Syed Q. Hussaini

Upper Esophageal Sphincter and Gastroesophageal Junction Pressure Changes Act to Prevent Gastroesophageal and Esophagopharyngeal Reflux During Apneic Episodes in Patients With Obstructive Sleep Apnea

BACKGROUND Gastroesophageal reflux (GER) is thought to be induced by decreasing intraesophageal pressure during obstructive sleep apnea (OSA). However, pressure changes in the upper esophageal sphincter (UES) and gastroesophageal junction (GEJ) pressure during OSA events have not been measured. The aim of this study was to determine UES and GEJ pressure change during OSA and characterize the GER and esophagopharyngeal reflux (EPR) events during sleep. METHODS We studied 15 controls, nine patients with GER disease (GERD) and without OSA, six patients with OSA and without GERD, and 11 patients with both OSA and GERD for 6 to 8 h postprandially during sleep. We concurrently recorded the following: (1) UES, GEJ, esophageal body (ESO), and gastric pressures by high-resolution manometry; (2) pharyngeal and esophageal reflux events by impedance and pH recordings; and (3) sleep stages and respiratory events using polysomnography. End-inspiration UES, GEJ, ESO, and gastric pressures over intervals of OSA were averaged in patients with OSA and compared with average values for randomly selected 10-s intervals during sleep in controls and patients with GERD. RESULTS ESO pressures decreased during OSA events. However, end-inspiratory UES and GEJ pressures progressively increased during OSA, and at the end of OSA events were significantly higher than at the beginning (P < .01). The prevalence of GER and EPR events during sleep in patients with OSA and GERD did not differ from those in controls, patients with GERD and without OSA, and patients with OSA and without GERD. CONCLUSIONS Despite a decrease in ESO pressure during OSA events, compensatory changes in UES and GEJ pressures prevent reflux.

Neurocognitive processing of esophageal central sensitization in the insula and cingulate gyrus

The cingulate and insular cortices are parts of the limbic system that process and modulate gastrointestinal sensory signals. We hypothesized that sensitization of these two limbic area may operate in esophageal sensitization. Thus the objective of the study was to elucidate the neurocognitive processing in the cingulate and insular cortices to mechanical stimulation of the proximal esophagus following infusion of acid or phosphate buffer solution (PBS) into the esophagus. Twenty-six studies (14 to acid and 12 to PBS infusion) were performed in 20 healthy subjects (18-35 yr) using high-resolution (2.5 x 2.5 x 2.5 mm(3) voxel size) functional MRI (fMRI). Paradigm-driven, 2-min fMRI scans were performed during randomly timed 15-s intervals of proximal esophageal barostatically controlled distentions and rest, before and after 30-min of distal esophageal acid or PBS perfusion (0.1 N HCl or 0.1 M PBS at 1 ml/min). Following distal esophageal acid infusion, at subliminal and liminal levels of proximal esophageal distentions, the number of activated voxels in both cingulate and insular cortices showed a significant increase compared with before acid infusion (P < 0.05). No statistically significant change in cortical activity was noted following PBS infusion. We conclude that 1) acid stimulation of the esophagus results in sensitization of the cingulate and insular cortices to subliminal and liminal nonpainful mechanical stimulations, and 2) these findings can have ramifications with regard to the mechanisms of some esophageal symptoms attributed to reflux disease.

Terminating motor events for TLESR are influenced by the presence and distribution of refluxate

Transient lower esophageal sphincter relaxation (TLESR) is frequently associated with reflux events and terminates with a primary or secondary peristaltic wave. However, it is unclear whether the presence and properties of the refluxate affect TLESR-termination events. The aims of this study were to determine the pattern of terminating esophageal motor activity after TLESR in healthy subjects and factors affecting the type of terminating motor event. Fifteen healthy subjects (7 men, age 18-56) were studied. High-resolution manometry and impedance/pH monitoring were performed simultaneously in supine position for 2 h after subjects took a 1,000-kcal meal (Awake Study). This procedure was repeated during the night under polysomnographic recording for 6-8 h after consuming a 1,000-kcal meal (Sleep Study). We categorized three types of TLESR-terminating motor events, primary peristalsis (PP), full secondary contraction (FSC), which propagated the entire esophagus, and partial secondary contractions (PSC), which started distal to the upper esophageal sphincter. Overall, 289 TLESR events were found. The percentages of TLESR events terminated by PP, FSC, and PSC were 22%, 14%, and 64%, respectively. TLESR events terminated by PP were less likely to be accompanied by reflux events. TLESR events terminated by FSC were significantly more likely to have evidence for proximal esophageal reflux and esophago-pharyngeal reflux. Findings were similar in awake and sleep states. We concluded that, in healthy recumbent subjects, the most common TLESR-termination event is a secondary contraction, rather than PP. Presence and distribution of the refluxate is a major influence on the type of terminating contraction.

