Meningeal carcinomatosis

Lymphomatous meningitis

Tuberculosis meningitis

Leukemia

Neurosarcoid

Fungal diseases

Tuberculosis meningitis

Fungal diseases

Neurosarcoid

Pyogenic meningitis

Lymphoma

Neurosyphilis

Clinical-laboratory (not imaging) diagnosis

Imaging may be normal early (FLAIR helpful)

Use imaging to detect complications (e.g., ventriculitis, hydrocephalus, subdural empyema, cerebritis/abscess, secondary ischemia, dural venous thrombosis)

CNS neoplasms (e.g., GBM, medulloblastoma, pineal tumors, choroid plexus tumors), extra-CNS primary tumors (breast, lung, melanoma common)

Look for other lesions (parenchyma, bone)

Involvement of leptomeninges or dura, more commonly in secondary lymphoma

Often affects both brain, spine

Cysts often in deep sulci, may incite intense inflammatory reaction

Cisternal NCC may appear racemose (multilobulated, grape-like), typically lacks scolex

Cisterns > parenchyma > ventricles

Best diagnostic clue: Cyst with “dot” (scolex) inside

Most common presentation of active CNS TB

Predilection for basal cisterns

Complications: Hydrocephalus, ischemia common

Look for extracerebral TB (pulmonary)

TB often mimics other diseases like neoplasm

Dural, leptomeningeal > > parenchymal disease

Lacy leptomeningeal enhancement typical

Look for infundibular stalk involvement

CXR may be helpful to assess for hilar/paratracheal lymphadenopathy (most have systemic disease)

Atrophy of affected hemisphere

Pial angioma enhances

Ipsilateral choroid plexus often enlarged

Abnormally prominent medullary (deep white matter), ependymal veins

Coccidioidomycosis, cryptococcus often basilar

T2* GRE: Hypointense hemosiderin deposition in 70-75% of patients with prior SAH

Meningeal involvement in AIDS (HIV or opportunistic infection > tumor)

Meningeal disease, usually with acute lymphoblastic leukemia (ALL)

Multiple lesions at multiple sites are suggestive of diagnosis

Giant or multiple cutaneous melanocytic nevi (GCMN) and

Benign, malignant CNS melanotic lesions occur

Foci of T1 hyperintensity (parenchymal melanosis) in amygdala or cerebellum

Diffuse/focal pial enhancement; may extend into parenchyma via perivascular spaces

Pre-contrast T1WI sulci/cisterns may be normal, iso-, or hyperintense

Neurofibromatosis found in ½ of patients (particularly NF2)

Rare, hamartomatous cortical/leptomeningeal malformation

Best diagnostic clue: Cortical mass with Ca++ (with or without cysts)

Increased signal in CSF on T1WI and FLAIR

Dialysis-dependent patient with end-stage renal disease

Contrast overload