Читать книгу The Esophagus - Группа авторов - Страница 154

Most patients with swallowing dysfunction have neural or muscular disorders that alter timing of events or muscular contraction rather than causing oral or pharyngeal structural damage. Some diseases affect a patient’s ability to self‐feed despite normal swallowing. Other diseases affect both the ability to feed and to swallow. For example, patients with Parkinson’s disease often have difficulty sitting and manipulating food as well as having abnormal bolus transfer [14].

About one‐fourth of cerebrovascular accidents cause dysphagia [14, 15]. In general, left‐sided strokes alter the oral phase of swallowing, whereas right‐sided strokes alter the pharyngeal phase [15, 16]. The corticobulbar pathways in the internal capsule can be damaged by large hemispheric strokes or small‐vessel disease. Acute strokes or small‐vessel disease resulting from hypertension, diabetes, or other causes can also affect the swallowing center in the pons and medulla [17].

Diseases that directly damage motor neurons in the swallowing center or cranial nerves in the skull base may result in bulbar palsy with oral and pharyngeal swallowing difficulties [18–22]. Lower motor neural destruction occurs in amyotrophic lateral sclerosis and 10–15% of patients with acute poliomyelitis [19, 20]. Some patients with a history of poliomyelitis have progressive disintegration of axon terminals in surviving but overworked residual motor neurons, resulting in pharyngeal muscle weakness caused by “post‐polio muscular atrophy” [21]. Meningeal carcinomatosis may also result in dysphagia. Unilateral pharyngeal paresis is often caused by destruction of motor nerves at the skull base or in the neck as a result of tumor, trauma, or surgery [10]. Abnormal transmission at the myoneural junction in myasthenia gravis may result in dysphagia that is initiated or exacerbated by prolonged swallowing.

Dysphagia resulting from inflammatory or endocrine‐related myopathies is potentially treatable [14]. Dermatomyositis and polymyositis directly damage the intrinsic or extrinsic muscles of the pharynx. Pharyngeal muscle myopathy may be caused by a variety of endocrine disorders, including hyperthyroidism, hypothyroidism, and Cushing’s syndrome [22].

The end result of these various neuromuscular disorders is poor timing of oral and pharyngeal events, or abnormal movement of oral and pharyngeal structures. A bolus may be directed in a normal fashion, but because of poor timing, the bolus may enter the laryngeal vestibule or nasopharynx. Laryngeal penetration is defined as passage of the bolus into the laryngeal vestibule either just before the swallow or during swallowing [23, 24]. Abnormal tongue motion, pharyngeal contraction, or epiglottic tilt may also lead to laryngeal penetration (Figures 6.7 and 6.8). Abnormal oral or pharyngeal movement may result from a structural abnormality or neuromuscular disorder. Abnormal epiglottic tilt or pharyngeal muscular contraction may also lead to stasis in either the valleculae or piriform sinuses, respectively. Marked stasis in the piriform sinuses may cause the bolus to overflow into the larynx through the interarytenoid notch when the patient breathes or subsequently swallows for a second time. Thus, overflow aspiration is defined as barium entering the laryngeal vestibule while the patient is breathing normally [23, 24] (Figure 6.9), or as barium entering the laryngeal vestibule as a result of poor timing when the patient swallows for a second time, and there is moderate stasis in the valleculae and piriform sinuses. Aspiration may also result from regurgitation of esophageal contents into the pharynx.

Figure 6.6 Representative frames from the pharyngeal phase of swallowing. (A) The bolus (b) has just entered the oropharynx. The soft palate (s) is rising to appose the posterior pharyngeal wall, but the velopharyngeal portal (arrow) is still open. The epiglottic tip is just beginning to tilt posteriorly. The laryngeal vestibule (l) is still open. (B) The bolus has just entered the hypopharynx. The soft palate (s) now apposes the posterior pharyngeal wall. The epiglottis (arrowhead) is partly obscured by the barium but is tilting. The pharyngoesophageal segment (arrow) remains closed. (C) The bolus is passing into the esophagus. Pharyngeal and laryngeal elevation is manifested by elevation of the hyoid bone (b) up underneath the mandible. The laryngeal vestibule is completely compressed and is no longer seen as an air‐filled space. The epiglottis (arrowhead) has tilted to appose the anterior wall of the hypopharynx. The posterior pharyngeal contraction wave (long arrow) is in the thyropharyngeal muscle. The pharyngoesophageal segment (short arrow, identified by redundant post‐cricoid mucosa on the opposite wall) is open. The C5 vertebral body is labeled 5 to allow a direct comparison to D. (D) The bolus has just passed through the pharynx. The pharynx and larynx have returned to their “resting” position. Compare the levels of the hyoid bone (b) and the pharyngoesophageal segment (thick arrow) on image C during swallowing and image D after swallowing. The epiglottic tip (arrowhead) has returned to its upright position. The soft palate now apposes the tongue, and the laryngeal vestibule is open. A small Killian–Jamieson diverticulum (thin arrow) is present. The C5 vertebral body is labeled 5.

Figure 6.7 Laryngeal penetration. (A) During drinking, barium enters the laryngeal vestibule (thick arrow). The anterior commissure (thin arrow) and true vocal cords (t) are identified. (B) Spot radiograph during phonation shows a huge epiglottic mass (arrows) with nodular mucosa (open arrow) as the cause of the laryngeal penetration.

Source: Reproduced from Rubesin [10], with permission.

Unilateral pharyngeal paresis should suggest vagal injury from the level of the pons to the recurrent laryngeal nerve, whereas abnormal epiglottic tilt as an isolated finding should suggest recurrent laryngeal nerve damage or intralaryngeal muscle problems. In general, however, the degree and types of swallowing dysfunction on barium swallows do not enable the radiologist to predict the underlying neuromuscular diseases causing this dysfunction.