Oropharyngeal dysphagia can be caused by a variety of etiologies, including neurological disorders, muscle lesions, structural abnormalities, and infections. Since Kaplan first reported the application of cricopharyngeal myotomy in 1951 to treat a patient with poliomyelitis with good results, cricopharyngeal myotomy has been widely used to treat oropharyngeal dysphagia of various etiologies. I. Oropharyngeal dysphagia The swallowing process is divided into oral preparatory phase, pharyngeal phase, and esophageal phase, and any abnormality in any of them, whether it is structural abnormality caused by the esophagus itself or extraesophageal lesions, or dynamic abnormality caused by the esophagus itself or with systemic diseases, can cause dysphagia. It can be divided into oropharyngeal and esophageal dysphagia according to the site, and oropharyngeal dysphagia is manifested as difficulty in swallowing at the beginning and difficulty in entering the esophagus with food mass obstructed in the pharyngeal cavity. Because of the close relationship between the oropharynx and swallowing, breathing and articulation functions, oropharyngeal dysphagia can include three manifestations: difficulty in advancing the food mass from the oropharynx to the cervical esophagus; pharyngeal-oral reflux and pharyngeal-nasal reflux after the food mass is obstructed; choking, misaspiration and dysarthria caused by the food mass remaining in the pharynx. Oropharyngeal dysphagia is a more common symptom, especially in the elderly, and it has been reported that 16% to 22% of people over 50 years of age have experienced oropharyngeal dysphagia. The causes are diverse and include the following categories: 1, neurological diseases: almost any disease of the central nervous system may cause oropharyngeal dysphagia, including cerebrovascular lesions, tumors, poliomyelitis, Parkinson’s disease and many other diseases, certain peripheral neuropathies such as vagus nerve injury can also cause oropharyngeal dysphagia. Neurological lesions produce symptoms due to disruption of the fine coordination of structures such as the tongue, soft palate, larynx, epiglottis, pharynx, and upper esophageal sphincter, of which cerebrovascular accidents are the most common. Two weeks after a unilateral hemispheric cerebrovascular accident 86% of patients have normal swallowing function, but if the lesion involves bilateral hemispheres, the brainstem or a larger area it is highly likely to cause severe and persistent dysphagia. 2, myogenic disease: either the motor end plate or the lesion of the muscle fiber itself may cause oropharyngeal dysphagia, commonly seen in: myasthenia gravis, polymyositis, oropharyngeal muscle atrophy, etc. 3, upper esophageal sphincter dysfunction: such as cricopharyngeal muscle dyslaxation, Zenker’s diverticulum. 4, local lesions: such as pharyngeal inflammation, tumors. 5.Other: oropharyngeal dysphagia can be a physiological defense response caused by gastroesophageal reflux; it can appear after head and neck surgery or radiotherapy. II. Anatomy and physiology of the upper esophageal sphincter (UES) The upper esophageal sphincter is functionally defined as the luminal high-pressure zone between the pharynx and the cervical esophagus. Its physiological role is to prevent air from entering the digestive tract during inspiration and to prevent regurgitation of esophageal contents into the hypopharynx causing aspiration. The upper esophageal sphincter opens briefly during swallowing to allow the passage of food masses into the esophagus, and during burping and vomiting to allow the passage of gas and gastric contents.The UES is anatomically composed of cartilage and muscle, with the cricopharyngeal cartilage extending from the anterior to the posterior medial surface of the posterior wall, which also includes the spoon cartilage and the internal spoon muscle, and the lateral and posterior walls, which are composed of muscles including the cricopharyngeal muscle, the hypopharyngeal constrictor, and the longitudinal muscles on the lateral side of the esophagus. The cricopharyngeal muscle is generally considered to be the main muscle that performs the function of the UES, and therefore the UES is often considered to be the cricopharyngeal muscle. The cricopharyngeal muscle emanates from the posterior lateral aspect of the cricoid cartilage and consists of transverse muscle fibers 25-35 μm in diameter, forming a horizontal muscular ring, but its muscle fiber orientation is not strictly parallel. Unlike most transverse muscles, the cricopharyngeal muscle is rich in elastic connective tissue, connected to the connective tissue skeleton, and contains both fast-contracting and slow-contracting muscle fibers, the latter being predominant, and its optimal initial length is 1.7 times its resting length, properties that allow the cricopharyngeal muscle to maintain resting tension and to extend and open when stressed. The available studies confirm that the peak pressure of the UES is consistent with the cricopharyngeal muscle site while the longitudinal muscle of the lateral esophagus does not histologically possess the properties of a sphincter; the cricopharyngeal muscle, but not the hypopharyngeal constrictor, maintains constant basal tension and opens during swallowing, and the electromyographic activity correlates with pressure changes in the UES; therefore, most authors agree that the cricopharyngeal muscle is the basis of UES function [10]. The results of esophageal manometry show that the UES high-pressure zone is located below the pharyngeal opening and is about 2-4 cm long; anatomically the high-pressure zone corresponds to the hypopharyngeal structures composed of cartilage and muscle, including: cricoid cartilage, spoon cartilage, subpharyngeal constrictor muscle and cricopharyngeal muscle, which is only about 1 cm long and cannot form a 2-4 cm high-pressure zone. Combined with the results of esophagography some scholars believe that the cricopharyngeal muscle constitutes the lower 1/3 of the UES and the subpharyngeal constrictor muscle constitutes its upper 2/3, and the opening of the UES includes the relaxation of the cricopharyngeal muscle and the subpharyngeal constrictor muscle, while the larynx should move forward and up. C. Indications for cricopharyngectomy The entry of food into the esophagus requires a combination of appropriate thrust from the oropharyngeal muscles, forward upward movement of the larynx, and