# paper.pdf ## Metadata - PDFFormatVersion=1.7 - Language=en-US - IsLinearized=true - IsAcroFormPresent=false - IsXFAPresent=false - IsCollectionPresent=false - IsSignaturesPresent=false - Author=Chris Varghese, Nicky Dachs, Gabriel Schamberg, Thomas Abell, Mohammad Al-Haddad, Timothy Robert Angeli-Gordon, Shahin Ayazi, Homira Ayubi, Mohammad Bashashati, Robert Bulat, Stefan Calder, Christopher Brian Cederwall, Bianca Chang, Leo Cheng, John Clarke, Charlotte Daker, Peng Du, Jon Erickson, Sven Eriksson, Asma Fikree, Daphne Foong, Mark Fox, Uday Chand Ghoshal, Mahesh Goenka, Rehan Haidry, William L. Hasler, Bu'Hussain Hayee, Vincent Ho, Gerald Holtman, Anthony Robert Hobson, I-Hsuan Huang, Daniel Keszthelyi, Sahib S. Khalsa, Natasha Koloski, Braden Kuo, David Kunkel, Mikaela Law, David Levinthal, Joy J. Liu, Prateek Mathur, Baharak Moshiree, Leila Neshatian, Catherine Ngo, Linda Nguyen, Nicholas R. Oblizajek, Henry P. Parkman, Sanjay Pandanaboyana, Alexander Podboy, Ali Rezaie, Amol Sharma, Sam Simmonds, Jonathan Sivakumar, Jarongkorn Sirimongkolkasem, Irene Sonu, Abigail Stocker, Joseph Sujka, Jan Tack, Charles Verdonk, Xiao Jing Wang, Douglas Weinstein, John Windsor, Nicha Wongjarupong, William Xu, Natalia Zarate-Lopez, Christopher N. Andrews, Armen A. Gharibans, Greg O'Grady - CreationDate=D:20260630111124+05'30' - Creator=Adobe InDesign 19.5 (Windows) - Keywords=Keywords: body surface gastric mapping; chronic nausea and vomiting syndromes; diagnostics; electrogastrography; electrophysiology; functional dyspepsia; gastroparesis; high-resolution electrogastrography - ModDate=D:20260630111306+05'30' - Producer=Adobe PDF Library 17.0; modified using iTextSharp™ 5.5.13.4 ©2000-2024 iText Group NV (AGPL-version) - Title=Expert Clinical Consensus on Body Surface Gastric Mapping Phenotypes for Gastroduodenal Disorders: ‘Auckland Classification’ v1.0 - Trapped=False - Custom.WPS-ARTICLEDOI=10.1111/nmo.70377 - Custom.WPS-JOURNALDOI=10.1111/(ISSN)1365-2982 - Custom.WPS-PROCLEVEL=3 - jav:journal_article_version=VoR - prism:doi=10.1111/nmo.70377 - pdfx:wps-articledoi=10.1111/nmo.70377 - pdfx:wps-journaldoi=10.1111/(ISSN)1365-2982 - pdfx:wps-proclevel=3 - dc:title=Expert Clinical Consensus on Body Surface Gastric Mapping Phenotypes for Gastroduodenal Disorders: ‘Auckland Classification’ v1.0 ## Contents ### Page 1 Neurogastroenterology & Motility REVIEW ![Open Access logo]() # Expert Clinical Consensus on Body Surface GastricMapping Phenotypes for Gastroduodenal Disorders:‘Auckland Classification’ v1.0 This is an open access article under the terms of the License, which permits use, distribution and reproduction in any medium,provided the original work is properly cited. © 2026 The Author(s). Neurogastroenterology & Motility published by John Wiley & Sons Ltd. Neurogastroenterology & Motility, 2026; 38:e70377 Chris Varghese ![ORCID logo]() | Nicky Dachs ![ORCID logo]() | Gabriel Schamberg ![ORCID logo]() | Thomas Abell | Mohammad Al-Haddad |Timothy Robert Angeli-Gordon ![ORCID logo]() | Shahin Ayazi | Homira Ayubi | Mohammad Bashashati | Robert Bulat |Stefan Calder | Christopher Brian Cederwall | Bianca Chang ![ORCID logo]() | Leo Cheng ![ORCID logo]() | John Clarke | Charlotte Daker ![ORCID logo]() |Peng Du | Jon Erickson | Sven Eriksson | Asma Fikree | Daphne Foong | Mark Fox | Uday Chand Ghoshal ![ORCID logo]() |Mahesh Goenka | Rehan Haidry | William L. Hasler ![ORCID logo]() | Bu'Hussain Hayee | Vincent Ho ![ORCID logo]() | Gerald Holtman |Anthony Robert Hobson | I-Hsuan Huang | Daniel Keszthelyi ![ORCID logo]() | Sahib S. Khalsa ![ORCID logo]() | Natasha Koloski |Braden Kuo | David Kunkel | Mikaela Law | David Levinthal | Joy J. Liu ![ORCID logo]() | Prateek Mathur |Baharak Moshiree | Leila Neshatian ![ORCID logo]() | Catherine Ngo | Linda Nguyen | Nicholas R. Oblizajek ![ORCID logo]() |Henry P. Parkman | Sanjay Pandanaboyana ![ORCID logo]() | Alexander Podboy | Ali Rezaie | Amol Sharma ![ORCID logo]() |Sam Simmonds | Jonathan Sivakumar | Jarongkorn Sirimongkolkasem | Irene Sonu | Abigail Stocker | Joseph Sujka |Jan Tack | Charles Verdonk | Xiao Jing Wang ![ORCID logo]() | Douglas Weinstein | John Windsor | Nicha Wongjarupong |William Xu ![ORCID logo]() | Natalia Zarate-Lopez | Christopher N. Andrews | Armen A. Gharibans | Greg O'Grady Correspondence: Greg O'Grady () Received: 23 February 2026 | Revised: 5 May 2026 | Accepted: 27 May 2026 Keywords: body surface gastric mapping | chronic nausea and vomiting syndromes | diagnostics | electrogastrography | electrophysiology |functional dyspepsia | gastroparesis | high-resolution electrogastrography ABSTRACT Introduction: Chronic gastroduodenal disorders remain challenging to manage, and new diagnostic approaches are needed tobetter delineate underlying causes and guide therapeutic decisions. Body Surface Gastric Mapping (BSGM) technologies combinehigh-resolution gastric myoelectrical activity measurements with symptom and psychological profiling to provide mechanisticinsights into gastric motor and sensory dysfunction. An International Working Group convened to derive the first consensusclassification of BSGM phenotypes (the “Auckland Classification”). Methods: A Technical Group conducted a systematic literature and clinical database review to identify objective test biomark-ers and candidate disease mechanisms. Evidence was synthesized across 50 studies (primarily in gastroparesis, chronic nauseaand vomiting, and functional dyspepsia), and BSGM phenotypes were mapped to existing treatment guidelines. Subsequently,iterative review and development of consensus was performed by a Consensus Group composed of international clinical expertsfamiliar with BSGM. Eleven statements underlying the classification were then derived and circulated as a final survey to estab-lish agreement. Results: Six BSGM phenotypes were endorsed: three defined by myoelectrical abnormalities (Dysrhythmic, High Frequency,and Low Meal Response) and three by characteristic symptom associations (Sensorimotor, Continuous, and Delayed OnsetSymptoms). Published studies plausibly linked these phenotypes to mechanisms including interstitial cell of Cajal depletion,vagal impairment, hypomotility, visceral hypersensitivity, gut-brain dysregulation, and small bowel dysfunction. Phenotypeswere also mapped to existing mechanism-based treatment guidelines. Ten out of the eleven statements had > 80% agreement. ![Society logo]() ![WILEY logo]() ### Page 2 Conclusions: The Auckland Classification, derived by international consensus, presents a structured framework for BSGM-defined patient phenotypes. Evidence and mechanism-based treatment options are suggested for each phenotype to provide afoundation for research, further validation, and a pathway for integrating BSGM into clinical care. ## 1 | Introduction Chronic gastroduodenal symptoms affect around 10% of theglobal population, with significant impacts to quality of life andhealthcare systems [], yet effective management remains aconsiderable unmet need []. A fundamental challenge has beeneffectively defining and diagnosing these disorders, with cur-rent frameworks presenting overlapping profiles with limitedspecificity for stratifying patients into clear and effective thera-peutic pathways []. Gastric emptying studies remain the only widely available testof gastric function []. Although gastric emptying testing isconsidered a diagnostic standard in gastroparesis, the tests lackspecificity for underlying disease mechanisms because severaldistinct physiological factors regulate emptying []. Thisheterogeneity contributes to variable test–retest reliability andmixed results when predicting treatment response and selectingtreatment options []. Tests assessing disease mecha-nisms beyond gastric emptying alone might offer more specificand effective therapeutic targets []. Additional tests of gastroduodenal function include antroduo-denal manometry (ADM), gastric accommodation testing (e.g.,barostat, single photon emission computed tomography, nutrientdrink, or satiety tests), and low-resolution electrogastrography(EGG) []. These tests have provided meaningful insightsinto mechanisms underlying gastroduodenal dysfunction andthe causes of dyspeptic symptoms after meals (e.g., Figure).However, in clinical practice they may be limited by low avail-ability, invasiveness, uncomfortable data acquisition, complexinterpretation, or inconsistent utility []. Consequently, caredecisions continue to be driven by symptom patterns and trial-and-error management []. The need for more accurate and mechanistic diagnoses moti-vated the development and clinical translation of a new non-invasive diagnostic test for assessing mechanisms underlyingchronic gastroduodenal symptoms []. This platform,Body Surface Gastric Mapping (BSGM), was built upon tech-nical advances in high-resolution electrophysiology, supersed-ing low-resolution EGG []. Research grade devices havematured, with an FDA-cleared clinical system first released in2023 (Gastric Alimetry, New Zealand), and recently approvedin pediatrics aged ≥ 12 years. This system combines BSGM withdigital symptom and psychological profiling in order