Cerebrovascular disease is the most common disorder causing neurogenic oral and oropharyngeal dysphagia (3). Swallowing disorders have been reported in 27% to 50% of patients suffering from CVAs (4). The incidence is not limited to severe strokes, because even patients with mild-to-moderate strokes have a poorer long-term outcome directly attributable to their swallowing disorder (5). Given the complex neurophysiology associated with swallowing, a wide range of stroke locations can result in dysphagia. The gamut of cerebrovascular events, from major occlusive events to multiple small-vessel ischemic areas due to diabetes and chronic hypertension, to almost imperceptible brainstem infarcts, can result in oropharyngeal dysphagia. The extent of resulting cerebral ischemia defines the clinical presentation of the disorder. It is obvious that large occlusive ischemic events will result in a more severe dysphagia due to insults at multiple areas controlling swallowing physiology. Patients with brainstem strokes usually present with the most difficult to rehabilitate swallowing disorders. The deficits related to the strokes can often be predicted based on the site of the lesion.
Cortical strokes usually result in significant oral dysphagia, as well. Left-sided hemispheric strokes tend to produce a greater degree of oral dysfunction than other sites. This type of deficit results in a greater risk of aspiration due to poor control of the food bolus in the mouth and early spill to the pharynx. Patients with a dominant hemisphere CVA also often exhibit drooling due to an apparent "swallow apraxia" (6). Right-sided hemispheric strokes tend to produce a dysphagia characterized by apparently normal oral propulsion with a delayed pharyngeal response, resulting in the presence of the bolus in the pharynx without laryngeal closure. The resultant dysphagia is usually silent, and therefore, more insidious. Of the previously listed brainstem strokes, the lateral medullary syndrome produces the most dramatic dysphagia.
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