Health Questions and Answers

Swallowing Disorders and Dysphagia

What is the most difficult substance to swallow?
Water. Swallowing involves several phases. First, a preparatory phase involves chewing, sizing, shaping, and positioning of the bolus on the tongue. Then, during an oral phase, the bolus is propelled from the oral cavity into the pharynx while the airway is protected. Finally, the bolus is transported into the esophagus. Water is the most difficult substance to size, shape, and contain in the oral cavity. This makes it the hardest to control as it is passed from the oral cavity into the pharynx. Thus, viscous foods are used to feed patients with oropharyngeal dysphagia.

What sensory cues elicit swallowing?
The sensory cues are not entirely known, but entry of food or fluid into the hypopharynx, specifically the sensory receptive field of the superior laryngeal nerve, is paramount. Swallowing may also be initiated by volitional effort, if food is present in the oral cavity. The required signal for initiation of the swallow response is a mixture of both peripheral sensory input from oropharyngeal afferents and superimposed control from higher nervous system centers. Neither is capable of initiating swallowing independent of the other. Thus, swallowing cannot be initiated during sleep when higher centers are turned off or with deep anesthesia to the oral cavity when peripheral afferents are disconnected.

What is flexible endoscopic evaluation of swallowing with sensory testing (FEESST)?
FEESST is an endoscopic test that allows direct visualization of the hypopharynx and larynx during swallowing evaluation. It can directly assess airway protection during a swallow. A thin, flexible endoscope is passed transnasally into the hypopharynx. Pooling of hypopharyngeal secretions is recorded and is used to gauge aspiration risk. Next, swallowing assessment is done with liquids (mixed with food coloring) of varying consistency, given serially to the patient and observed as they traverse the hypopharynx. Any penetration into the larynx (aspiration) is noted. Finally, discrete pulses of air are given, endoscopically, to the mucosa innervated by the superior laryngeal nerve to elicit the protective laryngeal adductor reflex. This results in brief closure of the vocal cords with or without a swallow. An intact reflex supports a low aspiration risk. FEESST is a safe procedure that can be performed at the bedside or office, and it does not require sedation.

What is the difference between globus sensation (globus hystericus) and dysphagia?
Globus sensation is the feeling of a lump in the throat. It is present continually and is not related to swallowing. It may even be temporarily alleviated during a swallow. Dysphagia is difficulty in swallowing and is noted by the patient only during swallowing.

Do patients accurately localize the site of dysphagia?
No. Patients with esophageal dysphagia localize the abnormal site correctly only 60-70% of the time. Patients incorrectly localize the site of dysphagia proximal to the actual site in the remainder. Differentiating between proximal and distal lesions may be difficult, based on the patient’s perception only. Patients with oropharyngeal dysphagia usually recognize that the swallow dysfunction is in the oropharynx. They may perceive food accumulating in the mouth or an inability to initiate a pharyngeal swallow. They can generally recognize aspiration before, during, or after a swallow. Associated symptoms, such as difficulty with chewing, drooling, coughing or choking after a swallow, are more suggestive of oropharyngeal than esophageal dysphagia.

What symptoms can be seen in oropharyngeal dysphagia?

  • Inability to initiate a swallow
  • Sensation of food getting stuck in the throat
  • Coughing or choking (aspiration) during swallowing
  • Nasopharyngeal regurgitation
  • Changes in speech or voice (nasality)
  • Ptosis
  • Photophobia or visual changes
  • Weakness, especially progressive toward the end of the day

What are the causes of oropharyngeal dysphagia?
Oropharyngeal dysphagia can result from propulsive failure or structural abnormalities of either the oropharynx or esophagus. Propulsive abnormalities can result from dysfunction of the central nervous system control mechanisms, intrinsic musculature, or peripheral nerves. Structural abnormalities may result from neoplasm, surgery, trauma, caustic injury, or congenital anomalies. If dysphagia occurs in the absence of radiographic findings, motor abnormalities may be demonstrable by more sensitive methods, such as electromyography or nerve stimulation studies. If all studies are normal, impaired swallowing sensation may be the primary abnormality

What causes oropharyngeal dysphagia in the elderly?

  1. 80% caused by neuromuscular disorders: Leading cause is cerebrovascular accidents (CVAs); others include Parkinson’s disease, myasthenia gravis, and dermatomyositis.
  2. 20% caused by structural disorders: Cancer is the most worrisome cause.