to offera comprehensive, non-invasive, and radiation-free diagnosticapproach []. There are now more than 50 clinicalstudies reported in the literature. The International Body Surface Gastric Mapping Working Group(herein “Working Group”) previously convened to conduct a tech-nical review and establish an evidence-based consensus on theprinciples, technical foundations, and clinical methods of BSGM[], and has also provided report interpretation guidelines [].The Working Group has now proceeded to review the availableclinical data, propose a consensus “Auckland Classification”for chronic gastroduodenal disorders based on BSGM, and mapthe phenotypes to potential therapeutic options. These develop-ments are intended to standardize terminology, guide future re-search, and inform clinical implementation of BSGM. ## 2 | Methods The Working Group is composed of gastroenterologists, surgeons,physiologists, psychiatrists, scientists, and bioengineers with rel-evant research and/or clinical experience, who convened to de-fine an inaugural classification scheme for BSGM. The WorkingGroup comprised two groups: first, a “Technical Group” compris-ing four expert clinicians, five clinical researchers and bioengi-neering specialists, and one health psychologist, who performedthe systematic review and collated a draft proposal; and second,a “Consensus Group,” comprised of more than 45 clinical and re-search experts familiar with BSGM (ranging from routine clinicaluse to familiarity with technology without previous research orclinical experience; the latter group being invited for their clinicalexpertise), who provided iterative review, feedback, and consen-sus. The “Consensus Group” was selected based on establishedresearch experience with BSGM technology and/or relevant clin-ical expertise in gastroduodenal disorders. Selection was aimed atincorporating geographical representation and including partici-pants from diverse clinical practice and research settings. ### 2.1 | Search Strategy A comprehensive literature search using Ovid Medline andEMBASE databases from inception to August 2025 was per-formed. The first search included the terms “body surface gas-tric mapping” OR “gastric mapping” OR “BSGM” OR “GastricAlimetry” OR “high-resolution electrogastrography” OR “HR-EGG,” and clinical and translational studies were retrieved. Asecond search then used society names to capture therapeuticguidelines. The latest guidelines published by the AmericanNeurogastroenterology and Motility Society (ANMS), EuropeanSociety of Neurogastroenterology and Motility (ESNM), AmericanCollege of Gastroenterology (ACG), American GastroenterologicalAssociation (AGA), British Society of Gastroenterology (BSG),and United European Gastroenterology (UEG) for “gastroparesis,”“chronic nausea and vomiting syndromes,” “functional dyspepsia,”and “gastric sensorimotor” disorders were additionally retrieved.BSGM biomarkers and BSGM phenotypes were defined and sub-sequently mapped to therapies from guidelines. Article bibliogra-phies were screened to ensure comprehensive literature capture. Studies on low-resolution EGG techniques and associated wear-able motility patches were excluded, as the Working Group ### Page 3 ![image]() agreed that low-resolution techniques are not clinically equiv-alent to BSGM and do not represent comparable services froma technical, clinical utility, resource requirement, or reimburse-ment viewpoint. The justification was that a minimum of 32 si-multaneous gastric electrodes are currently deemed necessaryto class as high-resolution recordings []. Clinical data arisingfrom single-channel electrophysiology were therefore not con-sidered relevant to inform the phenotyping classification, al-though low-resolution EGG studies provided valuable insightsinto foundational pathophysiology. ### 2.2 | Evidence Synthesis Based on the search results, a narrative synthesis of the evidenceas relevant to the proposed phenotyping scheme was integratedinto an initial working document by the Technical Group. Thestudy cohort, complementary diagnostic modality, and treatmentbeing investigated in each study are tabulated and referenced tosupport each phenotype, their proposed diagnostic criteria, pu-tative pathophysiology, and therapeutic research consideration.This synthesis detailed the evidence base for each BSGM pheno-type and informed the synthesis of the new classification system.Guided by other classification schemes for complex GI disorders,the Group aimed to prioritize a hierarchy of: (i) organic disor-ders/structural pathology; (ii) motor function; and (iii) abnor-mal sensitivity []. In addition, plausible (research-informing)therapeutic considerations anchored to existing guidelines wereidentified for future dedicated studies. Priority research gapsand directions for future work were identified. It is noted thatthis must not be considered as a therapeutic guideline. An initialdocument was then circulated to all members of the ConsensusGroup for review, comment, and iterative refinement across tworounds. Expert consensus was used to formalize and standard-ize phenotype definitions and nomenclature, potential contrib-utory mechanisms (summarized into a conceptual diagram inFigure), suggested mechanism-targeted therapies for furtherinvestigation, and future research prioritisation. A separate pe-diatric classification scheme is presently under development,with adolescent reference intervals now available []. ### 2.3 | Phenotype Prevalence An estimation of the prevalence was presented for each phe-notype, based on a multicenter database of patients that have Plain Language Summary The Auckland Classification v1.0, derived by interna-tional consensus, presents a structured framework forbody surface gastric mapping-defined patient pheno-types. This classification provides a foundation for re-search and a standardized pathway for integrating BSGMinto clinical care. ### Page 4 undergone BSGM and formal gastric emptying testing (furtherdetailed in Appendix). ### 2.4 | Consensus Voting and Agreement A modified Delphi approach, similar to what has been usedin previous GI consensus statements was employed [].Literature and expert inputs formed the basis of this document,reflecting a v1.0 classification. In this process, the TechnicalGroup shortlisted the initial phenotypes with correspondingproposed diagnostic criteria, putative pathophysiology's andclinical implications for each phenotype. This text was itera-tively refined across 2 rounds of feedback from the “ConsensusGroup.” Thereafter, the Technical Group distilled the refineddocument into 11 summary statements which all membersof the Consensus Group were invited to vote on using a stan-dard 6-point scale for assessment of agreement level: A+, agreestrongly; A, agree with minor reservation; A−, agree with majorreservation; D−, disagree with major reservation; D, disagreewith minor reservation; D+, disagree strongly []. The mem-bers were instructed to evaluate the phenotype definitions, theirclinical significance, and associated criteria based on appropri-ateness for a Version 1.0 framework. They were asked to spe-cifically evaluate phenotype criteria on their appropriatenessas a common language for standardized reporting, not as strictthresholds that supersede clinical judgment in the phenotyp-ing process. Per-statement agreement level was defined as thepercentage of responses rated either A+ or A. The statements,agreement level, and percentage of each rating are provided inTable. ## 3 | BSGM Methods The evidence synthesis presented below briefly covers the stan-dardized principles, protocols, and metrics for BSGM testing,before presentation of the “Auckland Classification” phenotypeconsensus. ### 3.1 | Principles and Protocols of BSGM Testing BSGM is indicated in patients with chronic gastroduodenalsymptoms in order to determine specific motor and sensorymechanisms contributing to symptoms, such as myoelectricaldysfunction, hypomotility, visceral hypersensitivity, and brain–gut axis contributions []. The test is used along-side clinical evaluation and other diagnostic tests as an aid todiagnosis. The principles and clinical methods of BSGM testing wererecently summarized in a separate technical review by theWorking Group []. In brief, BSGM summates all underlyinggastric myoelectrical activity, including both propagating slowwave potentials generated by the interstitial cells of Cajal (ICC),as well as associated smooth muscle potentials [].Cutaneous gastric signals are weak, being ~100× lower in ampli-tude than cardiac potentials []. Multiple limitations affectinglow-resolution EGG were therefore resolved to enable BSGM,with a particular focus on improving signal-to-noise ratio,artifact handling, signal loss due to variable gastric anatomy,and clinical uility []. The central innovation wasto employ high-resolution arrays of electrodes covering a widearea to maximally capture gastric activity []. These advanceshave been robustly validated against direct serosal recordings,demonstrating high fidelity []. As discussed below, in addi-tion to the acquisition of objective gastric myoelectrical activity,BSGM testing