Posterior hypothalamic activation in paroxysmal hemicrania
Article first published online: 17 FEB 2006
Copyright © 2006 American Neurological Association
Annals of Neurology
Volume 59, Issue 3, pages 535–545, March 2006
How to Cite
Matharu, M. S., Cohen, A. S., Frackowiak, R. S. J. and Goadsby, P. J. (2006), Posterior hypothalamic activation in paroxysmal hemicrania. Ann Neurol., 59: 535–545. doi: 10.1002/ana.20763
- Issue published online: 17 FEB 2006
- Article first published online: 17 FEB 2006
- Manuscript Revised: 26 OCT 2005
- Manuscript Accepted: 26 OCT 2005
- Manuscript Received: 29 JUN 2005
- Migraine Trust
- Wellcome Trust
Paroxysmal hemicrania (PH) is a severe, strictly unilateral headache that lasts 2 to 30 minutes, occurs more than five times daily, is associated with trigeminal autonomic symptoms, and is exquisitely responsive to indomethacin. The purpose of the study was to determine the brain structures active in PH.
Seven PH patients were studied using positron emission tomography (PET). Each patient was scanned in three states: (1) acute PH attack–off indomethacin; (2) pain-free–off indomethacin; and (3) pain-free after administration of intramuscular indomethacin 100mg. The scan images were processed and analyzed using SPM99.
The study showed no significant activations during state 1 compared with state 2, but there was relative activation of the pain neuromatrix in both states 1 and 2 compared with state 3. This suggests that there is persistent activation of the pain neuromatrix during acute PH attacks and during interictal pain-free states off indomethacin that is deactivated by the administration of indomethacin. In addition, the untreated PH state was associated with significant activation of the contralateral posterior hypothalamus and contralateral ventral midbrain, which extended over the red nucleus and the substantia nigra.
These activated subcortical structures may play a pivotal role in the pathophysiology of this syndrome. Ann Neurol 2006;59:535–545