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Ambulatory manometry in dyspepsia: walking a thin line
  1. Consultant Gastroenterologist,
  2. Gloucester Gastroenterology Group,
  3. Gloucestershire Royal Hospital,
  4. Great Western Road,
  5. Gloucester GL1 3NN, UK

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See article on page235

Fifteen years ago it was believed that motility studies would become to functional symptoms what endoscopy was (and still is) to ulcers, gallstones and cancer. Today, the ratio of endoscopic examinations to motility studies in most district general hospitals remains hundreds to one. There is no shortage of patients (about half the new referrals to gastroenterology outpatients are for functional symptoms), just no tests with which to make a positive diagnosis. The study by Wilmer et al from Leuven in Belgium illustrates why the early expectations of motility studies have not been realised (see page 235).

The starting point for the study was the belief that disturbed upper gut motility is responsible for functional dyspeptic symptoms. Others have shown that dyspeptic patients have abnormal motility.1 This study hoped to go one step further and link symptoms with specific patterns of dysmotility by using prolonged ambulatory motility studies. The logical extension of finding such a link is that the test would be able to distinguish those with and without the disorder and become clinically useful.

The investigators studied patients with “severe” symptoms and used the latest recording technology with both visual and computerised analysis of recordings. They found a high frequency of both qualitative and quantitative abnormalities of antrojejunal motility in the patient group. However, correlation of symptomatic episodes (there were 19 episodes in eight of 14 patients studied) with abnormal motility occurred only 21% of the time. In other words, there was a lot of abnormal motor activity in the absence of symptoms, and 79% of the time, when there were symptoms, the tracings were normal. Either the study design was unable to show a causal association when one exists, or there is none.

Three possible design errors that may have lead to missing a causal association include insufficiently sensitive manometric or analytical techniques, examination of the wrong segment of gut, or inappropriate selection of patients. It is difficult to imagine how, with available technology, the technical aspects of the study could be improved and the investigators gave good reasons to choose the antrum and upper intestine. Furthermore, identification of abnormal motor patterns suggests that the techniques and segment of gut chosen were appropriate. The failure of the study to link abnormalities with symptoms was probably unaffected by these factors. This leaves us with the possibility that either selection of patients affected the outcome, or that motility abnormalities are largely unconnected to functional dyspepsia.

We are told the patients had “severe” symptoms and that some had lost weight. There is no mention of other factors, unrelated to symptoms, that may have influenced referral and eventual inclusion into the study, nor whether the patients’ problems were solely physical. The focus on the severity of symptoms and the complete absence of other information tells us that the authors work under the presumption that symptoms are the most important driving force in consultation behaviour, and in referral for investigation and subsequently for secondary and tertiary opinions. This oversight ignores an emerging and increasingly respectable literature on somatisation2and everyday experience3 of unhappy, confused, anxious, and sometimes abused people with “severe” symptoms. Even weight loss (six of 14 patients had weight loss between 8 and 16 kg) occurs in the depressed or emotionally disturbed. Moreover, how do we know the patients did not have an eating disorder?

The response of functional gut symptoms to cognitive–behavioural therapy,4 hypnotherapy5 and psychotherapy6 lends weight to the belief that psychological factors play an important role in their genesis. Ignoring these factors at the point of selection into motility studies is asking for a confused result. Excluding patients with significant psychological disturbance may improve the correlation between symptoms and dysmotility. Alternatively, it is possible that dysmotility is the intermediate event between stress and symptoms and that exclusion of stressed patients will result in a convincing negative correlation. Disregarding behavioural and psychological factors is a common occurrence in high tech motility studies and so it is little wonder manometry is not getting very far in the clinical arena.

The best investigators of motility (of whom those from Leuven are typical) are very good at dealing with the technical challenges they face. The achievement of doing and analysing such studies must not be underestimated or undervalued. Therefore, it is a shame that so little effort (in this case none) goes into the behavioural, cognitive and psychological factors that are associated with functional symptoms. Ignoring these devalues the studies, leads to inconclusive conclusions and leaves motility studies out in the cold, perhaps for another 15 years. Can we persuade the famous physiologists from Leuven (and their brethren elsewhere) to join forces on an equal footing with psychologists who understand the nuances of consultation behaviour and the complex relationship of psychological distress to somatic symptoms? Only then can we hope to tease out those with a primary motility disorder and enable motility studies to come of age.

See article on page235


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