be expressed by a 'snoring index' based on sound intensity (14,15). Heavy snorers may exceed 70 to 80 dB intensity, obliging the bedpartner to leave the room and putting the snorer itself at risk of hypoacusia (16). An inspiratory flow limitation exists in both snorers and in patients with OSA (17). Subtle differences in snoring characteristics between apneic and nonapneic snorers have been recorded (13,14). Perez-Padilla et al have suggested that the quality of snoring sounds could help in detecting apneas among a group of snorers (11). Anatomic factors explain in part these differences: the site of airway narrowing is situated between the tongue base and the hyoid bone in 'simple' snorers, while being located at the velopalatal level in OSA (18). While the pharyngeal volume is not significantly different between snorers and nonsnorers (19), modem techniques, e.g. MRI, have provided evidence of a difference in pharynx shape between OSA or snorers and healthy subjects (the longer axis being in the coronal plane in the latter) (20). Bradley et al (21) and Hoffstein et al (14) have reported on a smaller pharyngeal cross-sectional area in snorers. An increase of pharyngeal wall compliance was reported by Brown et al (22) in patients with OSA.

MEDICALHYPOTHESES

The prevalence of snoring is higher in males and increases with age; two Italian studies found prevalences of 15% and 17% in middle-aged males (13,23). Among other risk factors for snoring, a weight excess, heavy cigarette or alcohol consumption, a history of respiratory symptoms, and use of hypnotics or tranquilizers were described (24).

Natural history of snoring: the 'Italian hypothesis' In 1983, Lugaresi et al reported five cases of heavy snorers, grouped into four categories (25): (a) subjects with heavy snoring and sporadic apneas; (b) subjects with heavy snoring and prolonged sequences of obstructive apneas; (c) subjects with obstructive apneas almost the whole length of sleep; (d) subjects with OSA and alveolar hypoventilation during wakefulness. They suggested the classification of 'heavy snorers disease' into four stages (0 to HI) corresponding to the clinical picture above. The same authors later speculated that snoring and severe OSA represent the extreme points of the natural history of heavy snorers disease (26). In recent years, a series of studies suggested that snoring and OSA are not only strongly associated, but that vibrations generated by the former could exert deleterious effects on upper airway wall structures, an effect similar to the structural changes induced by vibratory stress on isolated dog bronchi as reported by Sinclair and Roach (27). Effects of snoring on airway mucosa and submucosa, on pharyngeal muscles and pharyngeal motor nerves will be reviewed in that order, followed by some clinical observations.

Pharyngeal abnormalities in snorers M u c o s a and muscle

Edema and inflammatory cell infiltration of the soft palate m u c o s a were described by Cohn et al (28) in three snorers; the authors hypothesized that the lesions were due to vibratory trauma. If mucosal edema were to promote apnea, the finding could be compared to the induction of OSA in snorers by pharyngeal anesthesia blocking the surface receptors (29,30). Similar findings, associated with muscular and nervous fibers lesions (see below) were reported by Woodson et al (31). Pharyngeal muscle, as compared with diaphragm, has a predominance of fast glycolytic fibers, i.e. less endurance (32). According to Stauffer et al, the uvula of OSA patients contains more muscle and fat than that of control subjects, but these findings are difficult to interpret in the present

