Topical Nasal Anesthesia and Laryngopharyngeal Sensory Testing: A Prospective, Double-Blind Crossover Study

Laryngopharyngeal sensory discrimination testing (LPSDT) has become a popular means of detecting sensory deficits in patients with voice and/or swallowing complaints. During this procedure, transnasal fiberoptic laryngoscopy (TFL) using a specialized fiberoptic scope is performed in order to deliver discrete pulses of air to the laryngopharyngeal mucosa. Historically, topical anesthesia has been applied to the nasal mucosa to lessen discomfort during TFL. Because of the concern that topical nasal anesthesia could also anesthetize the laryngopharynx, it is usually not used during sensory testing. To prospectively compare LPSDT scores after the nasal administration of cocaine hydrochloride, oxymetazoline hydrochloride, and saline solution, we prospectively evaluated 15 subjects undergoing LPSDT. Each had the procedure performed on 3 separate occasions. Before examination, each patient was administered either 4% cocaine, 0.05% oxymetazoline, or saline solution by atomizer (2 sprays of 1-second duration to each naris). By the conclusion of the study, each patient had undergone sensory testing with each of the test agents. During each examination, the minimal air pulse eliciting the laryngeal adductor reflex was recorded for both sides of the laryngopharynx. Both patient and examiner were blinded to the test agent used. The mean sensory score for saline solution was 3.9 mm Hg. The sensory scores for oxymetazoline and cocaine were 3.4 and 3.5 mm Hg, respectively. When compared to saline solution and oxymetazoline independently, sensory testing of the laryngopharynx during which the nose was anesthetized with cocaine resulted in similar thresholds for eliciting the laryngeal adductor reflex (p = .40 and p = .85). We conclude that topical anesthesia can be applied to the nasal cavity during LPSDT without altering laryngeal sensation.

Breathing route influences upper airway muscle activity in awake normal adults

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21–38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.