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Migraines are a common primary headache disorder and can present variably. Typically they consist of debilitating headaches, accompanied by an aura in one-third of patients. Their etiology remains controversial, although changes in cerebral vessel reactivity are involved.
Migraines are broadly divided into those with and those without auras 7.
Migraines without aura usually consist of a headache that lasts 4 to 72 hours that is typically unilateral, moderate to severe and has a pulsating quality. The headache is often associated with photophobia, phonophobia and nausea and is worsened by physical activity 7.
Migraines with aura are usually preceded by focal neurological deficits, although in some individuals the aura can occur concurrently with the headache 7. The neurological deficits can be very varied and last 5 to 60 minutes and eventually fully resolve. They are followed by headache within an hour of onset 7.
In addition to auras and the headache, two other phases may be present: prodrome and postdrome. These may occur hours or even a couple of days before and after the migraine respectively. They typically comprise of one or more of the following: changes in mood, blurred vision, photophobia, phonophobia, fatigue, poor concentration and neck stiffness 7.
The classical explanation describes a headache (due to vasodilation) preceded by neurological symptoms, most classically visual (due to vasoconstriction).
This classic pattern is relatively uncommon accounting for ~10% of the migrainous patients and is unlikely to be an accurate reflection of the pathophysiology involved.
CT is usually unhelpful, except in cases of extensive cortical infarction.
In the vast majority of cases, MRI is normal. In hemiplegic migraines, venous dilatation can be seen on SWI MIP images contralateral to the hemiparesis, although this is not typical 3. Changes in cerebral perfusion have also been described 3.
MRI may demonstrate T2 hyperintensities in the white matter of the centrum semiovale, not dissimilar to small vessel deep white matter ischemic change. These are distinguished predominantly on history, although recent 3 T work 1 suggest that there is increased T2 signal in the cortex overlying white matter abnormalities as well as in the brainstem 1:
- migraine with aura: 8.1%
- migraine without aura: 2.2%
- controls: 0.7%
For MRI appearances consider:
- 1. Rocca M, Ceccarelli A, Falini A et al. Brain Gray Matter Changes in Migraine Patients with T2-Visible Lesions: A 3-T MRI Study. Stroke. 2006;37(7):1765-70. doi:10.1161/01.STR.0000226589.00599.4d - Pubmed
- 2. Kruit MC, Launer LJ, Ferrari MD et-al. Infarcts in the posterior circulation territory in migraine. The population-based MRI CAMERA study. Brain. 2005;128 (9): 2068-77. doi:10.1093/brain/awh542 - Pubmed citation
- 3. Karaarslan E, Ulus S, Kürtüncü M. Susceptibility-weighted imaging in migraine with aura. AJNR Am J Neuroradiol. 2011;32 (1): E5-7. doi:10.3174/ajnr.A1973 - Pubmed citation
- 4. Hamedani AG, Rose KM, Peterlin BL et-al. Migraine and white matter hyperintensities: the ARIC MRI study. Neurology. 2013;81 (15): 1308-13. doi:10.1212/WNL.0b013e3182a8235b - Free text at pubmed - Pubmed citation
- 5. Palm-Meinders IH, Koppen H, Terwindt GM et-al. Structural brain changes in migraine. JAMA. 2012;308 (18): 1889-97. doi:10.1001/jama.2012.14276 - Free text at pubmed - Pubmed citation
- 6. Butteriss DJ, Ramesh V, Birchall D. Serial MRI in a case of familial hemiplegic migraine. Neuroradiology. 45 (5): 300-3. doi:10.1007/s00234-003-0979-z - Pubmed
- 7. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. (2018) Cephalalgia : an international journal of headache. 38 (1): 1-211. doi:10.1177/0333102417738202 - Pubmed. Search the whole classification at