Abstract 116: Migraineurs Are More Susceptible to Infarct Growth in Acute Stroke
Epidemiological data indicate that migraine is an independent stroke risk factor. Recent data suggest that migraine mutations increase brain vulnerability to ischemia via excitatory mechanisms (Circulation 2012; 125:335). Migraine mutant mice developed higher number of ischemic depolarizations and accelerated infarct growth during hyperacute stroke, with worse tissue and neurological outcomes.
Here, we retrospectively assessed acute stroke evolution in patients with a reliably documented migraine history. In a blinded fashion, we analyzed the lesion volume on diffusion-weighted imaging (DWI), and the volume of perfusion defect on perfusion-weighted imaging (PWI) using mean transit time (MTT), from consecutive patients during the years 2003-2012 in the Massachusetts General Hospital stroke database. DWI-PWI mismatch was calculated on spatially co-registered DWI and MTT maps, as a marker for viable tissue at risk for infarction.
A total of 155 stroke patients had reliably documented presence or absence of a migraine history. Stroke patients with a history of migraine were younger and more often female, compared to stroke patients who never suffered from migraine. Migraineurs less frequently had coronary artery disease or diabetes. The frequency of posterior circulation lesions was significantly higher in migraineurs. Otherwise, groups were comparable.
In migraineurs with aura, a larger proportion of the perfusion defect showed DWI changes, resulting in smaller DWI/PWI mismatches. A significantly larger proportion of migraineurs with aura showed no mismatch (i.e., DWI/PWI>0.9), indicating that the entire perfusion defect was already infarcted (Table).
Our data show that a history of migraine, particularly with aura, is associated with accelerated acute infarct growth, consistent with data obtained in migraine mutant mice.
[Table. Diffusion-perfusion mismatch. *p=0.011 migraine vs no migraine, †p=0.002 migraine with aura vs no migraine]
Author Disclosures: K. Eikermann-Haerter: None. K. Park: None. J. Helenius: None. M. Velioglu: None. A. Daneshmand: None. M. Arsava: None. L. Pearlman: None. A. Ross: None. A. Negro: None. C. Ayata: None. H. Ay: None.
This research has received full or partial funding support from the American Heart Association, National Center.
- © 2014 by American Heart Association, Inc.