Introducing a Virtual Lesion Model of Dysphagia Resulting from Pharyngeal Sensory Impairment

Abstract

Background/Aims: Performing neurophysiological and functional imaging studies in severely affected patients to investigate novel neurostimulation techniques for the treatment of neurogenic dysphagia is difficult. Therefore, basic research needs to be conducted in healthy subjects. Swallowing is a motor function highly dependent on sensory afferent input. Here we propose a virtual peripheral sensory lesion model to mimic pharyngeal sensory impairment, which is known as a major contributor to dysphagia in neurological disease. Methods: In this randomized crossover study on 11 healthy volunteers, cortical activation during pneumatic pharyngeal stimulation was measured applying magnetoencephalography in two separate sessions, with and without pharyngeal surface anesthesia. Results: Stimulation evoked bilateral event-related desynchronization (ERD) mainly in the caudolateral pericentral cortex. In comparison to the no-anesthesia condition, topical anesthesia led to a reduction of ERD in beta (13-30 Hz) and low gamma (30-60 Hz) frequency ranges (p<0.05) in sensory but also motor cortical areas. Conclusions: Withdrawal of sensory afferent information by topical anesthesia leads to reduced response to pneumatic pharyngeal stimulation in a distributed cortical sensorimotor network in healthy subjects. The proposed paradigm may serve to investigate the effect of neuromodulatory treatments specifically on pharyngeal sensory impairment as relevant cause of neurogenic dysphagia.

Targeting the sensory feedback within the swallowing network—Reversing artificially induced pharyngolaryngeal hypesthesia by central and peripheral stimulation strategies

“…Activation following pneumatic stimulation was localized bilaterally mainly in areas corresponding to primary and secondary somatosensory and motor cortices, the supramarginal gyrus as well as the insula. To a lesser extent, activation was also found in prefrontal areas, as previously described (Muhle, Claus, et al, 2018). Activation intensity was relevantly lower than in the swallowing conditions, with the relatively strongest albeit small activation peaks found as follows: Condition Figures S2-S5).…”

Dysphagia in the intensive care unit: epidemiology, mechanisms, and clinical management

“…Stimulation levels are personalized at the start of the treatment to ensure that optimal levels of stimulation are delivered. PES is considered to target the afferent sensory feedback within the swallowing network that seems crucial for swallowing safety and efficacy of motor execution [126, 127]. PES may involve two postulated key modes of action: (a) facilitation of cortico-bulbar pathways [128] and (b) increase of swallowing processing efficiency in respective central nervous system areas [129], e.g., the right primary and secondary sensorimotor cortex and the right supplementary motor area.…”

FEES‐based assessment of pharyngeal hypesthesia—Proposal and validation of a new test procedure

“…[9][10][11][12][13][14] At the cortical level, reduced sensory input causes a decreased somatosensory swallowing activation 15,16 which also leads to an impaired motor coordination. [15][16][17] Pharyngeal sensation therefore provides key feedback for swallowing coordination at both the level of the brain stem and the cortex. Consistent with this model, the dissection of the laryngeal sensory nerves in animal models was associated with swallowing dysfunction and silent aspiration.…”

“…Cortical areas are associated with the volitional initiation and modulation of swallowing . At the cortical level, reduced sensory input causes a decreased somatosensory swallowing activation which also leads to an impaired motor coordination . Pharyngeal sensation therefore provides key feedback for swallowing coordination at both the level of the brain stem and the cortex.…”