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Role of Diffusion- and Perfusion-Weighted Magnetic Resonance Imaging

David C. Tong, MD; Alessandro Adami, MD; Michael E. Moseley, PhD; Michael P. Marks, MD

Arch Neurol. 2001;58:587-593.

Background  Acute diffusion-weighted (DWI) and perfusion-weighted (PWI) magnetic resonance imaging (MRI) findings may correlate with secondary hemorrhagic transformation (HT) risk in patients with stroke. This information could be of value, particularly in individuals being considered for thrombolytic therapy.

Objective  To determine the relationship between DWI and PWI findings and the risk of secondary HT in patients with acute stroke.

Design  Retrospective case series.

Setting  Academic medical center.

Patients  Twenty-seven patients with acute stroke capable of being evaluated with DWI/PWI 8 hours or less after symptom onset.

Main Outcome Measures  Apparent diffusion coefficient values, perfusion delay measurements, and subsequent MRI or computed tomographic scans detected HT.

Results  The mean ± SD apparent diffusion coefficient of ischemic regions that experienced HT was significantly lower than the overall mean ± SD apparent diffusion coefficient of all ischemic areas analyzed (0.510 ± 0.140 x 10^-3 mm²/s vs 623 ± 0.113 x 10^-3 mm²/s; P = .004). This difference remained significant when comparing the HT-destined ischemic areas with the non-HT–destined areas within the same ischemic lesion (P = .02). Patients receiving recombinant tissue-type plasminogen activator (rt-PA) experienced HT significantly earlier than patients not receiving rt-PA (P = .002). Moreover, a persistent perfusion deficit in the area of subsequent hemorrhage at 3 to 6 hours after the initial MRI scan was identified in significantly more patients who experienced HT than in those who did not (83% vs 30%; P = .03).

Conclusion  Both DWI and PWI scans detect abnormalities that are associated with HT. These findings support a role for MRI in identifying patients who are at increased risk for secondary HT following acute ischemic stroke.

From the Stanford Stroke Center, Palo Alto, Calif (Dr Tong); the Clinica Neurologica, Università di Verona, Verona, Italy (Dr Adami); and the Department of Radiology, Stanford Medical Center, Stanford, Calif (Drs Moseley and Marks).

Reprints: David C. Tong, MD, Stanford Stroke Center, 701 Welch Rd, Suite 325B, Palo Alto, CA 94304 (email: dct{at}stanford.edu).

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