Chest
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Previously, we and other investigators have described reversible loss of lung elastic recoil in patients with acute and persistent, moderate-to-severe, chronic, treated asthma who never smoked, and its adverse effect on maximal expiratory airflow. In four consecutive autopsies, we reported the pathophysiologic mechanism(s) has been unsuspected mild, diffuse, middle and upper lobe centrilobular emphysema. ⋯ As documented now in five cases, unsuspected microscopic mild centrilobular emphysema is the sentinel cause of loss of lung elastic recoil. This contributes significantly to expiratory airflow obstruction in never-smoking patients with asthma, with normal diffusing capacity and near-normal lung CT scan results.
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Cough originates from stimulation of structures innervated by the vagus nerve, including the airways and distal esophagus. Arnold nerve reflex describes the induction of cough by stimulation of the external auditory canal, which is innervated by the auricular branch of the vagus. Historically, the prevalence of this reflex has been reported in the range of 2% to 3% on the basis of studies of outpatients in otolaryngology practices, but has not been investigated in healthy volunteers or in patients with chronic cough. ⋯ The greater than 12 fold prevalence of Arnold nerve reflex in adults with chronic cough compared with healthy volunteers supports the concept of cough hypersensitivity syndrome (CHS), in which vagal hypersensitivity is proposed to underlie chronic refractory cough. The absence of increased prevalence among children with chronic cough suggests that cough hypersensitivity syndrome is an acquired condition, perhaps triggered by viral respiratory infection or other environmental factor.