What imaging findings distinguish PML in an HIV patient?

• A. Acute hemorrhagic lesions with mass effect.
• B. Enhancing ring lesions with significant edema.
• C. Subacute focal neurological deficits with non-enhancing demyelinating lesions on MRI, often without mass effect.
• D. Isolated diffuse atrophy.

Answer: (C)

In HIV patients, PML is a JC virus–driven demyelinating disease, so the imaging pattern reflects loss of myelin rather than a mass-forming infection. The hallmark is subacute focal deficits with non-enhancing demyelinating lesions in the white matter on MRI, often without mass effect or significant edema. On MRI, you typically see T2/FLAIR hyperintense lesions in the subcortical white matter (often parieto‑occipital and asymmetric), sometimes involving U-fibers, with little or no gadolinium enhancement. This lack of enhancement and edema contrasts with mass lesions like toxoplasmosis or lymphoma, which usually produce ring-enhancing lesions with edema or diffusion-restricted tissue. Diffusion and spectroscopy can vary but the absence of a mass effect and active enhancement is characteristic of PML, reflecting the primarily demyelinating, relatively inflammatory-sparing process in this setting.