The terminology used in describing esophageal motility disorders is not fully standardized. At Washington University we classify dysmotility using a simple scheme representing the two principal types of motor dysfunction (Figure 18-1). The first leads to impaired contraction in the esophageal body and/or lower esophageal sphincter (LES). Resultant hypomotility predisposes the patient to gastroesophageal reflux disease (GERD), either by increasing reflux events or delaying clearance of refluxate. The second type of motor dysfunction reflects inadequate or failed inhibition of contraction in these same regions or an imbalance between contraction and inhibition. Neural inhibitory effects are required for the correct timing of contraction in the esophageal body and for appropriate relaxation of the LES. The resultant
Diffuse esophageal spasm
Vigorous contraction wave abnormalities: High amplitude (nutcracker) Long duration Double and triple peaks
Hypertensive or poorly relaxing LES
FIGURE 18-1. A method for categorizing motor disorders of the distal esophagus and lower esophageal sphincter (LES) based on principal type of motor dysfunction. Some patients have a mixture of hypomotility and hypermotility features and cannot be classified solely into one branch. Hypermotility typically is associated with hypersensitivity to endogenous, intraluminal, and chemical stimuli, whereas hypomotility is associated with hyposensitivity. From Clouse (1997).
The swallowing process begins in the oropharyngeal phase. Oropharyngeal motor dysfunction results primarily from central nervous system (CNS), cranial nerve, and striated muscle disease, and motility disorders are common causes of oropharyngeal dysphagia. Control of motor activity shifts largely to the intramural nerve plexus once peristalsis passes the first several centimeters of esophagus, correlating with transition from striated to smooth muscle in the esophageal wall. Motor dysfunction in these distal regions is an important cause of esophageal symptoms, but unlike oropharyngeal dysphagia, structural lesions are more common causes of esophageal dysphagia. The subject of this chapter is the management of motility disorders involving the smooth-muscle region and chest pain related to motor dysfunction in that region.
Esophageal body hypomotility
Low wave amplitude
Complete peristaltic failure (without evidence of poor LES relaxation)
Nonspecific spastic disorders hypermotility manifests as rapid propagation or nonperi-staltic contraction in the esophageal body, exaggerated contraction response of high amplitude or broad duration, hypertension of the LES, and inadequate or incomplete LES relaxation. Advanced manifestations of hypermotility (no normal peristalsis and incomplete LES relaxation) typify achalasia. Less developed patterns of hypermotility that display intermittently normal peristalsis and LES relaxation are classified as spastic disorders. Some overlap occurs between spastic disorders and achalasia that cannot be fully differentiated manometrically.
One often-overlooked management aspect is concurrent esophageal sensory dysfunction. A variety of conditions associated with hypomotility also are associated with hyposensitivity to intraluminal stimuli, such as acid or distention. In contrast, conditions associated with hypermotility, particularly the spastic disorders, also are associated with increased sensation and symptom reproduction with such stimuli (hypersensitivity). Although these relationships are incomplete, co-occurrence of sensory and motility alterations is sufficiently common that the relationship should be considered in management.
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