SUMMARY1. To determine the afferent pathways mediating pharyngeal dilator muscle activation in response to negative airway pressure in man, we recorded genioglossus electromyogram (EMG) activity (via intra-oral bipolar surface electrodes) in response to 500 ms duration pressure stimuli of -15 and -25 cmH20 in normal, conscious, supine subjects relaxed at end-expiration; responses were compared before and after upper airway anaesthesia.2. Six rectified and integrated EMG responses were bin averaged for pressure stimuli applied with the glottis open (GO) and closed (GC) and to the outside of the face only (controls). Response magnitude was quantified as the ratio of the EMG activity for an 80 ms post-stimulus period (before the subject's reaction time for tongue protrusion) to an 80 ms pre-stimulus period.3. In eight subjects, upper airway anaesthesia reduced the EMG responses with GC to a level indistinguishable from controls. After anaesthesia, responses with GO remained higher than those with GC.4. With GC, the mean EMG responses decreased by 43 % after selective anaesthesia of the nasal mucosa (trigeminal nerves) in two subjects, 32 % after selective anaesthesia of the laryngeal mucosa (superior laryngeal nerves) in six subjects and by 21 % after selective anaesthesia of the oropharyngeal mucosa (glossopharyngeal and lingual nerves) in four subjects.5. We conclude that upper airway afferents mediate pharyngeal dilator muscle activation in response to negative pressure with GC and that subglottal receptors cause the increased activation with GO. With GC, the trigeminal and superior laryngeal nerves mediate an important component of the responses with the glossopharyngeal nerves playing a less important role.

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709pressure produced as a result of rupture of the aneurysm into the tight fascia1 compartment of the psoas and iliacus muscles. The cause of the sciatic palsy was attributed to direct pressure of a common iliac artery aneurysm impinging on the nerve trunks arising from L.V.4, L.V.5, S.V.1, and S.V.2.It is interesting to speculate on the mechanism of the lateral popliteal palsy recorded in our second case. It seems unlikely that direct pressure on the nerve trunks in the pelvis can be held responsible since the medial popliteal component of the sciatic nerve was not involved. Ischaemic neuropathy is rare since nerves receive a blood-supply from several anastomosing vessels. However, the sciatic nerve is supplied by a named vessel, the arteria comitans nervi ischiadici. It is conceivable that sudden occlusion of this vessel by embolism or thrombosis might result in ischaemic damage of vulnerable nerve-fibres, particularly in a limb already the site of extensive peripheral vascular disease. Although it is possible that the lateral popliteal palsy in our second case arose from some other cause, its development in a limb with extensive peripheral vascular disease shortly before the rupture of an abdominal aortic aneurysm makes it very likely that the neurological signs were related to the arterial disease. It is tempting to suggest that the aneurysm produced the peripheral nerve lesion either via ischaemia or pressure and that the consequent foot-drop caused the fall which precipitated aneurysmal rupture.