SILENT LARYNGOPHARYNGEAL SENSORY DEFICITS AFTER STROKE

Dysphagia and aspiration are two devastating sequelae of stroke. Recen t work has shown that laryngopharyngeal (LP) sensory deficits are asso ciated with aspiration in stroke patients with dysphagia. The phenomen on of silent LP sensory deficits, where the patient exhibits no subjec tive or objective evidence of dysphagia, yet has an LP sensory deficit , has not been previously described. The aim of this study was to eval uate the sensory capacity of the laryngopharynx in stroke patients who had no subjective or objective complaints of dysphagia. We determined the sensory threshold in the laryngopharynx using air pulse stimulati on of the mucosa of the pyriform sinus and aryepiglottic fold. Eightee n stroke patients (mean age 65.6 +/- 11.5 years) and 18 age-matched co ntrols were prospectively evaluated. Normal thresholds were defined as <4.0 mm Hg air pulse pressure (APP). Deficits were defined as either a moderate impairment in sensory discrimination thresholds (4.0 to 6.0 mm Hg APP) or a severe sensory impairment (>6.0 mm Hg APP). Stroke pa tients were followed up for 1 year to determine the incidence of aspir ation pneumonia (AP) as verified by chest radiography. In 11 of the st roke patients studied, either unilateral (n = 6) or bilateral (n = 5) severe sensory deficits were identified. The elevations in sensory dis crimination thresholds were significantly greater than those in age-ma tched controls (7.1 +/- 0.6 mm Hg APP versus 2.5 mm Hg APP; p < .01, W ilcoxon score). Among patients with unilateral deficits, sensory thres holds were severely elevated in all cases on the affected side compare d with the unaffected side (p < .01, Wilcoxon score). Moreover, the se nsory thresholds of the unaffected side were not significantly differe nt from those of age-matched controls. Aspiration pneumonia did not oc cur in the patients with normal LP sensation or in the patients with u nilateral severe LP sensory deficits. However, in the 5 patients with bilateral, severe LP sensory deficits, 2 developed AP, both within 3 m onths of their LP sensory test. The results of this study showed, for the first time, that stroke patients without subjective or objective c linical evidence of dysphagia could have silent LP sensory deficits. T hese impairments could contribute to the development of AP following s troke. The findings in this study suggest that LP sensory discriminati on threshold testing should not be restricted only to patients with cl inical dysphagia.