also routinely encompasses detailed subjectivesymptom profiling before and after ingestion of a standardizednutrient challenge, and an optional psychological screeningquestionnaire, with these results now being critical adjuncts tophenotyping. ### 3.2 | Test Protocol A standardized clinical BSGM testing protocol has been imple-mented per Figure []. This protocol includes a complete gas-tric meal cycle time of 4 h [], which is currently necessaryto apply normative ranges and phenotyping schemes [],although shorter protocols are still being investigated, includingin mental health research contexts []. The commercial GastricAlimetry System has regulatory clearance for use in patientsaged ≥ 12 years old []. The test is validated for a patient bodymass index (BMI) of up to 35 kg/m2, and whilst the test has beenanecdotally observed to be effective above this cutoff in selectedcases, caution should be exercised when applying the proposedclassification scheme to high BMI patients (see Appendix)[]. There is no cut-off for low BMI. BSGM performed through the Gastric Alimetry test also includestwo complementary diagnostic adjuncts delivered in a compan-ion App []. Firstly, a symptom profiling App, validated ina study of 79 patients, records typical foregut symptoms at min-imum 15-min intervals (e.g., nausea, pain, bloating, heartburn,stomach burn, upper gut pain, excessive fullness), as one-off mea-sures (early satiation after meal ingestion), or as discrete time-stamped events (e.g., vomiting, belching, reflux), with validatedpictograms to enhance the reliability of patient self-reporting[]. Clinically correlating the resultant symptom curvesand events to meal ingestion and gastric meal responses is in-tegral to test interpretation []. Secondly, a validated men-tal health survey is optionally provided in the Gastric Alimetrytest (the “Alimetry Gut Brain Wellbeing Survey”; AGBW) [],encompassing depression, anxiety and stress domains. This isincluded because psychological comorbidities are common, mayreflect shared disease mechanisms, and frequently track withdisorder severity [], while also correlating with specific phe-notypes (discussed below) []. Due to the multifactorialnature of GI symptoms (Figure), the Working Group recom-mends that these tools should be routinely employed alongsideBSGM testing if phenotyping is to be applied. A standardized meal is given during BSGM testing to provokea gastric meal response and symptoms, typically being a nu-trient/protein bar with nutrient drink, with variants to accom-modate dietary requirements or research protocols []. Therecommended standard meal is consumed over 10 min, andis ~450 kCal (in comparison to gastric emptying test protocolsof 255–320 kCal) []. The large meal size is motivated by theneed to provide a sufficient caloric load to stress gastric motor ### Page 5 ### Page 6 ### Page 7 ![Figure 2]() ### Page 8 function and provoke symptoms, offering a more sensitive physi-ological challenge than lower-calorie standards, although > 50%meal completion is presently considered sufficient for routinetest interpretation []. Tests involving smaller meal portions oreven fasting tests may still be interpretable; however, low gastricamplitudes and rhythm stability must then be interpreted withcaution []. Previous MRI studies have indicated that a min-imum meal volume (e.g., > 200 mL) is likely required to elicita reliable physiological response []. In addition, researchershave tested various meal compositions (e.g., egg meals, pancake,nutrient bars with water, liquid test meals), concluding that cal-orie load, as opposed to macronutrient content, appears to bethe key determinant in meal response metrics, such that patientsmay choose to bring their own meal if necessitated by dietaryrestrictions or rigid preferences []. ### 3.3 | Gastric Alimetry Test Biomarkers BSGM utilizes new metrics that overcome the limitations inher-ent in low-resolution EGG biomarkers, including susceptibility toartifacts, conflation of frequency with rhythm stability, and lackof correction for BMI []. The three key metrics derived fromBSGM are: Principal Gastric Frequency (PGF; reference interval:2.65–3.35 cpm), Gastric Alimetry Rhythm Index (GA-RI; ≥ 0.25),and BMI-adjusted amplitude (22–70 μV) (example spectrogramsummarized in Figure) []. Reference intervals for thesemetrics were established in a study of 110 healthy controls of di-verse age and ethnicity [], with strong test–retest reproduc-ibility shown at short (1 week) and long-term (> 6 month) intervals[], and resilience to vomiting should it occur during testing []. A fourth metric is reported, termed the Fed:Fasted AmplitudeRatio (ff-AR). However, the Working Group did not find anysupporting evidence for the diagnostic utility of ff-AR at thistime. They noted inherently high variability in control sub-jects and recommended that this metric be reserved for usein research applications or as a supporting metric in other-wise abnormal tests []. A fifth exploratory metric used inresearch studies, called the Meal Response Ratio (MRR), wasrecommended for ongoing evaluation as a potential replace-ment for ff-AR. This additional metric indicates the timingof the meal response and is calculated as the ratio of the av-erage amplitude in the first 2 h postprandially to that of thenext 2 h, with ratios < 1 found to be associated with delayedgastric emptying []. The core metrics are explained furtherin Appendix. The association between gastric amplitude and symptoms overthe test duration is also quantified by a correlation score between0 and 1, which aims to offer a proxy indicator of “sensorimo-tor disorders” (recommended cut-off > 0.5) that is, principallygastric hypersensitivity (Figure) []. Some Working Groupmembers queried whether disordered accommodation mightalso express a correlation of > 0.5; however, no data was found inthe literature review to support or refute this concept, indicatingan area for future research. Finally, a series of “symptom tags” recently received FDA clear-ance to objectively profile and categorize individual symptomseverity curves reported during testing. These tags include“meal induced,” “meal alleviated,” “late onset,” “sensorimotor”(correlation score > 0.5), and “continuous,” as recently describedin detail elsewhere []. Late-onset symptoms peak in the latepost-prandial period (hours 3+), a time typically associated withthe transition of chyme distal to the stomach, and have there-fore been considered a plausible indicator of symptoms of smallbowel origin []. ## 4 | Results ### 4.1 | BSGM Phenotypesand the Auckland Classification v1.0 Following BSGM metric development, the Working Group fo-cused on identifying a set of well-characterized “phenotypes”that can underpin disease classifications and clinical decisionmaking []. This was achieved by mapping phenotypes tosymptom and psychological profiles and to pathophysiologicalmechanisms (Figure) []. Here, we present this consensus classification scheme iterativelydeveloped by the Working Group [], termed the AucklandClassification v1.0, based on current accrued evidence from 50published studies identified in the literature review, and accumu-lated research and clinical experience among the Working Groupfrom over 4500 tests (refer to Appendix, Table for evaluatedstudies). The phenotypes presented here should be considered thefirst consensus classification scheme for BSGM, superseding allearlier interim schemes [], and they are intended to be usedalongside other diagnostic tests of gastric function such as emp-tying testing, if desired. In addition, a deterministic algorithm toobjectively ascertain the Auckland Classification from individualBSGM tests was developed by the Technical Group (presented inAppendix). This could be integrated into automated reportingtools in future versions of BSGM software. Six phenotypes were resolved by the Working Group andgrouped by motor or sensory predominance. These pheno-types are described in detail below along with currentlyidentifiable clinical considerations and research gaps. Thephenotypes are illustrated using representative case exam-ples in Figure. The consensus statements describing eachphenotype, quantitative criteria used in the automated clas-sification algorithm, and associated levels of agreement arereported in Table. Acknowledging the difficulty in assign-ing a strict threshold for classification, we establish two sets ### Page 9 ![image]() of criteria that correspond to the strength of the evidence foreach phenotype. Meeting the “Primary Criteria” for a pheno-type suggests stronger alignment with that phenotype thanonly meeting the “Secondary Criteria.” These sets of criteriaare used to prioritize phenotypes in the automated classifica-tion algorithm (see Table), which was subsequently appliedto a cohort of 176 patients to estimate the prevalence of eachphenotype (Appendix). Additional emerging phenotypesthat did not currently reach sufficient agreement for inclusionin the v1.0 Classification, but signal important ongoing re-search areas, are also addressed. Lastly, a summary diagramoffering research- oriented treatment considerations for eachphenotype is presented in Figure. ### 4.2 | Auckland Classification: Motor PredominantPhenotypes #### 4.2.1 | Dysrhythmic Phenotype 4.2.1.1 | Criteria. Sustained dysrhythmia as indicated bylow GA-RI values (refer to Table; e.g., Figure). 