Aim: To assess the pathophysiology and treatment of neurogenic dysphagia.
Methods: 46 patients with brain damage, 46 with neurodegenerative diseases and eight healthy volunteers were studied by videofluoroscopy while swallowing 3-20 mL liquid (20.4 mPa s), nectar (274.4 mPa s) and pudding (3931.2 mPa s) boluses.
Results: Volunteers presented a safe and efficacious swallow, short swallow response (< or =740 ms), fast laryngeal closure (< or =160 ms) and strong bolus propulsion (> or =0.33 mJ). Brain damage patients presented: (i) 21.6% aspiration of liquids, reduced by nectar (10.5%) and pudding (5.3%) viscosity (P < 0.05) and (ii) 39.5% oropharyngeal residue. Neurodegenerative patients presented: (i) 16.2% aspiration of liquids, reduced by nectar (8.3%) and pudding (2.9%) viscosity (P < 0.05) and (ii) 44.4% oropharyngeal residue. Both group of patients presented prolonged swallow response (> or =806 ms) with a delay in laryngeal closure (> or =245 ms), and weak bolus propulsion forces (< or =0.20 mJ). Increasing viscosity did not affect timing of swallow response or bolus kinetic energy.
Conclusions: Patients with neurogenic dysphagia presented high prevalence of videofluoroscopic signs of impaired safety and efficacy of swallow, and were at high risk of respiratory and nutritional complications. Impaired safety is associated with slow oropharyngeal reconfiguration and impaired efficacy with low bolus propulsion. Increasing bolus viscosity greatly improves swallowing function in neurological patients.