Altered Cortical Swallowing Processing in Patients with Functional Dysphagia: A Preliminary Study

Abstract

ObjectiveCurrent neuroimaging research on functional disturbances provides growing evidence for objective neuronal correlates of allegedly psychogenic symptoms, thereby shifting the disease concept from a psychological towards a neurobiological model. Functional dysphagia is such a rare condition, whose pathogenetic mechanism is largely unknown. In the absence of any organic reason for a patient's persistent swallowing complaints, sensorimotor processing abnormalities involving central neural pathways constitute a potential etiology.MethodsIn this pilot study we measured cortical swallow-related activation in 5 patients diagnosed with functional dysphagia and a matched group of healthy subjects applying magnetoencephalography. Source localization of cortical activation was done with synthetic aperture magnetometry. To test for significant differences in cortical swallowing processing between groups, a non-parametric permutation test was afterwards performed on individual source localization maps.ResultsSwallowing task performance was comparable between groups. In relation to control subjects, in whom activation was symmetrically distributed in rostro-medial parts of the sensorimotor cortices of both hemispheres, patients showed prominent activation of the right insula, dorsolateral prefrontal cortex and lateral premotor, motor as well as inferolateral parietal cortex. Furthermore, activation was markedly reduced in the left medial primary sensory cortex as well as right medial sensorimotor cortex and adjacent supplementary motor area (p<0.01).ConclusionsFunctional dysphagia - a condition with assumed normal brain function - seems to be associated with distinctive changes of the swallow-related cortical activation pattern. Alterations may reflect exaggerated activation of a widely distributed vigilance, self-monitoring and salience rating network that interferes with down-stream deglutition sensorimotor control.

Comparison of motor diagnoses by Chicago Classification versions 2.0 and 3.0 on esophageal high‐resolution manometry

“…In patients presenting with dysphagia, those with CWA meeting CC diagnostic criteria were most prevalent, followed by those with CWA without CC diagnoses, and only then by those without CWA or CC diagnoses symptoms like dysphagia, which in turn may interfere with downstream sensorimotor control of deglutition and generation of abnormal motor patterns. 26 These data suggest that CWA could represent a minor motor disorder which may not be pathognomonic for a defined motor diagnosis, but one which can potentially explain esophageal symptoms, particularly transit symptoms like dysphagia. Therefore, we believe it is important to recognize abnormalities in the contraction wave before designating a motility study as normal, using either of CC 2.0 and 3.0.…”

“…Many of the CWA have been linked to abnormal esophageal inhibitory function, with an inverse relationship between the degree of inhibition and the propagation velocity of deglutitive contraction, as well as an absence of inhibition in SC . Finally, functional magneto‐electroencephalographic studies demonstrate activation of cortical areas depicting vigilance and self‐monitoring in perceptive esophageal symptoms like dysphagia, which in turn may interfere with downstream sensorimotor control of deglutition and generation of abnormal motor patterns . These data suggest that CWA could represent a minor motor disorder which may not be pathognomonic for a defined motor diagnosis, but one which can potentially explain esophageal symptoms, particularly transit symptoms like dysphagia.…”

Impact of symptom burden and health‐related quality of life (HRQOL) on esophageal motor diagnoses

“…Further, cohorts with non-obstructive dysphagia and CWA have been demonstrated to have lower esophageal perception thresholds, higher reproduction of symptoms, as well as reproduction of CWA during balloon distension studies 24, 25 . Limited electroencephalographic evidence suggests abnormal cortical control of swallowing favoring hypervigilance, and potentially impacting downstream motor pathways 26 . Based on this data, CWA could be a marker of esophageal hypervigilance 21-23, 27 , and could represent a unique motor entity.…”

Neurophysiology and new techniques to assess esophageal sensory function: an update

“…14 Spastic CWAs, such as multiple peaked waves, exaggerated contraction vigor, and rapid peristalsis, can have symptom burden similar to disorders that are identified by the Chicago Classification of motor disorders, 15 despite the fact that many of these abnormalities do not fulfill criteria for major or minor motor disorders. 16 These spastic disorders may be associated with reduced peripheral perception thresholds for esophageal sensation, 17,18 altered central assimilation of esophageal perception with increased vigilance, 19,20 and interference with downstream sensorimotor control. 20 These data suggest that, in addition to impeding bolus transit in the esophagus, spastic disorders can indirectly generate symptoms from increased esophageal perception and vigilance.…”

“…16 These spastic disorders may be associated with reduced peripheral perception thresholds for esophageal sensation, 17,18 altered central assimilation of esophageal perception with increased vigilance, 19,20 and interference with downstream sensorimotor control. 20 These data suggest that, in addition to impeding bolus transit in the esophagus, spastic disorders can indirectly generate symptoms from increased esophageal perception and vigilance. Therefore, spastic disorders may be epiphenomena or markers of esophageal visceral hypersensitivity.…”