Chronic nasal obstruction (CNO) is a main complaint in ENT practice. It is often explained by structural deformities or edematous and inflamed nasal mucosa. In some cases, only little anatomical deformity or discrete obstructive mucosal inflammation is present even though patients complain of severe nasal obstruction. Our recent studies suggested that alteration of afferent neural pathways responsible for airflow perception, namely the intranasal trigeminal system may cause reduced subjective nasal patency that is perceived via trigeminal receptors located on the nasal cavity’s epithelium. These receptors respond to temperature changes, and to chemical substances such as eucalyptol which causes the same sensation of cooling as does increased airflow. The trigeminal system plays a crucial role in the pathogenesis of treatment-refractory and anatomically inexplicable CNO. In order to prove his involvement in the perception of nasal patency, we aimed to create a model for this pathogenesis of CNO.

We are carrying out a double-blind crossover study with 34 healthy participants. They are randomised for either treatment (local mucosal anesthetic) or placebo (saline solution) for the first study visit, and the opposite treatment for the second visit. We examine the intranasal trigeminal sensitivity using the Trigeminal Lateralization Task with eucalyptol. We further use questionnaires and Peak Nasal Inspiratory Flow to evaluate subjectively and objectively the nasal patency, respectively.

After 7 participants (preliminary results), trigeminal sensitivity (p=0.009) and subjective nasal patency (p=0.03) are significantly lower after nasal anesthetic than placebo. No difference was observed for objective nasal patency.

Our recent and current results shed light on trigeminal involvement in CNO, as we have shown that we can create a model of trigeminal dysfunction by local anesthetics. The created model opens the doors for future research concerning CNO.

Funding: FRQS; NSERC