Cerebral Hyperemia During Spontaneous Cluster Headaches With Excessive Cerebral Vasoconstriction to Hyperoxia
Version of Record online: 20 MAY 2005
Headache: The Journal of Head and Face Pain
Volume 31, Issue 4, pages 222–227, April 1991
How to Cite
Kawamura, J., Meyer, J. S., Terayama, Y. and Weathers, S. (1991), Cerebral Hyperemia During Spontaneous Cluster Headaches With Excessive Cerebral Vasoconstriction to Hyperoxia. Headache: The Journal of Head and Face Pain, 31: 222–227. doi: 10.1111/j.1526-4610.1991.hed3104222.x
- Issue online: 20 MAY 2005
- Version of Record online: 20 MAY 2005
- Accepted for Publication: February 2, 1991.
- Cited By
- cluster headache;
- cerebral blood flow;
Values for local cerebral blood flow (LCBF) were measured in three dimensions utilizing xenon enhanced computerized tomography among patients during spontaneously occurring cluster headaches, during headache-free intervals and immediately after terminating attacks by inhalation of 100% oxygen. Results were compared with values measured among age-matched normal volunteers. LCBF values measured in five cluster patients while headache-free did not differ from similar measures among age-matched normal volunteers. In three patients during attacks of spontaneously occurring cluster headache, LCBF values for temporal cortex, basal ganglia and subcortical white matter were increased. Immediately after terminating attacks of cluster by 100% oxygen inhalation for five minutes, LCBF values for temporal cortex and basal ganglia became significantly decreased below normal values in five patients with spontaneously occurring cluster headache. Prompt relief of head pain by inhalation of 100% oxygen is associated with abolition of the hyperperfusion of both cortical and subcortical brain structures that occurs during spontaneously occurring cluster headaches and is followed by excessive cerebrovascular constriction. It remains to be determined whether the cerebral hyperemia occurring during cluster headaches is causally related to the head pain or is secondary to the pain itself. Rapid termination of head pain by hyperoxia associated with excessive cerebral vasoconstriction suggests that this vascular phenomenon is unique to cluster headache and offers clues to its pathogenesis.