Snoring

Electroencephalography and Clinical Neurophysiology, 1975, 39 : 59-64 ~ Elsevier Scientific Publishing Company, Amsterdam -~ Printed in The Netherlands

59

SNORING E. LUGARESI,

G. COCCAGNA, P. FARNETI, M. MANTOVANI AND F. CIRIGNOTTA

Clinica delle Malattie Nert, ose e Mentali dell'Universitgt di Bologna, 40123 Boloqna (Italy)

(Accepted for publication: February 27, 1975)

Under the term hypersomnia with periodic apneas (H. P.A.) we have collected several clinical syndromes (Pickwickian syndrome, primary alveolar hypoventilation, alveolar hypoventilation secondary to stenosis of the upper airways), which are characterized by the onset and persistence during sleep of continuous apneas of a prevalently obstructive type. These obstructive apneas are the cause of the disturbance ; indeed, their disappearance after weight loss or tracheostomy leads to complete clinical recovery (Coccagna et al. 1972; Lugaresi et al. 1973). The majority of patients with H.P.A. have snored heavily for years or even decades, and this suggests a causal relationship between snoring and H.P.A. Verification of this hypothesis is the principal aim of this study. Snoring is an acoustic phenomenon produced by vibration of the soft palate and the faucial pillars. Both local anatomical factors (thickness of the faucial soft tissues, adenoidal and tonsillar hypertrophy, mandibular malformation, mucosal edema due to infection or excessive smoking, etc.) and functional factors which arise during sleep (hypotonia of the muscles of the pharynx and tongue) are responsible for its appearance. The relative positions of the tongue and soft palate established during sleep create the physical conditions under which air passing through a narrow orifice causes the soft palate to vibrate (Robin 1968). There are few polygraphic studies on snoring reported in the literature. Fischgold and Schwartz (1961) observed that snoring appears late in the night, at the end of the first sleep cycle and during subsequent cycles; it is present in all sleep stages, but most commonly in stages 2 and 4 and rarely during periods of rapid eye movement. According

to Duron (1972), snoring, which he considers a predominantly expiratory nasal dyspnea, is accompanied in light sleep stages by apneas which are initially central and later obstructive. MATERIALS AND METHODS

Eight male non-hypersomniac subjects aged from 27 to 63, who were identified or who identified themselves as heavy snorers underwent a total of 18 nocturnal polygraphic recordings lasting from physiological dozing off to awakening in the morning. In all cases simultaneous recordings were made of the EEG, the horizontal oculogram, EMG with surface electrodes of the mylohyoid muscle and an intercostal muscle on the mid-axillary line at the level of the 9th 10th intercostal space. In addition the movements of the thoracic wall were recorded by means of a bellows type tube placed over the anterior wall of the thorax and held in place by a belt; the expansible tube was connected to a piezoelectric transducer connected in turn to a DC preamplifier of the polygraph. Oral and nasal respirograms were obtained through small thermocouples placed respectively at the mouth and in one nostril. To record the intraesophageal pressure, a catheter equipped with a terminal balloon was introduced into the lower third of the esophagus through a nostril. The catheter was connected to a Statham P 23 Db transducer which was, in turn, connected to a manometric preamplifier of the polygraph. The sound of snoring was picked up by means of a small microphone suspended over the patient's head; the acoustic vibrations were recorded on a polygraphic channel. In four patients, in addition to these

E. LUGARESI el al.

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Fig. 1. Snoring in the different sleep stages. Simultaneous recording of the EEG (first two channels), horizontal electrooculogram (EOG), electromyogram of the mylohyoid muscle (mylohyoid EMG), phonogram, electromyogram of an intercostal muscle (interc. EMG), endoesophageal pressure; nasal and oral respirogram and thoracic pneumogram. Snoring noise increases progressively through non-REM sleep (stage 2 stage 4) and diminishes in REM sleep. EMG activity of the intercostal muscles and endoesophageal pressure increase with snoring: when the subject is snoring loudest (in stage 4), EMG activity and intrathoracic depression reach their maximum levels.

SNORING

61

parameters, the systemic arterial pressure was recorded by percutaneous cannulation of the radial artery with an Abbocath 20-G teflon needle. The needle was connected by teflon tubing to a Statham P 23 Db transducer and thence to a manometric preamplifier of the polygraph. The left arm, in which the needle was placed, was attached to the side of the bed by a strap which was long enough to permit limited movements, but which obliged the patient to sleep either on his back or on the left side. A three-way stopcock was placed between the connecting tube and the transducer through which periodic samples of arterial blood were taken during sleep for blood gas determination; the gas analysis values were determined immediately using a Radiometer apparatus (blood micro-system model BMS 3b; acid-base analyzer PHM 71 with PO2 module type PHA 930 and PCO2 module type PHA 931). The sleep stages were scored according to Dement and Kleitman (1957). B.GALL. 42 yrs.

