The cricopharyngeus muscle (CPM) is a key component of the upper esophageal sphincter (UES). In dysphagia, 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 the resultant clinical manifestation is solid food or solid and liquid dysphagia. Several diagnostic tools are available for dysphagia clinicians to distinguish CPD from other causes of UES dysfunction. For CPD, accurate diagnosis is paramount for the recommendation of appropriate treatment. In appropriately selected patients, intervention at the CPM may yield significant improvement in dysphagia.
| BTx | Botulinum toxin |
| CPB | Cricopharyngeus muscle bar |
| CPD | Cricopharyngeus muscle dysfunction |
| CPM | Cricopharyngeus muscle |
| FEES | Flexible endoscopic evaluation of swallowing |
| FOSS | Functional outcome swallowing scores |
| HRM | High-resolution impedance manometry |
| PCR | Pharyngeal constriction ratio |
| PES | Pharyngoesophageal segment |
| PSM | Pharyngeal squeeze maneuver |
| RLN | Recurrent laryngeal nerve |
| UES | Upper esophageal sphincter |
| VFSS | Video-fluoroscopic swallow study |
Key points
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The cricopharyngeus muscle (CPM) is one component of the upper esophageal sphincter, and the failure of its coordinated relaxation or expansion is termed cricopharyngeus muscle dysfunction (CPD).
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Many conditions cause CPD; the clinical manifestations vary from asymptomatic to profound dysphagia.
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The diagnosis of CPD may be accomplished with a combination of clinical and instrumental swallowing evaluations, including flexible endoscopic evaluation of swallowing, video-fluoroscopic swallow study, and high-resolution manometry.
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The success of intervention at the CPM relies heavily on the accuracy of diagnosis, which is often challenging.
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Patients with dysphagia with CPD who retain sufficient pharyngeal strength and hyolaryngeal elevation will fair best with interventions targeting the CPM.
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Interventions include nonsurgical, pharyngoesophageal segment dilation, botulinum toxin injection, and cricopharyngeus myotomy.
Introduction
The upper esophageal sphincter (UES) is a 2.5- to 4.5-cm high-pressure zone extending from the distal pharynx to the proximal esophagus. This anatomic region is also referred to as the pharyngoesophageal segment (PES). The cricopharyngeus muscle (CPM) is positioned in the transition zone between the inferior pharyngeal constrictor and cervical esophageal musculature, which compose the PES. The CPM is 1 to 2 cm wide and C shaped, attaching to the lateral portions of the cricoid cartilage without a median raphe. It is composed of a horizontal portion termed the pars fundiformis and an oblique portion known as the pars oblique . Uniquely composed of skeletal muscle and abundant connective tissue, the CPM small fibers originate and insert within the fibroelastic connective tissue. The CPM contains mostly slow type 1 muscle fibers but also fast type 2 fibers enabling baseline tonicity as well as rapid reflexive relaxation or tightening. Anatomic studies have demonstrated that the CPM receives dual innervation from the ipsilateral pharyngeal plexus and the recurrent laryngeal nerve (RLN). Sensory information is carried along the glossopharyngeal nerve and cervical sympathetics.
At rest, the tonically contracted UES protects against aspiration of refluxed gastric contents as well as aerophagia during respiration. Reflexive tightening of the UES is induced by esophageal distention or acid exposure, pharyngeal stimuli and emotional stress. During deglutition, eructation and vomiting, the UES reflexively opens. During swallowing, opening of the PES relies on CPM relaxation, anterosuperior movement of the hyolaryngeal complex, pharyngeal contraction, and distension by the passing bolus. Although the CPM is only one component of effective PES function, it is the only portion that actively participates in all reflexive relaxation and tightening activities. Consequently, the CPM is an important target for therapy in several disease processes affecting the UES. Cricopharyngeus muscle dysfunction (CPD) describes impaired or uncoordinated PES relaxation or expansion and results from a variety of causes as listed in Table 1 .
| Neoplastic | Oropharyngeal carcinoma Esophageal carcinoma Benign esophageal neoplasm Brainstem neoplasm |
| Neurologic/Neuromuscular | Cerebrovascular accident Traumatic brain injury Parkinson disease Amyotrophic lateral sclerosis Huntington chorea Inflammatory myopathy Spinocerebellar degeneration Syringobulbia Muscular dystrophy |
| Inflammatory/Autoimmune | Laryngopharyngeal reflux Pharyngitis Dermatomyositis Inclusion body myositis Polymyositis Scleroderma |
| Infectious/Toxic | Poliomyelitis Diphtheria Rabies Botulism Lead poisoning |
| Metabolic | Hyperthyroidism Myxedema Diabetes |
| Trauma/Iatrogenic | Foreign body Postsurgical changes Radiation therapy Aerodigestive injury |
| Other | Zenker diverticulum Idiopathic |
Introduction
The upper esophageal sphincter (UES) is a 2.5- to 4.5-cm high-pressure zone extending from the distal pharynx to the proximal esophagus. This anatomic region is also referred to as the pharyngoesophageal segment (PES). The cricopharyngeus muscle (CPM) is positioned in the transition zone between the inferior pharyngeal constrictor and cervical esophageal musculature, which compose the PES. The CPM is 1 to 2 cm wide and C shaped, attaching to the lateral portions of the cricoid cartilage without a median raphe. It is composed of a horizontal portion termed the pars fundiformis and an oblique portion known as the pars oblique . Uniquely composed of skeletal muscle and abundant connective tissue, the CPM small fibers originate and insert within the fibroelastic connective tissue. The CPM contains mostly slow type 1 muscle fibers but also fast type 2 fibers enabling baseline tonicity as well as rapid reflexive relaxation or tightening. Anatomic studies have demonstrated that the CPM receives dual innervation from the ipsilateral pharyngeal plexus and the recurrent laryngeal nerve (RLN). Sensory information is carried along the glossopharyngeal nerve and cervical sympathetics.
