Premium
Cluster Headache: The Ventilatory Response to Transient Hypoxia with Pure Nitrogen
Author(s) -
Shen Jie Ming,
Schaanning Jan,
White Linda,
Kruszewski Piotr,
Bjaanes Elisabeth,
Sjaastad Ottar
Publication year - 1993
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.1993.hed3309476.x
Subject(s) - cluster headache , pco2 , carotid body , hypoxia (environmental) , anesthesia , medicine , statistical significance , wilcoxon signed rank test , tidal volume , inhalation , respiratory system , cardiology , oxygen , mann–whitney u test , chemistry , carotid arteries , organic chemistry , migraine
SYNOPSIS 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 (N 2 ), until the arterial oxygen saturation (SaO 2 ) decreased to around 80%. Changes in ventilation (tidal volume, inspiratory minute ventilation (V I ), and end‐tidal PCO 2 (P ET CO 2 )), were analyzed breath‐by‐breath. Under basal conditions, cluster headache patients had a slightly higher SaO 2 and V I when compared to controls. P ET CO 2 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 N 2 , no significant difference was found in the rate of reduction of SaO 2 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. Chemoreceptor sensitivity of the carotid body, expressed as the slope of a regression curve obtained by plotting the increase in V I against the reduction in SaO 2 , 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.