A detailed neurological examination would, therefore, be an impor

A detailed neurological examination would, therefore, be an important part of the clinical evaluation of orophagyngeal dysphagia. It is equally important to look for peripheral skin and joint stigmata of scleroderma, CREST syndrome or systemic connective tissue disease, as these patients are at risk of esophageal hypomotility. Medications such as dopamine antagonists and anti-cholinergic agonists can lead to xerostomia

and esophageal dysmotility. The presence of xerostomia should be enquired, as treatment is simple and effective. In elderly patients, pill-induced ulceration and stricture should be suspected for those who take bisphosphonates and non-steroidal anti-inflammatory drugs. Finally, risk factors for esophageal and gastric cancers such as smoking, alcohol use, ethnic background and known family Selleckchem Wnt inhibitor history of upper gastrointestinal (GI) malignancy should be noted. It is important to remember that although healthy aging is related to certain neuromuscular

changes, it rarely leads to clinically significant dysphagia.2 Therefore, the presence of oropharyngeal dysphagia will always require a search for an underlying cause (Table 1). The biggest clue to the cause of a patient’s oropharyngeal dysphagia lies with age. Development of oropharyngeal dysphagia in an elderly person (age > 70 years) may relate to either an acute neurological event such as a stroke, or a progressive BGJ398 neurological disease such as Parkinson’s disease and Alzheimer’s. Zenker’s diverticulum is also more prevalent in the elderly. In contrast, degenerative motor neuron diseases must be suspected in younger patients. The causes of esophageal dysphagia can be broadly divided into either mechanical or dysmotility (Table 2). There selleck compound are, however, a number of conditions in which dysphagia is mediated by both mechanical and dysmotility mechanisms. Achalasia is a classic example of such a condition, where there is often a failure of peristalsis in the esophageal body with impaired

relaxation of the lower esophageal sphincter, leading to anatomical obstruction. Tumors in the region of the lower esophageal sphincter or gastric cardia can give rise to “pseudo-achalasia” with identical clinical presentation. Eosinophilic esophagitis has recently been recognized as an increasing common cause of dysphagia and food bolus impaction. Histologically, eosinophilic esophagitis is characterized by marked eosinophilic infiltration and associated inflammation in the esophagus and, in patients with longstanding disease, marked fibrosis of the esophageal wall. This, in turn, can lead to significant “stiffening,” luminal narrowing, and impaired peristalsis of the esophagus. The diagnosis of this condition heavily relies on clinical awareness, endoscopic features and esophageal biopsies.

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