Cluster headache: the ventilatory response to transient hypoxia with pure nitrogen.

To determine whether the carotid body plays a pathogenetic role in cluster headache, 20 cluster headache patients have been studied. Of these, 11 patients were in the interparoxysmal cluster phase, and 9 were in 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 saturation (SaO2) decreased to around 80%. Changes in ventilation (tidal volume, inspiratory minute ventilation (VI), and end-tidal PCO2 (PETCO2)), were analyzed breath-by-breath. Under basal conditions, cluster headache patients had a slightly higher SaO2 and VI when compared to controls. PETCO2 was significantly lower (P < 0.05) during the cluster period as measured by Wilcoxon signed rank test for paired data, and during remission, according to the Student's paired t-test, in comparison with controls. After exposure to N2, no significant difference was found in the rate of reduction of SaO2 between any of the groups. A higher absolute increase in VI, but a relative (%) decrease in VI at moderate hypoxia were measured, the differences between patients and controls being on the border of the level of significance. Chemoreceptor sensitivity of the carotid body, expressed as the slope of a regression curve obtained by plotting the increase in VI against the reduction 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.