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We describe in six men, recurrent episodes recurring over months or years, of sudden, brief complete obstruction to respiration followed by dyspnoea with loud inspiratory stridor lasting two to five minutes. Attacks occurred during wakefulness and/or sleep. In one patient an episode was witnessed endoscopically: the initial obstruction was seen to be caused by complete laryngeal closure. The false vocal cords then opened, but the vocal cords remained adducted and caused inspiratory stridor. The similarity of the attacks described by the other patients suggests that they were all caused by laryngeal closure. Furthermore, they could simulate the episodes by voluntarily adducting their vocal cords. The symptoms were usually preceded by a sensation of throat irritation and in four cases symptoms of upper respiratory infection were present. Associated features present in some of the patients included post-nasal discharge, snoring, sleep apnoea and gastro-oesophageal reflux. None was hypocalcaemic. Although stimulation of laryngeal receptors is known to produce reflex laryngeal closure, cough is the usual response during wakefulness. Treatment aimed at reducing upper airway irritation and voluntary inhibition of coughing appeared successful in reducing the incidence and severity of the episodes. Recognition of the condition is important as it may be confused with other causes of acute dyspnoea and it appears to respond to specific management.

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In a two year period 44 endobronchial resections using the Neodymium-YAG laser have been performed in 28 patients. The majority of cases had either bronchogenic carcinoma (57%) or metastatic carcinoma (18%) involving the bronchial tree. Adenoid cystic carcinoma, benign tumours, lymphoma, tracheal papillomatosis, Wegener's granulomatosis and benign stricture comprised the other cases. Rigid bronchoscopy and general anaesthesia were used in the majority. Symptomatic improvement of dyspnoea when relief of bronchial obstruction occurred was marked in ten of 17 cases, moderate in four and absent in three. Haemoptysis was markedly improved in two of three cases and obstructive pneumonitis resolved in one of two cases. Significant respiratory function improvement was observed in Raw (most sensitive), FEV11, FVC and TLC. Laser treatment restored the lumen to normal calibre in 52% (including all patients with tracheal lesions), to greater than half normal in 28% and to less than half normal in 20% of cases. Re-expansion of a collapsed lung or lobe occurred in seven of eight patients. In six of these patients laser treatment was the initial therapy resulting in immediate re-expansion and symptomatic relief prior to further therapy. In patients with bronchogenic carcinoma the mean time to retreatment or death was 72 days. For metastatic carcinoma this was 60 days. Two early deaths (3 hours, 36 hours) due to respiratory failure occurred in patients with very severe bilateral bronchial obstruction too advanced for effective clearance. Other complications included laryngeal oedema requiring prolonged intubation (1), bronchospasm (1), atrial fibrillation (1), and acute pulmonary oedema (1). Laser treatment provides effective palliation for bronchial obstruction and haemoptysis in selected proximal endobronchial cancers.