The term spastic disorders is applied to a wide spectrum of dysmotility (see Figure 18-1). These disorders are identified from patterns of hypermotility on manometric tracings or presence of tertiary or uncoordinated contractions during barium fluoroscopy. Unlike achalasia, where inhibitory nerve death results in regular evidence of motor dysfunction, the findings in spastic disorder are intermittent, vary in severity from swallow to swallow, and are intermixed with normal findings. The anatomic location of neural dysfunction is uncertain in spastic disorders, and no consistent pathologic abnormality has been detected. Abnormal modulation of motility through central mechanisms may be responsible in some cases.
Spastic disorders typically are discovered during the investigation of esophageal complaints when no structural explanation is present. Appropriate management must take several important facts into consideration (Clouse, 1997; Kahrilas, 2000). First, the manometric or radiologic findings are sufficiently nonspecific for symptoms that careful exclusion of other explanations, esophageal (eg, GERD) and nonesophageal (eg, cardiac), is still required. Second, concurrent abnormalities in esophageal sensation may be as important as motility abnormalities in producing symptoms. Despite the wide variety of spastic disorders (including diffuse esophageal spasm, nutcracker esophagus, and other nonspecific spastic disorders), there presently is no evidence that one should be managed different from another.
Once the spastic disorder is detected and alternative symptom explanations are excluded, management proceeds according to the algorithm shown in Figure 18-3. If the principal symptoms reflect disturbed transit (viz dysphagia or regurgitation), then the spectrum of treatments used for achalasia can be considered (Gui et al, 2003; Balaji and Peters, 2002). Because dysphagia also can be a symptom of altered sensation in these disorders, that is, a sense of disturbed transit without conspicuous obstruction to bolus movement, management approaches used for chest pain sometimes are appropriate. Before considering the more morbid procedures, including pneumatic dilatation or myotomy, it is essential that a relationship of symptoms to impaired transit be demonstrated. This can be accomplished by offering a radio-opaque pill at the time of a fluoroscopic barium swallow to see if symptoms are reproduced with lodging of the pill—usually at the level of the LES.
At my institution, PPIs and antidepressants, either alone or in combination, prove to be the most important management tools for these patients. A PPI trial, either empiric or as directed by findings on 24-hour pH monitoring, is the first step. Patients with refractory symptoms will receive a low dose TCA along with the PPI if there was a symptomatic response, if pathologic reflux has been demonstrated either by endoscopy or pH monitoring, if there was an association of symptoms with reflux events during the pH study, or in place of antireflux therapy if none of these features were present. TCAs appear superior in clinical practice to contemporary antidepressants (Clouse, 1994). I begin with nortriptyline 25 mg at bedtime with an escalation to 50 to 125 mg daily until symptomatic response occurs or side effects prevent further dose increment. In
patients with many somatic symptoms or unexplained syndromes, I start with 10 mg at bedtime. Nortriptyline and desipramine, metabolites of amitriptyline and imipramine, respectively, are better-tolerated TCAs because of their fewer side effects. Treatment for 6 to 24 months is typical in symptomatic responders before withdrawal is attempted. Patients with objective evidence of reflux disease need continuous antireflux therapy; "stepping down" to intermittent antireflux treatment should be tried for other subjects.
Rarely is surgery used in patients with spastic disorders. (Balaji and Peters, 2002). Chest pain is a poor indication, just as chest pain is the least responsive symptom to surgery for achalasia. Most patients with spastic disorders have stable patterns over time and symptoms wax and wane. Long esophageal myotomy is the surgical procedure of choice when esophageal body abnormalities are present; if poor LES relaxation is the dominant finding, a shorter myotomy as for achalasia is performed. Surgery typically is reserved for subjects with advanced spastic motor abnormalities that overlap with achalasia (sometime called "acha-lasia variants") in whom incomplete LES relaxation is well demonstrated and transit disturbances during radiography correlate well with symptoms.
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