Aren't disorders of motility observed whatever the etiology of these diverticula ?
T.P.J. Hennessy (Dublin)
Mediothoracic or parabronchial diverticula have a variable aetiology. They may be of acquired or congenital origin and may be traction or pulsion in type. Traction diverticula are likely to be true diverticula possessing a complete muscular layer, whereas pulsion diverticula are false diverticula due to protrusion of the mucosa and submucosa through the muscular layer.
Traction diverticula of the acquired type are found in association with contracted fibrotic lymph glands and the scar tissue of chronic granulomatous inflammation, often tuberculous in origin. The chronically infected lymph nodes adhere to the wall of the esophagus and subsequent contraction pulls out part of the esophageal wall forming a triangular or tent-shaped diverticulum with a wide neck and narrow fundus. If the inflammation is more acute an abscess may form which may perforate into the esophageal lumen or give rise to a fistulous communication with a bronchus.
Some mid-thoracic diverticula may be congenital in origin. Belsey  has suggested that parabronchial diverticula unassociated with motility disorders or chronically infected lymph glands may be enterogenous cysts or foregut duplications which have established a communication with the esophageal lumen. Alternatively, as suggested by Ishigami  who noted a fibrous attachment to the trachea in two cases, the diverticulum may be the result of an incomplete separation of trachea and esophagus and may represent an incomplete tracheo-esophageal fistula. Such diverticula may also be classified as traction in type.
Traction diverticula are usually small, may be multiple and tend to be asymptomatic unless complications such as fistula are present. Very rarely the development of a carcinoma in the diverticulum may account for the symptoms. Substernal pain and mild dysphagia sometimes occur. In the absence of complications an alternative source for these symptoms should be sought. Traction diverticula of either the congenital or acquired variety are not usually accompanied by an esophageal motility disorder.
In Kaye's  study of twelve patients with mid-esophageal diverticula, a variety of motor disorders was demonstrated. Five had diffuse spasm, one displayed a pattern of vigorous achalasia and the other six had a definite but unclassifiable motility disturbance. Only one patient showed evidence of tuberculous infection. The radiographic appearance of the diverticula in Kaye's patients is variable and although a few appear to have the characteristic tent-like shape of traction diverticula the majority resemble pulsion diverticula with a globular outline and a narrow neck. The significance of unclassified motor disorders is difficult to evaluate and their presence may be incidental rather than of etiological importance.
Many authors [4-6] believe that most mid-esophageal diverticula are pulsion in type and that they are due to disordered motility. Cross et al.  suggested three possible mechanisms by which diverticula could be created as a consequence of
increased intra-luminal pressure. These mechanisms involved disordered peristalsis proximally and diffuse spasm in the distal half of the esophagus giving rise to a high pressure zone with protrusion of the mucosa through an anatomical weak spot. The proximal disorder could be either diminished or increased peristalsis. The net result, they believed was a functional obstruction in the mid-esophagus.
Maximum distention of the diverticulum can be demonstrated radiologically to coincide with maximum lower esophageal pressure. They attempted to combine the concepts of pulsion and traction by suggesting that high intraluminal pressure is assisted by traction from infected nodes from outside the esophageal wall in the formation of the diverticulum.
Gastroesophageal reflux and hiatus hernia have been identified in association with mid-esophageal diverticula. The possibility of a secondary motor disorder in the etiology of the diverticulum must be considered in these circumstances.
Para-bronchial (mid-esophageal) and epiphrenic diverticula may co-exist and it is of interest to note that myotomy and diverticulectomy performed in the treatment of an epiphrenic diverticulum brought about regression in the size of the associated mid-thoracic diverticula.
In summary, it would seem reasonable to suggest that most mid-esophageal diverticula are pulsion in type and are associated with and probably induced by an esophageal motility disorder. However, traction diverticula whether acquired or congenital have a different etiology and esophageal dysmotility is not a feature. Nevertheless, disordered motility is a common phenomenon in the esophagus and may co-exist with traction diverticula without being implicated in their etiology.
Surgical treatment of mid-esophageal diverticula is rarely indicated and most reported series of surgically treated patients are small. The results of excision, however, appear to be very satisfactory. Esophageal myotomy should be included in the procedure if a recognized motility disorder has been identified by manometry prior to operation.