Etiology
Upper airway abnormalities are a key component of the syndrome and thus nasal and/or sinus disease is the central causative factor. Seasonal and occupational triggers are recognized risk factors in some people. Other nonspecific triggers of cough include aerosols (e.g., perfumes, air freshener), change in room temperature, air conditioning, and pollen; however, these triggers are not necessarily specific for upper airway cough syndrome.
Pathophysiology
The pathophysiology is yet to be fully understood. It has been proposed that noxious irritation of the upper airway by either direct physical or chemical irritation results in upregulation of the afferent limb of the cough reflex. This may arise from stimulation of cough receptors located in the hypopharynx or larynx due to secretions translocating from the nose and/or sinuses stimulating the receptors directly; however, the role of nasal discharge in causing chronic cough remains contentious. The fact that some people have troublesome nasal symptoms and copious postnasal drip in the absence of a chronic cough indicates that a more complex interaction and upregulation of neuroregulatory processes may be present.[12]
Many features of upper airway cough syndrome overlap with general features of a cough hypersensitivity syndrome (i.e., a clinical syndrome characterized by troublesome coughing often triggered by low levels of thermal, mechanical, or chemical exposure).[4][13] Several features are common to both syndromes, and thus a component of neural hypersensitivity is likely to be present in both.[14] Moreover, it is becoming increasingly apparent that in some patients chronic cough may coexist with other clinical features of laryngeal hypersensitivity. This is best conceptualized as an inappropriate or maladaptive response of the glottis (e.g., cough, inspiratory wheeze, or globus) to an otherwise innocuous stimulus (e.g., perfume exposure).[15]
The concept of a unified airway has also been proposed as a pathophysiologic factor whereby both the upper and lower airways may be linked by a common local inflammatory process.[16] The precise mechanism underpinning this relationship remains to be determined; however, several studies have established that nasal stimulation (e.g., allergen provocation) in patients with allergic rhinitis results in increased lower respiratory tract symptoms (e.g., wheeze, dyspnea, cough).
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