4.2.1.2 | Pathophysiological Considerations. Disrup-tions in gastric myoelectrical activity and/or ICC networkintegrity are now established to play a role in the pathophysi-ology of several gastroduodenal disorders []. Multiplestudies, including a recent meta-analysis, confirmed that ICC ### Page 10 ![image]() ![image]() network depletion, commonly in association with a decline inanti-inflammatory macrophages, is a pathological hallmarkof severe gastroduodenal disorders, regardless of gastric emp-tying status []. This “Cajal-opathy” representsa distinct neuromuscular disorder that is not accounted for incurrent disease classifications []. The clinical relevanceof this condition is supported by the finding that more severeICC depletion correlates with higher rates of delayed gastricemptying, although patients with ICC depletion can be foundanywhere on a disease spectrum across functional dyspepsia/chronic nausea and vomiting syndromes and gastroparesis []. A growing body of evidence indicates that the DysrhythmicPhenotype, defined by sustained dysrhythmia with GA-RI ### Page 11 < 0.25, offers a plausible diagnostic indicator for ICC depletionwith neuromuscular dysfunction []. While this link-age is logical, based on evidence from translational studies usinginvasive serosal mapping in which degraded ICC networks anddysrhythmias were observed [], direct evidence cur-rently rests on limited data using single-channel EGG meth-ods, which showed that patients with ICC depletion displayedsignificantly reduced normal slow wave activity and increasedtachygastria in both fasting and fed states compared to thosewith intact networks []. Additional studies employing BSGMare therefore recommended, while noting that the traditional ac-quisition of full thickness biopsies from the stomach is challeng-ing and invasive. Gastric emptying may be preserved or delayed,depending on whether sufficient electromechanical couplingoccurs to facilitate effective bolus propagation []. Symptomdrivers in this phenotype are likely to include abnormal motorfunction, together with concomitant immune activation mech-anisms []. In a recent cohort of 210 patients with chronicgastroduodenal symptoms, 19% of patients showed this pheno-type []. Rates of this phenotype tend to vary between 10%and 30% depending on referral population (Table). Symptomprofiles varied, but were most commonly meal-induced in overtwo thirds. The literature review also identified advanced systemic sclero-sis as a potential cause of sustained gastric dysrhythmia, poten-tially related to fibrosis []. Numerous other causes of gastricdysrhythmia have been described in the literature, includingmotion sickness, short-acting opiates, excessive gastric volumeloading, vasopressin, and glucagon []. These factors aretypically avoided during BSGM testing. In addition, transientdysrhythmias have been observed, typically in the early post-prandial period, and often correlated to post-prandial distress[]. This phenomenon is currently poorly understood and re-quires further research regarding mechanisms and implica-tions []. 4.2.1.3 | Therapeutic Research Directions. The Dys-rhythmic Phenotype has been associated with comorbiditiesincluding diabetes and neuropathic diagnoses, plausibly relatedto pathophysiologic mechanisms discussed above []. Poor gly-cemic control is known to be a potential trigger for ICC deple-tion []. This may be reversible with tightening of glycemiccontrol, which should therefore be prioritized in affected dia-betic patients to recover ICC network function [], howeverit remains to be determined whether BSGM findings revert tonormal with ICC restoration. In addition, Sadaka et al. showedin adolescents that the Dysrhythmic Phenotype was completelycorrelated with a neuropathic diagnosis by ADM in a cohortof 15 patients, with further validation studies now awaited []. The Dysrhythmic Phenotype has also been associated withgreater severity of symptoms, particularly in children. Humphreyet al. demonstrated worse symptoms in adolescents with theDysrhythmic Phenotype compared to all other patients, includ-ing more severe upper gut pain and nausea, as well as higherdisability scores and reduced quality of life []. Sadaka et al.similarly found more severe symptoms of nausea and bloatingcompared to all other patients in their adolescent study []. Anadult study of 43 patients with chronic nausea and vomiting andmatched controls showed that symptoms correlated with theDysrhythmic Phenotype when present; whereas symptoms cor-related with mental health parameters in patients with normalspectral metrics []. Similar findings have since been shownin successive cohorts of increasing size, demonstrating the po-tential of phenotyping to plausibly distinguish subgroups by dis-ease mechanisms []. Overall, the Dysrhythmic Phenotypeis therefore currently viewed as indicative of a relatively severegroup of patients with true gastric neuromuscular disorders,potentially requiring a higher intensity of medical management[]. In the absence of disease-modifying therapies, therapy for theDysrhythmic Phenotype is currently focused on optimizing gas-tric motor function, symptom control, and nutritional support.ICC depletion may be expected to impair antral contractilityand antro-pyloric-duodenal coordination, which may impactthe breakdown of solid food (trituration) and gastric emptying[]. Dietary modification in favor of low volume, small parti-cle size diets is currently recommended to support gastroduode-nal transit and alleviate antral distension []. However, theWorking Group notes that phenotype-guided dietary studies arecurrently lacking, indicating a priority area for future research[]. While symptom management may include antiemetics,emerging evidence suggests that prokinetics may be disadvanta-geous in this cohort [], with additional validation pending ina prospective study (NCT06854120). Neuromodulators are alsoused in patients with gastroduodenal symptom disorders, espe-cially those without gastric emptying delay [], which canbe further informed by mental health overlays given that thisphenotype is known to be predisposed to depression and stressassociations []. As noted above, the Dysrhythmic Phenotype may requiretreatment escalation owing to the underlying neuromusculardysfunction, such that comprehensive multidisciplinary inputwith dietitians, nutritional support teams, and psychological/psychiatric support may be necessary []. Currently,the specific prevalence of advanced nutritional support require-ments and success rates (e.g., nasogastric, nasojejunal, or par-enteral nutrition) in this phenotype is unknown, presenting avaluable area for future research to guide prognostic counselingand proactive management. Data is limited, but in treatment re-fractory settings where gastric emptying is delayed, this groupmay be carefully considered, with shared clinician-patient de-cision making, for gastric per oral endoscopic pyloromyotomy(GPOEM), in view of high response rates in one cohort study[]. The role of gastric electrical stimulation in this phenotypeis currently being investigated, under the hypothesis that moresevere ICC depletion is correlated with lower response rates[]. #### 4.2.2 | High Frequency Phenotype 4.2.2.1 | Criteria. Stable high frequency activity as indi-cated by the Principal Gastric Frequency (refer to Table; e.g.,Figure). 4.2.2.2 | Pathophysiological Considerations. The stom-ach normally operates within a tight frequency range, with anupper bound of 3.35 cpm for the normative Principal Gastric ### Page 12 Frequency range []. The Working Group observed thatsmall frequency elevations of ~0.25 cpm may occur inciden-tally, including during the luteal phase of the menstrual cycleor with progesterone-based contraceptives, such that borderlineor transient frequency abnormalities may be inconsequentialand should be interpreted cautiously []. In addition, lowfrequency (< 2.65 cpm) was considered an emerging phenotypeonly, with clinical relevance currently uncertain, and is dis-cussed subsequently in the manuscript. Autonomic innervation is known to modulate gastric fre-quency (although specific linkages require further resolu-tion) [], and the High Frequency Phenotype has mostcommonly been observed in the context of presumed vagalneuropathy or injury [], although it can also be idiopathic.In patients with long-term type 1 diabetes, Xu et al. foundthat 28% of participants exhibited abnormally high gastricfrequencies, typically being those with more severe chronicGI symptoms and having established peripheral neuropathyand higher HbA1c []. In these patients, gastric frequencydeviation (absolute difference between PGF and 3.0 cpm) waspositively correlated with bloating, upper gut pain, nausea,vomiting, and excessive fullness, as well as total symptomsand reduced quality of life. In a separate study, Xu et al. fur-ther investigated gastric myoelectrical abnormalities in asmall cohort of patients experiencing persistent symptomsfollowing fundoplication []. Elevated frequencies were ob-served in those with presumed vagal nerve injury (observed atthe time of surgery), again with positive correlations betweenfrequency deviation and symptom severity. This emerging evidence therefore suggests that the HighFrequency Phenotype could serve as an indicator of severevagal nerve dysfunction, although the mechanism, sensitivity,and specificity of this association remain to be determined.This insight is consistent with evidence from low-resolutionEGG studies, which similarly demonstrated persistent ele-vations in gastric frequency in subsets of patients followingvagotomy and has additional support from studies in animalmodels []. This phenotype is observed in ~10% of gas-troduodenal patients (Table), while noting the significantprevalence modifiers of diabetes and post- surgical presenta-tions []. 