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Brainstem Dysfunction in Chronic Migraine as Evidenced by Neurophysiological and Positron Emission Tomography Studies *
Author(s) -
Aurora Sheena K.,
Barrodale Patricia M.,
Tipton Reda L.,
Khodavirdi Ani
Publication year - 2007
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.1526-4610.2007.00853.x
Subject(s) - transcranial magnetic stimulation , migraine , brainstem , somatosensory system , positron emission tomography , pathophysiology , medicine , chronic migraine , neuroscience , cortex (anatomy) , cerebral cortex , stimulation , psychology
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 ( 18 F‐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.