Cricopharyngeal dysphagia

The cricopharyngeal muscle, or upper esophageal sphincter (UES), corresponds to the most inferior portion of the inferior constrictor muscle. It creates a sphincter separating the hypopharynx from the esophagus, preventing the inlet of air into the esophagus during inspiration and esophageal reflux into the pharynx. It is myoelectrically silent at rest and active during swallowing.

Cricopharyngeal dysphagia arises from dysfunction of the cricopharyngeal muscle, which can be primary or secondary to a number of pathological conditions, including cerebrovascular accidents, amyotrophic lateral sclerosis, oculopharyngeal muscular dystrophy and skull basal lesion. Oropharyngeal dysphagia is the clinical presentation and possibly correlates with aspiration or penetration of liquid or food into the upper airways. During manometry, incomplete relaxation of the UES or an increase in intrabolus pressure may be demonstrated (Fig. 32.1).

Cricopharyngealmuscle dysfunction has been traditionally treated with surgical myotomy, mechanical dilatation or plexus neurectomy. Localized injections of botulinum neurotoxin (BoNT) into the dorsomedial or ventrolateral parts of the muscle have also been successfully performed endoscopically, percutaneously (Fig. 32.1a) and eventually under CT or fluoroscopic control, with or without electromyographic (EMG) guidance (Fulmer et al., 2011). Unfortunately, there are no standards or guidelines and the administered dose reported ranges widely between 10 and 120 U onabotulinumtoxinA, usually selected on the basis of symptom severity.