Posterior circulation territory lesions in migraine

We investigated the relationship between migraine and specific structural changes in regions of the posterior circulation territory in a population-based MRI-study of 295 migraineurs and 140 controls. A total of 27 migraineurs (9%) and 2 controls (1.5%; p<0.005) had posterior circulation lesions, including small (silent) pontine and cerebellar infarcts and confluent pontine hyperintensities. Subjects with lesions were significantly older, had higher blood pressures and cholesterol levels. However, after controlling for cardiovascular risk factors, migraineurs remained at 6-fold increased risk, compared to controls, with highest risks for those with migraine with aura. Introduction Migraine is a prevalent, neurovascular disorder: at least 6% of the males and 15% of the females in the adult general population have at least one disabling migraine attack per year. Several studies have demonstrated marked instability of the cerebral blood flow (CBF) between attacks, spreading oligemia (hypoperfusion) during the aura-phase, and both hyperand hypoperfusion during the headache-phase of attacks.’-6 Whether such changes contribute to structural brain damage is unknown, although several studies suggest, that migraine attacks, notably those with aura, may lead to cerebral ischemia or infarction, most frequently in the brain areas supplied by the vertebrobasilar arterial system? We conducted an MRI study to examine the association of migraine and structural brain changes in a population-based sample. In the current report, we show data on prevalence, location and characteristics of lesions in the posterior circulation brain areas. Materials and methods The sample is from the GEM study, which is based on a cohort of 6039 Dutch adults aged 20-60 yrs, including 863 migraineurs, who participated in a population-based study of cardiovascular risk factors5 Migraine was assessed according to IHS criteria6 in a multistage procedure that included a semi-structured clinical interview by telephone. Migraine diagnosis was conducted blind to an individual’s profile of cardiovascular risk factors and disease, which were assessed by interview and clinical exam at the study center. From the cohort aged 30-60 yrs, we randomly selected for MR imaging of the brain, 134 migraineurs without aura (MO), 161 migraineurs with aura (MA) and 140 controls who were frequency matched to the cases by sex, 5-yr age strata and region of residence. Total brain MR images were acquired on a 1.0 T and a 1.5 T system with 48 contiguous 3 mm axial slices. Pulse sequences were comparable between the systems, and included a proton density and T2-weighted FSE and a FLAIR sequence. Blinded to clinical status, a neuroradiologist read all images to identify infarcts and hyperintensities. Infarcts were nonmass parenchymal defects, with a signal intensity approaching that of CSF on all sequences; hyperintensities were bright on all sequences. Brain areas supplied by the vertebrobasilar arterial system were identified according to topographical To estimate the risk (Odds Ratio, OR) for posterior circulation lesion in migraineurs vs. controls, we controlled for demographic and cardiovascular risk factors. Results Of all identified infarcts, the majority was located within the posterior circulation (34 of 60 infarcts; 54%). There were no supratentorial posterior circulation infarcts. Sixteen migraineurs (5.4% of all migraineurs; 13 MA, 3 MO) had 33 cerebellar and 1 pontine infarct; 1 control (0.7%) had 1 cerebellar infarct. Infarcts were always small (2-20 mm diameter), without corresponding clinical signs, and involved, in all but one case, the cerebellar artery border zones. In 1 control and 11 migraineurs (3.7%; 4 MO, 7 MA) we found confluent hyperintense lesions in the pons. These lesions always involved the paramedian central basis pontis. No other structural brain changes were identified in the posterior circulation territories. In total, structural brain changes in the posterior circulation were more prevalent in migraineurs (n=27, 9.2%0) compared to controls (n=2, 1.5%; p<0.005). MA were more affected (n=20, 12.4%) than MO (n=7, 5.2%). As shown in the table, those with posterior circulation lesions were significantly older, and those with pontine hyperintensities had more often hypertension and higher cholesterol levels, compared to those without such lesions. Table No lesion Cerebellar Pontine P Value Characteristics (N=406) (N=17) (N=12) post.circ. infarct hyperint.