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First published on May 23, 2007
This version was published on July 1, 2007
Neuro Oncol 2007 9(3):373-377; DOI:10.1215/15228517-2007-015
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Case Studies

Diffusion and perfusion imaging in subacute neurotoxicity following high-dose intravenous methotrexate

April F. Eichler, Tracy T. Batchelor and John W. Henson

Pappas Center for Neuro-Oncology (A.F.E., T.T.B., J.W.H), Neurology Service (A.F.E., T.T.B., J.W.H.), Division of Neuroradiology (J.W.H.), and Department of Radiology (J.W.H.), Massachusetts General Hospital, Boston, MA 02114; and Harvard Medical School, Boston, MA 02115 (A.F.E., T.T.B., J.W.H.); USA

Address correspondence to John W. Henson, Pappas Center for Neuro-Oncology, 55 Fruit Street, Yawkey 9E, Boston, MA 02114, USA (henson{at}helix.mgh.harvard.edu).

Methotrexate (MTX) is a widely used chemotherapeutic agent that can cause acute, subacute, and chronic neurological complications. Subacute MTX neurotoxicity is manifest by abrupt onset of focal cerebral dysfunction occurring days to weeks after MTX administration, usually in children. We describe the neuroimaging features of an adult patient with primary CNS lymphoma who presented with transient aphasia and right hemiparesis 12 days after receiving intravenous high-dose MTX (8 g/m2) chemotherapy. Imaging within 1 h of symptom onset showed bilateral symmetrical restricted diffusion involving white matter of the cerebral hemispheres. CT angiogram and dynamic susceptibility MRI showed no evidence of vasospasm or perfusion defect. MRI five days later showed near-complete resolution of the abnormalities. MRI 31/2 months later showed normal diffusion but new hyperintense T2-weighted signal changes in the subcortical white matter corresponding to previous areas of restricted diffusion. The absence of vascular or perfusion abnormalities suggests that transient cytotoxic edema in white matter may explain the syndrome of subacute MTX neurotoxicity.

Key Words: adult • diffusion • methotrexate • neurotoxicity







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Copyright 2007 by Society for Neuro-Oncology