Acute-onset migrainous aura mimicking acute stroke: MR perfusion imaging features

Abstract

Background and purpose: In a very limited number of cases, acute migrainous aura may mimic acute brain infarction. The aim of this study was to recognize patterns of MR perfusion abnormalities in this presentation.

Materials and methods: One thousand eight hundred fifty MR imaging studies performed for the suspicion of acute brain infarction were analyzed retrospectively to detect patients with acute migrainous aura not from stroke. All patients were examined clinically by 2 neurologists and underwent a standard stroke MR imaging protocol, including PWI. Two radiologists reviewed the perfusion maps visually and quantitatively for the presence, distribution, and grade of perfusion abnormalities.

Results: Among 1850 MR imaging studies, 20 (1.08%) patients were found to have acute migrainous aura. Hypoperfusion was found in 14/20 patients (70%) with delayed rMTT and TTP, decreased rCBF, and minimal decrease in rCBV. In contrast to the typical pattern in stroke, perfusion abnormalities were not limited to a single vascular territory but extended to >1. Bilateral hypoperfusion was seen in 3/14 cases. In 11/14 cases, hypoperfusion with a posterior predominance was found. TTP and rMTT were the best maps to depict perfusion changes at visual assessment, but also rCBF maps demonstrated significant hypoperfusion in quantitative analysis. In all patients, clinical and imaging follow-up findings were negative for stroke.

Conclusions: Acute migrainous aura is rare but important in the differential diagnosis among patients with the suspicion of acute brain infarction. Atypical stroke perfusion abnormalities can be seen in these patients.

Fig 1.

Quantitative evaluation of perfusion maps with region-of-interest measurements of the affected and normal side. A, rMTT. B, TTP. C, rCBF, D, rCBV.

Fig 2.

A–F, A 17-year-old male patient with acute onset of aphasia and right-sided paresthesias: DWI findings were negative for ischemic brain infarction initially (A) and during follow-up (F). B–E, PWI demonstrates hypoperfusion in the posterior cerebral and, to a lesser degree, in the middle cerebral vascular territories on the left side—most pronounced in TTP (grade 3) and rMTT (grade 2) maps. rCBF maps demonstrated hypoperfusion grade 2; rCBV maps demonstrated hypoperfusion grade 1. G–J, Follow-up PWI after 24 hours shows complete resolution of hypoperfusion.

Fig 3.

A 24-year-old male patient presenting with acute-onset aphasia, visual reduction, and right-sided paresthesias. Initial PWI (A–D) shows apparent hypoperfusion, best outlined in rMTT (grade 3) and TTP (grade 3). rCBF maps demonstrate hypoperfusion grade 2. In rCBV maps, no visible hypoperfusion is demonstrated. E–H, Follow-up PWI after 24 hours shows complete resolution of hypoperfusion in all maps.

Fig 4.

A 19-year-old female patient presenting with scintillating scotomata and left-sided hemiparesis and hemisensory symptoms. A–D, PWI 100 minutes after the onset of symptoms demonstrates hypoperfusion in the entire right hemisphere, delineated on rMTT (grade 3) and TTP (grade 3), rCBF (grade 2), and rCBV (grade 1). Follow-up PWI after 28 hours and after treatment with IV salicylates (E–H) shows no remaining hypoperfusion.