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Association of Sustained Oxyhemoglobin Desaturation and Onset of Cluster Headache Attacks
Author(s) -
Kudrow Lee,
Kudrow David B.
Publication year - 1990
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.1526-4610.1990.hed3008474.x
Subject(s) - hypoxemia , cluster headache , anesthesia , medicine , oxygen saturation , peripheral , pulse oximetry , cluster (spacecraft) , cardiology , oxygen , migraine , chemistry , organic chemistry , computer science , programming language
SYNOPSIS Ten episodic cluster headache patients in their active cluster period, ten patients in remission and five control subjects were monitored for minute to minute changes in oxygen saturation (SaO2) and pulse rate before and after nitroglycerin (NTG) administration. A transient but significant decrease in SaO2 and increase in pulse rate of 25 minutes duration occurred following NTG in all groups. These changes may reflect physiologic hemodynamic effects of NTG as a smooth muscle relaxant. Subsequently, SaO2 levels and pulse rate recovered to baseline values in remission and control groups. In contrast, SaO2 values in the active cluster group decreased further and after an extended period culminated in cluster headache attacks in 10/10 patients. Three major changes, therefore, distinguished active cluster patients from remission and control groups. First, the magnitude of oxygen desaturation increased after the physiological effects of NTG ceased. Second, oxygen desaturation was sustained for an additional 9 to 30 minutes duration. Third, the hypoxemic state culminated in attacks in all cases. Our findings suggest that the active cluster period may be characterized by an impaired mechanism to autoregulate, and thus compensate, for hypoxemia. It is further proposed that persistence of hypoxemia and the cluster attack onset may share a common mechanism, coupling the two events. We suggest that abnormal central and/or peripheral chemoreceptor activity may be responsible for these events.