Migraine

Migraines are common, consisting of often debilitating headaches, accompanied by an aura in one-third of patients. Their aetiology remains controversial, although changes in cerebral vessel reactivity are involved.

The classical explanation 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 only 10% or so of the migrainous population and is unlikely to be an accurate reflection of the pathophysiology involved. 

Radiographic features

CT

CT is usually unhelpful, except in cases of extensive cortical infarction.

MRI

In the vast majority of cases, MRI is normal. Sometimes, venous dilatation can be seen on SWI MIP images (Case 1) although this is not typical.

MRI may demonstrate T2 T2 hyperintensities in the white matter of the centrum semiovale, not dissimilar to small vessel deep white matter ischaemic change. These are distinguished predominantly on history, although recent 3T work (Rocca 2006) suggest that there is increased T2 signal in the cortex overlying white matter abnormalities as well as in the brain stem ¹.

In some cases foci of cerebellar infarction, usually in the posterior cerebral artery territory, develop. This is most frequently seen in patients with severe and frequent migraines with aura. In one study (Kruit 2005) the prevalence of MRI detected infarcts was ²:

• migraine with aura: 8.1%
• migraine without aura: 2.2%
• controls: 0.7%

Differential diagnosis

For MRI appearances consider

• chronic small vessel deep white matter ischaemic change
• multiple sclerosis / demyelination
• cerebral vasculitis