Chronic nausea and vomiting syndromes (NVSs) are prevalent and debilitating disorders. Putative mechanisms include gastric neuromuscular disease and dysregulation of brain-gut interaction, but clinical tests for objectively defining gastric motor function are lacking. A medical device enabling noninvasive body surface gastric mapping (BSGM) was developed and applied to evaluate NVS pathophysiology. BSGM was performed in 43 patients with NVS and 43 matched controls using Gastric Alimetry (Alimetry), a conformable high-resolution array (8 × 8 electrodes; 20-mm interelectrode spacing), wearable reader, and validated symptom-logging app. Continuous measurement encompassed a fasting baseline (30 minutes), 482-kilocalorie meal, and 4-hour postprandial recording, followed by spectral and spatial biomarker analyses. Meal responses were impaired in NVS, with reduced amplitudes compared to controls (median, 23.3 microvolts versus 38.0 microvolts, P < 0.001), impaired fed-fasting power ratios (1.1 versus 1.6, P = 0.02), and disorganized slow waves (spatial frequency stability, 13.6 versus 49.5; P < 0.001). Two distinct NVS subgroups were evident with indistinguishable symptoms (all P > 0.05). Most patients (62%) had normal BSGM studies with increased psychological comorbidities (43.5% versus 7.7%; P = 0.03) and anxiety scores (median, 16.5 versus 13.0; P = 0.035). A smaller subgroup (31%) had markedly abnormal BSGM, with biomarkers correlating with symptoms (nausea, pain, excessive fullness, early satiety, and bloating; all r > 0.35, P < 0.05). Patients with NVS share overlapping symptoms but comprise distinct underlying phenotypes as revealed by a BSGM device. These phenotypes correlate with symptoms, which should inform clinical management and therapeutic trial design.
Importance Chronic nausea and vomiting syndromes (NVS) are prevalent and debilitating disorders. Putative mechanisms include gastric neuromuscular disease and dysregulation of brain-gut interaction, but clinical tests for objectively defining gastric motor function are lacking. Objective A novel medical device enabling non-invasive body surface gastric mapping (BSGM) was developed and applied to evaluate NVS pathophysiology. Design A case-control study where BSGM was performed in NVS patients and matched controls using Gastric Alimetry (Alimetry, New Zealand), comprising a conformable high-resolution array (8x8 electrodes; 20 mm inter-electrode spacing), wearable Reader, and validated symptom logging App. Continuous measurement encompassed a fasting baseline (30 min), 482 kCal meal (10 min), and 4-hr post-prandial recording. Setting Multicenter study in Auckland, New Zealand and Calgary, Canada. Participants 43 NVS patients (gastroparesis and Rome IV chronic NVS) and 43 matched controls. Main outcomes and measures Symptom severity and quality of life were measured using Patient Assessment of Upper Gastrointestinal Disorders-Symptom Severity Index (PAGI-SYM), Gastroparesis Cardinal Symptom Index (GCSI), and Patient Assessment of Upper Gastrointestinal Disorders-Quality of Life (PAGI-QOL) instruments. Health psychology metrics included the State Trait Anxiety Inventory Short Form (STAI-SF) and Patient Health Questionnaire-2 (PHQ-2) questionnaires. Spectral analyses including frequency, amplitude, and fed-fasting power ratio. Spatial biomarker analyses included spatial frequency stability and average spatial covariance. Results Meal responses were impaired in NVS, with reduced amplitudes compared to controls (median 23.3 vs 38.0 microV, p<0.001), impaired fed-fasting power-ratios (1.1 vs 1.6, p=0.02), and disorganized slow-waves (spatial frequency stability 13.6 vs 49.5; p<0.001). However, two distinct NVS subgroups were evident with indistinguishable symptoms (all p>0.05). A majority (62%) had normal BSGM studies (all biomarkers non-significant vs controls) with increased psychological comorbidities (43.5% vs 7.7%; p=0.03) and anxiety scores (median 16.5 vs 13.0; p=0.035). A smaller subgroup (31%) had markedly abnormal BSGM, with test biomarkers correlating with symptoms (nausea, pain, excessive fullness, early satiety, bloating; all r>0.35, p<0.05). Conclusions and Relevance NVS patients share overlapping symptoms, but comprise distinct underlying phenotypes as revealed by a novel BSGM device. These phenotypes correlate with symptoms, which should inform clinical management and allocations into therapeutic trials.