Why is a brain stem stroke more likely to cause severe oropharyngeal dysphagia than a hemispheric stroke?
The swallowing center is situated bilaterally, in the reticular substance below the nucleus of the solitary tract, in the brain stem. Efferent fibers from the swallow centers travel to the motor neurons controlling the swallow musculature located in the nucleus ambiguus. Therefore, brain stem strokes are more likely to cause the most severe impairment of swallowing with difficulty in initiating a swallow or absence of the swallow response.

When is it appropriate to evaluate stroke-related dysphagia?
About 25-50% of strokes will result in oropharyngeal dysphagia. Most stroke-related swallowing dysfunction improves spontaneously within the first 2 weeks. Unnecessary diagnostic or therapeutic procedures, such as percutaneous gastrostomy, should be avoided immediately after a cerebrovascular accident. When symptoms persist beyond the 2-week period, swallowing function should be evaluated.

Is a barium swallow examination adequate to evaluate oropharyngeal dysphagia?
No. A barium swallow focuses on the esophagus, is done in a supine position, and takes only a few still images as the barium passes through the oropharynx. Therefore, aspiration may be missed if a conventional barium swallow is ordered.
Oropharyngeal dysphagia is best evaluated with a cineradiographic or videofluoroscopic swallowing study, commonly called the modified barium swallow. The oropharyngeal swallow is rapid and transpires in less than 1 second, images must be obtained and recorded at a rate of 15-30/sec to capture adequately the motor events. The recorded study can be played back in slow motion for careful evaluation. This study is done with the patient in the upright position and resembles normal eating position more than the conventional barium swallow.

Can childhood polio cause dysphagia to develop years later in adulthood?
Yes, even if the initial presentation did not include bulbar involvement. The post polio syndrome is a disorder of the medullary motor neuron resulting from new or continuing instability of previously injured motor neurons. Typically, the syndrome consists of new musculoskeletal symptoms, such as weakness and atrophy in previously affected muscles. Patients become symptomatic 25-35 years after the original illness, and even muscular units (limb or bulbar) that appeared untouched in the original infection may develop signs of clinical weakness. Bulbar neuron involvement was reported previously in only 15% of patients with the acute infection. Recent studies demonstrate that some bulbar muscle dysfunction can be demonstrated in all patients with post polio syndrome, although few report dysphagia. Swallowing problems are most severe in patients with bulbar involvement at the onset.

What is the characteristic feature of dysphagia in myasthenia gravis?
Myasthenia gravis is an autoimmune disorder characterized by progressive destruction of acetylcholine receptors at the neuromuscular junction. It affects the striated portion of the esophageal musculature. A distinct feature is increased muscle weakness with repetitive muscle contraction, such that dysphagia worsens with repeated swallows or as the meal progresses. Resting to allow reaccumulation of acetylcholine in nerve endings improves pharyngoesophageal functions and symptoms simultaneously. Muscles of facial expression, mastication, and swallowing are frequently involved, and dysphagia is a prominent symptom in more than one third of cases. An anticholinesterase antibody test is about 90% sensitive in diagnosing myasthenia gravis. If clinical suspicion is strong, a therapeutic trial with an acetylcholinesterase inhibitor, such as Tensilon, or a cholinomimetic, such as Mestinon, should be considered even in the absence of the anticholinesterase antibody.

What is a Zenker’s diverticulum?
A diverticulum of the hypopharynx. It is located posteriorly in an area of potential weakness at the intersection of the transverse fibers of the cricopharyngeus and the obliquely oriented fibers of the inferior pharyngeal constrictors, also called the Killian’s dehiscence.

Is a Zenker’s diverticulum the result of an obstructive or propulsive defect?
Obstructive defect. Previously, it was believed that the pathogenesis of the diverticulum was due to abnormally high hypopharyngeal pressures caused by defective coordination of upper esophageal sphincter (UES) relaxation during pharyngeal bolus propulsion. It is now known that Zenker’s diverticulum is caused by a constrictive myopathy of the cricopharyngeus (poor sphincter compliance). Increased resistance at the cricopharyngeus and increased intrabolus pressures above this relative obstruction cause muscular stress in the hypopharynx with herniation and diverticulum formation. Thus, Zenker’s diverticulum is an obstructive rather than propulsive disease.

