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. 2009;301(24):2594-2595 (doi:10.1001/jama.2009.933)JAMATobias
Kurth; Christophe Tzourio
Observation, Not a DiseaseMigraine and Cerebral Infarct-like
Lesions on MRI: An
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areas.Neurology, Other; Radiologic Imaging; Magnetic Resonance
ImagingNeurology; Cerebrovascular Disease; Neuroimaging; Headache;
Migraine;
the same issueRelated Articles published in
. 2009;301(24):2563.JAMAAnn I. Scher et al.Migraine Headache in
Middle Age and Late-Life Brain Infarcts
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Several points should be considered when interpretingthe
findings of the AGES-Reykjavik Study. First, classifica-tion of
migraine and migraine aura was based on relativelybroad,
self-reported measures, limiting comparisons withother studies. The
prevalence of migraine with aura (63%)was substantially higher than
estimates from other popu-
lation-based studies, which raises concerns about
misclas-sification or biased selection processes. The prevalence
ofmigraine with aura in the CAMERA study was also rela-tively high
(55%). However, it would be difficult to ex-plainwhy thesepotential
misclassification biases shouldcausean association between migraine
with aura and infarct-likelesions in prospective data.
Second, the nature of the infarct-like lesions observed onthe
MRI remains elusive. In the study by Scher et al and inthe CAMERA
study, infarct-like lesions were defined as hav-ing a size of at
least 4 mm and being surrounded by an areaof highsignal intensity
on FLAIR (fluid-attenuatedinversion-recovery) images. However,
these criteria were not appliedto lesions in the cerebellum, ie,
the region with higher fre-
quency of infarct-like lesions among patients with mi-graine.
These less specific criteria may increase the diffi-cultyto
distinguish, for example, between infarct-like lesionsand enlarged
perivascular space (ie, the Virchow-Robinspace), which is
particularly problematic in the intratento-rial region because of
reduced image quality due to closeproximities of anatomic
structures. Thus, some lesions mightbe of a different nature and
perhaps of no particular pathol-ogy. Alternatively, if these
lesions are infarcts, the messagewould be alarming, raising
concernsabout the potential long-term consequences of migraine on
brain structure and func-tion. However, such a conclusion does not
fit current con-cepts of the rather benign course of common
migraine on
the brain, particularly in the absence of relevant clinical
cog-nitive or other functional decline.10 In addition, with the
ex-ception of the extremely rare familiar hemiplegic form
ofmigraine that is caused by specific gene mutations, indi-viduals
with migraine do not have cerebellar symptoms.
Third, how does this observation fit with the
establishedassociation between migraine and ischemic stroke?11-14
Sev-eral differences exist when comparing the association be-tween
migraine and silent infarct-like lesions with the asso-ciation
between migraine and ischemic strokes. Clinicallyrelevantstrokes
among patientswithmigraine occur most of-ten in supratentorial
regions and do not cluster in particularlocations in
population-based samples.14 The association be-
tween migraine andischemic stroke is apparent in women andmen,
stronger in younger age, andnot detectable in older agegroups of
most studies.11,13 In addition, specificsubgroups ex-ist in which
the association is particularly strong, includingthose with the
combination of smoking and oral contracep-tive use,12,14 low
cardiovascular risk profile,11,14 or a specificgenetic
polymorphism.15 There is currently littleevidence thatthe
mechanisms leading to infarct-like lesions are similar tothe ones
leading to ischemic strokes, but subgroups may ex-
ist in which mechanisms overlap. Furthermore,migraine
andmigraine aura are heterogeneous disease entities and pri-mary
formsshouldbe distinguished from migrainecaused byother conditions
or diseases.In some patients,arterial wall dis-sections could play
a role in migraine, but cervical artery dis-sections are too rare
to explain increased risk of stroke or si-
lent lesions in the posterior circulation.
13
In summary, the clinical implications of the AGES-Reykjavik
study7 should be interpreted with caution. In theabsence of the
source and the nature of infarct-like lesionsand the absence of
clinical symptoms or consequences, itis premature to conclude that
migraine has hazardous ef-fects on the brain. In this regard, brain
scans among pa-tients with migraine should not be initiated to
detect silentbrain lesions but to rule out rare secondary forms of
mi-graine among those patients with atypical migraine formsor
migraine courses. However, the study raises importantquestions. New
studies examining the association of mi-graine with structural
brain changes and brain functionshould improve understanding of the
associations and per-
haps further unveil migraine-specific mechanisms.
Financial Disclosures:Dr Kurth reported receiving
investigator-initiated researchfunding from McNeil Consumer &
Specialty Pharmaceuticals, Merck, the Na-tional Institutes of
Health, and Wyeth Consumer Healthcare; being a consultantto i3 Drug
Safety and to World Health Information Science Consultants, LLC;
andreceivinghonorariafrom Genzyme, Merck,and Pfizerfor educational
lectures. DrTzourio reported receiving investigator-initiated
research funding from the FrenchNational Research Agency (ANR) and
receiving fees from Sanofi-Synthelabo forparticipationon a data
andsafety monitoringboard andfrom MerckSharp& Dohmefor
participation on a scientific committee.
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