timely opening of the upper esophageal sphincter, while cricopharyngectomy can only solve the problem of opening of the cricopharyngeal muscles, so cricopharyngectomy cannot solve all oropharyngeal dysphagia. The ideal indications are: 1. oropharyngeal dysphagia caused by the failure of the upper esophageal sphincter to open 2. the patient has sufficient thrust of the oropharynx on the food mass and the food mass passes smoothly in the oropharynx 3. normal or nearly normal laryngeal movements 4. no severe gastroesophageal reflux 5. no dysarthria or aphasia 6. patients with cerebrovascular accidents should be operated after 6 months of observation In the preoperative examination, dynamic barium esophagogram is the most widely used and the most classical method. It is convenient to observe the abnormality of pharynx and upper esophageal sphincter. During swallowing, barium occupies more than 50% of hypopharynx or barium retention in upper esophageal sphincter area can be considered as abnormal opening of upper esophageal sphincter. However, the evaluation of pharyngeal peristalsis is not sensitive enough. Esophageal manometry has been increasingly used in recent years, and it can provide quantitative data to evaluate whether coordination and relaxation are abnormal. However, most scholars currently believe that the determination of resting pressure is not meaningful because there is some overlap between the ranges of normal and abnormal values, and because the determination of resting pressure is affected by a variety of factors such as stress, sleep, and respiration, and the normal value itself is controversial. However, some scholars believe that the accuracy of manometry can reach 90% higher than that of dynamic barium esophagogram, and the simultaneous application of both is more instructive. There is not much literature on the contraindications of cricopharyngeal myotomy, and it is generally believed that oropharyngeal inability to advance the food mass is an absolute contraindication. The cricopharyngeal myotomy is a shaping procedure, and most authors use the following method The patient is placed in the supine position with general anesthesia and head tilted to the right. An incision is made at the anterior border of the left sternocleidomastoid muscle, and the sternocleidomastoid muscle is freed and retracted posteriorly and laterally to cut the scaphohyoid muscle, middle thyroid vein, and inferior thyroid artery, exposing the trachea and esophagus. The laryngeal recurrent nerve is protected and the trachea and esophagus are retracted forward to expose the posterior wall of the esophagus. The cricopharyngeal muscle is identified in the posterior midline, and the muscle is incised from 2 cm below the inferior border of the cricopharyngeal muscle to the level of the thyroid hyoid membrane for a full length of approximately 6 cm. The muscle flap is freed to one side and resected to avoid later healing of the muscle layer. A more extensive excision has been recommended but not accepted. V. Surgical complications It is generally believed that cricopharyngeal myotomy is a relatively safe procedure with few postoperative complications such as wound infection, temporary vocal cord paralysis, and pharyngeal or esophageal fistulae, if they occur at all, are relatively easy to manage. However, in the early literature, the perioperative mortality rate was as high as 20%, and further analysis revealed that most of these patients had severe respiratory dysfunction, low pulmonary ventilation and coughing and sputum production, and most died of pulmonary infection after surgery. The complication rate was greatly reduced after later strengthening the screening of patients. Loizou et al. operated on 25 patients with oropharyngeal dysphagia due to motor neurological disease, and 15 patients had different degrees of improvement. 20 of 40 patients with oropharyngeal dysphagia due to neurogenic disease by Poirier et al. had disappearance of dysphagia after surgery, and 7 patients had improvement of dysphagia after surgery. The postoperative dysphagia improved in 7 cases. In addition, he summarized the English literature before 1996, in which: 86 cases of cerebrovascular lesions, with significant improvement in 22 cases and moderate improvement in 35 cases; 55 cases of amyotrophic lateral sclerosis, with significant improvement in 25 cases and moderate improvement in 14 cases; 22 cases of bulbar palsy and pseudobulbar palsy, with significant improvement in 1 case and moderate improvement in 8 cases; 66 cases of other central nervous system lesions, with significant improvement in 6 cases; 12 cases of trauma There were 66 cases of other central nervous system lesions, with significant improvement in 6 cases; 12 cases of trauma, with significant improvement in 3 cases and moderate improvement in 1 case; and 21 cases of peripheral nervous system lesions, with significant improvement in 7 cases and moderate improvement in 3 cases. Overall, about 75% of the patients who met the indications were likely to improve to varying degrees. VII. Some alternative methods There are some alternatives to cricopharyngeal myotomy that aim to open the upper esophageal sphincter with less trauma and improve dysphagia. The main ones include: endoscopic laser cricopharyngeal myotomy for patients with poor general condition and high risk; balloon dilation, which may work best when cricopharyngeal muscle fibrosis is suspected; botulinum toxin injection, which can be performed percutaneously or transendoscopically and is applied to patients with non-relaxed cricopharyngeal muscle, with little trauma and can be performed under local anesthesia; all are still in the experimental stage and cannot replace conventional cricopharyngeal myotomy yet. In conclusion: in oropharyngeal dysphagia of various etiologies, if the oropharyngeal muscles can produce appropriate thrust, the forward upward laryngeal movement is basically normal and the opening of the upper esophageal sphincter is impaired, cricopharyngeal myotomy is a more mature treatment with good results and low complication rate, but careful screening of cases is required. In addition, although it is traditionally called cricopharyngectomy, it can be seen from the surgical operation that it actually includes part of the inferior pharyngeal constrictor muscle and the upper esophageal longitudinal muscle, so it may be more reasonable to call it upper esophageal sphincterotomy.