RESULTS

Snoring is an almost exclusively inspiratory noise which arises during dozing off (stage la) and intensifies progressively with the deepening of non-REM sleep. It weakens and becomes discontinuous during REM sleep, but persists during bursts of rapid eye movements. Occasionally a very intense inspiratory noise is followed by a less intense expiratory noise. The number of noise-producing respiratory movements increases with the deepening of slow sleep; during REM sleep they occur at the same rate as during light sleep. During snoring we observed a clear increase in the EMG activity of the intercostal muscles and an abnormal intrathoracic depression: the louder the snoring, the greater the increase in the EMG activity of the intercostal muscles and in the intrathoracic inspiratory depression (Fig. 1). During sleep in heavy snorers, the negative intrathoracic pressure is often high, even in Sleep St.2

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Fig. 2. Obstructive apnea recorded during snoring in stage 2 sleep (arrows indicate inspiration). Initially the patient is s~rin.g (see Phone), with some effort required for inspiration (see intercostal EMG and endoesophageal pressure); the snoring ceases and the intercostal muscle activity slackens off: simultaneously the air flow through the upper airways stops while the thoracic movements persist and the endoesophageal pressure remains higher than in wakefulness (obstructive apnea). About 20 sec later the respiratory movements become more energetic, ventilation resumes and the snoring reappears. (The values of endoesophageal pressure during wakefulness in the same subject are indicated in Fig. 1.)

62

z. LUGARESIet al.

periods when the patient is not snoring. In a very obese snorer, during wakefulness, the inspiratory intrathoracic depression was markedly greater than normal; this indicates that heavy snorers may present incomplete obstruction of the upper airways even during wakefulness. Moreover, habitual snorers may present obstructive apneas which appear primarily during light sleep (stages 1-2)and REM sleep. The apneas are favored by weakening of the central breathing: this is documented by diminution in the E M G activity of the intercostal muscles (Fig. 2). In heavy snorers the obstructive apneas may occur in long series (Fig. 3). In our experience with six healthy non-snorers, alveolar ventilation

B.G.50 yrs.

during sleep varied substantially from that of wakefulness but the PaCO2 values never, in any sleep stages, rose above the physiological level (45 mmHg). In contrast, heavy snorers may show fairly marked states of hypoventilation during sleep, especially during REM sleep when the obstructive apneas are most frequent and prolonged. In one of our cases a mild bronchopneumonia provoked a particularly intense nocturnal state of alveolar hypoventilation. In the five cases in which the systemic arterial pressure was recorded, during snoring the pressure rose above wakefulness levels even during deep slow sleep stages, when a physiological decrease of approximately 15~0 should

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SNORING

63

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Fig. 4. Behavior of the systemic arterial pressure during sleep in eight normal subjects (dotted line) and eight heavy snorers (solid line). In normals the pressure decreases progressively and significantly through the successive stages of non-REM sleep; in R E M sleep the pressure values are similar to those of stage 2. In heavy snorers the systolic pressure increases progressively and significantly from wakefulness through stages 1, 2, 3, 4 and undergoes a further rise in R E M sleep ( P < 0.01). The differences for the diastolic pressure are significant only between slow and R E M sleep (P< 0.05).

assumed that snoring, as a dynamic hypnogenic stenosis of the upper airways, shows clear symptomatic and physiopathological affinities with the respiratory disturbance of H.PA,. However, as snoring is an extremely widespread phenomenon (according to some statistics, 9 % of the population snores) and since H.P.A. is a rare syndrome (we have seen 30 cases in 7 years), it must be admitted that the passage from one to the other occurs only exceptionally. In any case, during sleep the heavy snorer suffers respiratory difficulty which can affect alveolar ventilation, the systemic arterial pressure and, very likely, the pulmonary pressure as well. It is probable that, over a period of years, this ventilatory and hemodynamic situation has adverse effects on the cardiac muscle. If these hypothetical effects of snoring are confirmed by further research, the problem of preventing and curing phenomena such as obesity, which produce heavy snoring, assumes a hitherto unsuspected importance. SUMMARY

have occurred (Coccagna et al. 1971) (Fig. 4); in addition, it underwent marked respiratory oscillations. It is quite probable that the hypoventilation produced by snoring would be reflected even more clearly in the pulmonary arterial pressure, but as yet we have no data on this. DISCUSSION

