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Stroke. 2004;35:506-507
Published online before print January 22, 2004, doi: 10.1161/01.STR.0000115529.14410.CF
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(Stroke. 2004;35:506.)
© 2004 American Heart Association, Inc.


Original Contributions

Editorial Comment—Can MRI Reliably Detect Hyperacute Intracerebral Hemorrhage? Ask the Medical Student

Italo Linfante, MD, Guest Editor

Neuro Endovascular Surgery Interventional NeuroRadiology, University of Miami Jackson Memorial Hospital, Miami, Florida

Although never formally tested, a CT is required to exclude intracerebral hemorrhage (ICH) in acute stroke prior to thrombolysis. Therefore, centers that use MRI in acute stroke must in addition obtain a CT to safely rule out ICH.

Despite traditional skepticism, MRI is intrinsically able to detect hyperacute ICH. Such capability is based on the magnetic susceptibility effect of deoxyhemoglobin. In ICH, hemoglobin extravasates in an environment with a low O2 concentration, low pH, and high CO2. Because of the Bohr effect, such changes promote the formation of deoxyhemoglobin extending from the periphery of the hematoma toward the center. Deoxyhemoglobin has 4 unpaired electrons and is therefore paramagnetic ({chi} >0). As such, it produces magnetic inhomogeneities that result in local T2* relaxation enhancement. Obviously, the MR contrast of deoxyhemoglobin is highly dependent on the mode of imaging acquisition. For instance, deoxyhemoglobin induced signal loss (darkening) is most pronounced in sequences that are T2* weighted such as conventional gradient echo (GE) and both spin-echo and gradient-echo echo-planar sequences.1

Atlas and Thulborn reported signal loss on long TR/TE, and GE images in a rat model of ICH.2 Distinctive signal loss was present at the earliest imaging time point (1 hour after the induction of the hematoma). Several authors reported clearly detectable changes on T2*-weighted imaging in patients with ICH imaged between 23 minutes and 6 hours after symptom onset.3,4 In 5 patients with ICH imaged within 2 hours after symptom onset, distinctive patterns of hyperacute ICH and absence of signs of ischemic stroke were the hallmark features of this diagnosis. The hyperacute hematoma appears to be composed of 3 distinct areas: (1) center: isointense to hyperintense signal on T2* and T2-weighted imaging; (2) periphery: hypointense (deoxyhemoglobin) mostly on T2*-weighted imaging; (3) rim: hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, representing vasogenic edema encasing the hematoma.4

These preliminary clinical observations were put to test by Fiebach et al.5 This study is a prospective, multicentric, blinded, randomized trial involving 124 patients: 62 patients with ICH and 62 controls. The authors measured sensitivity, specificity, accuracy, positive and negative predictive value of a multisequence MRI protocol in detecting ICH within 6 hours after symptom onset. Twenty-nine patients were imaged within the first 3 hours, 20 within the second hour. Three experienced readers identified ICH with 100% sensitivity and 100% accuracy. In addition, 3 students in the final year of medical school, who did not have formal training in MRI, identify ICH with a sensitivity of 95%.

This landmark article provides level I evidence that MRI can reliably detect ICH within 6 hours after symptom onset.

The data have critical implications for the care of acute stroke patients. Because ICH is a potentially lethal complication of thrombolytic treatment, evidence of prior hemorrhage is an absolute contraindication.6 Evidence of microbleeds on MRI is present in 38% to 66% of patients with primary ICH and in 26% of patients with ischemic stroke. Kidwell et al reported that 12% of 41 patients had microbleeds on MRI obtained pre-thrombolysis that were not visible on CT.7 Fiebach et al also reported that a T2*-weighted sequence identified microbleeds not visible on CT.5 Because all the major thrombolytic trials used CT before thrombolysis, the incidence of microbleeds in this patient population is not known. The data are worrisome since in the NINDS trial 20% of all symptomatic ICH occurred outside the arterial territory of the presenting stroke.8 The article of Fiebach et al provides further evidence that MRI should be "the gold standard" in screening for hematomas and microbleeds prior to thrombolysis.