INTRODUCTION:Body surface gastric mapping (BSGM) is a new noninvasive test of gastric function. BSGM offers several novel and improved biomarkers of gastric function capable of differentiating patients with overlapping symptom profiles. The aim of this study was to define normative reference intervals for BSGM spectral metrics in a population of healthy controls.METHODS:BSGM was performed in healthy controls using Gastric Alimetry (Alimetry, New Zealand) comprising a stretchable high-resolution array (8 × 8 electrodes; 196 cm2), wearable Reader, and validated symptom-logging App. The evaluation encompassed a fasting baseline (30 minutes), 482 kCal meal, and 4-hour postprandial recording. Normative reference intervals were calculated for BSGM metrics including the Principal Gastric Frequency, Gastric Alimetry Rhythm Index (a measure of the concentration of power in the gastric frequency band over time), body mass index (BMI)–adjusted amplitude (μV), and fed:fasted amplitude ratio. Data were reported as median and reference interval (5th and/or 95th percentiles).RESULTS:A total of 110 subjects (55% female, median age 32 years [interquartile range 24–50], median BMI 23.8 kg/m2 [interquartile range 21.4–26.9]) were included. The median Principal Gastric Frequency was 3.04 cycles per minute; reference interval: 2.65–3.35 cycles per minute. The median Gastric Alimetry Rhythm Index was 0.50; reference interval: ≥0.25. The median BMI-adjusted amplitude was 37.6 μV; reference interval: 20–70 μV. The median fed:fasted amplitude ratio was 1.85; reference interval ≥1.08. A higher BMI was associated with a shorter meal-response duration (P = 0.014).DISCUSSION:This study provides normative reference intervals for BSGM spectral data to inform diagnostic interpretations of abnormal gastric function.
Background Electrogastrography (EGG) non‐invasively evaluates gastric function but has not achieved common clinical adoption due to several technical limitations. Body Surface Gastric Mapping (BSGM) has been introduced to overcome these limitations, but pitfalls in traditional metrics used to analyze spectral data remain unaddressed. This study critically evaluates five traditional EGG metrics and introduces improved BSGM spectral metrics, with validation in a large cohort. Methods Pitfalls in five EGG metrics were assessed (dominant frequency, percentage time normogastria, amplitude, power ratio, and instability coefficient), leading to four revised BSGM spectral metrics. Traditional and revised metrics were compared to validate performance using a standardized 100‐subject database of BSGM tests (30 min baseline; 4‐h postprandial) recorded using Gastric Alimetry® (Alimetry). Key Results BMI and amplitude were highly correlated (r = −0.57, p < 0.001). We applied a conservative BMI correction to obtain a BMI‐adjusted amplitude metric (r = −0.21, p = 0.037). Instability coefficient was highly correlated with both dominant frequency (r = −0.44, p < 0.001), and percent bradygastria (r = 0.85, p < 0.001), in part due to misclassification of low frequency transients as gastric activity. This was corrected by introducing distinct gastric frequency and stability metrics (Principal Gastric Frequency and Gastric Alimetry Rhythm Index (GA‐RI)TM) that were uncorrelated (r = 0.14, p = 0.314). Only 28% of subjects showed a maximal averaged amplitude within the first postprandial hour. Calculating Fed:Fasted Amplitude Ratio over a 4‐h postprandial window yielded a median increase of 0.31 (IQR 0–0.64) above the traditional ratio. Conclusions & Inferences The revised metrics resolve critical pitfalls impairing the performance of traditional EGG, and should be applied in future BSGM spectral analyses.
Burst-suppression electroencephalography (EEG) patterns of electrical activity, characterized by intermittent high-power broad-spectrum oscillations alternating with isoelectricity, have long been observed in the human brain during general anesthesia, hypothermia, coma and early infantile encephalopathy. Recently, commonalities between conditions associated with burst-suppression patterns have led to new insights into the origin of burst-suppression EEG patterns, their effects on the brain, and their use as a therapeutic tool for protection against deleterious neural states. These insights have been further supported by advances in mechanistic modeling of burst suppression. In this Perspective, we review the origins of burst-suppression patterns and use recent insights to weigh evidence in the controversy regarding the extent to which burst-suppression patterns observed during profound anesthetic-induced brain inactivation are associated with adverse clinical outcomes. Whether the clinical intent is to avoid or maintain the brain in a state producing burst-suppression patterns, monitoring and controlling neural activity presents a technical challenge. We discuss recent advances that enable monitoring and control of burst suppression.
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