127

SNORING AND OBSTRUCTIVE SLEEP APNEA

context as the authors did not examine a group of nonapneic snorers (33). Of particular interest are the results of Smime et al (34), who found a reduction of type IIb fibers in the pharyngeal muscles of snorers as compared with nonsnorers. Even in healthy young subjects the mechanical characteristics of pharyngeal muscles are clearly different from those of other respiratory muscles: when compared with the diaphragm, the endurance of sternohyoid muscle fibers is less (35), while the rate of firing of the genioglossus motoneurons is obviously more abrupt (36). Suratt et al reported on the augmentation of the upper airway muscle activation in OSA (37); their results have been recently confirmed by the careful metabolic studies of S6ri~s et al (38,39). An animal model of upper airway obstruction and sleep apnea - - the English bulldog (40) - - also showed that an altered pattern of usage and a chronic load imposed on the upper airway dilator muscles lead to myopathic changes (41). Cohn et al found myolysis of soft palate muscular fibers in three heavy snorers (28) whose recorded sounds had an average frequency of 71 Hz; the authors speculate that myolysis was secondary to vibratory trauma. Snoring may occasionally contain high-frequency components, capable of damaging tissue by micro-streaming and cavitation (42). Some snorers develop hypoxemia (43) which can also contribute to upper airway muscle fatigue (44).

in palatal muscular tonus. Concentrating on vowel emission, Fiz et al found a decrease in maximum frequency and in the number of harmonics for 'e' and for 'i' (50); they concluded that vocalization of vowel 'i' is the best able to distinguish OSA patients. An interesting clinical-physiological study was carded out by Larsson et al (51), adapting to the upper airways a method originally elaborated for the study of temperature thresholds recognition at the skin. The results indicated a significant impairment of temperature detection, and the authors discussed three hypotheses: (a) pharyngeal mucosal thickening; (b) sensory neuropathy ((a) and (b) both due to snoringrelated vibrations); (c) stretching of pharyngeal wall structures during the obstructed inspiratory efforts.

Nerve fibers

Conclusion

Woodson et ai in the study already quoted above (31) reported focal degeneration of myelinated nerve fibers in heavy snorers and patients with sleep apnea (no differences between these groups) as compared with a control group. The structural abnormalities of myofibrils of the pharyngeal muscles were attributed by Edstrom et al (45) to motor neuron lesions, similar to those seen in vibration-induced neuropathy (46).

Clinical observations in heavy snorers An unusual speech disorder was noticed in OSA patients by Moran (47), who coined the term 'hot potato voice'. His observations were confirmed and extended by Monoson and Fox (48,49) who proceeded to a detailed analysis of speech samples in separate groups of OSA patients, COPD patients and healthy controls. A discriminant function based on abnormal resonance, articulation and phonation correctly classified 63% of the apneics and 96.3% of the healthy controls. The speech alteration was tentatively explained by the mucosal edema and alteration

May snoring be of benefit? The high-frequency oscillating pressures generated by snoring may help maintain upper airway patency by activating pharyngeal dilator muscles as reported by Sullivan et al (52,53). According to the Australian authors, a reduction of this reflex might be a mechanism by which snoring evolves to sleep apnea. Thus, contrary to all the facts reviewed above, snoring might have a life-protecting role!

Can we conclude from this that snoring causes or promotes obstructive sleep apnea? On existing evidence, obviously not: only a few of the criteria for causation in epidemiological studies are fulfilled (54). What we know is that snorers and patients with OSA have tissular damage in common (mucosal, muscular and nervous histologic lesions) and that these lesions are compatible with a deleterious effect of chronic vibration. We need to know many more things: 1. We do not understand why some OSA patients declare that they do not snore (55). 2. We need to better quantify and analyse the snoring sound (56), not only in the sleep laboratory, but also in field conditions, in unattended home recordings. According to Hoffstein et al (57) the 'snoring profile' can distinguish the apneic from the non-apneic snorer. 3. We need much more data on histologic lesions in heavy snorers; combined with simultaneous recording of snoring sound, these would make possible the assessment of a dose-response relationship. 4. Finally, what we bitterly need are longitudinal studies in non-apneic snorers, followed to assess

128 the incidence of OSA in this group. The few prospective studies published to date concern patients with OSA at the beginning of the study (58), thus being inappropriate to answer the question. An influence of snoring on the natural history of upper airway obstruction was suggested 13 years ago; the time has come to prove or disprove it using well-established facts.

Acknowledgement The author is indebted to Professor J.-L. Racineux (Angers, France) for his comments on a preliminary version of the paper. Mr B. Phrhit typed the manuscript.

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