4.2.2.3 | Therapeutic Research Directions. Based onlimited data, clinical experience, and associations with dia-betic neuropathy, members of the Working Group considerthe High Frequency Phenotype as a possible emerging indi-cator of a treatment-refractory disease. This position hasearly support from initial observations in patients referredfor GPOEM, which reported a 0% response rate amonghigh-frequency patients and significant overall differencesin gastric frequency between responder and non-respondergroups []. A multi- center prospective study is therefore inprogress to validate and extend these preliminary findings(NCT06381349). Given the emerging associations with neuropathy or vagal nerveinjury in this phenotype, a plausible therapeutic approach, par-ticularly in patients at high risk, such as long-term diabetics, maytherefore be directed at the control of neuropathic symptoms[]. Multidisciplinary care incorporating dietitians, painservices, as well as diabetologists to optimize glycemia shouldbe prioritized, and as a research opportunity, pharmacologicalconsiderations could encompass peripheral neuromodulator-based pharmacotherapy or gabapentinoids []. Given theputative association with neuropathy, escalation in therapy fortreatment-refractory patients might also include non-invasivevagal nerve stimulation [], or gastric electrical stimula-tion, particularly when nausea and vomiting are predominant[]; however, a paucity of current data necessitates fur-ther research before clinical recommendations can be provided.Further research is also needed to determine whether specificsubgroups could benefit from revisional gastric drainage proce-dures, and whether acupuncture techniques may have a validtherapeutic role []. Importantly, the Working Group notes that this group appearsdistinct from patients with systemic autonomic dysfunction. Ina series of 80 patients treated at a tertiary US center, generalizeddysautonomia in the domains of cardiovagal function, axonalsudomotor function, and postural orthostatic tachycardia wasassociated with delayed gastric emptying, but was not associatedwith spectral abnormalities such as elevated gastric frequencies[]. If autonomic contributors are suspected, pancreatic poly-peptide sham feeding test of vagal function or direct autonomicfunction testing may be pursued. #### 4.2.3 | Low Meal Response Phenotype 4.2.3.1 | Criteria. Low and/or delayed gastric activity inresponse to a meal, as indicated by Meal Response Ratio (MRR)and BMI-Adjusted Amplitude, and meal induced symptoms(refer to Table; e.g., Figure). 4.2.3.2 | Pathophysiological Considerations. TheLow Meal Response Phenotype is characterized by relativelyweak or delayed neuromuscular reaction immediately afterthe meal, in the presence of a normal gastric rhythm, oftenseen in association with post-prandial distress. A delayedmeal response may follow in the third hour, often correlat-ing to the abatement of symptoms (e.g., Figure) []. Thisphenotype may be present despite the spectral metrics beingwithin reference intervals, standing in contrast with spec-tral abnormality-based phenotypes (e.g., concomitant Dys-rhythmic Phenotype), which are associated with more severepost-prandial distress []. In a study of 151 patients, thisphenotype was seen in 11.2% of patients with normal gas-tric emptying, and 25% of patients with delayed emptying(also refer Table) []. Note that high-amplitude responseswere considered an emerging phenotype with uncertain clin-ical relevance at this time and are discussed subsequently inthe manuscript. To objectively quantify this phenotype, Varghese et al. recentlyintroduced the MRR, which as noted above, is currently cal-culated as the average amplitude in the first 2 h postprandiallydivided by the following 2 h. In normal tests, gastric amplitudein the first 2 h generally exceeds that of hours 3–4 (MRR > 1.0).While the Technical Group considered several approaches toquantify this phenotype, including reduced overall amplitudes ### Page 13 (e.g., < 22 μV), an MRR < 1.0 was considered most suitable at thecurrent time (refer to discussion) []. This decision was basedon emerging data linking MRR < 1.0 with delayed gastric emp-tying []. However, qualitative observations of spectrogramsremain informative; specifically, relatively low amplitudes inthe first two post-prandial hours (i.e., < 30 μV) may convey ther-apeutic significance even if the strict ratio criteria are border-line, based on limited data []. In a first cohort study implementing this metric, 42.9% of pa-tients with MRR < 1 had delayed gastric emptying, comparedto 16.7% of those with a normal MRR [], possibly caused byproximal fundic retention []. An additional possible contrib-utor to a Low Meal Response Phenotype is comorbid constipa-tion, which can suppress post-prandial gastric activity and delaymeal responses without altering rhythm stability via cologastricreflexes []. 4.2.3.3 | Therapeutic Research Directions. This phe-notype is commonly observed across adult patients withgastroparesis, FD, and nausea and vomiting disorders [].Consistent with these observations, Humphrey et al. alsoidentified this phenotype in approximately one-third of ado-lescent patients with FD or gastroparesis, again with associ-ated symptom correlations to the first two post-prandial hours[]. Overall, the Low Meal Response Phenotype is thereforeconsidered to offer a diagnostic aid to identify post-prandialhypomotility, although specific motility correlates are stillbeing evaluated []. Emerging real-world evidence recently demonstrated that theLow Meal Response Phenotype experienced the best symp-tomatic response to prokinetics []. Of note, these patientshad BMI-adjusted amplitudes at the lower end of the nor-mative ranges in the first two post-prandial hours [], andlower than those of prokinetic non-responders. This findingrequires further verification and is being actively investi-gated in an ongoing multicentre cohort study (NCT06854120).Given evidence of weak myoelectrical activity immediatelyafter the meal and association with delayed emptying [], itis hypothesized that this phenotype may be responsive to lowvolume, easily digestible, low residue diets to promote transit[]. However, it is acknowledged that research linking di-etary options to clinical outcomes is currently lacking acrossall phenotypes, and previous inconsistent findings may stemfrom the heterogeneity of more coarsely defined patient pop-ulations. Early evidence also suggests the timing of the mealresponse may be modulated through simple, non-invasivevagally- directed therapies such as resonance breathing (slowdiaphragmatic breathing to increase heart rate variability andactivate the parasympathetic nervous system) or non-invasivevagal nerve stimulation [], which has also been shownto alleviate myoelectrical abnormalities induced by a highgastric volume load []. As noted above, clinical members of the Working Group havealso observed a high prevalence of comorbid constipation in thisgroup, which may compound delayed meal responses [], al-though no published studies have reported this association todate []. Management of constipation may therefore pres-ent another actionable therapeutic option when the Low MealResponse Phenotype is detected. Further study of this correla-tion for potential causality needs to be explored. ### 4.3 | Auckland Classification:Sensory- Predominant Phenotypes #### 4.3.1 | Sensorimotor Phenotype 4.3.1.1 | Criteria. Symptoms tightly correlated to the gas-tric amplitude as supported by a high correlation score (> 0.5)(refer to Table; e.g., Figure). 