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Background Maturation of pharyngeal swallowing during neonatal oral feeding is unknown. Our objective was to evaluate pharyngeal functioning using high‐resolution manometry (HRM) during nutritive oral stimulus and test the hypothesis that pharyngeal contractility and regulation are distinct in preterm‐born infants. Methods High‐resolution manometry data during oral milk feeding were analyzed for pharyngeal contractile (PhCI, mm Hg cm s) and regulatory (number and frequency of pharyngeal contractions and bursts, pharyngeal activity‐to‐quiescence ratio, upper esophageal sphincter nadir pressure) characteristics in 23 preterm (<38 weeks’ gestation) and 18 full‐term‐born infants at term maturation. Mixed linear models and stepwise regression methods were used. Results Despite more oral feeding experiences (P < 0.05), preterm infants (vs full‐term), consumed less milk volume (P < 0.001), had lesser pharyngeal contractions within bursts (P = 0.04), lower pharyngeal contraction frequency (P < 0.01), and lower pharyngeal activity (P = 0.03), but higher PhCI per individual contraction (P = 0.01). PhCI is higher for longer PMA (P < 0.05), higher UES nadir pressures (P < 0.05), and lower pharyngeal contraction frequency (P < 0.05). Conclusions Nutritive oral milk stimulus provoked pharyngeal contractility characteristics is distinct in preterm‐born. Despite more oral nutritive experiences, preterm infants had underdeveloped excitatory and inhibitory rhythmic activity. Cranial nerve IX and X effects on sensory‐motor responses and feedback (excitation‐inhibitory rhythm regulation) remain immature among preterm‐born even at full‐term maturational status. We speculate the relationship between PhCI and UES regulatory activity contributes to the observed differences in preterm and full‐term infants.

PhCI is a novel reliable metric capable of distinguishing (1) proximal and distal pharyngeal activity, (2) effects of oral and pharyngeal stimulation, and (3) effects of prolonged stimulation. Changes in pharyngeal contractility with maturation, disease, and therapies can be examined with PhCI.

Objective Eating difficulties coupled with cardiorespiratory spells delay acquisition of feeding milestones in convalescing neonates, and the mechanisms are unclear. Aims were to examine and compare the pharyngoesophageal–cardiorespiratory (PECR) response characteristics: (a) in control neonates and those with recurrent bradycardia spells; and (b) during pharyngeal stimulation when bradycardia occurs versus when no bradycardia occurs. Methods Preterm infants ( N = 40, 27 ± 3 weeks gestation), underwent concurrent pharyngoesophageal manometry, electrocardiography, respiratory inductance plethysmography, and nasal airflow thermistor to evaluate pharyngoesophageal motility, heart rate (HR), and respiration during graded abrupt pharyngeal sterile water stimuli. Infants with recurrent bradycardia ( N = 28) and controls ( N = 12) were evaluated at 38 (38–40) and 39 (38–40) weeks postmenstrual age, respectively. Comparisons were performed (a) between study and control groups; and (b) among HR responses of <80 BPM, 80–100 BPM, and >100 BPM. Results Overall, characteristics of PECR responses in infants with a history of recurrent bradycardia (vs. controls) did not differ ( p > .05). However, when pharyngeal stimulus induced severe bradycardia (<80 BPM): prolonged respiratory rhythm change, increased pharyngeal activity, increased esophageal dysmotility (as evidenced by prolonged esophageal inhibition and motor activity), and prolonged lower esophageal sphincter relaxation were noted (all p < .05). Conclusions In control infants and those with recurrent bradycardia, pharyngeal stimulation results in similar PECR response characteristics. However, when severe bradycardia occurs, PECR response characteristics are distinct. The mechanisms of severe bradycardia spells are related to abnormal prolongation of vagal inhibitory effects on cardiorespiratory rhythms in conjunction with prolonged esophageal inhibition and delays with terminal swallow.

OBJECTIVE: To identify esophageal sensitivity phenotypes relative to acid (S Acid ), bolus (SBolus), acid and bolus (S Acid+Bolus ), and none (S None ) exposures in infants suspected with gastroesophageal reflux disease (GERD). METHODS: Symptomatic infants (N=279) were evaluated for GERD at 42(40–45) weeks postmenstrual age using 24-hour pH-impedance. Symptom associated probability (SAP) for acid and bolus components defined esophageal sensitivity: 1) S Acid as SAP≥95% for acid (pH<4), 2) S Bolus as SAP≥95% for bolus, 3) S Acid+Bolus as SAP≥95% for acid and bolus, or 4) S None as SAP<95% for acid and bolus. RESULTS: Esophageal sensitivity prevalence (S Acid , SBolus, SAcid+Bolus, S None ) was 28(10%), 94(34%), 65(23%), and 92(33%) respectively. Emesis occured more in SBolus and S Acid+Bolus vs S None (p<0.05). Magnitude (#/day) of cough and emesis events increased with S Bolus and S Acid+Bolu s vs S None (p<0.05). S Acid+Bolus had increased acid exposure vs S None (p<0.05). Distributions of feeding and breathing methods were distinct in infants with S Bolus vs S None (both, p<0.05). Multivariate analysis revealed that arching and irritability events/day were lesser at higher PMAs (p<0.001), greater for infants on NCPAP (p<0.01), with S Bolus and S Acid+Bolu s (p<0.05). Coughs/day was greater at higher PMAs (p<0.001), for infants with gavage and transitional feeding methods (p<0.02), with S Bolu s and S Acid+Bolus (p<0.05) but lesser with Trach (p<0.001). Number of emesis events/day were greater with SBolus and SAcid+Bolus (p<0.001). Sneezes/day decreased for infants on Trach (p=0.02). CONCLUSIONS: Feeding and breathing methods can influence the frequency and type of aerodigestive symptoms. We differentiated esophageal sensitivity phenotypes in NICU infants referred for GERD symptoms using pH-Impedance. Acid sensitivity alone was rare, which may explain poor response to acid suppressives; aerodigestive symptoms were predominantly linked with bolus spread. Magnitude of esophageal acid exposure and esophageal sensitivity to bolus spread may explain the pathophysiological basis for symptoms.