Migraine and Structural Changes in the Brain

Summary and Comment |
September 19, 2013

Migraine and Structural Changes in the Brain

  1. Peter J. Goadsby, MD, PhD, DSc

A meta-analysis finds some evidence of abnormalities, but their clinical relevance remains unclear.

  1. Peter J. Goadsby, MD, PhD, DSc

The authors undertook a systematic review and meta-analysis of structural changes in the brain of migraine patients, focusing on white-matter abnormalities, infarct-like lesions, and volumetric changes in the gray and white matter, using both population- and clinic-based data .

Compared with nonmigraine controls, patients with migraine with aura (but not those with migraine without aura) had a significant but modestly increased appearance of white-matter abnormalities (odds ratio, 1.68; 95% confidence interval, 1.07–2.65). Infarct-like lesions were significantly more common in migraine-with-aura patients than in migraine-without-aura patients (OR, 1.44; 95% CI, 1.02–2.03) but were no more common in either group than in controls. The data suggest a pattern of brain volume loss in migraineurs involving the bilateral insula and frontal/prefrontal, temporal, parietal, and occipital cortices, the anterior cingulate cortex, basal ganglia, and cerebellum. Migraineurs also had volume gain in the dorsolateral pons and periaqueductal gray matter.


These valuable data present some very challenging issues from a pathophysiological perspective. First, there is much good news. Migraine-without-aura patients are not at any important risk for either white-matter abnormalities or infarct-like lesions. Moreover, prospective studies show no cognitive penalty for migraine or for these MRI changes (BMJ 2011; 342:c7357; Cephalalgia 2011; 31:1291; and JAMA 2012; 308:1889). Physicians can thus continue with current practice recommendations that, in patients with migraine and a normal examination, no imaging is required. The infarct-like lesions remain an issue; given that they are no more common in migraine with or without aura than in controls, migraine itself is, arguably, no reason to image. Rather, any concern regarding cerebrovascular disease should be dealt with on its own merits. The volumetric changes, as the authors say, are a research tool. They reinforce the major physiology-related question the review exposes: Are structural brain changes part of the migraine condition (i.e., static and associated with the disorder) or are they a consequence (i.e., progressive in some way with disorder activity), and would that have management implications? As there is no cognitive or other penalty for migraine, and the abnormalities seem static, with the caveat that much more longitudinal data are needed, perhaps the findings simply mark the inheritance of migraine. Resolving this question is hugely important and will require a well-funded, large-scale, population-based imaging study. Perhaps this can be one of the goals of the new large-scale NIH brain-imaging project. To understand what happens with time to the human brain in health and disease would be a wonderful legacy for the next generation.

Editor Disclosures at Time of Publication

  • Disclosures for Peter J. Goadsby, MD, PhD, DSc at time of publication Consultant / Advisory board AstraZeneca; Allergan; ATI; Boeringher-Ingelheim; Boston Scientific; Bristol-Myers Squibb; Coherix; Colucid; Eli-Lilly; MAP Pharmaceuticals; Medtronic; Merck Sharp & Dohme; Neuralieve; Neuraxon; Neuro Therapeutics Pharma; Pfizer Speaker's bureau Allergan; Merck Sharp & Dohme Grant / research support Boston Scientific; GlaxoSmithKline; MAP Pharmaceuticals; Merck Sharp & Dohme; Neuralieve; U.S. Department of Defense Royalties American Headache Society; MedicoLegal Leadership positions in professional societies American Headache Society (Board Member); International Headache Society (President)


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