Our clinical findings may be summarized as follows: (1) Snoring is an inspiratory noise (or primarily inspiratory) related to incomplete obstruction of the upper airways. It begins with dozing off and becomes progressively stronger and more continuous with the deepening of nonREM sleep. Snoring during REM sleep has approximately the same intensity and continuity as in stage 2. (2) Snorers suffer obstructive apneas, particularly in stage 2 and REM sleep. Heavy snorers may present protracted sequences ofapneas and a state of alveolar hypoventilation. (3) In heavy snorers the systemic arterial pressure remains at relatively high levels and undergoes large respiratory oscillations. On the basis of these findings, it may be

Eight heavy snorers underwent nocturnal polygraphic recordings. The principal results are the following : 1. Snoring is an inspiratory (or primarily inspiratory) noise linked to subobstruction of the upper airways. It appears with falling asleep (stage 1) and intensifies progressively through the deepening of slow sleep; in REM sleep it becomes discontinuous and is comparable to stage 2 snoring in intensity. 2. In heavy snorers, obstructive apneas are always present and particularly abundant during light sleep (stage 2) and REM sleep. 3. In heavy snorers during sleep the systemic arterial pressure reaches and remains at levels higher than those of wakefulness instead of diminishing normally. 4. Some degree of alveolar hypoventilation is associated with snoring when the apneas are especially abundant. These findings confirm the existence of significant polygraphic analogies between snoring and hypersomnia with periodic apneas and indicate that snoring may represent the first phase in the development of this syndrome.

64 Moreover, the effects of snoring on alveolar ventilation and the systemic pressure during sleep suggest that heavy, constant snoring has physiopathological implications for the cardio-circulatory apparatus. RESUME LE RONFLEMENT

Huit grands ronfleurs ont 6t6 soumis /~ enregistrements polygraphiques nocturnes. Les principaux r6sultats obtenus sont indiqu6s cidessous: 1. Le ronflement est un bruit inspiratoire (ou prrdominance inspiratoire) 1i6 "fila subobstruction des voies arriennes suprrieures. I1 se manifeste drj~ durant l'assoupissement sphase 1) et devient d'autant plus intense que le sommeil lent devient plus profond. Durant le sommeil paradoxal il devient discontinu et son intensit6 ressemble ~ celle de la phase 2. 2. Des apnres obstructives sont toujours prrsentes chez les grands ronfleurs: elles sont particuli~rement frrquentes durant le sommeil 16ger (phase 2) et le sommeil paradoxal. 3. Chez les grands ronfleurs la tension artrrielle systrmique, qui diminue pendant le sommeil des sujets normaux, se maintient au contraire il des valeurs plus ~lev~es que pendant la veille. 4. Un certain degr6 d'hypoventilation alv6olaire accompagne le ronflement (lorsque les aF.~6es sont particuli6rement nombreuses). Les r6sultats confirment l'existence d'importantes analogies polygraphiclues entre ron-

E. LUGARESIet al. flement et hypersomnies avec apnres p~riodiques; ils suggrrent en outre que le ronflement reprrsente la premirre 6tape de l'evolution de ce syndrome. Les effets du ronflement sur la ventilation alvrolaire et la tension arterielle systrmique durant le sommeil suggrrent en outre que le ronflement, lorsqu'il est trrs intense, peut avoir des rrpercussions significatives sur l'appareil cardio-circulatoire.

REFERENCES COCCAGNA, G., MANTOVANI,M., BRIGNAN1,F., MANZINk A. and LUGARESI, E. Arterial pressure changes during spontaneous sleep in man. Electroenceph. clin. Neurophysiol., 1971, 31 : 277-281. COCCAGNA, G., MANTOVANI, M., BRIGNANk F., PARCHI, C. and LUGARESI, E. Tracheostomy in hypersomnia with periodic breathing. Bull. Physio-path. resp., 1972,8: 1217-1227. DEMENT, W. and KLEITMAN, N. Cyclic variations in EEG during sleep and their relation to eye movements, body motility and dreaming. Electroenceph. clin. Neurophysiol., 1957, 9:637 690. DURON, B. La fonction respiratoire pendant le sommeil physiologique. Bull. Physio-path. resp. 1972, 8: 10311057. FISCHGOLD, a . and SCHWARTZ, B. A. A clinical, electroencephalographic and polygraphic study of sleep in the human adult. In G. E. W. WOLS~NHOLM and M. O'CONNOR (Eds.), The nature o f sleep. Churchill, London, 1961 : 209~36. LUGARESI, E., COCCAGNA, G., MANTOVANI, M. and BRIGNANI, F. Effects of tracheostomy in;two cases of hypersomnia with periodic breathing. J. Neurol. Neurosurq. Psychiat., 1973, 36: 15-26. ROBIN. I. G. Snoring. Proc. roy. Soc. Med., 1968, 61: 575 582.