No abstract

Metoclopramide, the only drug approved by the FDA for treatment of diabetic gastroparesis, but used off-label for a variety of other gastrointestinal indications, has many potentially troublesome adverse neurologic effects, particularly movement disorders. In this article, we comprehensively review the indications and side effects of metoclopramide, and describe some common pitfalls and strategies to minimize the medicolegal risks to the prescribing physician. Metoclopramide accounts for nearly a third of all drug-induced movement disorders, a common reason for a malpractice suit. The entire spectrum of drug-induced movement disorders, ranging from subtle to life-threatening, can ensue from its use; akathisia and dystonia are generally seen early in the course of metoclopramide-induced movement disorders, whereas tardive dyskinesia and parkinsonism seem to be more prevalent in chronic users. Female sex, age and diabetes are the major risk factors for metoclopramide-induced movement disorders. It is therefore incumbent on gastroenterologists and other prescribing physicians to become familiar with the adverse neurologic effects associated with the use of metoclopramide, and to take appropriate preventive and defensive measures.

Heartburn occurs in the presence as well as the absence of acid reflux. We searched for a motor correlate of heartburn. Twelve subjects with heartburn were studied with 24-h synchronized pressure, pH, and high-frequency intraluminal ultrasound (HFIUS) imaging of the esophagus. The HFIUS images were analyzed every 2 s for a period of 2 min before and 30 s after the onset of heartburn during 20 acid reflux-positive and 20 acid reflux-negative heartburn episodes. The esophageal muscle thickness was measured as a marker of contraction. Esophageal pressure and HFIUS images were recorded during the Bernstein test in 15 subjects. Sustained esophageal contractions (SECs) were identified during 13 of 20 heartburn episodes associated with acid reflux and 15 of 20 heartburn episodes without acid reflux. SECs were detected during 2 of 40 matched control periods only (P < 0.05). The duration of SECs was 44.9 +/- 26.9 s. The Bernstein test reproduced heartburn symptoms in 8 of 15 subjects. SECs were identified during 6 of 8 (75%) Bernstein-positive and in 1 of 7 (14.3%) Bernstein-negative tests (P = 0.04). We conclude that a SEC precedes both spontaneous and induced heartburn symptoms and may be the cause of heartburn sensation.

Purpose The natural history and outcome of patients with gastroparesis is not well known. The aim of this study was to identify the clinical or pathophysiological characteristics, if any, that may be helpful in predicting therapeutic response in this condition. Methods This is a retrospective study of a cohort of patients who presented to a tertiary referral center with symptoms suggestive of gastroparesis. All patients were evaluated by scintigraphic measurement of gastric emptying and symptoms were scored using a modification of the Gastroparesis Cardinal Symptom Index (GCSI). Treatment generally included conservative measures such as antiemetics, prokinetics, tricyclic antidepressants and analgesics as well as various more invasive interventions in selected patients. Response to treatment was defined as a change in the overall GCSI score of two-thirds or more as compared with baseline. Results Out of a total of 93 patients, 69 patients met the eligibility criteria. Of these, 29 patients had diabetes mellitus and 40 patients had gastroparesis of non-diabetic etiology. Out of 69 patients, 49 were responders (71%) and 20 were non responders (29%). The cause (diabetic vs. non-diabetic) of gastroparesis or the presence of delayed emptying did not correlate with response. However, the severity of stomach distension, bloating subscale score and the global GCSI score at baseline presentation were predictive of response by multivariate analysis. Conclusion Higher global GCSI score, bloating subscale score, and severity of stomach distension at baseline presentation correlate with an unfavorable response in gastroparetic patients. On the other hand, neither the etiology of gastroparesis nor associated delay in gastric emptying appeared to be important in the clinical response. Patients with symptoms of typical gastroparesis but without delays in gastric emptying may be a distinct syndrome with a greater proportion of males than classical gastroparesis.