Acute-Onset Migrainous Aura Mimicking Acute Stroke: MR Perfusion Imaging Features

Discussion

A subset of migraine attacks may manifest with acute neurologic symptoms (ie, aura) that can also be found in acute stroke.¹ These symptoms occur before the migrainous headache. Cases with predominantly motor symptoms are also referred to as “hemiplegic migraine.”²⁵ According to the International Headache Society,⁴ these forms are diagnosed clinically by accurate patient history and neurologic examination. However, substantial problems may arise in the acute phase because accurate information is often incomplete or difficult to obtain.³ Distinguishing between migrainous aura, cerebral ischemia, and Todd paralysis following a seizure may be difficult. In our series, no one had a previous history of migraine with acute neurologic deficits. Thus, a certain dilemma arises because an accurate differential diagnosis is mandatory for correct treatment.

Stroke MR imaging has demonstrated its clinical importance in the work-up of acute brain infarction.^7,26 Perfusion abnormalities in acute brain infarction usually comprise hypoperfusion in a defined (mostly single) vascular territory.¹¹

There are reports that certain perfusion abnormalities may be found in migraine by using PWI; however, these are limited to case studies.^17⇓–19

Since 2005, we have examined all patients with acute stroke who are potentially candidates for thrombolysis or mechanical intervention, primarily with stroke MR imaging. From 1850 consecutive patients with acute stroke symptoms, 20 patients with migraine that mimicked acute stroke (1.08% of all patients) were found. In the case of standard unenhanced CT, these patients would probably have been treated with systemic thrombolysis, which is risky and delays specific antimigrainous treatment.

Perfusion abnormalities were found in 70% (14/20 patients). That implies that—if migrainous aura is present—perfusion abnormalities are frequent. In each case, the perfusion abnormality was detected by visual evaluation, which was performed in the first step of the study evaluation. Subsequent quantitative analysis did not reveal any further cases with significant perfusion abnormalities. This finding demonstrates that visual assessment, which is usually performed in the acute setting, also seems to be adequate to show migraine-associated perfusion abnormalities. Quantitative assessment—which takes additional time—does not seem to be mandatory in the acute setting.

Of these 14 cases showing perfusion abnormalities, increased perfusion was not seen in any. In our opinion, this was due to the fact that all patients were examined in the stage of migrainous aura, where neurologic deficits—but not headache—were the dominant symptom. Even in 1 patient with a prolonged symptom history for 3 days, no headache was present, similar to findings in other reports.¹⁶ Some published studies report hyperperfusion; however, this is during the headache stage, 6–24 hours after the onset of symptoms.^{2,17,19⇓–21,24} Others report hypoperfusion during the migrainous aura.^{2,14,18,22,23,27}

These findings emphasize that early MR imaging examination is crucial to detect the perfusion abnormalities. This correlates with the presumed pathogenesis of migraine, which includes a combination of vascular and neuronal factors.^28,29 The finding of occipital predominance of vasoconstriction during the aura is supported by our data because we found a posterior predominance of hypoperfusion (71.4%).

The striking point is that in all cases, >1 vascular territory was affected, which holds the greatest potential to differentiate migraine from stroke, where hypoperfusion is usually limited to a single vascular territory. In 4 of 14 patients (28.6%), the entire hemisphere was hypoperfused. A possible differential diagnosis for this pattern of hypoperfusion is severe stenosis of the extracranial vessels. However, this can be ruled out by MRA of the extracranial vessels.

Concerning the 4 PWI maps, we found that quantitative evaluation of the perfusion abnormalities was not much more striking than visual inspection. In the visual assessment, TTP was significantly superior, followed by rMTT (Table 2). TTP and rMTT were positive for hypoperfusion in all positive cases except 1, in which only subtle findings (grade 1) were seen in TTP, with the other maps having negative findings. Notably, all except 1 of the cases positive for hypoperfusion also showed changes in rCBF.^21,27 On quantitative analysis, rCBF demonstrated the most pronounced changes, followed by rMTT and TTP. The Spearman correlation test revealed significant correlation for TTP, rMTT, and rCBF between visual and quantitative analysis, except for rCBV. This may be due to the color-coding of the lookup table in combination with window and center settings that we use that encode the rCBF map predominantly with dark colors, blue and black. However, the quantitative results can be better appreciated if the rCBF images are windowed and centered with extremely narrow values. Of course, in the acute clinical setting, visual evaluation is used first because it is the fastest approach (“time is brain”). In cases of doubt, however, additional quantitative evaluation with calculation of ratios in the different maps between the affected and the normal hemisphere may be performed.

In all patients, clinical follow-up was available. All showed complete resolution of the symptoms, spontaneously or after treatment with analgesics. MR imaging follow-up was performed in 14/20 patients (70%) and showed complete resolution of hypoperfusion in all cases.

A limitation of this study is its retrospective design, describing only patterns of perfusion anomalies. Sensitivities or specificities cannot be provided and must be the topic of further research. PWI in patients with migraine during headache will be a topic of further research in a prospective setting. The comparison of visual-versus-quantitative assessment of PWI also warrants further research.