“…Structural changes may limit one's ability to coordinate breathing and swallowing, or generate adequate pressure for high velocity airflows during cough. These may include: (1) altered compliance of the chest wall, (2) weak/spastic inspiratory (e.g., diaphragm, external intercostals) and expiratory (e.g., abdominals, obliques, internal intercostals) muscles, (3) vocal fold and upper airway pathologies ( 6 , 10 , 12 , 18 , 19 ). Disruptions in neural signaling of sensorimotor pathways may also contribute to hypotussia, including dysfunctional signal reception, transmission, processing, and/or output in one, or several neural substrates: (1) pulmonary, tracheobronchial, and laryngeal receptors that receive cough stimuli input ( 10 , 12 , 25 – 27 ), (2) vagal afferents of the airways that transmit sensory input to the central nervous system, including internal superior (iSLN) and recurrent laryngeal nerves (RLN) [Box A ] ( 10 , 25 , 26 ), (3) central pattern generators (CPG) for swallow, cough, and breathing integrate sensory input to generate a reconfigured respiratory CPG (rRCPG) to execute cough [Box B ] ( 4 , 28 ), and (4) subcortex and cortical structures involved with filtering, perceiving, and processing discriminative and affective characteristics of the sensory stimuli, leading to execution of volitional cough, or suppression/augmentation of reflexive cough ( 4 , 10 , 12 , 13 , 25 – 27 , 29 ).…”