4.3.1.2 | Pathophysiological Consideration. The Senso-rimotor Phenotype indicates cases with stable rhythmic activity,with the critical distinction that symptom curves correlate withgastric myoelectrical activity (i.e., increasing and decreasing inunison with a correlation score > 0.5). Together, these associa-tions indicate that gastric motility has an integral relationshipwith symptom genesis in the Sensorimotor Phenotype, whichis therefore a plausible indicator of gastric hypersensitivity(Figure) []. This phenotype is seen in ~25% of patients(Table). GI hypersensitivity can be associated with past enteric infec-tions, immune activation, dysbiosis, and intestinal permeabilityto chemicals (e.g., acid) and luminal antigens [], and in fe-males, estrogen-mediated effects on enterochromaffin cells maybe contributory []. It is proposed that mechanical stimuli,including distension and contractions trigger hypersensitizedviscerosensory pathways []. Symptoms typically aremeal-induced, correlate with gastric activity, and subside as thestomach empties and motility wanes; although mixed symptomprofiles are also observed in some patients, indicating that over-lapping phenotypes should be considered. Interestingly, a recentcohort study of 258 patients showed that this phenotype cor-relates strongly with higher anxiety scores (although not stressor depression), indicating a gut-brain link []. This finding isconsistent with other studies linking chronic GI hypersensi-tivity disorders to anxiety and hypervigilance []. On recentdatabase analysis, ~9% of patients with chronic gastroduodenalsymptoms exhibited this phenotype, but higher rates have beenobserved in different populations []. 4.3.1.3 | Therapeutic Research Directions. Giventhe putative link to visceral sensitization, promising treat-ment directions in this phenotype may also be focused onavoidance of trigger foods and neuromodulation medications.Estrogen-containing contraceptives that are plausibly linked toincreased visceral sensitivity could be substituted for alterna-tive contraceptive methods in women []; however, fur-ther research is required to confirm the benefit of this approach.Similarly, NSAIDs are linked to increased gastroduodenalpermeability [], allowing luminal antigens to triggerinflammation and sensitize visceral afferents []. A ther-apeutic approach to improve barrier dysfunction and restoremucosal integrity, such as avoiding NSAIDs or trialing PPIs,may reduce further sensitisation []. Again, the WorkingGroup acknowledges further research is needed in this area.Buspirone could also be considered when impaired accommo-dation is suspected [], while pain-targeted neuromodulators, ### Page 14 including tricyclic antidepressants (TCAs), mirtazapine,or serotonin-norepinephrine reuptake inhibitors (SNRIs),might be beneficial when pain symptoms show a sensorimo-tor correlation []. Importantly, neuromodulators shouldbe individualized to dominant symptoms, including favoringselective serotonin reuptake inhibitors (SSRIs) when comorbidanxiety is present, with expert involvement if possible [].Non-pharmacological interventions, including psychologicalsupport such as cognitive behavioral therapy and gut-directedhypnotherapy, are also worthwhile research directions thatcould offer additive benefit []. Two recent studies raise the hypothesis that therapies directedat gastric emptying may be relevant in the SensorimotorPhenotype. In one study, Kumar et al. showed a strong re-lationship between gastric emptying rate and sensorimotorsymptoms (not observed for other phenotypes), while Ayubiet al. demonstrated an 80% GPOEM response rate [].These studies indicate that further research into the potentialrole of prokinetics and pylorus- directed therapies in these pa-tients is warranted. #### 4.3.2 | Continuous Phenotype 4.3.2.1 | Criteria. Stable symptom profiles independentof meal or gastric amplitude (refer to Table; e.g., Figure). 4.3.2.2 | Pathophysiological Considerations. This phe-notype is characterized by normal gastric spectral activity, butwith a high continuous symptom burden. Symptoms must beelevated, remain stable throughout the test duration (i.e., withina 3-point range out of 10), and not correlate with the meal or gas-tric amplitude, implying that gastric myoelectrical activity, asmeasured by BSGM, does not contribute here to changes insymptoms []. The continuous pattern is common, observedin > 20% of patients, regardless of gastroparesis, FD, or chronicnausea and vomiting diagnoses (Table) []. The Continuous Phenotype has demonstrated consistent group-level associations with psychological comorbidities, includinghigher rates of depression, stress, and anxiety, indicating plau-sible linkage to a centrally-mediated sensitization etiology insome patients []. Centrally-mediated linkages withinthe Continuous Phenotype are further supported by emergingdata showing worse sleep and more severe illness perceptions(including higher perceived consequences, identified experi-ence, concern, and emotional response—unpublished work). 4.3.2.3 | Therapeutic Research Directions. Given thatsymptoms in the Continuous Phenotype do not correlate withmeal ingestion, motility indices, or gastric emptying [],the Working Group noted that exclusion of organic diseaseremains an important consideration in patients with continuoussymptoms, regardless of psychological comorbidities, and partic-ularly when presentations are atypical (e.g., symptoms of rapidonset, older ages, or accompanied by recent weight loss). Inthe absence of organic pathologies, the Continuous Phenotype isotherwise considered a plausible indicator of centrally-mediatedsymptoms/central sensitization in selected patients, based onthe key features discussed above; that is, normal motility [],meal-unrelated symptoms [], high psychological comor-bidity []; and cognitive associations (unpublished data).This is particularly true when an individual patient's AGBWscreening scores are supportive. However, members of the Work-ing Group also noted the need for further research into otherpotential contributors to symptoms in individuals with the Con-tinuous Phenotype, including immune activation with highcirculating levels of inflammatory mediators, and bacterialovergrowth states, to avoid unduly grouping these patients intoa common mechanism at this time []. Specific therapeutic options in patients exhibiting the ContinuousPhenotype are under evaluation, with limited data revealed onliterature review. However, in view of the above considerations,lifestyle modification including sleep optimization, regular ex-ercise, avoidance of triggers, and stress management are cur-rently deemed important []. Specialist psychological orpsychiatric evaluation and targeted interventions also warrantconsideration when central sensitization is clinically consideredand AGBW scores are high, based on which psychological axisis most affected []. Cessation or modulation of hormonalcontraception triggers could also be trialed, owing to the emerg-ing marked relationship between estrogen, GI sensitization, andmore severe chronic GI symptoms [], as well asknown associations between progesterone and nausea and vom-iting []. In selected cases, and with expert guidance, thisgroup may additionally benefit from SSRIs [] and advancedbrain-gut directed therapies, for example, cognitive behavioraltherapy or gut-directed hypnotherapy []. Together with holistic patient care strategies, targeted neuro-modulation options for specific symptoms are also consideredrelevant, based on existing guidelines for chronic gastroduode-nal disorders. Generally, in patients with gastroduodenal symp-tom disorders, SSRIs have been recommended when depressionor anxiety symptoms are predominant, TCAs or SNRIs whenpain is predominant, and tetracyclic antidepressants whenearly satiation, nausea, vomiting, and weight loss are present[]. In other guidance, TCAs have been recommendedif global foregut symptoms are treatment-refractory or there isevidence of comorbid irritable bowel syndrome []. Notably,the use of TCAs and other anticholinergic medications shouldbe balanced against their side effects, including sedation andconstipation []. ### 4.4 | Auckland Classification: Other Phenotypes #### 4.4.1 | Delayed Onset Symptoms Phenotype 4.4.1.1 | Criteria. Symptoms predominantly emerge afterthe majority of postprandial gastric activity is complete (refer toTable; e.g., Figure). 4.4.1.2 | Pathophysiological Consideration. The DelayedOnset Symptoms Phenotype describes symptoms that occur afterthe majority of the gastric meal response cycle (timing indicatedby MRR ≥ 1), suggesting a small bowel contribution to symptomgenesis []. This concept is supported by gastric emptyingstudies showing that certain symptom profiles are sustained afterthe majority of the meal has exited the stomach []. This pattern ### Page 15 could therefore plausibly implicate small bowel pathology suchas duodenal eosinophilia, hypersensitivity [], aberrantneuronal or hormonal feedback loops [], bacterial overgrowth[], dumping syndromes (including following foregut surgery)[], and/or small bowel dysmotility []; however, furtherresearch is required to directly confirm these associations. Thisphenotype may include motor and/or sensory contributors. 