Dysphagia in neurological diseases: a literature review

M Panebianco, R Marchese-Ragona, S Masiero, D A Restivo, M Panebianco, R Marchese-Ragona, S Masiero, D A Restivo

Abstract

Dysphagia is defined as an impairment of this complex and integrated sensorimotor system. It is estimated that 400,000 to 800,000 individuals worldwide develop neurogenic dysphagia per year. Neurogenic dysphagia is typically occurring in patients with neurological disease of different etiologies. A correct and early diagnosis and an appropriate management of dysphagia could be useful for improving patient's quality of life and may help to prevent or delay death. In the present review, we discuss thoroughly the anatomy and physiology of swallowing and also the pathophysiological mechanisms involved in impaired swallowing, as well as the diagnosis, management, and potential treatments of neurogenic dysphagia. Assessment of neurogenic dysphagia includes medical history, physical exam, and instrumental examinations (fiberoptic endoscopic evaluation of swallowing, videofluoroscopic swallowing study, electromyography). Pharmacological treatment of these problems includes oral anticholinergic drugs. Surgical myotomy of the cricopharyngeal muscle showed an important improvement of oropharyngeal dysphagia associated to upper esophageal sphincter hyperactivity. Chemical myotomy of the upper esophageal sphincter by local injections of botulinum toxin type A into the cricopharyngeal muscle has been proposed as an alternative less invasive and less unsafe than surgical myotomy.

Keywords: Dysphagia; Neurological diseases; Swallowing.

Conflict of interest statement

Dr. Restivo, Dr. Marchese-Ragona, Dr. Di Stefano, and Dr. Panebianco declare that have no conflict of interest related to the content of this article. The authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership, or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge, or beliefs) in the subject matter or materials discussed in this manuscript.

Figures

Fig. 1
Fig. 1
The figure shows the central program generator (CPG) located in the medulla oblongata and corresponding to the nucleus tractus solitaries (NTS), which receive both ascending and descending inputs and project to the ipsilateral brainstem nucleus such as nucleus ambiguous (NA); nucleus of V, VII, IX, X and XII cranial nerves; and C1–C3 tract of the cervical medulla. The existence of two CPGs can explain the recovery of the swallowing function after lesion of one CPG
Fig. 2
Fig. 2
The figure shows EMG recording of the IC (top trace) and CP (bottom trace) in a health subject during voluntary swallowing, using concentric needle electronic. At the activation of the IC corresponds a relaxation of UES allowing that the bolus passes from the pharynx to the esophagus. Calibration: gain, 200 μ V/D; sweep, 500 ms/D

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Source: PubMed

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