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The upper oesophageal sphincter (UOS) remains closed at rest as a result of a combination of intrinsic muscle tone and passive pressure from the anterior mass of the larynx. This tonic activity is augmented during inspiration, thus preventing oesophageal air penetration each time intrathoracic pressure falls. UOS tonic pressure undergoes a further augmentation if the tubular oesophagus is distended—a protective reflex against oesophagopharyngeal regurgitation. Once oral preparation of an ingested bolus is complete, UOS tonic activity is abolished during the pharyngeal phase of a swallow. As the laryngopharynx elevates and shortens to engulf the bolus, the simultaneous forward tug of the rising hyoid on the anterior UOS wall brings about mechanical opening of the sphincter.
The nature of the deglutition reflex remains somewhat mysterious. The trigger to the onset of the ultra-rapid pharyngeal phase of swallowing is only semireflexive. All of us at times select the preferred moment of swallow—when we feel the bolus has been sufficiently chewed, when the social moment is right. Equally all of us have been caught out by the premature onset of a swallow reflex—when the bolus still feels too big to be swallowed, but seems to be escaping precipitately from the oropharynx. The elements of the swallow “reflex” which have been demonstrated experimentally to be under volitional control include the force of tongue and pharyngeal contraction,1 the duration of hyoid elevation2 and the extent of UOS opening.3
Until recently, the anterior pillars of the fauces were believed to be the site for afferent stimulation of the pharyngeal swallow reflex. The anterior pillars were subjected to “sensitisation” by application of cold laryngeal mirrors, in (almost certainly fruitless) attempts to facilitate the swallow reflex. The Chicago group, however, showed that prior to swallowing, the bolus collected on the tongue base—that is, in the oropharynx, distal to the oral cavity and the anterior faucial pillars.4 Moreover, it has been shown that a bolus of food reaches the vallecula prior to swallow onset in up to 50% of swallows.5 6
The epiglottic edge seems to be the most sensitive trigger zone for swallowing6 and is innervated by the vagus. Magnetic stimulation of either the trigeminal or vagal nerve evokes pharyngo-oesophageal EMG responses. Also, muscle responses to cortical stimulation are facilitated by vagal stimulation.7 Such modification of central swallow reflexes represents one method by which deglutition dynamics in the pharyngo-oesophageal segment adapt to alterations in bolus properties—for example, by enhanced and earlier UOS opening with increasing bolus volumes.
Swallowing is a precarious business because of the common upper channel for ingestion and respiration. A major function of the larynx is sphincteric—to protect the airway at moments of uncoordinated swallowing and respiration. The upper airway is normally protected from laryngeal penetration by deglutition apnoea, even in the minority of normal swallows which occur in inspiration.
A few years ago, the group in Wisconsin characterised, first in animals and later in humans, a number of reflexes which modify the normal resting and deglutitive patterns of pharyngo-oesophageal motility, most of which seem to enhance airway protection. These include the oesophagoglottal closure reflex, a protective closure of the upper airway introitus in response to abrupt oesophageal distension. This reflex is likely to protect the airway at times of notable gastro-oesophageal reflux, when there is a risk of oesophagopharyngeal reflux and laryngeal acid penetration. The reflex may be supported by a second laryngeal protective phenomenon, a pharyngoglottal adduction reflex, which is triggered by pharyngeal entry of very small amounts of fluid, especially in younger people.8
The group, lead by Reza Shaker, have also described a pharyngo-UOS contractile reflex where the stimulation of glossopharyngeal afferents by hypopharyngeal fluid evokes a vagal efferent tonic response in the UOS. Larger fluid volumes evoke a reflex pharyngeal swallow. These responses, which are abolished by topical pharyngeal anaesthesia, account for the difficulty encountered in early attempts at pharyngeal manometry with perfused catheter systems. In healthy volunteers the threshold volume for UOS contraction is only 0.1 ml if infused rapidly, but around 1 ml with slow infusion.
It is suggested that the UOS contraction response to the presence of extremely small amounts of fluid protects against aspiration. This protection may be brought about by three mechanisms. Firstly, the UOS tonic pressure augmentation reduces the risk of further oesophagopharyngeal reflux. Secondly, if fluid enters the proximal pharynx, as in the experimental situation, the UOS contraction may assist a sufficient fluid build up in the pharynx to provoke the related pharyngeal swallow, which clears the pharynx and also closes the glottis. Finally, Shaker’s work on glottic closure during deglutition suggests that the pharyngo-UOS contractile reflex is accompanied by closure of the laryngeal inlet.
There seems to be little direct observation of the respiratory and other motor effects, if any, of fluid entering the pharynx as a result of oesophagopharyngeal reflux, one of the proposed aetiological factors in so called acid laryngitis. Shaker’s team now report the effects of cigarette smoking on the UOS contractile and swallow reflex which follow experimental pharyngeal water infusion (see page 537). Smoking increased the threshold of the pharyngeal reflexes. This report also indicates an absence of the pharyngo-UOS contractile reflex in three of the 20 subjects. This may reflect the natural variation in pharyngeal reflexes (e.g. the gag reflex).
The most direct explanation for the group’s findings is that cigarette smoke acts as a sensory depressant in the upper aerodigestive tract. Olfaction and taste are diminished in smokers, whose oropharyngeal mucosa is chronically thickened, as evinced by the reduced rate of aphthous ulceration in smokers. This argument does not, however, take account of the known abolition of the reflexes after topical anaesthesia, nor does it explain the acute incremental threshold rise after smoking. The authors examine a number of other mechanisms,9 but do not consider the role of nicotine induced arousal10 on pharyngeal reflex activity.
Shaker’s team has made unique contributions to the understanding of the pathophysiology of pharyngolaryngeal coordination. Nonetheless, their latest paper should not let us lose sight of the fact that the principal effects of cigarette smoking on the respiratory tract are much more severe, and direct, than merely the diminution of pharyngeal fluid responsiveness.
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