A 42-year-old man presents with a 6-month history of progressive dysphagia to both solids and liquids, regurgitation of undigested food, and retrosternal chest pain. Upper endoscopy reveals a dilated esophagus with retained food debris and a tightly closed lower esophageal sphincter (LES) that requires gentle pressure to pass. The structure marked **A** in the diagram shows these characteristic findings. High-resolution esophageal manometry confirms failed LES relaxation with 100% failed peristalsis and no esophageal pressurization. Which of the following pathophysiologic mechanisms BEST explains the manometric findings in this patient?
A. Fibrosis and shortening of the esophageal muscle layers causing spastic contractions and premature peristalsis
B. Degeneration of the dorsal motor nucleus of the vagus nerve leading to increased parasympathetic tone
C. Mechanical obstruction of the GE junction by a malignant stricture causing progressive dysphagia to solids before liquids
D. Loss of inhibitory neurons in the myenteric (Auerbach) plexus resulting in unopposed cholinergic tone and failure of LES relaxation
Explanation
Why option 1 is correct
Achalasia is a primary esophageal motility disorder characterized by loss of inhibitory neurons (containing nitric oxide and VIP) in the myenteric (Auerbach) plexus of the distal esophagus and LES. This neuronal loss results in unopposed cholinergic tone, producing failure of LES relaxation on swallowing and absent or disordered peristalsis in the esophageal body—exactly the manometric pattern seen in this patient (failed LES relaxation with 100% failed peristalsis and no pressurization, consistent with Type I achalasia per Chicago Classification v4.0). The clinical presentation of dysphagia to BOTH solids and liquids is a key differentiator from mechanical obstruction and reflects the primary motility defect. (Chicago Classification v4.0; ACG Achalasia Guideline 2020)
Why each distractor is wrong
Option 2: While pseudoachalasia from malignancy must be ruled out on endoscopy (especially in patients >55 with short symptom duration and rapid weight loss), mechanical obstruction typically causes dysphagia to solids BEFORE liquids—opposite to this patient's presentation. Moreover, manometry would show normal LES relaxation with mechanical obstruction, not failed relaxation.
Option 3: Degeneration of the dorsal motor nucleus would impair parasympathetic outflow and cause decreased (not unopposed) cholinergic tone, resulting in a patulous LES and aspiration—not achalasia. The dorsal motor nucleus is not the primary pathology in achalasia.
Option 4: Spastic contractions and premature peristalsis are features of Type III (spastic) achalasia, not Type I (classic) achalasia. This patient's manometry shows 100% failed peristalsis with NO pressurization, not spastic contractions—a fundamentally different pathophysiology.
High-YieldNEET PG
Achalasia = loss of inhibitory neurons in Auerbach plexus → unopposed acetylcholine → failed LES relaxation + absent peristalsis; dysphagia to BOTH solids and liquids (not solids-first) is the clinical clue.
Chicago Classification v4.0; ACG Achalasia Guideline 2020
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