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Introduction Dysphagia is one of the most important and prognostically relevant complications of acute stroke. Pharyngeal Electrical Stimulation (PES) is a treatment device that enhances cortical reorganization for the restoration of swallowing function after cerebral injury. Furthermore, it was shown that PES leads to a temporary increase of Substance P (SP) level in saliva but not serum in healthy adults. The neuropeptide SP likely acts as a neurotransmitter in the pharyngeal mucosa and enhances the swallow and cough reflex. Post-stroke dysphagia may be related to reduced SP-levels. Here, we investigated the association of PES treatment in neurointensive care patients suffering from severe post-stroke dysphagia and salivary SP level, as well as a possible link between SP level and decannulation success after PES. Material and methods In this prospective single-center study, 23 tracheotomized stroke patients from our neurological intensive care unit were included. Due to severe and persisting dysphagia and according to the protocol for standardized endoscopic evaluation of tracheotomy decannulation in critically ill neurologic patients, participants could not be decannulated. Comorbidities that are known to likely cause dysphagia were not an exclusion criterion in contrast to other studies investigating on PES. 10 min of PES were applied on three consecutive days (= one treatment cycle). Three patients received multiple stimulation cycles. Saliva samples were collected prior to and directly after each treatment. To determine SP concentration, Enzyme-linked immunosorbent assay (ELISA) was performed. Results After the first treatment cycle 60% (n = 14) of all participants, respectively 73% (n = 7) of patients without comorbidities that likely cause dysphagia were decannulated. There was a close relation between increase of SP directly after the treatment and stimulation success (= decannulation). In 89% (n = 9) of patients without clinical improvement of dysphagia, SP levels remained stable or even decreased; 79% (n = 11) of successfully treated patients showed a post-stimulation increase of SP. Applying logistic regression analysis, increased SP level showed to be independently predictive of improved swallowing function after PES (p Conclusion The increase of salivary SP level following PES may indicate treatment success and SP therefore possibly acts as a biomarker of an improved swallowing function following PES.

Objective Dysphagia is a frequent and outcome-relevant complication of various neurological disorders, whose treatment options are still limited. Lately, neuromodulatory treatment devices have come into focus to enhance adaptive plasticity in the cortical swallowing network. However, performing neurophysiological and functional imaging studies to investigate these novel neurostimulation techniques for the treatment of neurogenic dysphagia in severely affected patients is difficult. Therefore, basic research needs to be conducted in healthy subjects instead. Here, we propose a virtual peripheral sensory lesion model to mimic pharyngeal sensory impairment, which is known to be a major contributor to dysphagia in neurological disease, as swallowing is a motor function highly dependent on sensory afferent input. Methods In this randomized crossover study on 11 healthy volunteers, cortical activation during pneumatic pharyngeal stimulation was measured applying 275-channel magnetoencephalography (MEG) in two separate sessions, with and without pharyngeal surface anesthesia. Individual source reconstruction was performed applying a linear constraint minimum variance (LCMV-) beamformer algorithm and significant differences between conditions were assessed with a nonparametric permutation test. Results Pneumatic pharyngeal stimulation evoked bilateral event-related desynchronization (ERD) mainly in the primary and secondary sensorimotor areas located in the caudolateral pericentral cortex, the insula, the prefrontal cortex and the supramarginal gyrus. In comparison to the no-anesthesia condition, topical pharyngeal anesthesia led to a virtual lesion in this network, indicated by a reduction of ERD in beta (13–30 Hz) and low gamma (30–60 Hz) frequency ranges (p Conclusions Withdrawal of sensory afferent information by topical surface anesthesia leads to reduced response to pneumatic pharyngeal stimulation in a distributed cortical sensorimotor network in healthy subjects thereby mimicking the situation in patients with dysphagia related to sensory impairment. Significance The proposed virtual sensory lesion paradigm may serve to investigate the effect of neuromodulatory treatments specifically on pharyngeal sensory impairment as relevant cause of neurogenic dysphagia.