Abstract

The overlap of symptoms experienced by subjects with visceral hypersensitivity and those with motility disorders often confounds clinical diagnosis. The ascertainment of the physiological mechanisms responsible for GI symptoms is often challenging for clinicians and investigators alike. As a result, treatment of these disorders is largely empiric, often based on patient symptoms rather than on the underlying pathophysiology. Although slowed gastric motility is the defining feature of gastroparesis, the correlation between gastric emptying time and symptom severity is not well established [1, 2]. Such a correlation would simplify the treatment of gastroparesis since accelerating gastric motility with prokinetic agents would have a high probability of improving the cardinal symptoms of nausea, vomiting, heartburn, bloating, upper abdominal pain, and postprandial fullness. Despite no demonstrated correlation, it is evident in clinical practice that a subset of gastroparesis patients respond well to prokinetic agents, whereas others are refractory to treatment. Predicting the patient subset that is likely to respond to prokinetics would be of great clinical use, since it would reduce the number of patients unnecessarily exposed to ineffective treatments and associated adverse drug effects. If such a biomarker correlating symptom with a measurable process is to emerge, it will be essential to segregate patients with ‘‘pure’’ (homogeneous) motility disorders from those with visceral hypersensitivity. Albeit an oversimplification of a heterogeneous group, this population can be thought of as on a spectrum, with pure motility disorders on one extreme, and pure sensory disorders on the other. According to the paradigm, pure prokinetic therapy would have minimal effect on symptom alleviation in patients with pure sensory dysfunction, since their symptoms are generated by visceral neural hypersensitivity, not hypomotility. On the other extreme, patients with pure motility disorders would in theory benefit from prokinetic agents since they treat the underlying pathophysiology. In actual clinical practice, most patients have mixed etiology, which impedes successful treatment. Without a biomarker correlating gastrointestinal symptoms to motility or other measures, empiric therapies are the norm. The wireless motility capsule (WMC) is a modality used to assess multiregional gut motility in this patient population that has been increasingly used, mostly at advanced tertiary care centers. The WMC is a pill-sized device that travels throughout the gastrointestinal tract for 5 days after ingestion, continuously sampling intraluminal pH, temperature, pressure, and motility parameters. Unlike conventional antroduodenal manometry, the enhanced capabilities of the WMC support the simultaneous and convenient measurement of antroduodenal contractility and transit enabling regional or full gut assessment of motility. In this issue of Digestive Diseases and Sciences, Arora et al. [3] highlight this complexity in their article ‘‘Clinical utility of wireless motility capsule in patients with suspected multiregional gastrointestinal dysmotility.’’ They characterize their patients with suspected motility disorders using WMC testing, reporting multiregional dysmotility in nearly half of their sizable population of patients with upper and lower GI symptoms, in concordance with K. Barshop Pritzker School of Medicine, University of Chicago, Chicago, IL, USA

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