No abstract

.-The pathogenesis of achalasia involves the degeneration of enteric and autonomic nervous systems with resultant effects on esophageal motility. The neural degeneration could affect visceral sensation in achalasia. The aim of this study was to examine mechanosensitivity and chemosensitivity in patients with achalasia. Perceptual responses to esophageal distension and acid perfusion were assessed in nine achalasia patients and nine healthy subjects. Mechanosensitivity was evaluated using a barostat with a doublerandom staircase distension protocol. Responses were graded as follows: 0, no sensation; 1, initial sensation; 2, mild discomfort; 3, moderate discomfort; and 4, pain. Chemosensitivity was graded along a visual analog scale after perfusion of saline and 0.1 N HCl. Barostat pressure-volume relationships were used to report esophageal body compliance. Barostat pressures for initial sensation and mild discomfort were not significantly different for patients and controls. The pressures for moderate discomfort (37.9 Ϯ 3.5 vs. 25.7 Ϯ 2.4 mmHg; P Ͻ 0.05) and pain (47.8 Ϯ 2.3 vs. 32.2 Ϯ 3.5 mmHg; P ϭ 0.002) were significantly higher in achalasics than controls. Seven of the eight achalasia patients never reached pain thresholds at the maximum distension pressure (50 mmHg). Sensation to acid perfusion was significantly lower in achalasics compared with controls (2.2 Ϯ 1.2 vs. 6.7 Ϯ 1.7 cm; P Ͻ 0.05). Compliance was significantly increased in patients with achalasia compared with controls. We conclude that both mechanosensitivity and chemosensitivity are significantly diminished in achalasia patients compared with controls. Also, initial sensation and pain sensation are differentially affected in achalasics. These findings suggest that neuropathic defects in achalasia may manifest themselves in visceral sensory and motor dysfunction. motility; esophageal motility disorders; visceral sensitivity; noncardiac chest pain ACHALASIA IS AN ESOPHAGEAL motility disorder characterized histopathologically by degeneration of ganglia of the myenteric plexus. The pathology may follow a continuum ranging from inflammation of the myenteric plexus with neuronal degeneration to complete aganglionosis (7). Loss of neurons within the dorsal motor nucleus and degenerative changes of vagal nerve fibers have also been described. The resulting motor deficits have been well characterized by manometry and include aperistalsis of the esophageal body and failure of the lower esophageal sphincter (LES) to relax with deglutition although manometric variability has been described (10). Functional obstruction of the LES leads to impaired esophageal emptying that is manifest clinically as progressive dysphagia, regurgitation, and weight loss. Serious complications of retained material in the esophagus exist, including stasis mucosal injury, chronic aspiration, and delayed transit of nutrients and medications.In contrast to the pathophysiology of motor dysfunction, little is known about the integrity of esophageal sensory perception in patients wit...

No abstract

No abstract