The palatopharyngeus forms the palatopharyngeal arch (posterior pillar of the fauces) and connects the soft palate to the pharyngeal wall and larynx. Its palatine origin means it depresses the soft palate while its insertion into the thyroid cartilage elevates the larynx, making it act simultaneously on two structures to coordinate swallowing. The posterior pillar is the landmark for posterior tonsillectomy incisions.
| Origin | Palatine aponeurosis and posterior hard palate |
|---|---|
| Insertion | Blends with the pharyngeal constrictors and inserts on the posterior thyroid cartilage lamina |
| Nerve Supply | Pharyngeal plexus via the vagus nerve (CN X) |
| Blood Supply | Ascending palatine artery |
| Actions |
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|---|
During swallowing the palatopharyngeus simultaneously helps narrow the soft palate descent while pulling the larynx superiorly, coordinating the two movements needed to seal the nasopharynx and protect the airway.
Weakness of palatopharyngeus contributes to velopharyngeal insufficiency, with hypernasal speech and nasal regurgitation, and to dysphagia in vagal nerve lesions. Uvulopalatopharyngoplasty (UPPP) for obstructive sleep apnoea trims and repositions the posterior tonsillar pillar containing this muscle to widen the oropharyngeal airway; over-aggressive resection can itself cause velopharyngeal insufficiency. In sphincter pharyngoplasty for velopharyngeal insufficiency, flaps containing palatopharyngeus are raised from the posterior pillars and attached to the posterior pharyngeal wall to create a narrower, dynamic velopharyngeal port.
Not externally palpable. Visible as the posterior tonsillar pillar fold on oral examination and assessed by nasopharyngoscopy.
Vagal nerve palsy weakens palatopharyngeus, contributing to velopharyngeal insufficiency and dysphagia.
Excessive resection of the posterior pillar and soft palate during sleep apnoea surgery causes hypernasal speech and nasal regurgitation of liquids, which may need speech therapy or pharyngoplasty.
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