The Internal Superior Laryngeal Nerve in Humans: Evidence for Pure Sensory Function.

OBJECTIVES: To determine if the internal branch of the superior laryngeal nerve (iSLN) provides direct motor innervation to the interarytenoid muscle, a laryngeal adductor critical for airway protection. We studied the iSLN-evoked motor response in the interarytenoid and other laryngeal muscles. If the iSLN is purely sensory, there will be no detectable short latency motor response upon supramaximal stimulation, indicating the absence of a direct efferent conduction path. STUDY DESIGN: Intraoperative case series. METHODS: In seven anesthetized patients undergoing laryngectomy for unilateral laryngeal carcinoma, the iSLN of the unaffected side was electrically stimulated intraoperatively with 0.1-ms pulses of progressive intensities until supramaximal stimulation was reached. Electromyographic responses were measured in the ipsilateral interarytenoid, thyroarytenoid, and cricothyroid muscles. RESULTS: None of the subjects exhibited short-latency interarytenoid motor responses to iSLN stimulation. Supramaximal electrical stimulation of the intact iSLN evoked ipsilateral motor responses with long latencies: 18.7-38.5 ms in the interarytenoid (n = 6) and 17.8-24.9 ms in the thyroarytenoid (n = 5). Supramaximal stimulation of the recurrent laryngeal nerve evoked ipsilateral motor responses with short latencies: 1.6-3.9 ms in the interarytenoid (n = 6) and 1.6-2.7 ms in the thyroarytenoid (n = 6). CONCLUSION: The iSLN provides no functional efferent motor innervation to the interarytenoid muscles. The iSLN exclusively evokes an interarytenoid motor response via afferent activation of central neural circuits that mediate the laryngeal reflex arc. These findings suggest that the role of the iSLN in vital laryngopharyngeal functions, such as normal swallowing and protection of the airway from aspiration, is purely sensory. LEVEL OF EVIDENCE: 4 Laryngoscope, 131:E207-E211, 2021.

Sensory dysphagia: A case series and proposed classification of an under recognized swallowing disorder.

BACKGROUND: Although sensory feedback is a vital regulator of deglutition, it is not comprehensively considered in the standard dysphagia evaluation. Difficulty swallowing secondary to sensory loss may be termed "sensory dysphagia" and may account for cases receiving diagnoses of exclusion, like functional or idiopathic dysphagia. METHODS AND RESULTS: Three cases of idiopathic dysphagia were suspected to have sensory dysphagia. The patients had (1) effortful swallowing, (2) globus sensation, and (3) aspiration. Endoscopic sensory mapping revealed laryngopharyngeal sensory loss. Despite normal laryngeal motor function during voluntary maneuvers, laryngeal closure was incomplete during swallowing. The causes of sensory loss were identified: cranial neuropathy from Chiari malformation, immune-mediated neuronopathy, and nerve damage from prior traumatic intubation. CONCLUSIONS: Sensory loss may cause dysphagia without primary motor dysfunction. Sensory dysphagia should be classified as a distinct form of swallowing motility disorder to improve diagnosis. Increasing awareness and developing appropriate assessment tools may advance dysphagia care.