Ann Otol Rhinol Laryngol 111:2002 ENDOSCOPIC BOTULINUM TOXIN INJECTION EOR CRICOPHARYNGEAL DYSPHAGIA MAHESH S, PARAMESWARAN, MD AHMED M. S. SOLIMAN, MD PHILADELPHIA, PENNSYLVANIA Twelve patients underwent 17 endoscopic injections of botulinum toxin type A in the cricopharyngeus muscle for the treatment of dysphagia and cricopharyngeal spasm over a 3-year period. The patient's charts were reviewed, Preoperative and postoperative symptoms, examination, and swallowing studies were reviewed. Eleven of the 12 patients had improvement in their symptoms, which lasted for a mean of 3,8 months. Two patients elected cricopharyngeal myotomy for permanent correction of their dysphagia. There was 1 case of postoperative neck cellulitis in an immunocompromised patient undergoing simultaneous excision of a thyroglossal duct cyst. We conclude that endoscopic injection of botulinum toxin is a relatively safe and viable technique for the treatment of dysphagia associated with cricopharyngeal spasm. It requires simple tools readily available to otolaryngologists. Larger, prospective controlled studies are necessary to establish its effectiveness and role in the management of this condition, KEY WORDS — botulinum toxin, cricopharyngeus, dysphagia. INTRODUCTION The cricopharyngeus (CP) muscle (upper esopha- geal sphincter) attaches to the lateral aspect of the cricoid cartilage and separates the hypopharynx from the esophagus. It is innervated by the recurrent la- ryngeal nerves and pharyngeal plexus. When func- tioning properly, this sphincteric muscle maintains esophageal closure during inspiration and between swallows, and briefly relaxes in coordination with the swallow to allow for bolus transit. It prevents the reflux of gastric and esophageal contents into the hy- popharynx during inspiration. It also prevents air from entering the esophagus during inspiration, Dys- phagia may result from CP muscle dysfunction. The diagnosis of CP muscle spasm or hypertonic- ity begins with careful history-taking and can be con- firmed with a wide variety of studies, including modi- fied barium swallow study, esophageal manometry, and electromyography (EMG) of the CP muscle, which show persistent spasm of the CP muscle dur- ing the swallow,'-5 Symptoms may include a cervi- cal "block" dysphagia in which primarily solid foods get caught up at the cricoid level. Patients may also describe choking symptoms, multiple attempts at swallowing the bolus, and nasopharyngeal reflux. Consequences may include weight loss, aspiration pneumonia, episodes of asphyxia due to airway ob- struction, use of alternative food consistencies, and dependence on nonoral feedings,^ A wide variety of disorders may affect the CP mus- cle and cause dysphagia. These include 1) various neurologic disorders such as amyotrophic lateral scle- rosis or multiple sclerosis, 2) cerebral vascular acci- dents, 3) injuries to the pharyngeal plexus of nerves or the recurrent laryngeal nerves during head and neck surgery, 4) pharyngeal diverticula, and 5) idio- pathic conditions,^'^ Symptoms of CP dysphagia have been treated in the past with mechanical dilation, pharyngeal plexus neurectomy, and CP myotomy,''^ McKenna and De- do'' reported on their experience in performing 54 CP myotomies; they advocate patient selection based on careful history-taking alone. Patients with CP dys- phagia may have previously had normal findings on manometric or cineradiographic studies. They advo- cate CP myotomy as both a diagnostic and a thera- peutic modality in patients with CP dysphagia,' More recently, botulinum toxin type A (Botox) has been advocated for the diagnosis and management of CP dysphagia.^''O'" Botox has been used effec- tively for the treatment of a number of hyperkinetic disorders, such as blepharospasm, torticollis, orofa- cial dystonia, spasmodic dysphonia, and CP spasm that resulted in poor voice in tracheoesophageal punc- ture speakers.'2.13 Botulinum exotoxin is a large pro- tein molecule that after intramuscular injection binds rapidly and irreversibly to the presynaptic choliner- gic nerve terminals. It thereby impairs the release of acetylcholine at the neuromuscular junction, causing a dose-related weakness of the innervated muscle. Its effects are mainly localized to the area in which it is administered, resulting in a process referred to as From the Department of Otolaryngology-Head and Neck Surgery, Temple University School of Medicine, Philadelphia, Pennsylvania, Presented at the meeting of the American Broncho-Esophagological Association, Palm Desert, California, May 14-15, 2001. CORRESPONDENCE — Ahmed M, S, Soliman, MD, Dept of Otolaryngology-Head and Neck Surgery, Temple University School of Medicine, 3400 N Broad St, Kresgc 102, Philadelphia, PA 19140, 871