The cricopharyngeal muscle (CPM) is essential for normal deglutition. Pharyngeal dysphagia commonly results from impaired or uncoordinated CPM dilation. Dysfunction of the CPM has also been implicated in the genesis of Zenker's (pharyngoesophageal) diverticulum. Despite the CPM's significance, little is understood about its morphology. We studied CPM biopsy specimens from 20 patients with Zenker's diverticulum and from 5 fresh cadaver patients with detailed histologic techniques to include fiber size and shape and adenosine triphosphatase, reduced nicotinamide adenine dinucleotide, trichrome, succinate dehydrogenase, cytochrome C oxidase, periodic acid-Schiff reaction, oil red O, acid phosphatase, Congo red, crystal violet, and monoadenylate deaminase stains. The normal CPM has unique morphological characteristics, with some myofibers having staining properties that are a hybrid between striated muscle and muscle spindle. The variable orientation of the muscle fibers is also different from that of most other striated musculature. Of the 20 Zenker CPM specimens, 4 specimens did not reveal any significant differences from controls (2 of which had insufficient amounts of tissue for complete analysis). In the remaining 16 specimens, several abnormalities existed, including excessive size variation (16/16), grouping of atrophic fibers (9/16), target or targetoid formations (4/16), cores (2/16), and ragged red fibers (2/16). The final pathological pattern of the 16 specimens was neurogenic in 7, myopathic in 4, and mixed (with neurogenic predominance) in the remaining 5. Two specimens contained significant lymphocytic inflammatory infiltrates. We conclude that the unique neuromuscular function of the CPM in deglutition is likely due to its fiber orientation and the hybrid nature of some of the myofibers. Morphological disturbances of the CPM impair its dilation and may account for the development of Zenker's diverticulum. This disturbance is most often due to progressive denervation of the CPM.
Abstract Objectives/Hypothesis Although the cricopharyngeus muscle is a ring‐like structure, unilateral cricopharyngeal dysfunction can produce significant dysphagia. This entity has not been well described in the literature. The aims of the study were to identify the characteristic findings on videofluoroscopic swallow studies in patients with dysphagia secondary to unilateral cricopharyngeal dysfunction, to note the associated vagal nerve injury, and to evaluate patient outcomes following ipsilateral cricopharyngeal myotomy. Study Design Retrospective clinical investigation. Methods The clinic charts, electromyographic tests, videostroboscopic examinations, and videofluoroscopic swallow studies were reviewed from a series of patients who presented to our institution from 1993 to 2001 with dysphagia and findings on videofluoroscopic swallow studies suggestive of unilateral cricopharyngeal dysfunction on posterior–anterior view. In patients treated with ipsilateral cricopharyngeal myotomy, postoperative findings on swallow studies and patient outcomes were also reviewed. Results Eighteen patients demonstrated findings characteristic of unilateral cricopharyngeal muscle dysfunction on videofluoroscopic swallow study. The common feature was a unilateral shelf‐like barrier at the cricopharyngeus on the posterior–anterior view with pooling of liquid bolus in the ipsilateral pyriform sinus and episodic shunting to the contralateral side. Eight patients did not have evidence of cricopharyngeal dysfunction (ie, cricopharyngeal bar) on lateral films. Of the 18 patients, 14 had histories consistent with vagal injury secondary to trauma (n = 2), neoplastic involvement (n = 7), iatrogenic injury (n = 2), or central nervous system disease (n = 3). Results of videostroboscopic examinations demonstrated vocal fold motion impairment in 14 patients, and electromyographic test results confirmed unilateral vagal injuries in those who underwent electromyographic testing (n = 6). In the remaining 4 of 18 patients, videostroboscopic examinations demonstrated normal vocal fold abduction but impaired lengthening with a posterior glottic gap, and electromyographic test results (n = 4) indicated unilateral superior laryngeal nerve involvement. Of the 15 patients treated with ipsilateral cricopharyngeal myotomy, 1 patient required postoperative esophageal dilations for an esophageal stricture distal to the cricopharyngeus, whereas the remaining 14 patients had functional resolution of their dysphagia. Conclusion In patients presenting with dysphagia and evidence of unilateral vagal injury, careful assessment of posterior–anterior view on videofluoroscopic swallow study should be included to evaluate for unilateral cricopharyngeal dysfunction.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)