Progressive multifocal leukoencephalopathy in AIDS: are there any MR findings useful to patient management and predictive of patient survival? AIDS Clinical Trials Group, 243 Team

Abstract

Background and purpose: While MR findings in progressive multifocal leukoencephalopathy (PML) have been described previously, usually in retrospective studies with limited sample size, what has not been well addressed is whether any are predictive of longer survival. Our participation in a large prospective clinical trial of AIDS patients with biopsy-proved PML and MR correlation allowed us to test our hypothesis that certain MR features could be found favorable to patient survival.

Methods: The patient cohort derived from a randomized multicenter clinical trial of cytosine arabinoside for PML. Pretreatment T1- and T2-weighted noncontrast images (n = 48) and T1-weighted contrast-enhanced images (n = 45) of 48 HIV-positive patients with a PML tissue diagnosis as well as the follow-up images in 15 patients were reviewed to determine signal abnormalities, lesion location and size, and the presence or absence of mass effect, contrast enhancement, and atrophy, and to ascertain the frequency of these findings. A statistical analysis was performed to determine if any MR abnormalities, either at baseline or at follow-up, were predictive of patient survival.

Results: No MR abnormalities either on univariate or multivariate analysis significantly correlated with patient survival, with the exception of mass effect, which was significantly associated with shorter survival. The mass effect, however, always minimal, was infrequent (five of 48). More severe degrees of cortical atrophy and ventricular dilatation, lesion location and size, and other MR variables were not predictive of outcome.

Conclusion: Except for mass effect, we found no MR findings predictive of the risk of death in patients with PML. The mass effect, however, was so infrequent and minimal that it was not a useful MR prognostic sign.

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.

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).

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.)

fig 5.

PML progression. A–D, Axial T2-weighted images before (3700/150/2) (A and B) and at 4½-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.