Hyperreflective rhinitis is a highly reactive nasal disease caused by excessive reflex of sensory nerve axons in the nasal cavity. Previously, it was classified under vasomotor rhinitis as the "sneezing type." With the understanding of neuropeptide substance P, this condition has been recognized as a distinct type of rhinitis. Wolf (1988) referred to it as hyperreflective nasal disease.

bubble_chart Pathological Changes

Primary afferent neurons of sensory nerves belong to unmyelinated C fibers. When sensory nerves are stimulated retrogradely, the terminals of C fibers release substance P (SP). SP is a neuropeptide composed of 11 amino acids, which causes local vasodilation, increased vascular permeability, and tissue edema. Experiments have found that SP can also induce mast cells to release histamine. Animal studies have shown that retrograde stimulation of the intranasal sensory branch of the trigeminal nerve in experimental animals can lead to nasal mucosal congestion, increased vascular permeability, and mucosal edema. Even if animals are pretreated with anticholinergic drugs (atropine), β-receptor blockers, histamine antagonists, or antiallergic agents, these neurogenic inflammatory responses cannot be prevented. These characteristics are identical to the local reactions induced by exogenous SP. However, when animals are pretreated with a large dose of capsaicin (the active component of hot peppers) before sensory nerve stimulation, the aforementioned reactions do not occur. Capsaicin selectively destroys unmyelinated C fibers.

From the above, it can be concluded that the neurogenic inflammation of the nasal mucosa caused by retrograde stimulation of sensory nerves is a local axon reflex, with SP acting as the neurotransmitter for this neural activity. Physical, chemical, and inflammatory stimuli can all trigger axon reflexes. Under normal conditions, the intact nasal mucosal epithelium protects against excessive local stimulation. The neuropeptide-degrading enzyme neutral endopeptidase (NEPase) present in the nasal mucosa continuously breaks down excess SP. Through these two mechanisms, the threshold for local axon reflexes is maintained at a normal level. However, when the mucosal epithelium is injured or NEPase activity is reduced due to exogenous or endogenous stimuli, the threshold for local axon reflexes decreases, leading to hyperreactivity of the nasal mucosa.

It closely resembles other highly reactive nasal diseases, but the symptoms appear and disappear rapidly, lasting for a short duration. Sneezing is the main symptom, accompanied by grade I intermittent stuffy nose, with no significant nasal discharge. After the symptoms subside, everything can return to normal. Many patients report onset after a common cold, with symptoms disappearing after persisting for a period. Nasal endoscopy often shows no changes, and nasal secretion smears typically reveal no characteristic findings.

bubble_chart Diagnosis

Due to the similarity of symptoms with other hyperreactive nasal diseases, diagnosis through {|###|}pulse taking and palpation{|###|} is relatively difficult. The following conditions may suggest this disease: ①Symptoms appear and disappear rapidly, mainly sneezing, possibly accompanied by {|###|}grade I stuffy nose{|###|}; ②{|###|}stuffy nose{|###|} is intermittent and short-lived; ③Rare nasal discharge; ④Both allergen skin tests and nasal secretion cytology tests are negative; ⑤Antihistamines and anticholinergic drugs show limited efficacy; ⑥The entire course often presents in stages, with remission periods longer than active phases.

Recent reports indicate elevated SP levels in nasal lavage fluid or serum among hyperreactive nasal diseases patients compared to healthy individuals (1992).

bubble_chart Treatment Measures

Topical intranasal corticosteroids and antihistamines are the first-line treatments for this condition. If symptoms occur frequently, anterior ethmoidal neurectomy may be considered.