4.4.1.3 | Therapeutic Research Directions. This patternwas less common (Table). In one study of 210 patients, it wasseen in 4.3% where a previous hierarchical phenotyping frame-work was applied [], but when seen, it typically associateswith pain, bloating, and burning symptomatology []. Dueto the plausible associations with small bowel activity as notedabove, this phenotype warrants additional diagnostic work upfocusing on small intestinal pathologies. ### 4.5 | Emerging Phenotypes Additional phenotypes have been proposed and assessed in theliterature []. While the Working Group did not find suffi-cient evidence to include these phenotypes in the current corev1.0 set, they represent key areas for future research and evalua-tion, and likely hold unresolved clinical potential such that theymay be included in future versions. Their presence is thereforeindicated in the Auckland Classification's automated algorithmto provide clinical insights and standardize future research(refer Appendix and Table for proposed thresholds). The twomost promising emerging phenotypes are: • “Low Frequency” Phenotype: tests with frequencies belowthe normative range are observed infrequently [],except that very low frequencies (2.0–2.3 cpm) are typicalafter sleeve gastrectomy or other gastric surgeries involvingresection of the native pacemaker region, including someesophagogastrectomy procedures []. The dominantpacemaker appears to typically remodel, often with reducedstability and frequency []. However, a lack of identi-fied symptom or clinical correlations in the evaluated liter-ature concerning low frequencies means that clinical utilitywas currently deemed speculative • “High Amplitude” Phenotype: High amplitude activity isobserved more commonly and could reflect relative gas-tric hyperactivity, but motility correlates are currentlyunknown. Members of the Working Group noted that thisfinding may be observed if BSGM is performed in patientswith gastrostomy tubes, where the stomach wall is pulledup very close to the electrode array, potentially giving an ar-tifactually high voltage reading. However, high amplitudemay also be seen in patients without tubes, with severalWorking Group members pointing to plausible links to dis-tal resistance to flow (e.g., pyloric dysfunction), based onprevious low-resolution EGG studies []. However,it is worth noting that the lack of BMI-adjustment of low-resolution EGG amplitudes may confound this association,as may medication-related effects on amplitude (as seen inesophageal manometry, see []). Further research is nowrequired to resolve these potential associations and any im-plications for pyloric therapies. It is important to note that BSGM does not evaluate severalimportant elements critical to gastric function and symptoms,including fundic accommodation, pyloric function, and duo-denal immune activation. Patient reported symptom type andseverity in relation to the meal stimulus given during BSGMtesting highlight whether symptoms are meal-responsive ormeal-unrelated and will provide additional data that may pointto alternative causes []. In conjunction with mentalwellbeing screening tools, these data might enable treatmentstrategies to be matched to current standard of care approaches,such as the Rome criteria for gastroduodenal disorders of gut-brain interaction []. ## 5 | Discussion This consensus paper presents the Auckland Classification v1.0,establishing an inaugural standardized framework for the in-terpretation of BSGM for patients with chronic gastroduodenalsymptoms in clinical practice. Based on evidence synthesizedfrom 50 published studies and a dataset of over 4500 clinicaltests, the Working Group has defined six principal phenotypestogether with an algorithmic workflow for application of the sys-tem in practice. These definitions aim to standardize reportingand research methodologies, facilitating the ongoing transitionof BSGM from technical validation to clinical application. Aswith the evolution of the Chicago Classification [], the firstversion of this diagnostic framework is intended as an iterativebaseline that will be subject to refinement as the evidence basematures. Current diagnostic labels, such as functional dyspepsia andgastroparesis defined by the Rome Criteria and the results ofgastric emptying studies, frequently overlap, lack specificity interms of disease mechanisms, and do not satisfactorily predictresponses to pharmacological or other interventions with cer-tainty []. The aim of the new Auckland Classificationis to phenotype patients with chronic gastroduodenal symp-toms into discrete and biologically plausible mechanistic sub-groups based on BSGM technology. By categorizing patientsinto Motor Predominant (Dysrhythmic, High Frequency,Low Meal Response), Sensory Predominant (Sensorimotor,Continuous), and Delayed Onset Symptoms Phenotypes, thisclassification aims to provide additional objective and ac-tionable biomarkers for mechanisms that were previously de-scribed but difficult to identify using existing tests in clinicalpractice []. For example, the Dysrhythmic Phenotype pres-ents a plausible non-invasive surrogate for the ICC depletionand associated neuromuscular dysfunction that is known tounderpin a spectrum of GI dysfunction [], while theSensorimotor Phenotype offers a plausible indicator of gas-tric hypersensitivity, and the Continuous Phenotype supportscentral sensitization in selected patients with risk factors andindicators []. Using BSGM to delineate subgroups thatrespond to distinct therapeutic approaches would be a majoradvance in the management of patients with these challengingconditions. Importantly, this overarching hypothesis can betested. Validation in prospective studies is now essential, withearly data suggesting that phenotype-guided management,such as prokinetics for the Low Meal Response Phenotype,GPOEM for the Dysrhythmic Phenotype, or neuromodulators ### Page 16 for the Sensorimotor Phenotype, may improve therapeuticprecision and outcomes compared to empiric trial-and- error[]. The integration of BSGM into clinical workflows thereforehas potential to address key limitations of current testingmodalities. While 4-h gastric emptying scintigraphy (GES) re-mains the standard for assessing transit, it does not elucidatethe mechanism of delay and therefore does not provide suffi-ciently specific therapeutic targets, nor does it identify pathol-ogy in patients with normal emptying []. Moreover, withthe exception of the Nottingham Test Meal protocol [],existing methods for assessing gastric emptying do not assessgastric sensation by recording patient symptoms during gas-tric filling or emptying. The Working Group views BSGM ascomplementary to GES and other diagnostics that assess tran-sit time (i.e., wireless motility capsule, breath testing), withtheir combined use allowing for the differentiation of gas-tric myoelectrical dysfunction from transit delays, resultingin an overall substantially higher combined diagnostic yieldfor any gastric motility abnormality []. Importantly,the Auckland Classification's phenotypes go beyond some ofthe limitations of gastric emptying testing alone, by achiev-ing superior and more specific symptom and psychologi-cal correlations across broad disease categories as reviewedhere. The two tests may also be performed synchronously inpractice, so long as meals can be successfully harmonized[]. This enhanced mechanistic clarity supported thepresentation of a provisional, research-guiding, therapeu-tic algorithm presented in this review. This algorithm usescurrent society guidelines to identify the range of availabletherapeutic options, rather than seeking to reconcile differentrecommendations between societies (e.g., regarding G-POEM)[]. As the first consensus classification for BSGM, this frameworkhas several limitations and is expected to evolve. First, whilethe phenotypes are supported by translational and clinical co-hort studies, direct validation against histopathology (e.g., ICCcounts), vagal nerve testing, or motility correlates (e.g., ADM)remain limited and would benefit from expansion [].Second, the algorithmic framework for automated implemen-tation of the scheme (Appendix) currently includes a mix ofrobust quantitative cut-offs guided by reference intervals, emerg-ing linkages estimated from current experience and clinicalresearch studies, and those included based on Working Groupconsensus. We invite the broader GI community to challengeand test this framework to facilitate its continuous improve-ment. Third, the current classification is derived primarily fromadult data; while adolescent studies show consistent patterns, adedicated pediatric classification is currently in development toaccount for developmental physiology []. Fourth, we have pri-marily considered the proposed phenotypes in isolation; whilethe algorithmic framework supports the reporting of mixed phe-notypes, the clinical significance of co-occurring phenotypesis not yet well-understood. Lastly, emerging phenotypes andimportant areas for future investigation have been identified,including novel biomarkers such as spatial wave propagationmetrics that could be integrated in future as technical capabili-ties advance []. The most challenging phenotype for the technical group to objec-tively quantify in the Auckland Classification v1.0 was the LowMeal Response Phenotype. The Fed:Fasted Amplitude Ratio (ff-AR) was not found to be sufficiently discerning, as high fastingbaselines are common in both control and patient data [], andno associations were identified with either symptoms or clinicaloutcomes on literature review. This