region of a peptic stricture [135] (Figure 6.73B). In such cases, the pseudodiverticula most likely occur as a sequela of scarring from reflux esophagitis.
When viewed en face on double‐contrast esophagrams, esophageal intramural pseudodiverticula can sometimes be mistaken for tiny ulcers. When viewed in profile, however, they often appear to be “floating” or “levitating” outside the wall of the esophagus without any apparent communication with the lumen [135] (Figure 6.73B), whereas true esophageal ulcers are almost always seen to communicate directly with the lumen. This sign is extremely helpful for differentiating esophageal intramural pseudodiverticula from ulcers.
Figure 6.72 Traction diverticulum. Double‐contrast view shows a triangular outpouching (straight arrow) from the left lateral wall of the mid esophagus. Also note a clump of calcified lymph nodes (curved arrow) in the adjacent pulmonary hilum. This traction diverticulum presumably was caused by scarring from old tuberculous disease in the mediastinum.
Esophageal motility disorders
Achalasia
Achalasia can be classified as primary when it occurs as an idiopathic condition involving the myenteric plexus of the esophagus or as secondary when it is caused by other underlying conditions, most commonly malignant tumor involving the GEJ (especially carcinoma of the gastric cardia and fundus). Primary achalasia is characterized by absent primary peristalsis in the body of the esophagus and incomplete relaxation of the lower esophageal sphincter, manifested on barium studies by tapered, beak‐like narrowing of the distal esophagus directly adjacent to the GEJ [136] (Figure 6.74). In advanced disease, the esophagus can become massively dilated and tortuous distally (also known as a “sigmoid esophagus”). Because of the slow, insidious progression of symptoms, affected individuals typically have longstanding dysphagia when they seek medical attention.
Figure 6.73 Esophageal intramural pseudodiverticulosis. (A) Double‐contrast view shows multiple flask‐shaped outpouchings throughout the esophagus in a patient with diffuse esophageal intramural pseudodiverticulosis. Also note a focal stricture (arrow) in the upper thoracic esophagus. (B) Double‐contrast view in another patient shows a mild peptic stricture in the distal esophagus with multiple pseudodiverticula clustered together in the region of the stricture. When viewed en face, the pseudodiverticula could be mistaken for tiny ulcers. When viewed in profile, however, these structures (arrows) appear to be floating outside the esophagus without communicating with the lumen. This feature is characteristic of pseudodiverticula.
Source: Reproduced from Levine MS. Radiology of the esophagus. Philadelphia: WB Saunders, 1989, with permission.
In contrast, secondary achalasia usually results from tumor at the GEJ that simulates the findings of primary achalasia because of destruction of ganglion cells in the distal esophagus. As a result, secondary achalasia is also characterized by absent peristalsis in the body of the esophagus and beak‐like narrowing near the GEJ. In secondary achalasia, however, the length of the narrowed segment is often considerably greater than that in primary achalasia because of spread of tumor into the distal esophagus [137] (Figure 6.75). The narrowed segment also may be asymmetric, nodular, or ulcerated because of underlying tumor in this region. In some cases, barium studies may reveal other signs of malignancy in the region of the gastric cardia and fundus. The clinical history also is extremely helpful, as patients with primary achalasia almost always have longstanding dysphagia, whereas patients with secondary achalasia are usually older individuals (over 60 years of age) with recent onset of dysphagia (<6 months) and weight loss [137]. As a result, it is often possible to differentiate these conditions on the basis of the clinical and radiographic findings.
Figure 6.74 Primary achalasia. Single‐contrast esophagram shows a markedly dilated esophagus filled with debris. Also note beak‐like narrowing (arrow) of the distal esophagus near the gastroesophageal junction in this patient with longstanding achalasia.
Diffuse esophageal spasm
Patients with diffuse esophageal spasm typically present with recurrent chest pain, dysphagia, or both. Diffuse esophageal spasm is sometimes manifested on barium studies by intermittently absent or weakened primary esophageal peristalsis with simultaneous, lumen‐obliterating, nonperistaltic contractions that compartmentalize the esophagus, producing a classic corkscrew appearance [136] (Figure 6.76A). In a study by Prabhakar et al., however, most patients had nonperistaltic contractions of mild‐to‐moderate severity that did not obliterate the lumen [138], so the absence of a corkscrew esophagus on barium studies in no way excludes this diagnosis. It has also been found that the majority of patients with diffuse esophageal spasm have impaired opening of the lower esophageal sphincter on barium studies with the tapered, beak‐like distal esophageal narrowing classically associated with achalasia [138] (Figure 6.76B). When these patients present with dysphagia, they may have a marked clinical response to treatment with the Clostridium botulinum toxin or endoscopic balloon dilatation [138]. Achalasia and diffuse esophageal spasm therefore may represent opposite ends of a spectrum of related esophageal motility disorders.
Figure 6.75 Secondary achalasia caused by bronchogenic carcinoma. Double‐contrast view shows a mildly dilated esophagus with beak‐like distal narrowing (straight arrows). Unlike the patient with primary achalasia in Figure 6.74, however, the narrowed segment extends 4–5 cm above the gastroesophageal junction. Also note the large mass (curved arrow) abutting the right side of the mediastinum in a patient with bronchogenic carcinoma that had metastasized to the gastroesophageal junction. (Aspirated barium is seen at the right lung base.).
Source: Reproduced from Levine MS. Radiology of the esophagus. Philadelphia: WB Saunders, 1989, with permission.
Presbyesophagus
Older patients often have intermittent weakening of primary peristalsis and multiple non‐peristaltic contractions in the absence of esophageal symptoms, a relatively common manifestation of aging known as presbyesophagus [136]. In other normal patients, there may be splitting of the barium column at or near the level