T1230 TLESR Termination By Swallows: A Chance Event

The advent of pharmacological agents that inhibit TLESRs has increased the need for accurate objective identification and scoring of these events. The only current objective criteria were published over 10 years ago (Am.J.Physiol,1995;268:G128-13) and have not been subject to rigorous evaluation. Aims: To assess the performance of the TLESR criteria with regard to intraand inter-assessor variability and to improve them where necessary. Methods: Two 3-hour post-prandial esophageal manometric and pH recordings were performed at least 1 week apart in 20 healthy volunteers. Each recording was duplicated and all recordings were given a unique identifier, creating two datasets of 40 recordings. The recordings were analysed by 5 experienced observers for the occurrence of TLESRs based on their expert opinion. Scored TLESRs were also analysed for the presence of the original 4 criteria as well as inhibition of the crural diaphragm (ID), a prominent after-contraction (AC), acid reflux and an esophageal common cavity. Results: For TLESRs based on the observers expert opinion, the overall inter-observer agreement was 59% (range 56-67%) and the intra-observer agreement 75% (60-89%). When TLESRs were restricted to those fulfilling the original criteria, inter-observer agreement fell to 46% (40-53%) and the intra-observer agreement to 60% (44-67%). Cleaning the recordings by removal of technically flawed sections (up to 20% of any one recording) improved inter and intra-observer agreement by 5%. Inclusion of additional criteria (ID and AC) for the identification of TLESRs in the second dataset resulted in interand intra-observer agreements of 62% (52-70%) and 69% (53-79%) respectively, close to those based on the observers expert opinion (64% (56-71%), 71% (61-80%). A consensus analysis performed collectively by 3 observers and based on the new criteria (original ± ID and AC) resulted in agreement between the paired recordings of 84%. The remaining disagreement was largely the result of technical difficulties with the recordings.Conclusions: The original criteria for the definition of TLESRs allows for substantial interand intra-observer variability. Incorporation of additional objective criteria reduces the variability. However, the highest level of intra-observer agreement can be achieved by consensus analysis.

80 Upper Esophageal Sphincter and Gastroesophageal Junction Pressure Changes Act to Prevent Reflux During Obstructive Sleep Apnea in GERD Patients

Introduction: Gastroesophageal reflux (GER) is thought to be induced by deceasing intraesophageal pressure during obstructive sleep apnea (OSA). However, pressure changes in the upper esophageal sphincter (UES) and gastroesophageal junction (GEJ) pressure during OSA events have not been measured. Aims: Determine UES and GEJ pressure change during OSA and characterize the GER and esophago-pharyngeal reflux (EPR) events during sleep. Methods: We studied 12 controls, 5 GERD without OSA and 6 GERD with OSA patients for 6-hours post-prandially during sleep. We concurrently recorded: a) UES, GEJ and esophageal body (ESO) pressures with a high-resolution manometric system. b) pharyngeal and esophageal reflux events by impedance and pH recordings. c) sleep stages and respiratory events using polysomnogram. End inspiration UES, GEJ and ESO pressures over intervals of OSA were averaged in GERD/OSA patients and compared to average values for randomly selected ten-second intervals during sleep in controls and GERD patients. Results: Total sleep time was 309±46, 317±39 and 306±58 minutes in controls, GERD and OSA patients, respectively. Our findings confirm previous reports of decreasing ESO pressures during OSA events, however, end-inspiratory UES and GEJ pressures at the end of OSA events were significantly higher than those at the beginning of OSA (p<0.01, Table 1). End-expiratory pressure in UES, GEJ and ESO at the beginning of OSA was not changed during OSA. Only two GER events during OSA were recorded in OSA patients. The incidence of GER and EPR events during sleep in GERD/OSA patients did not differ from those in controls and GERD patients (Table 2). Conclusion: Despite a decrease in ESO pressure during OSA events, compensatory changes in UES and GEJ pressures prevent GERD patients with OSA from having an increase in reflux events.