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Aspiration is a common result of stroke, and may lead to lung infections and pneumonia. Cough may prevent this aspiration and thus prevent the pneumonia. We review the four types of cough usually used to assess aspiration risk: voluntary cough (VC), reflex cough (RC), the laryngeal expiration reflex (LER), and cough on swallow (CoS). VC is easy to test but starts with an inspiration that may cause aspiration, and is controlled by cortico-brainstem pathways that may not be involved in influencing aspiration. RC also starts with an inspiration, and requires instrumental intervention, but is more relevant to protecting the lungs. The LER starts with an expiration, so is 'anti-aspiration', and is easy to test, but its neural mechanisms have not been fully analysed. CoS can be tested at the same time as direct observations of aspiration, but little is known about its neural mechanisms. Each method has its advocates, and the purpose of the review is to discuss how each may be applied and how the information from each may be assessed and valued.

Twelve distinguished scientists attended the workshop, heard three presentations, and took part in the discussions. Fontana first described his unpublished studies on cough in exercise and during hyperventilation with healthy subjects. Both activities depressed cough induced by inhalation of distilled water aerosol (fog). The possible mechanisms were discussed. Gibson then described the successful use of speech therapy to treat chronic cough, and discussed the possible mechanisms, centering on the role of the larynx and its neural control. A comparison was made with the ability of speech and laughter to precipitate cough. Widdicombe discussed the scanty literature on the effect of singing and playing wind instruments on cough, most of the evidence being anecdotal. In the discussion periods several matters for future study arose. It is usually not clear if the modulation of cough, its depression, enhancement or excitation, arose primarily at peripheral sites (reflexes from the airways), or at a cortical level, or both. Nor is it clear whether the same results would be obtained with provoked cough and with spontaneous cough. But all three aspects of 'behavioual' changes in cough sensitivity (exercise, speech and music) could be further explored, and current techniques should make this possible.

The Third International Symposium on Cough focused on acute and chronic cough, both clinical and basic science. Cough is a defensive and clearing mechanism, and can cause discomfort and nuisance; it is also an important symptom of many chronic airway diseases. In this Symposium, several issues concerning the relationship of cough to disease processes, different types of cough, and the concept of idiopathic cough will be discussed. Characterization of cough receptor(s) and identification of peripheral and central mechanisms for cough sensitization are current areas of investigation for delineating the cause of chronic cough. Peripheral mechanisms may be most important for acute cough such as after viral infections. The role of pathological changes at the level of the airway mucosa and of cortical pathways will be reviewed. Finally, therapeutic inhibition of the cough reflex remains an area of active research.

Both PAF (10 microM) and bradykinin (0.1-10 microM) increased lysozyme (from submucosal gland serous cells (+138 and +45% for PAF, 10 microM, and bradykinin, 1 microM, respectively) and albumin (mainly active epithelial transport; +387 and +108%) outputs into the ferret tracheal lumen in vitro and reduced the negativity of the potential difference (PD: -33 and -17%) across the trachea. Since PAF can cause bronchial smooth muscle hyperresponsiveness, we tested whether these effects were interactive, and if PAF would increase the actions of bradykinin. The bradykinin-induced lysozyme and albumin outputs were more than trebled and the PD change was enhanced by PAF, after the immediate secretory effects of the latter had returned to baseline. The secretory and PD responses to PAF were all prevented by the PAF-antagonist WEB 2086 and by a combination of the free-radical scavengers catalase and SOD, indicating that PAF may act on specific receptors to release free-radicals. Nedocromil sodium inhibited the increase in lysozyme and albumin outputs produced by PAF, but had no effect on the PD response. None of the tracheal responses to bradykinin was modified by WEB 2086, catalase and SOD, or nedocromil sodium. The secretory and PD hyperresponsiveness to bradykinin caused by PAF was prevented by WEB 2086 and by catalase and SOD. Nedocromil sodium greatly inhibited the lysozyme and albumin hyperresponsiveness but had no effect on the PD response. Thus PAF may release more than one type of radical which have differential effects on serous cells and albumin transport compared with PD; nedocromil sodium may act only against the radical causing the secretory effects.

Twelve posters were presented in the section on Basic Research. They were discussed in a session chaired by Paul Davenport (Gainesville, US) and Marian Kollarik (Boston, US), with each poster presenter first briefly describing his/her poster.