Cerebellar Hypoperfusion in Migraine Attack: Incidence and Significance.

BACKGROUND AND PURPOSE: Patients diagnosed with migraine with aura have an increased lifetime risk of ischemic stroke. It is not yet clear whether prolonged cortical hypoperfusion during an aura increases the immediate risk of cerebellar infarction because it may induce crossed cerebellar diaschisis and subsequent tissue damage. To address this question, we retrospectively analyzed potential relationships between cortical oligemia and cerebellar hypoperfusion in patients with migraine with aura and their potential relation to small infarct-like cerebellar lesions. MATERIALS AND METHODS: One hundred six migraineurs who underwent MR imaging, including DSC perfusion, were included in the study. In patients with apparent perfusion asymmetry, we used ROI analysis encompassing 18 infra- and supratentorial ROIs to account for differences in regional cerebral blood flow and volume. The presence of cerebellar hypoperfusion was calculated using an asymmetry index, with values of >10% being considered significant. RESULTS: We observed perfusion asymmetries in 23/106 patients, 22 in patients with migraine with aura (20.8%). Cerebellar hypoperfusion was observed in 12/23 patients (52.2%), and crossed cerebellar diaschisis, in 9/23 patients (39.1%) with abnormal perfusion. In none of the 106 patients were DWI restrictions observed during migraine with aura. CONCLUSIONS: Cerebellar hypoperfusion and crossed cerebellar diaschisis are common in patients with migraine with aura and cortical perfusion abnormalities. Crossed cerebellar diaschisis in migraine with aura may be considered a benign phenomenon because we observed no association with DWI restriction or manifest cerebellar infarctions, even in patients with prolonged symptom-related perfusion abnormalities persisting for up to 24 hours.

Whole-Brain Susceptibility-Weighted Thrombus Imaging in Stroke: Fragmented Thrombi Predict Worse Outcome.

BACKGROUND AND PURPOSE: The prevalence and clinical importance of primarily fragmented thrombi in patients with acute ischemic stroke remains elusive. Whole-brain SWI was used to detect multiple thrombus fragments, and their clinical significance was analyzed. MATERIALS AND METHODS: Pretreatment SWI was analyzed for the presence of a single intracranial thrombus or multiple intracranial thrombi. Associations with baseline clinical characteristics, complications, and clinical outcome were studied. RESULTS: Single intracranial thrombi were detected in 300 (92.6%), and multiple thrombi, in 24 of 324 patients (7.4%). In 23 patients with multiple thrombi, all thrombus fragments were located in the vascular territory distal to the primary occluding thrombus; in 1 patient, thrombi were found both in the anterior and posterior circulation. Only a minority of thrombus fragments were detected on TOF-MRA, first-pass gadolinium-enhanced MRA, or DSA. Patients with multiple intracranial thrombi presented with more severe symptoms (median NIHSS scores, 15 versus 11; P = .014) and larger ischemic areas (median DWI ASPECTS, 5 versus 7; P = .006); good collaterals, rated on DSA, were fewer than those in patients with a single thrombus (21.1% versus 44.2%, P = .051). The presence of multiple thrombi was a predictor of unfavorable outcome at 3 months (P = .040; OR, 0.251; 95% CI, 0.067-0.939). CONCLUSIONS: Patients with multiple intracranial thrombus fragments constitute a small subgroup of patients with stroke with a worse outcome than patients with single thrombi.