Citation: Goadsby PJ (2006) The Migrainous Brain: What You See Is Not All You Get? PLoS Med3(10): e404. https://doi.org/10.1371/journal.pmed.0030404
Published: October 17, 2006
Copyright: © 2006 Peter J. Goadsby. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The author received no specific funding for this article.
Competing interests: The author has declared that no competing interests exist.
Migraine is an episodic brain disorder  that affects about 15 percent of the population [2,3]. The disorder can be highly disabling , and has been estimated to be the most costly neurological disorder in the European Community, costing more than €27 billion per year .
Two clinical forms are commonly seen: migraine with aura and migraine without aura . Aura in this context is defined as a recurrent disorder manifesting in attacks of reversible focal neurological symptoms, usually developing gradually over a period of five to 20 minutes and lasting for less than 60 minutes. These symptoms are typically visual , and are often described as bright jagged lines (fortification spectra) that move across the visual field, often followed by visual loss (scotoma).
The phenomenon of migraine has been known since antiquity. Now there are new data on anatomical alterations in the visual motion-processing regions. Do these new data shed light on aura, or perhaps illuminate more basic principles about the migrainous brain? Is the traditional view—that the migrainous brain is structurally normal—incorrect?
A New Study of the Visual Motion-Processing Network in Migraine
In a new study published in PLoS Medicine, Granziera and colleagues  used magnetic resonance imaging to perform high-resolution measurements of cortical thickness and diffusion tensor imaging to study the anatomy of the motion-processing network in patients with migraine and in healthy controls. The authors found significant differences between patients and controls in MT+ and V3A, both motion-processing visual cortical regions . These differences were seen both in patients who experienced migraine with aura and patients who experienced migraine without aura.
These data need to be considered in the light of recent structural imaging suggesting, in a study of a random sample of patients with migraine, that those with aura may be particularly at risk for brain lesions on magnetic resonance imaging . The data also need to be seen in the context of no detected change in voxel-based morphometry (a computational approach to neuroanatomy that measures differences in local concentrations of brain tissue) in the brains of patients with migraine . However, voxel-based morphometry is probably not as sensitive as the technique used by Granziera and colleagues in their new study.
The phenomenon of migraine has been known since antiquity.
The authors of the new study suggest that the findings may be used as a biomarker. Certainly the findings will not be useful as diagnostic tools, since they overlap with healthy controls, and it still remains simpler, and indeed the gold standard, to take a history from the patient. Moreover, it will be important to see whether the changes seen in Granziera and colleagues' study occur in other primary headaches.
It does seem likely that the findings relate to migraine given the motion sensitivity of migraineurs  and the very obvious travel sickness that younger migraineurs so often report. Indeed the literature on vertigo in migraine  further colours a landscape that suggests migraineurs have very distinct perceptual motion problems. For the clinician, one could take home the message from this new study that patients with migraine might be expected to present some often curious clinical features of motion sensitivity, and the new data give a strong biological context to an otherwise somewhat soft history.
The Experimental Homologue of the Migraine Aura
Cortical spreading depression (a wave of neuronal and glial depolarisation, followed by long-lasting suppression of neural activity) as described in animals  is likely to be the experimental homologue of the migraine aura. Cortical spreading depression and migraine aura share many features, and recent demonstrations of phenomena similar to cortical spreading depression during aura in patients are convincing .
Do Granziera and colleagues' new data provide more information about aura? The authors believe the changes may have been caused by aura, and by inference suggest that because patients with migraine without aura have the same changes, they have clinically silent aura. An alternative view would be that the inherited basis for migraine is responsible for a developmental change that leads to the structural differences, and has no relationship to aura. Motion sensitivity is as marked in children with migraine as adults with migraine, and there are no longitudinal data examining whether the structural changes progress with time. The authors' silent aura hypothesis would predict increasing change with age, especially with attack frequency, while the alternative trait hypothesis presented here would predict a static defect. More research will provide the answer, and certainly the question is tractable.
Is there more change in the migrainous brain than we have previously thought? I think the new data show that after four millennia, migraine still has many more secrets to be uncovered. A common disorder such as migraine needs extensive and in-depth study. Brain imaging is an important part of that work. For patients and physicians alike, the new data certainly plant migraine firmly in the brain in terms of the fundamental problem and its most crucial manifestations. The neurobiology of migraine is complex and its study rewarding.