Magnetic resonance imaging has proven to offer unique information in acute stroke.9 A multisequence MRI protocol is sensitive to early ischemia, can exclude nonstroke diagnosis, can predict the likelihood of hemorrhagic transformation, and can detect the arterial occlusion.9–11 In addition, by imaging the complex blood flow and tissue dynamics of early ischemia, MRI can guide therapeutic decisions based on tissue viability rather than rigid time intervals.9,12 Moreover, ultrafast MRI stroke protocols take only 5 to 20 minutes to perform and by reliably detecting hyperacute ICH, they can now be used as the sole imaging study prior to thombolysis.5,13


*    References
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*References
 
1. Edelman RR, Johnson K, Buxton R, Shoukimas G, Rosen BR, Davis KR, Brady TJ. MR of hemorrhage: a new approach. AJNR. 1986; 7: 751–756.[Abstract]

2. Atlas SW, Thulborn KR. MR detection of hyperacute parenchymal hemorrhage of the brain. AJNR. 1998; 19: 1471–1477.[Abstract]

3. Schellinger PD, Jansen O, Fiebach JB, Hacke W, Sartor K. A standardized MRI stroke protocol: comparison with CT in hyperacute intracerebral hemorrhage. Stroke. 1999; 30: 765–768.[Abstract/Free Full Text]

4. Linfante I, Llinas RH, Caplan LR, Warach S. MRI features of intracerebral hemorrhage within 2 hours from symptom onset. Stroke. 1999; 30: 2263–2267.[Abstract/Free Full Text]

5. Fiebach JB, Schellinger PD, Gass A, Kucinski T, Siebler M, Villringer A, Ölkers P, Hirsch JG, Heiland S, Wilde P, et al, for the Kompetenznetzwerk Schlaganfall B5. Stroke magnetic resonance imaging is accurate in hyperacute intracerebral hemorrhage: a multicenter study on the validity of stroke imaging. Stroke. 2004; 35: 502–506.[Abstract/Free Full Text]

6. The National Institute of Neurological Disorders and Stroke t-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995; 333: 1581–1587.[Abstract/Free Full Text]

7. Kidwell C, Saver J, Villablanca J, et al. Magnetic resonance imaging detection of microbleeds before thrombolysis: an emerging application. Stroke. 2002; 33: 95–98.[Abstract/Free Full Text]

8. NINDS t-PA Stroke Study Group. Intracerebral hemorrhage after intra-venous t-PA for ischemic stroke. Stroke. 1997; 28: 2109–2118.[Abstract/Free Full Text]

9. Baird AE, Warach S. Magnetic resonance imaging of acute stroke. J Cereb Blood Flow Metab. 1998; 18: 583–609.[CrossRef][Medline] [Order article via Infotrieve]

10. Selim M, Fink J, Kumar S, Caplan LR, et al. Predictors of hemorrhagic transformation after intravenous rt-PA: prognostic value of the initial apparent diffusion coefficient and diffusion-weighted lesion volume. Stroke. 2002; 33: 2047–2052.[Abstract/Free Full Text]

11. Linfante I, Llinas RH, Selim M, et al. Clinical and vascular outcome in internal carotid artery versus middle cerebral artery occlusions after intravenous tissue plasminogen activator. Stroke. 2002; 33: 2066–2071.[Abstract/Free Full Text]

12. Kidwell CS, Alger JR, Saver JL. Beyond mismatch: evolving paradigms in imaging the ischemic penumbra with multimodal MRI. Stroke. 2003; 34: 2729–2735.[Abstract/Free Full Text]

13. Sunshine JL, Tarr RW, Lanzieri CF, et al. Hyperacute stroke: ultrafast MR imaging to triage patients before therapy. Radiology. 1999; 212: 352–332.





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