CLUSTER HEADACHE - THE VENTILATORY RESPONSE TO TRANSIENT HYPOXIA WITHPURE NITROGEN

To determine whether the carotid body plays a pathogenetic role in clu ster headache, 20 cluster headache patients have been studied. Of thes e, 11 patients were in the interparoxysmal cluster phase, and 9 were i n remission. Comparison was made with healthy subjects matched for sex , age, and smoking habits. Transient hypoxia was induced by inhalation of 1-8 breaths of 100% nitrogen (N2), until the arterial oxygen satur ation (SaO2) decreased to around 80%. Changes in ventilation (tidal vo lume, inspiratory minute ventilation (V(I)), and end-tidal PCO2 (P(ET) CO2)), were analyzed breath-by-breath. Under basal conditions, cluster headache patients had a slightly higher SaO2 and V(I) when compared t o controls. P(ET)CO2 was significantly lower (P < 0.05) during the clu ster period as measured by Wilcoxon signed rank test for paired data, and during remission, according to the Student's paired t-test, in com parison with controls. After exposure to N2, no significant difference was found in the rate of reduction of SaO between any of the groups. A higher absolute increase in V(I), but a relative (%) decrease in V(I ) at moderate hypoxia were measured, the differences between patients and controls being on the border of the level of significance. Chemore ceptor sensitivity of the carotid body, expressed as the slope of a re gression curve obtained by plotting the increase in V(I) against the r eduction in SaO2, showed no statistical difference between the groups. The results do not support the hypothesis of a pathogenetic role for the carotid body in cluster headache.