Cough is one of the most important defensive reflexes. However, extensive non- productive cough is a harmful mechanism leading to the damage of human airways. Cough is initiated by activation of vagal afferents in the airways. The site of their convergence is particularly the nucleus of the solitary tract (nTS). The second-order neurons terminate in the pons, medulla and spinal cord and there is also the cortical and subcortical control of coughing.Upper airway cough syndrome (UACS) - previously postnasal drip syndrome - is one of the most common causes of chronic cough together with asthma and gastroesophageal reflux. The main mechanisms leading to cough in patients with nasal and sinus diseases are postnasal drip, direct irritation of nasal mucosa, inflammation in the lower airways, upper airway inflammation and the cough reflex sensitization. The cough demonstrated by UACS patients is probably due to hypersensitivity of the upper airways sensory nerve or lower airways sensory nerve, or a combination of both. Further studies are needed to clarify this mechanism.

• MeSH
• Chronic Disease MeSH
• Capsaicin adverse effects   MeSH
• Cough chemically induced   physiopathology   MeSH
• TRPV Cation Channels agonists   physiology   MeSH
• TRPA1 Cation Channel agonists   physiology   MeSH
• Humans MeSH
• Sensory Receptor Cells drug effects   physiology   MeSH
• Vagus Nerve drug effects   physiopathology   MeSH
• Nasal Mucosa drug effects   physiopathology   MeSH
• Syndrome MeSH
• Trachea drug effects   physiopathology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Capsaicin MeSH
• TRPV Cation Channels MeSH
• TRPA1 Cation Channel MeSH
• TRPA1 protein, human MeSH Browser
• TRPV1 protein, human MeSH Browser