Abstract

Cinefluorography and videofluorography were used to record and analyze functional swallowing deficits of 12 dogs with spontaneously occurring oropharyngeal dysphagias and six experimental dogs with selected neurectomies. Ten of the 12 dogs had dysphagias affecting the cricopharyngeal stage of the oropharyngeal phase of swallowing. Two dogs had mixed oropharyngeal dysphagias. Clinical signs of cricopharyngeal dysphagia could not be differentiated from those of dysphagias due to pharyngeal or mixed oropharyngeal deficits. Signs of cricopharyngeal dysphagia consisted of: 1) repeated attempts to swallow; 2) excessive head movement; 3) dropping food from the mouth after unsuccessful swallowing attempts; 4) reingestion of dropped food. Nine of these dogs had cinefluorographic evidence of asynchrony between the normal pharyngeal contraction and relaxation, and subsequent cricopharyngeal relaxation and contraction. Only one dog demonstrated a consistent cricopharyngeal non‐opening (achalasia). Seven of the dogs responded dramatically to cricopharyngeal myotomy. Two dogs with mixed oropharyngeal dysphagias had poor contractility of the pharyngeal muscles in addition to cricopharyngeal dysphagia. Clinical and cinefluorographic evaluation following cricopharyngeal myotomy of one dog verified exacerbation of functional deficits due to the iatrogenic cricopharyngeal chalasia. Esophagopharyngeal reflux accentuated the contrast medium retention in the pharynx and laryngotracheal aspiration. The need was stressed for careful differentiation between cricopharyngeal dysphagia and dysphagias involving the pharyngeal stage. Four experimental dogs with selective bilateral neurectomies of branches of the glossopharyngeal (IX) and vagus (X) nerves were evaluated clinically and cinefluorographically in an attempt to identify the pathogenesis of cricopharyngeal dysphagia. The variable results in the four dogs and the observed recovery in two dogs suggested that peripheral motor nerve deficits are not a major cause of cricopharyngeal dysphagia. Glossopharyngeal neurectomy in two dogs induced a profound functional disorder involving the pharyngeal and cricopharyngeal stages and the esophageal phase of swallowing. This would support a new hypothesis that the glossopharyngeal nerve is sensory to the esophagus as well as the pharynx, and may play a major role in disorders of the pharynx, upper esophageal sphincter, and esophagus, including congenital or acquired megaesophagus.

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