finding is also consistentwith low-resolution EGG studies, which generally failed to findgroup-level differences in “dominant power” changes betweenfasting and fed states []. The ff-AR metric may thereforebe deprioritised in future []. Instead, the MRR was adoptedto capture meal response timing. While MRR < 1 correlates withdelayed emptying, symptoms, and possibly prokinetic response[], it lacks specificity in isolation as healthy con-trols can also exhibit late peaks, despite a normative mean > 1(1.18 ± 0.42; unpublished data). Furthermore, strict amplitudecut-offs (< 22 μV) lacked sensitivity, with prokinetic respondersoften showing higher values up to 30 μV []. Therefore, clin-ical assessment of this phenotype is currently more complex,requiring simultaneous evaluation of meal response profile (asmeasured by MRR), strength (as measured by BMI-adjustedamplitude), and symptom severity in response to meals. The in-clusion of symptoms was considered necessary to separate thisclinical phenotype from the physiological findings that may alsooccur in healthy controls, and is supported by precedents in theChicago Classification v4.0 []. Further iteration is anticipatedas ongoing prokinetic responder studies mature across our con-sortium (including NCT06854120). Several additional areas of further investigation were also elu-cidated by the Working Group during iterative feedback stages.First, the Delayed Onset Symptoms phenotype fell below theconsensus threshold of 80%, identifying this as a target area forfurther validation studies. As this is a relatively low prevalencephenotype, larger series are anticipated to clarify its clinical rel-evance. Second, several Working Group members identified theoccurrence of meal responsive symptoms that do not meet thethreshold for a sensorimotor correlation. Further, it is acknowl-edged that the present BSGM literature is still emerging, andfurther independent reproduction of early reports is desirable.Further work is required to evaluate patients who do not fallwithin the current classification, which may lead to thresholdadjustments in future versions. We further emphasize that, as a foundational scheme, theAuckland Classification v1.0 should be viewed as a platformfor future development (refer Appendix, Table for list ofongoing studies). While further elucidation of mechanistic as-sociations, the “emerging” phenotypes, and the expansion ofnormative data across broader demographic groups are import-ant focus areas, the highest priority work for the next iterationof the Auckland Classification is the ongoing validation of theproposed therapeutic algorithm through prospective trials. Wealso anticipate that future versions will incorporate increasinglyrigorous methodologies, including patient involvement, as theframework matures. The current resource requirements for con-ducting a standardized BSGM test protocol are also presented inAppendix, which may change as future methodologies evolve. In conclusion, the Auckland Classification v1.0 formalizesa standardized clinical nomenclature and system for Body ### Page 17 Surface Gastric Mapping. By moving beyond symptom-basedlabels toward mechanism-based phenotyping, this consensusframework provides a structured approach for clinical decision-making and a foundation for the next generation of research ingastroduodenal disorders. ## Author Contributions C.V., G.O., A.A.G., G.S., N.D., and D.F. contributed literature review,drafting, and figure preparations. All authors contributed critical re-view, edits, methodological review, and appraisal. ## Affiliations 1Department of Surgery, The University of Auckland, Auckland, NewZealand |2Mayo Clinic, Rochester, Minnesota, USA |3AlimetryLtd, Auckland, New Zealand |4University of Louisville, Louisville,Kentucky, USA |5Indiana University School of Medicine,Indianapolis, Indiana, USA |6Auckland Bioengineering Institute,University of Auckland, Auckland, New Zealand |7Te Wananga oAotearoa, Auckland, New Zealand |8Allegheny Health Network,Pittsburgh, Pennsylvania, USA |9King's College Hospital NHSFoundation Trust, London, UK |10Dell Medical School, Universityof Texas at Austin, Austin, Texas, USA |11Johns Hopkins University,Baltimore, Maryland, USA |12Wellington Hospital, Wellington, NewZealand |13Cedars- Sinai, Los Angeles, California, USA |14StanfordUniversity, Stanford, California, USA |15Waitemata District HealthBoard, Auckland, New Zealand |16Washington and Lee University,Lexington, Virginia, USA |17University College London, London,UK |18School of Medicine, Western Sydney University, Sydney,New South Wales, Australia |19Klinik Arlesheim and Universityof Zurich, Zurich, Switzerland |20Apollo Multispeciality Hospitals,Kolkata, West Bengal, India |21Cleveland Clinic London, London,UK |22Mayo Clinic, Scottsdale, Arizona, USA |23PrincessAlexandra Hospital; University of Queensland, Brisbane, Queensland,Australia |24Functional Gut Clinic, London, UK |25Tri- ServiceGeneral Hospital, National Defense Medical University, Taipei,Taiwan |26Maastricht University Medical Center, Maastricht, theNetherlands |27Laureate Institute for Brain Research (LIBR), UCLA,Los Angeles, California, USA |28Vagelos College of Medicine,Columbia University, New York, New York, USA |29University ofCalifornia, San Diego, California, USA |30University of PittsburghMedical Center, Pittsburgh, Pennsylvania, USA |31FeinbergSchool of Medicine, Northwestern University, Chicago, Illinois,USA |32Atrium Health, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA |33Hoag Digestive Health Institute,Newport Beach, California, USA |34Temple University Schoolof Medicine, Philadelphia, Pennsylvania, USA |35FreemanHospital, Newcastle, UK |36Medical University of South Carolina,Charleston, South Carolina, USA |37University of Melbourne,Melbourne, Victoria, Australia |38Chulalongkorn University,Bangkok, Thailand |39University of South Florida, Tampa, Florida,USA |40University Hospitals Leuven, Leuven, Belgium |41FrenchArmed Forces Biomedical Research Institute, Bretigny-sur- Orge,France |42Hackensack Meridian Jersey Shore University MedicalCenter, Neptune City, New Jersey, USA |43Bangkok Hospital Pattaya,Chonburi, Thailand |44Department of Gastroenterology, University ofCalgary, Calgary, Alberta, Canada ## Acknowledgments Open access publishing facilitated by The University of Auckland,as part of the Wiley - The University of Auckland agreement via theCouncil of Australasian University Librarians. ## Funding This work was supported by the New Zealand Health Research Council. ## Disclosure International Body Surface Gastric Mapping Working Group. Technical Group: Chris Varghese, Nicky Dachs, Gabriel Schamberg,Armen A. Gharibans, Daphne Foong, Mikaela Law, Stefan Calder,Charlotte Daker, Christopher N. Andrews, Greg O'Grady. Consensus Group: David Levinthal, Baharak Moshiree, Braden Kuo,Catherine Ngo, Sahib S. Khalsa, Charles Verdonk, William L. Hasler,Xiao Jing Wang, Nicholas R. Oblizajek, Thomas Abell, Henry P.Parkman, Linda Nguyen, Ali Rezaie, Irene Sonu, David Kunkel, JonErickson, Vincent Ho, Anthony Robert Hobson, Daniel Keszthelyi,Leila Neshatian, Jan Tack, Christopher Brian Cederwall, BiancaChang, I-Hsuan Huang, Mohammad Bashashati, Joseph Sujka, RehanHaidry, Bu'Hussain Hayee, Homira Ayubi, Mohammad Al-Haddad,Sven Eriksson, Shahin Ayazi, Sanjay Pandanaboyana, Mark Fox, JohnClarke, Gerald Holtman, Natasha Koloski, Robert Bulat, Amol Sharma,Joy J. Liu, Douglas Weinstein, Uday Chand Ghoshal, Mahesh Goenka,Asma Fikree, Natalia Zarate-Lopez, Prateek Mathur, Abigail Stocker,Peng Du, Leo K. Cheng, Timothy R. Angeli- Gordon, Sam Simmonds,William Xu, Jonathan Sivakumar, John A. Windsor, JarongkornSirimongkolkasem, Nicha Wongjarupong, Alexander Podboy. ## Conflicts of Interest A.A.G., S.C., G.S., N.D., and G.O. hold grants and intellectual propertyin GI electrophysiology. Several authors are members of University ofAuckland Spin-out companies: The Insides Company (GO), and AlimetryLtd. (A.A.G., S.C., G.S., N.D., G.O., C.V., D.F., M.L., S.S., J.W., P.D., C.D.,and C.N.A.). The remaining authors have no relevant conflicts. ## Data Availability Statement The data that supports the findings of this study are available in the of this article. ## References - 1. A. D. Sperber, S. I. Bangdiwala, D. A. Drossman, et al., “WorldwidePrevalence and Burden of Functional Gastrointestinal Disorders,Results of Rome Foundation Global Study,” Gastroenterology 160 (2021):99–114.e3. - 2. C. J. Black, D. A. Drossman, N. J. Talley, J. Ruddy, and A. C. 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Table S1: List of studies evaluated by the technicalgroup to inform the Auckland Classification v1.0. Table S2: Proposedalgorithmic implementation of Auckland Classification version 1.0. ABSGM test is evaluated against every criteria listed in the table. Whenone or more criteria is met, the automated classification is determinedas the highest priority criteria or criterion. Table S3: Prevalence ofAuckland Classification v1.0 phenotypes by gastroduodenal disorderdiagnosis. Table S4: List of ongoing body surface gastric mapping stud-ies (excludes completed and published studies).