Dysphagia in multiple sclerosis (MS) occurs in 31.3%. In Parkinson’s disease (PD), dysphagia occurs approximately in 50%. It is estimated that dysphagia occurs in approximately 65% of acute stroke patients. It is generally agreed that stroke is the most common cause of ND. The reported incidence of dysphagia in specific neurologic diseases is variable, owing in part to patient selection methods and evaluation methods (e.g., questionnaires, clinical evaluation, diagnostic evaluation). It is estimated that 400,000 to 800,000 individuals worldwide develop neurogenic dysphagia per year. 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. 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. Neurological problems that cause dysphagia can be categorized in many different ways: anatomic location of the lesion (e.g., central nervous system, peripheral nervous system or muscle), pathogenetic mechanism of disease (e.g., ischemic injury or degenerative process), etiology, or clinic presentation (e.g., dementia or movement disorders). Neurogenic dysphagia (ND) is typically occurring in patients with neurological disease of different etiologies (see T able 1), and it is associated to high mortality, morbidity, and social costs. Dysphagia is defined as an impairment of this complex and integrated sensorimotor system. About 50 pairs of striated cranial muscles are excited and/or inhibited sequentially allowing the bolus transit from the mouth to the stomach. During a swallow, different levels of the central nervous system from the cerebral cortex to the medulla oblongata are involved. Swallowing is defined as the semiautomatic motor action of the muscles of respiratory, oropharyngeal, and gastrointestinal tract that propels the food from oral cavity to the stomach and protects airway from food, liquids, and other substances. 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. Surgical myotomy of the cricopharyngeal muscle showed an important improvement of oropharyngeal dysphagia associated to upper esophageal sphincter hyperactivity. Pharmacological treatment of these problems includes oral anticholinergic drugs. Assessment of neurogenic dysphagia includes medical history, physical exam, and instrumental examinations (fiberoptic endoscopic evaluation of swallowing, videofluoroscopic swallowing study, electromyography). Neurogenic dysphagia is typically occurring in patients with neurological disease of different etiologies.
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