Multiple Enhancing Lesions, General
Karen L. Salzman, MD
DIFFERENTIAL DIAGNOSIS
Common
Metastases, Parenchymal
Multiple Sclerosis
Neurocysticercosis
Abscess (Multiple)
Less Common
ADEM
Opportunistic Infection, AIDS
Tuberculosis
Lymphoma, Primary CNS
Neurosarcoid
Glioblastoma Multiforme
Rare but Important
Vasculitis
Lyme Disease
Lymphoma, Intravascular (Angiocentric)
Parasites, Miscellaneous
Susac Syndrome
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
Superficial enhancement is usually vascular or inflammatory
Nodular cortical/subcortical enhancement is characteristic for hematogenous metastases & embolic disease
Ring-enhancing lesions have numerous etiologies: Gliomas (40%), metastases (30%), abscesses (8%), demyelinating disease (6%)
Thick, irregular (“shaggy”) rim-enhancing lesions are usually malignant
DWI MR may help differentiate lesions
Helpful Clues for Common Diagnoses
Metastases, Parenchymal
Discrete enhancing parenchymal masses at gray-white interface
Account for up to 50% of all brain tumors
80% hemispheres, 15% cerebellum, 3% basal ganglia (BG)
Enhancement: Punctate, solid, or ring
Primary tumor often known
Multiple Sclerosis
Multifocal periventricular & callososeptal T2 hyperintensities in a young adult
Active demyelination enhances transiently
Incomplete ring or “horseshoe shaped” enhancement is classic
May be nodular, ring, or semilunar
Neurocysticercosis
Cyst with scolex in convexity subarachnoid spaces is typical
Four stages: Vesicular, colloidal vesicular, granular nodular, nodular calcified
Vesicular: No enhancement typical; may see discrete, eccentric scolex enhancement
Colloidal vesicular: Thick cyst wall enhances; enhancing marginal nodule
Granular nodular: Thickened, retracted cyst; nodular or ring enhancement
Nodular calcified: Small calcified lesion, rare minimal enhancement
Abscess (Multiple)
DWI + & T2 hypointense rim classic
Four stages: Early cerebritis, late cerebritis, early capsule, late capsule
Early cerebritis: No/patchy enhancement
Late cerebritis: Intense but irregular rim enhancement
Early capsule: Well-defined, thin-walled enhancing rim thicker on side near cortex
Late capsule: Cavity collapses, thickened enhancement of capsule especially side near cortex
Septic emboli → multiple lesions
Helpful Clues for Less Common Diagnoses
ADEM
Multifocal T2 hyperintense lesions 1-2 weeks after viral infection or vaccination
Variable patterns of enhancement, incomplete ring classic
May be punctate, ring, or peripheral
Predilection for subcortical white matter
Bilateral, but asymmetric lesions
Opportunistic Infection, AIDS
Toxo: Multiple ring-enhancing lesions with surrounding edema in deep & superficial brain typical
Enhancement: Smooth, nodular or target (central nodule & peripheral rim)
Involves BG & gray-white junctions
Aspergillosis: Hemorrhagic, multifocal, poorly defined, enhancing lesions
Solid or rim enhancement
Tuberculosis
TB meningitis is most frequent manifestation, more common in children
Basilar meningitis & parenchymal lesions highly suggestive of TB
Tuberculomas: Typically parenchymal, supratentorial; solid or ring-enhancing
Lymphoma, Primary CNS
Enhancing lesions in periventricular white matter (WM) or BG
Majority supratentorial but deep gray nuclei are commonly involved
Often involve corpus callosum & extend along ependymal surfaces
Immunocompetent: Strong homogeneous enhancement
Immunocompromised: Peripheral enhancement with central necrosis or homogeneous enhancement
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