Cricopharyngeal dysphagia

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

Cricopharyngeal dysphagia arises from its dysfunction which can be primary or secondary to a number of pathological conditions including cerebrovascular accidents, amyotrophic lateral sclerosis, oculopharyngeal muscular dystrophy, skull basal lesion, etc. Oropharyngeal dysphagia is the clinical presentation, and possibly correlates with aspiration or penetration of liquid or food in the upper airways. During manometry an incomplete relaxation of the UES or an increased intrabolus pressure may be demonstrated (Figure 17.1a).

Cricopharyngeal muscle dysfunction has been traditionally treated with surgical myotomy, mechanical dilation, or plexus neurectomy. Localized injections of botulinum toxin (BoNT) into the dorsomedial or ventrolateral parts of the muscle have also been successfully performed endoscopically by means of electromyographic (EMG) guidance, or percutaneously with EMG guidance (Figure 17.1b) and eventual computerized tomography or fluoroscopic control (Moerman, 2006). Unfortunately, there are no standards or guidelines and the administered dose ranges widely between 10 and 120 (mouse) units of Botox® per patient, usually selected on the basis of symptom severity. Local injections are relatively simple, safe (complication rate about 7%) and effective, although the effect wanes after 4–6 months (Moerman, 2006). Injection in the horizontal part of the muscle and an adequate (i.e., high enough) starting dose are predictors of greater efficacy.