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From the Department of Radiology (T.N.N.), Centre hospitalier de lUniversité de Montréal, Hôpital Notre Dame, Montréal, Québec; and the Department of Neurology (G.R., L.H.S., E.E.S.), Stroke Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Address correspondence and reprint requests to Dr. Eric E. Smith, MGH Stroke Service, VBK 802, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114; e-mail: eesmith{at}partners.org
A 77-year-old man presented with acute dysarthria and right hemiparesis. He was treated with IV tPA, after a head CT excluded hemorrhage, at 2.5 hours. Routine MRI at eight hours revealed an 8.8 cm3 right frontal lesion with mixed T1 hypointensity/isointensity, T2 hyperintensity, increased central apparent diffusion coefficient (ADC), peripheral hypointensity on susceptibility, and nodular peripheral gadolinium enhancement (figure), suggesting hemorrhage. ADC was decreased in the left precentral gyrus, consistent with acute infarction. At 12 hours, the patient developed a left hemipare-sis. Head CT showed the right frontal lesion had increased to 58.7 cm3. Cryoprecipitate and platelets were administered, followed by surgical evacuation of a pathologically confirmed hematoma.
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Differentiation of hyperacute hemorrhage from other MRI lesions relies on the recognition of the peripheral T2 hypointensity and susceptibility effect caused by the early appearance of deoxygenated hemoglobin.1 MRI has been shown to be as sensitive as CT for hyperacute hemorrhage.1 If there is diagnostic uncertainty, however, rapid referral for CT is indicated. We hypothesize that the gadolinium enhancement re-flected ongoing contrast extravasation from ruptured vessels and indicated a propensity to hematoma expansion, which was observed on the follow-up CT.2 Detection of post-thrombolysis hyperacute hemorrhage on MRI should prompt close observation for hematoma expansion.
Footnotes
Disclosure: The authors report no conflicts of interest.
References
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