At rest, the tonically contracted UES protects against aspiration of refluxed gastric contents as well as aerophagia during respiration. Reflexive tightening of the UES is induced by esophageal distention or acid exposure, pharyngeal stimuli and emotional stress. During deglutition, eructation and vomiting, the UES reflexively opens. During swallowing, opening of the PES relies on CPM relaxation, anterosuperior movement of the hyolaryngeal complex, pharyngeal contraction, and distension by the passing bolus. Although the CPM is only one component of effective PES function, it is the only portion that actively participates in all reflexive relaxation and tightening activities. Consequently, the CPM is an important target for therapy in several disease processes affecting the UES. Cricopharyngeus muscle dysfunction (CPD) describes impaired or uncoordinated PES relaxation or expansion and results from a variety of causes as listed in Table 1 .
| Neoplastic | Oropharyngeal carcinoma Esophageal carcinoma Benign esophageal neoplasm Brainstem neoplasm |
| Neurologic/Neuromuscular | Cerebrovascular accident Traumatic brain injury Parkinson disease Amyotrophic lateral sclerosis Huntington chorea Inflammatory myopathy Spinocerebellar degeneration Syringobulbia Muscular dystrophy |
| Inflammatory/Autoimmune | Laryngopharyngeal reflux Pharyngitis Dermatomyositis Inclusion body myositis Polymyositis Scleroderma |
| Infectious/Toxic | Poliomyelitis Diphtheria Rabies Botulism Lead poisoning |
| Metabolic | Hyperthyroidism Myxedema Diabetes |
| Trauma/Iatrogenic | Foreign body Postsurgical changes Radiation therapy Aerodigestive injury |
| Other | Zenker diverticulum Idiopathic |
Evaluation of CPD
Accurately diagnosing CPD is challenging but essential for therapeutic decision making. Individuals with poor CPM relaxation but intact laryngeal elevation and pharyngeal contraction generally respond well to surgical CPM intervention. However, those demonstrating intact CPM behavior with impaired pharyngeal strength or hyolaryngeal elevation are more appropriate candidates for therapy than surgery. Dysphagia clinicians rely on several diagnostic tools to identify and differentiate pharyngeal weakness, poor hyolaryngeal elevation, loss of PES elasticity, and impaired CPM relaxation. Available tools include the clinical swallow evaluation, flexible endoscopic evaluation of swallowing (FEES), video-fluoroscopic swallow study (VFSS) and manometry of the pharynx, and UES.
Clinical Swallow Evaluation
Information gathered during the clinical swallow evaluation is useful for generating a hypothesis for the cause or site of dysphagia and for choosing a potential instrumental tool for further swallowing assessment. A history of solid food or combined solid food and liquid dysphagia suggests impaired pharyngeal strength, PES dysfunction, or an esophageal cause, whereas isolated dysphagia to thin liquids indicates laryngopharyngeal sensory impairment or oropharyngeal dysphagia. Furthermore, patients identifying their dysphagia as cervical may have a pharyngeal or UES abnormality, whereas those localizing complaints to the chest assuredly have an esophageal cause for their dysphagia.
The physical examination is helpful in assessing hyolaryngeal mobility. Poor palpable elevation of the hyoid bone or thyroid notch during a dry swallow reveals a probable cause for poor PES distension. During bolus trials, repeated swallows or throat clearing after swallowing suggests hypopharyngeal residue, which is frequently encountered with PES dysfunction or pharyngeal weakness.
Although the clinical swallow evaluation is important for the initial evaluation of patients complaining of dysphagia, it is inadequate to fully characterize all phases of swallowing and definitively identify the sites of abnormality. Furthermore, previous studies have shown that a bedside swallow evaluation may fail to detect aspiration in up to 40% of individuals.
FEES
A potentially useful component of the office-based dysphagia evaluation is FEES. It is particularly important for assessing laryngopharyngeal anatomy as well as sensory and motor integrity. Although FEES does not directly evaluate PES function, the presence of pooled hypopharyngeal secretions with intact pharyngeal strength assessed by the pharyngeal squeeze maneuver (PSM) ( Fig. 1 ) indicates obstruction at the PES. However, observing an impaired PSM suggests pharyngeal weakness as a potential cause for dysphagia but reveals little regarding PES function.
Video-fluoroscopy
Improved evaluation of PES opening is afforded during the VFSS. Impaired CPM function may manifest radiographically as a cricopharyngeus muscle bar (CPB) with varying degrees of obstruction or complete PES obstruction ( Fig. 2 ). To improve interpretation and comparison of sequential studies, Leonard and colleagues reported validated displacement and timing measures that allow extraction of objective data from VFSS. Particularly important for assessing CPM function are the PES opening size and duration; laryngohyoid approximation; oropharyngeal and hypopharyngeal transit times; and pharyngeal constriction ratio (PCR), which is a surrogate measure for pharyngeal strength. The PES opening enlarges with increasing bolus size and is, on average, smaller in adults older than 65 years. CPBs are frequently encountered during VFSS and were identified in nearly one-third of a cohort of nondysphagic elderly (>65 years of age) individuals. Such incidental findings lend support to measuring the PES opening because it remains adequate in many individuals with radiographic evidence of CPBs. Furthermore, measurement of the PES opening preoperatively and postoperatively in patients with obstructing CPM dysfunction helps to quantify the effect of the intervention.