What therapies can be used to improve swallowing?

The goal of swallow therapy is to help minimize the risk of aspiration and to optimize oral delivery of nutrition.
Direct swallow therapies attempt to improve the swallow physiology. Examples include treatment of the primary disease, oral and maxillofacial prosthetics, cricopharyngeal myotomy, and swallow maneuvers, such as the supraglottic swallow.
Compensatory techniques help elimiate symptoms but do not change the swallowing dysfunction. They include adjustment of the patient’s head and neck, changing food viscosity, and optimizing the volume and rate of food delivery.
Indirect swallow therapies address the neuromuscular coordination needed for swallowing. Examples include exercise regimens for tongue coordination and chewing.

Which patients are ideal candidates for swallow therapy?
Patients who are mentally competent and motivated have the best results with swallow therapy. Therapy is most effective for aspiration (during and after swallow) and unilateral pharyngeal paresis.

What are the etiologies of dysphagia in gastroesophageal reflux disease?

  1. Inflammation: 30% of patients with esophagitis experience dysphagia.
  2. Stricture: dysphagia occurs when the lumen diameter is less than 11-13 mm.
  3. Peristaltic dysfunction: this is seen with advanced disease.
  4. Hiatus hernia: up to 30% of patients with a hiatus hernia may have dysphagia.

When is botulinum toxin (BTX) used for dysphagia?
BTX has been best studied in dysphagia due to achalasia. Achalasia is caused by selective loss of inhibitory neurons at the LES, resulting in unopposed (tonic) excitation of the LES. BTX injection into the distal esophagus can reduce LES pressure by blocking acetylcholine release from the presynaptic cholinergic nerve terminals in the myenteric plexus. Surgical myotomy is the definitive treatment for achalasia, because repeated BTX therapy is required to maintain efficacy. Ideal candidates for BTX are the elderly and those at high operative risk.
Surgical cricopharyngeal myotomy is the treatment of choice for Zenker’s diverticulum. Endoscopic injection of BTX into the diverticular spur, as an alternative to surgery, has shown favorable results in case reports. BTX in Parkinson’s disease with dysphagia, due to impaired relaxation of the UES, has also shown marked improvement by videofluoroscopic and electromyographic studies. Potential side effects include persistent stenosis and the risk of local BTX diffusion into the larynx or hypopharynx.

Last updated: March 15, 2010

Reference:

  • Aviv JE, Kaplan ST, Thomson JE, et al: The safety of flexible endoscopic evaluation of swallowing with sensory testing (FEESST): An analysis of 500 consecutive evaluations. Dysphagia 15(1):39-44, 2000.
  • Cook IJ, Gabb M, Panagopoulos V, et al: Pharyngeal (Zenker’s) diverticulum is a disorder of upper esophageal sphincter opening. Gastroenterology 103:1229-1235, 1992.
  • Cook IJ, Kahrilas PJ: AGA technical review of management of oropharyngeal dysphagia. Gastroenterology 116:455-478, 1999.
  • Kahrilas PJ, Logemann JA, Lin S, Ergun G: Pharyngeal clearance during swallowing: A combined manometric and videofluoroscopic study. Gastroenterology 103:128-136, 1992.
  • Kolbasnik J, Waterfall WE, Fachnie B: Long term efficacy of botulinum toxin in classical achalasia: A prospective study. Am J Gastroenterol 94:3434-3439, 1999.
  • Ramsey DJ, Smithard DG, Kalra L: Early assessment of dysphagia and aspiration risk in acute stroke patients. Stroke 34(5):1252-1257, 2003.
  • Restivo DA, Palmeri A, Marchese-Ragona R: Botulinum toxin for cricopharyngeal dysfunction in Parkinson’s disease. N Engl J Med 346(15):1174-1175, 2002.
  • Sonies BC, Dalakas MC: Dysphagia in patients with the post-polio syndrome. N Engl J Med 324:1162-1167, 1991.
  • Spechler S: American Gastroenterological Association technical review on treatment of patients with dysphagia caused by benign disorders of the distal esophagus. Gastroenterology 117(1):229-233, 1999.
  • Spinelli P, Ballardini G: Botulinum toxin type A (Dysport) for the treatment of Zenker’s diverticulum. Surg Endosc 17(4):660, 2003.

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