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Fig. 1.— Overview of the evaluation of chronic cough in an adult. ACE-I: angiotensin converting enzyme inhibitor; PEF: peak expiratory flow; PNDS: post-nasal drip syndrome; GORD: gastro-oesophageal reflux disease. Fig. 2.— Therapeutic algorithm. ACE: angiotensin-converting enzyme; GORD: gastro-oesophageal reflux disease. Fig. 3.— Investigational algorithm. CT: computed tomography. Fig. 4.— Diagnostic algorithm for the approach to children with chronic cough. ENT: ear, nose and throat; PFT: pulmonary function testing; BAL: bronchoalveolar lavage; CT: computed tomography; tbc: total blood count; CMV: cytomegalovirus; PCR: polymerase chain reaction; MRI: magnetic resonance imaging; NO: nitric oxide; BHR: bronchial hyperresponsiveness. CONTENTS Chronic cough, here defined as a cough of >8 weeks duration, is a common and frequently debilitating symptom 1, 2 that is often viewed as an intractable problem. However, theexperience of specialist cough clinics is that a very high success rate, in the order of 90%, can be achieved (table 1⇓) 3–15. The key to successful management is to establish a diagnosis and to treat the cause of cough. Truly idiopathic cough is rare and misdiagnosis common, particularly because of the failure to recognise that cough is often provoked from sites outside the airway. These guidelines aim to distil the lessons from these reports and provide a framework for a logical care pathway for patients with this highly disabling symptom. View this table: Table 1— Commonest causes of chronic cough in patients investigated in specialist clinics There are three common causes of chronic cough that arise from three different anatomical areas. This varied presentation explains the major reason for the success of multidisciplinary cough clinics compared with general clinics 16. As asthma, reflux and rhinitis are the realms of different specialists who have little experience in the diagnosis of conditions outside their expertise, a patient with chronic cough may not undergo full evaluation. This problem is exacerbated by the frequently atypical presentation of …

International audience; Cough is defensive airway reflex subjected to a high degree of cortical control. Not surprisingly, all cough motor patterns can be mimicked and reflex cough be inhibited up to complete suppression, at least to a certain extent. Reflex cough differentiates from other airway reflex responses for its characteristic 3-phase motor pattern, and such pattern is maintained when coughing is produced voluntarily. Despite these and some other similarities, voluntary and reflex cough differ in many important respects, suggesting different neural control of the respiratory and non-respiratory musculature implicated in the generation of the cough modalities. This paper focuses the motor features that differentiate voluntary and reflex cough efforts, and highlights the importance of functional assessment of coughing in the diagnostic workup of respiratory and extra-respiratory diseases affecting the production of voluntary and reflex cough.

The panel considered the different types of cough in terms of basic mechanisms and clinical manifestations; both experimentally and clinically cough could occur in single efforts and as 'bouts' or 'epochs'. There were different definitions of cough but, provided the definition used was clear, this did not seem to be a major concern. The methods available for determining the nature or type of clinical cough were discussed, in particular automated cough counting in the clinic and more sophisticated methods available in the laboratory. With regard to semantics, there has been great variation in the names used; this applies to nervous sensors for cough, to cough reflexes and epochs, to clinical names for cough, and to cough sounds. Some simplification and uniformity of nomenclature seemed desirable although, provided the use of a name was clear, little confusion probably existed. The panel felt that the cough nomenclature would evolve with time and would prove to be useful for investigators, clinicians and coughers.

1 The effects of exposure of the ferret trachea in vitro to platelet activating factor (PAF) were examined on methacholine-induced smooth muscle contraction, mucus volume and lysozyme outputs, and albumin transport across the tracheal epithelium. 2 Methacholine (0.1–30 μm) produced concentration-dependent increases in tracheal smooth muscle tone and mucus volume, lysozyme and albumin outputs from the trachea. 3 The concentration-response curves for methacholine-induced smooth muscle contraction, mucus volume and lysozyme outputs were all shifted upwards after exposure of the trachea to PAF (1 μm) with a significant increase in maximum response for each variable. The EC50 values for methacholine-induced smooth muscle contraction and mucus volume output were significantly reduced after PAF exposure suggesting an increase in the potency of methacholine. The concentration-response curve for methacholine-induced albumin output was shifted downwards after PAF exposure with a greatly reduced maximum but no change in the EC50 for methacholine. 4 PAF-induced hyperresponsiveness of methacholine-induced smooth muscle contraction, mucus volume and lysozyme outputs was not affected by indomethacin, FPL55712, or mepyramine and cimetidine, but was prevented by catalase and superoxide dismutase (SOD), and by WEB2086. Similarly, PAF-induced inhibition of methacholine-stimulated albumin output was prevented by catalase and SOD, and by WEB2086. 5 We conclude that PAF induces hyperresponsiveness of ferret tracheal smooth muscle and submucosal gland secretion (including lysozyme secretion from serous cells) to methacholine. This hyperresponsiveness is probably produced by receptor-mediated release of oxygen free-radicals. The inhibition of methacholine-induced albumin flux suggests a loss of epithelial function which is also probably mediated by release of free-radicals. The mechanism by which the free-radicals produce the changes in responsiveness to methacholine, and the cellular source of the free-radicals, remain to be established.

1. The effects of asphyxia, hypoxia, hypercapnia, stimulation of peripheral chemoreceptors, pneumothorax and breathing through resistances have been investigated on laryngeal resistance to airflow in anaesthetized cats, with and without bilateral vagotomy below the origin of the recurrent laryngeal nerves. 2. Resistance to airflow of the innervated larynx was usually measured with the larynx isolated in situ with constant flow from the trachea to a pharyngeal opening, and expressed by the relationship between translaryngeal pressure and airflow. 3. Asphyxia, hypoxia and hypercapnia each stimulated breathing and decreased laryngeal resistance to airflow, in both the inspiratory and expiratory phases. After vagotomy the effect was reduced, abolished or (usually) reversed to a laryngeal constriction, especially in expiration. 4. Intra-arterial injections of potassium cyanide (to stimulate carotid body chemoreceptors) caused a short apnoea or an augmented breath followed by hyperpnoea, concurrently with expiratory constrictions of the larynx. The responses were usually stronger after bilateral vagotomy. 5. Pneumothorax caused tachypnoea, inspiratory dilatations and expiratory constrictions of the larynx. The responses were abolished by vagotomy. 6. Imposition of respiratory resistances dilated the larynx, in inspiration and expiration, while complete closure of trachea caused expiratory constrictions of the larynx. These changes did not depend on intact vagal pathways. 7. The results are discussed in terms of nervous control of the larynx in the different conditions.