Background: Antroduodenal manometry (ADM) is the gold standard to diagnose myopathy vs neuropathy in patients with upper gastrointestinal (GI) disorders. ADM however, is an invasive and costly test. Body surface gastric mapping (BSGM) is an emerging noninvasive technique for measuring gastric myoelectrical activity. In a previous collaboration, we identified the normal range for Pediatric BSGM metrics. We aim in this study to evaluate the degree of correlation between BSGM and ADM findings.
Methods: We performed BSGM simultaneously with the clinically indicated ADM on 13 pediatric patients (12 female, age 10-19 yrs, BMI 21±3 kg/m²). We used high-resolution water-perfused ADM catheters consisted of 16 sensors (3cm spacing), and the BSGM-64 electrodes arrays (8x8 grid; 20mm spacing). We used Nausea Severity Scale (NSS) to assess nausea severity 2 weeks prior to the ADM; in addition, we recorded realtime individual symptom levels using Gastric Alimetry validated symptom logging app at 15-mins intervals during the test. Total and individual symptom burden score were obtained. We followed standardized manometry protocol; 4 hours of fasting, provocative testing, and a meal with >1 hour of postprandial recordings leading to a shorter BSGM post-prandial monitoring period. ADM tracings categorized patients into neuropathy, myopathy, postprandial hypomotility, or normal. We computed standardized BSGM metrics including principal gastric frequency, BMI-adjusted amplitude, and Gastric Alimetry Rhythm Index (GA-RI).
Results: ADM studies showed neuropathy (n=4), myopathy (n=1), post-prandial hypomotility (n=4), and normal manometry(n=4). All 4 patients with neuropathy on ADM had lower rhythm stability as measured by BSGM GA-RI (0.16±0.03 vs 0.36±0.17; p=.008) (Figure 1), which was accompanied by higher scores of nausea (8.2±1.2 vs 2.9±2.4; p<.001) and bloating (7.3±0.9 vs 2.5±1.9; p<.001) throughout the test. ADM neuropathy correlated 100% with BSGM low rhythm stability (Table 1). To our observation, the overall reported real-time nausea for all patients during the test (mean 4.54/10) was lower than the reported NSS during the 2 weeks before the test (mean 6.69/10). Real-time total symptom burden score in all patients were captured (range 0-44.7, mean 25.7, median 29.5). Normal ADM were consistent with normal BSGM phenotype in 75% of cases, whereas 75% of ADM studies with postprandial hypomotility were found to have normal BSGM (Table 1). Other BSGM metrics, principal gastric frequency (2.9±0.3 vs 2.9±0.1 cpm, p=.8) and BMI-adjusted amplitude (25±7 vs 35±9 µV; p=.08) had no significant correlation with ADM patterns.
Conclusion: When clinical presentations of Pediatric Gastroparesis and Functional Dyspepsia overlap, Low Rhythm Stability phenotype of BSGM is able to identify neuropathy with comparable result to ADM and significant association with nausea and bloating.

Beth skaggs

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