- 1. Goadsby PJ, Lipton RB, Ferrari MD (2002) Migraine: Current understanding and treatment. New Engl J Med 346: 257–270.PJ GoadsbyRB LiptonMD Ferrari2002Migraine: Current understanding and treatment.New Engl J Med346257270
- 2. Lipton RB, Stewart WF, Diamond S, Diamond ML, Reed M (2001) Prevalence and burden of migraine in the United States: Data from the American Migraine Study II. Headache 41: 646–657.RB LiptonWF StewartS. DiamondML DiamondM. Reed2001Prevalence and burden of migraine in the United States: Data from the American Migraine Study II.Headache41646657
- 3. Steiner TJ, Scher AI, Stewart WF, Kolodner K, Liberman J, et al. (2003) The prevalence and disability burden of adult migraine in England and their relationships to age, gender and ethnicity. Cephalalgia 23: 519–527.TJ SteinerAI ScherWF StewartK. KolodnerJ. Liberman2003The prevalence and disability burden of adult migraine in England and their relationships to age, gender and ethnicity.Cephalalgia23519527
- 4. Menken M, Munsat TL, Toole JF (2000) The global burden of disease study: Implications for neurology. Arch Neurol 57: 418–420.M. MenkenTL MunsatJF Toole2000The global burden of disease study: Implications for neurology.Arch Neurol57418420
- 5. Andlin-Sobocki P, Jonsson B, Wittchen HU, Olesen J (2005) Cost of disorders of the brain in Europe. Eur J Neurol 12(Suppl 1): 1–27.P. Andlin-SobockiB. JonssonHU WittchenJ. Olesen2005Cost of disorders of the brain in Europe.Eur J Neurol12Suppl 1127
- 6. Headache Classification Committee of The International Headache Society (2004) The international classification of headache disorders. Second edition. Cephalalgia 24(Suppl 1): 1–160.Headache Classification Committee of The International Headache Society2004The international classification of headache disorders. Second edition.Cephalalgia24Suppl 11160
- 7. Russell MB, Iversen HK, Olesen J (1994) Improved description of the migraine aura by a diagnostic aura diary. Cephalalgia 14: 107–117.MB RussellHK IversenJ. Olesen1994Improved description of the migraine aura by a diagnostic aura diary.Cephalalgia14107117
- 8. Granziera C, DaSilva AFM, Snyder J, Tuch DS, Hadjikhani N (2006) Anatomical alterations of the visual motion processing network in migraine with and without aura. PLoS Med 3: e402.C. GranzieraAFM DaSilvaJ. SnyderDS TuchN. Hadjikhani2006Anatomical alterations of the visual motion processing network in migraine with and without aura.PLoS Med3e402DOI: 10.1371/journal.pmed.0030402. DOI: 10.1371/journal.pmed.0030402.
- 9. Tootell RB, Mendola JD, Hadjikhani NK, Ledden PJ, Liu AK, et al. (1997) Functional analysis of V3A and related areas in human visual cortex. J Neurosci 17: 7060–7078.RB TootellJD MendolaNK HadjikhaniPJ LeddenAK Liu1997Functional analysis of V3A and related areas in human visual cortex.J Neurosci1770607078
- 10. Kruit MC, van Buchem MA, Hofman PA, Bakkers JT, Terwindt GM, et al. (2004) Migraine as a risk factor for subclinical brain lesions. JAMA 291: 427–434.MC KruitMA van BuchemPA HofmanJT BakkersGM Terwindt2004Migraine as a risk factor for subclinical brain lesions.JAMA291427434
- 11. Matharu MS, Good CD, May A, Bahra A, Goadsby PJ (2003) No change in the structure of the brain in migraine: A voxel-based morphometric study. Eur J Neurol 10: 53–58.MS MatharuCD GoodA. MayA. BahraPJ Goadsby2003No change in the structure of the brain in migraine: A voxel-based morphometric study.Eur J Neurol105358
- 12. Drummond PD (2002) Motion sickness and migraine: Optokinetic stimulation increases scalp tenderness, pain sensitivity in the fingers and photophobia. Cephalalgia 22: 117–124.PD Drummond2002Motion sickness and migraine: Optokinetic stimulation increases scalp tenderness, pain sensitivity in the fingers and photophobia.Cephalalgia22117124
- 13. Dieterich M, Brandt T (1999) Episodic vertigo related to migraine (90 cases): Vestibular migraine? J Neurol 246: 883–892.M. DieterichT. Brandt1999Episodic vertigo related to migraine (90 cases): Vestibular migraine?J Neurol246883892
- 14. Lauritzen M (1994) Pathophysiology of the migraine aura. The spreading depression theory. Brain 117: 199–210.M. Lauritzen1994Pathophysiology of the migraine aura. The spreading depression theory.Brain117199210
- 15. Hadjikhani N, Sanchez del Rio M, Wu O, Schwartz D, Bakker D, et al. (2001) Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci U S A 98: 4687–4692.1.N. HadjikhaniM. Sanchez del RioO. WuD. SchwartzD. Bakker2001Mechanisms of migraine aura revealed by functional MRI in human visual cortex.Proc Natl Acad Sci U S A9846874692.1