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Published Online
on October 15, 2009

Stroke. 2009
Published online before print October 15, 2009, doi: 10.1161/STROKEAHA.109.558163
A more recent version of this article appeared on December 1, 2009
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Submitted on May 17, 2009
Revised on August 8, 2009
Accepted on August 28, 2009

Normal Cortical Energy Metabolism in Migrainous Stroke. A 31P-MR Spectroscopy Study

Ursula G. Schulz DPhil*; Andrew M. Blamire PhD; Paul Davies MD; Peter Styles PhD; and Peter M. Rothwell PhD

From the Stroke Prevention Research Unit (U.G.S., P.M.R.), University Department of Clinical Neurology, and MRC Biochemical and Clinical Magnetic Resonance Unit (P.S.), Department of Biochemistry, University of Oxford, John Radcliffe Hospital, Oxford; Newcastle Magnetic Resonance Centre (A.M.B.), Newcastle University, Newcastle, UK; and Department of Neurology (P.D.), Northampton General Hospital NHS Trust, Northampton, United Kingdom.

* To whom correspondence should be addressed. E-mail: ursula.schulz{at}clneuro.ox.ac.uk.

Background and Purpose—Previous 31P–magnetic resonance spectroscopy (31P-MRS) studies have shown that cerebral cortical energy metabolism is abnormal in migraine and that cortical energy reserves decrease with increasing severity and duration of aura. Migrainous infarction is a rare complication of migraine with aura, and its pathophysiology is poorly understood. We used 31P-MRS to determine whether migrainous stroke shows similar interictal abnormalities in cortical energy metabolism as severe, prolonged aura.

Methods—We used 31P-MRS to study patients with a diagnosis of either migrainous infarction or migraine with persistent aura without infarction (aura duration >7 days) according to International Headache Society criteria. We compared clinical presentation and metabolite ratios between patient groups. We also studied healthy controls with no history of migraine.

Results—Patients with persistent aura without infarction had lower phosphocreatine-phosphate (PCr/Pi) ratios (mean±SD, 1.61±0.10) compared with controls (1.94±0.35, P=0.011) and with patients with migrainous stroke (1.96±0.16, P<0.0001). These differences were present in cortical tissue only. In migrainous stroke patients, the metabolite ratios did not differ significantly from those of controls without migraine.

Conclusions—The differences in cortical energy reserves between patients with migrainous stroke and in those with migraine with persistent aura suggest that the pathomechanisms of these conditions differ and that migrainous infarction does not simply represent a particularly severe form of migrainous aura. This finding supports the revised International Headache Society criteria, which now distinguish between migrainous infarction and migraine with persistent aura without infarction.


Key words: MR spectroscopy • migraine with aura • pathophysiology • migraine pathogenesis