Characteristics of Cricopharyngeal Dysphagia After Ischemic Stroke

Abstract

ObjectiveTo evaluate the characteristics of cricopharyngeal dysfunction (CPD), the frequency, and correlation with a brain lesion in patients with first-ever ischemic stroke, and to provide basic data for developing a therapeutic protocol for dysphagia management.MethodsWe retrospectively reviewed the medical records of a series of subjects post-stroke who underwent a videofluoroscopic swallowing study (VFSS) from January 2009 to December 2015. VFSS images were recorded on videotape and analyzed. CPD was defined as the retention of more than 25% of residue in the pyriform sinus after swallowing. The location of the brain lesion was assessed using magnetic resonance imaging.ResultsAmong the 262 dysphagic patients with first-ever ischemic stroke, 15 (5.7%) showed CPD on the VFSS. Patients with an infratentorial lesion had a significantly higher proportion of CPD than those with a supratentorial lesion (p=0.003), and lateral medullary infarction was identified as the single independent predictor of CPD (multivariable analysis: odds ratio=19.417; confidence interval, 5.560–67.804; p<0.0001). Compared to patients without CPD, those with CPD had a significantly prolonged pharyngeal transit time, lower laryngeal elevation, and a higher pharyngeal constriction ratio and functional dysphagia scale score.ConclusionOverall, the results support the notion that an impaired upper esopharyngeal opening is likely related to the specific locations of brain lesions. The association of CPD with lateral medullary infarction can be explained based on the regulation of the pharyngolaryngeal motor system by the motor neurons present in the dorsal nucleus ambiguus. Overall, the results reveal the relation between CPD and the problems in the pharyngeal phase as well as the severity of dysphagia.

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“…Ischemic stroke is the second most common type critical disease worldwide and leads to mortality and permanent dysfunction, including cricopharyngeal dysfunction (21,22). Brain injury induced by cerebral ischemia is the cause of exacerbations and damage mechanisms, including inflammatory response, oxidative stress, apoptosis and mitochondrial dysfunction (23–26).…”

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“… Pharyngeal construction ratio (PCR): evaluated by VFSS. It is the ratio of pharyngeal area at maximal contraction to pharyngeal area at rest [ 2 ]. The calculation formula: PCR = PA max /PA hold (PA max refers to the minimum area of the pharyngeal cavity when contracting during oral swallowing in the image of the VFSS, and PA hold refers to the maximum area of the pharyngeal cavity with a 1 ml bolus in the patient’s mouth in the resting state).…”

“…Functional swallowing occurs due to a series of well-coordinated movements that allow transport of food bolus from the oral cavity into the stomach while avoiding passage of food bolus into the airway [ 1 ]. Dysphagia occurs due to neurological disorders that impair the transport of food from the oral cavity to the stomach efficiently and/or safely [ 2 ] and is associated with an increased risk of pulmonary complications, dehydration, malnutrition, and mortality [ 1 , 3 ]. Dysphagia is a common complication in stroke patients with a morbidity rate between 20 and 90%, depending on the assessment methods [ 4 ].…”

“…The cricopharyngeal muscle is main muscle responsible for UES function [ 5 ]. This muscle remains in a contracted position during respiration, preventing air from entering into the esophagus and relaxes and opens during swallowing or vomiting [ 2 ]. Cricopharyngeal dysfunction (CPD), characterized by difficulty of food bolus entering the esophagus, occurs often due to 3 main factors: cricopharyngeal muscle spasm, incomplete laryngeal movement, and insufficient descending pressure of the bolus [ 2 ].…”

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“…One common etiology of CP dysfunction includes stroke, one of the leading causes of dysphagia. A study by Yang et al[ 38 ] utilizing videofluoroscopic imaging to assess swallowing function in patients suffering from dysphagia due to stroke found an incidence of CP dysfunction to be 5.7% among first-time ischemic stroke patients. This incidence increased to 14.3% among those with infratentorial lesions and decreased to 2.8% among those with supratentorial lesions, suggesting focal lesions, primarily to the dorsal motor nucleus of the vagus, to be the primary culprit[ 38 ].…”