• 한국임상수의학회지
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• 제35권2호
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• pp.50-52
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• 2018

A 6-month-old castrated male poodle presented with a cough, dysphagia, and regurgitation. Cricopharyngeal achalasia (CPA) was diagnosed by clinical history and a fluoroscopic examination. The animal received a botulinum toxin (BTX) injection but symptoms had not resolved by three days after injection. Thus, a cricopharyngeal and thyropharyngeal muscle myotomy was performed and immediately the clinical signs resolved. This report describes successful correction of CPA with myotomy after failure of BTX injection in a dog.

• 한국임상수의학회지
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• 제34권4호
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• pp.291-294
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• 2017

An 8-month-old Chow-Chow dog presented with dysphagia and regurgitation, and was diagnosed with cricopharyngeal dysphagia (CPD). Cricopharyngeal myotomy did not improve the clinical signs. Three months after the initial surgery, a subtotal myectomy of cricopharyngeal muscle with partial thyropharngeal myotomy was performed. The clinical improvement was maintained for more than one year after the second surgery. Subtotal myectomy of cricopharyngeal muscle can be considered for dogs with CPD that do not respond to myotomy.

• Journal of Chest Surgery
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• 제31권4호
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• pp.432-435
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• 1998

특발성 윤상인두근 무이완증은 드물게 발생하는 식도 연하장애이다. 이는 연하작용시 윤상인두근의 이완불능으로 인해 발생하며 식도조영검사상 돌출된 윤상인두근간의 특징적 소견을 보인다. 치료는 윤상인두근 절개술이 가장 효과적이다. 본 순천향대학교 천안병원 흉부외과에서는 상부식도괄약근 무이완증의 61세 여자 환자에게 국소마취 하에서 윤상인두근 절개술을 시행하여 문헌 고찰과 함께 보고하는 바이다.

• 대한기관식도과학회지
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• 제13권2호
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• pp.9-16
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• 2007

Cricopharyngeal dysphagia(CPD), a common condition in the dysphagic patient, refers to the dysfunction of the upper esophageal sphincter complex(UESC), which is composed of the cricopharyngeus, inferior pharyngeal constrictor and the upper segment of the cervical esophagus. Primary CPD is the disease entity solely confined to dysfunctional UESC, while secondary CPD encompasses various conditions that accompany UESC dysfunction. For proper diagnosis and treatment of such entity, a thorough understanding of the complex anatomy and physiology of the upper esophageal sphincter. Adequate relaxation of the cricopharyngeal muscle in conjunction with anterosuperior excursion of the larynx by suprahyoid muscles and propulsion of food bolus are prerequisite for normal swallow, mechanisms of which if altered result in cricopharyngeal dysfunction. Of the various methods used for the diagnosis of cricopharyngeal dysphagia, videofluoroscopy remains the method of choice. Mechanical dilatation of the cricopharayngeus, cricopharyngeal myotomy and botulinum toxin injection and head-lift exercise have been used in clinical practice to relieve dysphagia in such patients. Such procedures have therapeutic effect in primary CPD, but so often fail to relieve swallowing dysfunction in patient with secondary CPD. We herein explain ancillary procedures that support these primary treatment options, which lead to successful treatment of dysphagia.

• 대한후두음성언어의학회지
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• 제30권2호
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• pp.77-81
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• 2019

Dysphagia may result from dysfunction of any of the components involved in the complex neuromuscular interaction of swallowing. Hyperfunction of any of the muscles involved in swallowing is a frequent cause of dysphagia. The cricopharyngeus muscle (CPM) is a key component of the upper esophageal sphincter. Cricopharyngeus muscle dysfunction (CPD) refers to the muscle's failure to appropriately and completely relax or expand during deglutition. A variety of disease processes may cause CPD and accurate diagnosis is paramount for appropriate treatment. In appropriately selected patients, intervention at the CPM may yield significant improvement in dysphagia. Interventions include nonsurgical, pharyngoesophageal segment dilatation, botulinum toxin (BoNT) injection, and criccopharyngeal myotomy. Injections of BoNT in patients with CPD have been reported to result in marked relief of dysphagia. Different techniques for instilling BoNT into the CPM have been described. Awake, in-office CPM BoNT injection with electromyography and/or fluoroscopic or ultrasound guidance is performed transcervically or via flexible endoscopy. Operative CPM BoNT injection involves rigid laryngoscopy and esophagoscopy with direct visualization of the CPM. BoNT should be prepared in low-volume, high-concentration dilutions to minimize the potential for undesired diffusion of the toxin. The effects of BoNT occur within weeks of injection and typically last up to 5 or 6 months.