From the Swedish Headache Center, Seattle, WA, USA (Drs. Aurora, Barrodale, and Ms. Tipton); Neurosicence Division, Advanced Bionics, Valencia, CA, USA (Dr. Khodavirdi).
Brainstem Dysfunction in Chronic Migraine as Evidenced by Neurophysiological and Positron Emission Tomography Studies*
Article first published online: 7 JUN 2007
Headache: The Journal of Head and Face Pain
Volume 47, Issue 7, pages 996–1003, July/August 2007
How to Cite
Aurora, S. K., Barrodale, P. M., Tipton, R. L. and Khodavirdi, A. (2007), Brainstem Dysfunction in Chronic Migraine as Evidenced by Neurophysiological and Positron Emission Tomography Studies. Headache: The Journal of Head and Face Pain, 47: 996–1003. doi: 10.1111/j.1526-4610.2007.00853.x
This article is the winner of the 2007 Harold G. Wolff Award.
- Issue published online: 7 JUN 2007
- Article first published online: 7 JUN 2007
- Accepted for publication April 19, 2007.
- chronic migraine;
- positron emission testing;
- transcranial magnetic stimulation
Background.—The pathophysiology of chronic migraine (CM) is not fully understood. We aimed to examine transcranial magnetic stimulation (TMS) indices of cortical excitability in patients with CM and also performed PET studies to ascertain if there were any areas of activation and inhibition for possible correlation.
Methods.—Excitability of the cortex was assessed by a reliable parameter of magnetic suppression of perceptual accuracy (MSPA) profiles using transcranial magnetic stimulation in 25 patients with CM. Of these 10 patients were also studied with (18F-FDG PET) scans.
Results.—MSPA demonstrated decreased inhibition in CM compared to normal controls and episodic migraine. The percentage of letters reported correct at 100 ms was 84.37 for CM compared to 19.14 for normal controls and 57.41 for episodic migraine. The PET evaluation in 10 subjects demonstrated increased cerebral metabolism in areas of in the brainstem compared to the global flow. There were also decreased areas of cerebral metabolism in the medial frontal and parietal as well as the somatosensory cortex.
Conclusions.—Patients with CM appear to be characterized by reduced visual suppression correlating with high cortical excitability. In a cohort of these subjects there was brainstem activation and inhibition in certain areas of the cortex suggesting a potential dysfunction in the inhibitory pathways.