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E-055 FLAIR hyperintensities on MRI in M2 occlusion
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  1. K Dakay1,
  2. M Jayaraman2,
  3. R McTaggart2,
  4. S Yaghi1,
  5. G Jindal3,
  6. S Cutting1
  1. 1Neurology, Warren Alpert Medical School of Brown University, Providence, RI
  2. 2Diagnostic Imaging, Neurosurgery, Warren Alpert Medical School of Brown University, Providence, RI
  3. 3Diagnostic Imaging, Warren Alpert Medical School of Brown University, Providence, RI

Abstract

Background M2 segment occlusion of the middle cerebral artery is a potentially debilitating cause of stroke, and the data is unclear on the optimal method of treatment for these patients. FLAIR hyperintense vessels (FHV) on MRI have been postulated to be correlated with ischemic penumbra, and we sought to evaluate the incidence of this radiologic finding in patients with M2 occlusion. Additionally, the prognosis of M2 occlusion stroke is unclear, and we studied the incidence of deterioration as well as the incidence of interventional treatment at our center.

Methods We retrospectively reviewed patients admitted to our comprehensive stroke center with an acute ischemic stroke due to occlusion of an M2 branch of the middle cerebral artery who underwent MRI brain during their hospitalization, and analyzed their clinical and imaging features. The M2 segment was defined as distal to the first bifurcating branch. FLAIR hyperintense vessels were defined as a linear hyperintensity present on two or more slices conforming to the location of the middle cerebral artery. Neurologic deterioration was defined as a decline by more than 4 NIHSS points or a sustained new neurologic deficit.

Results A total of 98 patients were treated at our center for M2 occlusion from 2012–2017. 71 patients (72%) received an MRI brain during their hospitalization and were included in this analysis. FLAIR hyperintense vessels were present in a total of 30 (42.3%). 20 patients (28.2%) deteriorated during their stay, and FHV were present in 12/20 of these patients. Of the 51 patients who did not deteriorate, FHV were present in only 17 of them. Patients who deteriorated appeared to be more likely to have FHV than those who did not deteriorate (47% difference, CI 21.4243–63.4427, p = 0.0004). Figure 1 demonstrates the presence of FHV in a patient which resolved after mechanical thrombectomy, supporting the hypothesis that FHV represents the ischemic penumbra.

Abstract E-055 Figure 1

Pre-treatment MRI showed extensive FLAIR hyperintense vessels. Repeat imaging one day after endovascular therapy was artifact-limited, but showed resolution of the FLAIR hyperintense vessels.

Conclusion FHV may be a risk factor for neurologic decline in patients with M2 occlusion, though more data is needed to determine the utility of FHV in assessing risk of neurologic worsening. Our analysis did not take into account differences between treated and untreated patients; prior studies have suggested FHV correlates with ischemic penumbra and may correlate with better collateral circulation. Further studies are needed to correlate FHV with perfusion imaging and outcome adjusted for treatment.

Disclosures K. Dakay: None. M. Jayaraman: None. R. McTaggart: None. S. Yaghi: None. G. Jindal: None. S. Cutting: None.

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