Non-allergic rhinitis: a case report and review

Abstract

Rhinitis is characterized by rhinorrhea, sneezing, nasal congestion, nasal itch and/or postnasal drip. Often the first step in arriving at a diagnosis is to exclude or diagnose sensitivity to inhalant allergens. Non-allergic rhinitis (NAR) comprises multiple distinct conditions that may even co-exist with allergic rhinitis (AR). They may differ in their presentation and treatment. As well, the pathogenesis of NAR is not clearly elucidated and likely varied. There are many conditions that can have similar presentations to NAR or AR, including nasal polyps, anatomical/mechanical factors, autoimmune diseases, metabolic conditions, genetic conditions and immunodeficiency. Here we present a case of a rare condition initially diagnosed and treated as typical allergic rhinitis vs. vasomotor rhinitis, but found to be something much more serious. This case illustrates the importance of maintaining an appropriate differential diagnosis for a complaint routinely seen as mundane. The case presentation is followed by a review of the potential causes and pathogenesis of NAR.

Figure 1

Preoperative CT scan of the head. A preoperative CT scan of the head with intrathecal contrast was done to localize the CSF leak. The frontal view is shown here. The scan shows a defect in the cribriform plate with confluent CSF extension into several bilateral ethmoid air cells, evidenced by the higher intensity signal of the contrast. Secondarily, there is mucosal thickening in the ethmoid and maxillary sinuses.

Figure 2

Etiology of CSF Rhinorrhea. CSF leak can be attributed to the following causes: Accidental trauma from a closed head injury (44%), surgical trauma (29%), tumors (22%), spontaneously due to increased intracranial pressure (ICP) (3-4%, but in some series are as high as 15-20%) and congenital skull base deformities (rare)[8-10].

Figure 3

Balance of autonomic inputs into nasal mucosa of patients with vasomotor rhinitis (VMR). Central nervous system stimulation causes release of tachykinins, substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinin A (NKA) that result in inhibition of the sympathetic nervous system and shift the balance towards the parasympathetic response. Noradrenaline and neuropeptide tyrosine (NPY) cause vasoconstriction and relief of nasal congestion. Vasodilators acetylcholine (Ach), vasoactive intestinal peptide (VIP) and nitric oxide (NO) cause nasal congestion and glandular secretion [33].