Swallow Syncope

Swallow syncope incorporates two separate conditions:

1. a pharyngeal form which is usually associated with pain (“syncopal glossopharyneal neuralgia”)
2. an oesophageal variety, also known as “oesophageal” or “deglutition syncope” (fig. 7)[1].

The first isolated case description dates to 1906 (Mackenzie, 1906). Based on the fact that up to date there are only about sixty single cases reported (DEUCHAR & TROUNCE, 1960;Basker & Cooper, 2000), swallow syncope is probably rare.

The clinical presentation of glossopharyngeal neuralgia is a patient with (seemingly) spontaneous overwhelming pain in a jaw, tongue or throat. In some patients this pain can be triggered by touching a certain spot in the oral cavity, or by talking or swallowing. Among all patients with glossopharyngeal neuralgia, syncope seems a rare complication (Rushton et al., 1981).

In the oesophageal variety syncope typically occurs during or shortly after swallowing. Several reports point especially to cold drinks as the culprit (Rainford, 1975;Brick et al., 1978;Olshansky, 1999). Syncope triggered by belching has been reported (Kim et al., 2005).There are some that report that mention retro-sternal pain induced by swallowing as a trigger. Several cases report oesophageal syncope during recovery from myocardial infarction. Swallowing syncope is characterised by a slow or absent pulse.

Pathophysiology

The pathophysiology of both entities is poorly understood. The possible neurological pathways and mechanisms that might be involved in swallow syncope cannot be explained on the basis of any known normal reflex (Basker & Cooper, 2000). Oesophageal syncope is often ascribed to a vagovagal reflex (i.e. both afferent and efferent stimulus through the vagus nerve)(Piek et al., 1988); however this merely describes part of the peripheral functional anatomy.

In many cases of oesophageal syncope functional, endoscopic and radiological studies reveal oesophageal abnormalities including diverticulum, hiatal hernia, achalasia, stricture and neoplasms (Basker & Cooper, 2000). Although such co-morbidity may be over-reported, in the total clinical picture these case reports may be an argument to commence an in depth gastro-oesophageal evaluation.

Treatment

There are several therapeutic options.

1. First, in case of overt oesophageal lesions, these should be treated.
2. Secondly, if feasible, modification of antihypertensive drugs should be considered.

Surgical or pharmacological destruction of (the oesophageal branches of) the vagus nerve has shown not to be successful. Based on predominantly positive therapeutic response in over a dozen cases, the treatment of choice of oesophageal syncope is insertion of a cardiac demand pacemaker (Basker & Cooper, 2000). Management of persisting neuralgia is symptomatic.

References

1. Basker MR and Cooper DK. Oesophageal syncope. Ann R Coll Surg Engl. 2000 Jul;82(4):249-53.