Oropharyngeale Dysphagie als Neurogeriatrisches Syndrom

Dysphagia dimensions and risks

Oropharyngeal dysphagia encompasses impaired efficiency (insufficient oral intake causing malnutrition and dehydration) and impaired safety (airway invasion causing aspiration and pneumonia). These complications worsen outcomes, frailty, and quality of life in neurological and geriatric patients.

Instrumental assessment is essential

Clinical screening (e.g., water swallow tests, indirect signs, laryngeal elevation) shows limited sensitivity and specificity. Instrumental diagnostics—videofluoroscopy and FEES—serve as complementary gold standards; FEES enables bedside visualization and sensory testing, while videofluoroscopy depicts all swallowing phases but requires radiation exposure and cooperation.

Phenotype-guided, disease-specific management

Dysphagia phenotypes include premature spillage, delayed swallow reflex from reduced sensitivity, pharyngeal residue (valleculae, piriform sinuses, UES timing), pharyngeal movement disorders (e.g., freezing), fatigue, and complex issues. Their distribution differs by disease and guides targeted therapies, oral hygiene, nutrition, and PEG timing.

The continuing education “Oropharyngeale Dysphagie als Neurogeriatrisches Syndrom,” organized by Klinik Barmelweid and presented by Priv.-Doz. Dr. Bendix Labeit, addresses definition, diagnosis, phenotyping, and management of neurogenic oropharyngeal dysphagia. The course defines dysphagia along the dimensions of inefficiency (risk of malnutrition and dehydration) and safety (risk of penetration/aspiration and pneumonia), emphasizing impacts on morbidity, mortality, and quality of life. Neuroanatomy and control of swallowing are reviewed, and a phenotype-based approach is proposed in line with a recent systematic review and classification; severity metrics such as the Rosenbek Penetration-Aspiration Scale are referenced. Key phenotypes include premature spillage from impaired oral bolus control, delayed swallow trigger due to sensory deficits, pharyngeal residue in the valleculae and piriform sinuses from reduced pharyngeal contraction or limited upper esophageal sphincter opening, oropharyngeal movement disturbances (including “freezing” in Parkinsonian syndromes), and fatigability in myasthenia gravis (illustrated by a positive edrophonium/Tensilon response). Clinical screening (e.g., water swallow tests, Volume-Viscosity Swallow Test, and indirect signs such as wet voice or cough) is discussed, with clear limitations in sensitivity/specificity and silent aspiration; instrumental gold standards remain videofluoroscopic swallowing study and fiberoptic endoscopic evaluation of swallowing, each with distinct advantages and constraints. Management integrates disease-specific therapies (e.g., dopaminergic medication for Parkinson’s disease; acetylcholinesterase inhibitors and immunotherapy for myasthenia gravis), logopedic/behavioral interventions, and phenotype-guided strategies, including targeted approaches for upper esophageal sphincter dysfunction where appropriate. Supportive measures include rigorous oral hygiene, consistency and viscosity adaptation, early nutritional assessment with timely consideration of enteral feeding (PEG) before significant weight loss when aligned with patient goals, avoidance of prophylactic antibiotics to prevent aspiration pneumonia, and guideline-concordant decisions against enteral nutrition in advanced dementia.