Progressive Multifocal Leukoencephalopathy in AIDS: Are There Any MR Findings Useful to Patient Management and Predictive of Patient Survival?
M. Judith Donovan Post
,a,
Constantin Yiannoutsosa,
David Simpsona,
John Boossa,
David B. Clifforda,
Bruce Cohena,
Justin C. McArthura and
Colin D. Hallathe AIDS Clinical Trials Group, 243 Team
a From the Department of Radiology, Section of Neuroradiology, University of Miami School of Medicine/Jackson Memorial Medical Center, Miami (M.J.D.P.); the Harvard School of Public Health, Statistical & Data Analysis Center, AIDS Clinical Trials Group, Boston (C.Y.); the Department of Clinical Neurophysiology, Mount Sinai School of Medicine, New York (D.S.); the Department of Neurology and Laboratory Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven (J.B.); the Department of Neurology, Washington University School of Medicine, St Louis (D.B.C.); the Department of Neurology Northwestern University School of Medicine, Chicago (B.C.); the Departments of Neurology and Epidemiology, Johns Hopkins University, Baltimore (J.McA.); and the Department of Neurology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill (C.D.H.).
View larger version (144K):
[in a new window]
|
FIG 1. Signal characteristics of PML.
A and B, Axial MR studies show low-signal-intensity lesions on T1-weighted (533/25/1) image (A) and hyperintense lesions on T2-weighted (2000/80/1) image (B) in the centrum semiovale bilaterally, subcortical white matter, and corpus callosum. Note the asymmetrical white matter involvement, with the left cerebral hemispheric white matter more severely affected.
| |
View larger version (95K):
[in a new window]
|
FIG 2. Supratentorial and posterior fossa PML.A and B, Axial T2-weighted images (3700/150/2) show involvement of the medulla (arrow, A), right temporal lobe white matter, right thalamus, and right internal and external capsules, with mild cortical atrophy and no mass effect. Note the asymmetrical involvement of PML, with the right cerebral hemisphere affected to a much greater degree than the left. (Note also the maxillary sinus and left mastoid opacification.)
FIG 3. Cerebellar PML. Axial T2-weighted image (2000/80/1) shows bilateral hyperintense lesions in the cerebellar white matter (right greater than left).
| |
View larger version (191K):
[in a new window]
|
FIG 4. Marked progression of PML documented by serial MR studies.
A and B, Axial T2-weighted images (3500/95/1) show the right frontal lobe confluent hyperintense signal abnormalities extending from the periventricular white matter to the subcortical white matter, with much milder white matter involvement in the right parietal lobe and minimal involvement of the left cerebral hemisphere.
C, Axial T1-weighted image (600/15/1) shows corresponding low signal abnormalities in the affected white matter on the right as well as minimal mass effect on cortical sulci.
D–F, Eight weeks later, marked progression of disease is evident with extension and increasing confluence of the right frontal and parietal lobe lesions, corpus callosum involvement, and greater involvement of the left cerebral hemisphere. Also seen is an increase in white matter low signal abnormality on axial T1-weighted image (600/15/1). Patient died 7 days after this study. (Biopsy tract is also evident in the right cerebral hemisphere.)
| |
View larger version (259K):
[in a new window]
|
FIG 5. PML progression.
A–D, Axial T2-weighted images before (3700/150/2) (A and B) and at 4 -month follow-up (2500/96/1) (C and D) show worsening of PML as evidenced by increasing cortical atrophy and ventricular dilatation, as well as by further extension of bilateral white matter disease.
| |
