Cluster Headache: Oxygen Saturation and End‐Tidal CO 2 During and Without Attack

SYNOPSIS Twenty‐eight cluster headache patients were examined either in emission (n=10), in the interparoxysmal period (“cluster phase”) (n=12), or during spontaneously occurring (n=7), or nitroglycerin provoked (n=7) attacks. Fourteen healthy controls participated in the study. Oxygen saturation (SaO 2 ), end‐tidal CO 2 (PCO 2 ), and respiratory rate (R.R.) were recorded for the controls and the patients during the different phases of cluster headache. Both PCO 2 and SaO 2 tended to be lower during the interparoxysmal period of the cluster phase when compared to the control group or to the remission. During both nitroglycerin‐provoked and spontaneous attacks, PCO 2 and SaO 2 tended to respectively decease and increase, both when compared with the “cluster phase” and with the period immediately prior to attack (“pre‐attack”). Hence the “pre‐attack” state may, on an average, be characterized by a slight hypoxia and a slight hyperventilation. Marked, clinically observable hyperventilation was present only in the occasional cluster headache patient. There was no SaO 2 decrease from the “cluster phase” (inter‐paroxysmal period) to the period immediately preceding the attack (“pre‐attack”), and SaO 2 “dips” preceding an attack were only observed in one cluster headache patient. As demonstrated previously by our group, a considerable lowering of SaO 2 (i.e. partly to £83%) does only exceptionally lead to attack (Zhao et al, 1990). This observation combined with the evidence presented herein may seem to indicate that the slight pre‐attack oxygen desaturation probably is too small to be a symptom‐producing factor in cluster headache ‐ be it in the spontaneously occurring or in the induced attack. Slight O 2 desaturation and hyperventilation may, however, be subtle reflections of an underlying dysfunction in autonomic control systems.