Aetiology
Little is known about the aetiology of the NAR conditions. It has been proposed that, in response to local mucosal injury, a compensatory response might over-amplify axonal release of neuropeptides, which then initiate the vascular and glandular responses characteristic of NAR.[7] The most popular mechanism postulated for vasomotor rhinitis patients has been an autonomic imbalance between the sympathetic and parasympathetic nervous system, resulting in parasympathetic hyperactivity leading to nasal congestion and drainage.[8] Parasympathetic responses are largely responsible for increased blood flow leading to engorgement of venous sinusoids, plasma extravasation, and increased release of secretions of mucus-secreting cells.
Otherwise, as a diagnosis based on exclusion, the aetiological factors in NAR are also largely negative risk factors. It is more likely to be the diagnosis in those with no family history of allergies, onset of symptoms after age 35, no seasonal symptoms, and no symptom exacerbation by cats. It is positively associated with triggers such as temperature changes, diesel and car exhaust, tobacco smoke, perfumes and fragrances, incense, cleaning products, newsprint, hairspray, and alcoholic beverages, spicy foods, or eating.[9]
Pathophysiology
Several studies have investigated the role of neuropeptides causing autonomic imbalance in NAR patients. Studies have demonstrated that a number of neuropeptides are released from sensory nerves, including substance P, neurokinin A, and calcitonin-gene-related peptide, which may play a significant role in physiological changes (vasodilatation and mucus hypersecretion) observed in patients with NAR.[7][10] It has also been demonstrated that vasoactive intestinal peptide, a component of the parasympathetic system, induces acetylcholine release that intensifies glandular secretory responses and vasodilation in the nasal mucosa. A central neurological mechanism has been postulated based on a functional magnetic resonance imaging study that demonstrated significant changes in central nervous system blood flow patterns in response to odourants in NAR patients off versus on intranasal azelastine, a topical antihistamine previously approved for the treatment of NAR.[11] Subsequently, it has been demonstrated that intranasal capsaicin, a transient receptor potential vanilloid subfamily, member 1 (TRPV1) agonist, was effective in the treatment of patients with a significant component of NAR, suggesting a role for TRP receptors in this disorder.[12] It has now been demonstrated that azelastine can also activate TRPV1 ion channels.[13] With continued exposure, TRPV1 ion channels can be desensitised. These findings support a neurogenic mechanism of action in NAR. These ion channels may be the first interface between the external environment resulting in neurogenic responses that cause upregulation of the parasympathetic nervous system, resulting in vasodilation and increased mucus secretion.[14]
Immunohistochemical studies have examined T-cell subsets in the nasal mucosa of allergic and non-allergic subjects and found some overlap as well as distinct differences between the two populations. These findings suggested that the cells involved in the early stages of inflammation differ between allergic and NAR subjects, but the number of mast cells in both groups seems to correlate with the respective infiltrating CD8+ T-lymphocyte populations.[15] The inflammatory profile differs between subsets of NAR, with inflammatory eosinophils present in non-allergic rhinitis with eosinophilia syndrome but absent in other sub-types.[16][17]
Classification
Non-allergic rhinitis with eosinophilia syndrome
Non-allergic but inflammatory, as indicated by eosinophils present on nasal smear.
Vasomotor rhinitis (VMR)
Non-allergic and non-inflammatory, with no eosinophils on nasal smear. Can be acute or chronic. VMR is also known as 'autonomic rhinitis', 'non-allergic rhinopathy', and 'idiopathic non-allergic rhinitis'.[1][3][4]
Other sub-types
Other sub-types include atrophic rhinitis, senile rhinitis, gustatory rhinitis, drug-induced rhinitis, hormonal rhinitis, and occupational rhinitis.[1]
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