Causes of Esophageal Chest Pain

The location and radiation patterns of esophageal chest pain often mimic cardiac angina, mandating a thorough investigative approach. Pain is produced by diseases involving the mucosa and esophageal wall as well as by noxious luminal stimuli. GERD is the most commonly identified etiology of discrete esophageal pain episodes that are differentiated from heartburn. At least 40% of patients with otherwise unexplained chest pain will have evidence of pathologic reflux, either as esophagitis at endoscopy or elevated acid exposure time on ambulatory pH monitoring. Of the remainder, at least one-third will have close association of chest pain episodes with acid reflux events, although their responsiveness to acid suppressant therapy is reduced compared with those having pathologic reflux.

If no objective measure of GERD is present in patients with otherwise unexplained chest pain, the patient is diagnosed with functional chest pain, even if the pain seems acid provoked (Clouse et al, 1999). Studies using acid, balloon distension and electrical stimulation of the esophagus as sensory stimulants, and symptoms or direct physiologic measures of brain activity as the response, demonstrate that the primary abnormality is a misinterpretation of stimulus significance in the CNS. These observations may help explain the high prevalence of anxiety and affective disorders in patients with unexplained chest pain, disorders that can influence central perception of somatic signals and pain reporting. Either the distorted processing of esophageal sensory information or the comorbid psychiatric disturbances may be responsible for autonomic reactivity that also appears a part of the syndrome. This discussion is germane to understanding the relationship of unexplained chest pain to esophageal motil-ity disorders, as a certain degree of motor dysfunction, especially hypermotility, may be produced by this pathophysiology. Figure 18-2 illustrates these relationships and provides a conceptual framework for the treatment strategies outlined in this chapter, particularly for the spastic disorders.

Brain-Gut Axis

Environment

Heightened sensorimotor activity

I Gut luminal/ \ mucosal

Heightened sensorimotor activity

I Gut luminal/ \ mucosal

ENS

Functional esophageal symptoms

FIGURE 18-2. A model of the pathophysiologic elements involved in functional chest pain and other functional esophageal symptoms. Heightened sensory and motor activity, reflecting underlying errors in central signal processing and possibly exaggerated autonomic response to these processing errors, are the core abnormalities. These features are provoked by luminal stimuli (such as acid and distention) at the level of the enteric nervous system (ENS) and by psychological and cognitive influences at the level of the central nervous system (CNS). Each box represents a potential treatment target.

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