Purpose Of Review: Despite the wide prevalence of gastro-esophageal reflux disease (GERD), the neurophysiological mechanisms underlying heartburn perception in the esophagus of patients with GERD remains incompletely understood. Recent studies have highlighted the potential influence sensory afferent nerves innervating the oesophageal epithelium may have on heartburn pathogenesis. The purpose of this review is to consider the current understanding of esophageal afferent neuronal innervation, including the nociceptive role of acid-sensing receptors expressed on these sensory nerves, in relation to pain perception in the esophagus of GERD patients.
Recent Findings: Central and peripheral pathways of sensitization following noxious stimulation of nociceptive receptors expressed on afferent nerves can regulate the strength of sensory nerve activation in the esophagus, which can result in the amplification or suppression of afferent signal transmission. The localization and characterization of mucosal sensory afferent nerves vary between GERD phenotypes and may explain the heterogeneity of symptom perception in patients with apparently similar levels of reflux.
Summary: In this review, we discuss the relevance of afferent esophageal innervation in heartburn perception, with a particular focus on the pathways of reflux-induced activation of nociceptive nerves.
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http://dx.doi.org/10.1097/MOG.0000000000000749 | DOI Listing |
JAMA Ophthalmol
January 2025
Department of Ophthalmology, Casey Eye Institute, Oregon Health & Science University, Portland.
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Center for Advancing Neurotechnological Innovation to Application - CRANIA, University Health Network, Toronto, ON, Canada.
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Daniel Baugh Institute for Functional Genomics and Computational Biology, Department of Pathology and Genomic Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Loss of cardiac physiological function following myocardial infarction (MI) is accompanied by neural adaptations in the baroreflex that are compensatory in the short term, but then become associated with long-term disease progression. One marker of these adaptations is decreased baroreflex sensitivity, a strong predictor of post-MI mortality. The relative contributions of cardiac remodelling and neural adaptation in the sensory, central brainstem and peripheral ganglionic loci to baroreflex sensitivity changes remain underexplored.
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Smell and Taste Center, Department of Otorhinolaryngology: Head and Neck Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. Electronic address:
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View Article and Find Full Text PDFJ Neurophysiol
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Institute of Sport and Sport Science, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
In a recently developed associative rehabilitative brain computer interface system, electroencephalography is used to identify the most active phase of the motor cortex during attempted movement and deliver precisely timed peripheral stimulation during training. This approach has been demonstrated to facilitate corticospinal excitability and functional recovery in patients with lower limb weakness following stroke. The current study expands those findings by investigating changes in corticospinal excitability following the associative BCI intervention in post-stroke patients with upper limb weakness.
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