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CASE 1

40 year old male with history of AIDS, CD4 count of 39

Findings

Periventricular FLAIR signal hyperintensity with associated enhancement

Differential

Primary CNS Lymphoma (EBV)

Toxoplasma encephalitis (T. Gondii)

PML (JC)

HIV Encephalitis (HIV)

CMV Encephalitis (CMV)

Differential

Primary CNS Lymphoma (EBV)

Enhancing lesions with surrounding edema

Multiple lesions 50%

Variable signal on T2; isointense or hypointense on T1

Basal Ganglia, deep white matter

More likely to cross corpus callosum or occur in periventricular areas than toxoplasmosis

Can be > 4cm

Toxoplasma encephalitis (T. Gondii)

PML (JC)

HIV Encephalitis (HIV)

CMV Encephalitis (CMV)

Differential

Primary CNS Lymphoma (EBV)

Toxoplasma encephalitis (T. Gondii)

Thin-walled ring-enhancing lesions, surrounding edema; rarely diffuse encephalitis

Multiple lesions 80%

Usually hyperintense with hypointense rim on T2 (can have decreased signal in central areas from calcium and hemorrhage)

Basal Ganglia, G/W junction; parietal, frontal, thalamus

PML (JC)

HIV Encephalitis (HIV)

CMV Encephalitis (CMV)

Differential

Primary CNS Lymphoma (EBV)

Toxoplasma encephalitis (T. Gondii)

PML (JC)

Multiple areas of demyelination, without contrast-enhancement or edema

Bilateral, asymmetric; hypointense on T1, hyperintense on T2

Can see atypical enhancing lesions with immune reconstitution syndrome

Periventricular and subcortical white matter (rarely grey matter)

HIV Encephalitis (HIV)

CMV Encephalitis (CMV)

Differential

Primary CNS Lymphoma (EBV)

Toxoplasma encephalitis (T. Gondii)

PML (JC)

HIV Encephalitis (HIV)

Indistinct lesions in subcortical white matter

Symmetric; hyperintense on T2

CMV Encephalitis (CMV)

Differential

Primary CNS Lymphoma (EBV)

Toxoplasma encephalitis (T. Gondii)

PML (JC)

HIV Encephalitis (HIV)

CMV Encephalitis (CMV)

Scattered micronodules in the cortex, BG, brain stem, and cerebellum

Large ventricles with periventricular enhancement/hyperintensity on T2

Ring-enhancing lesions with edema

Differential

Primary CNS Lymphoma (EBV)

Ring-enhancing lesions, surrounding edema

Multiple lesions 50%

Variable signal on T2; isointense or hypointense on T1

Basal Ganglia, deep white matter

More likely to cross corpus callosum or occur in periependymal areas than TE

Can be > 4cm

Toxoplasma encephalitis (T. Gondii)

Thin-walled ring-enhancing lesions, surrounding edema; rarely diffuse encephalitis

Multiple lesions 80%

Usually hyperintense with hypointense rim on T2 (can have decreased signal in central areas from calcium and hemorrhage)

Basal Ganglia, G/W junction; parietal, frontal, thalamus

PML (JC)

Multiple areas of demyelination, without contrast-enhancement or edema

Bilateral, asymmetric; hypointense on T1, hyperintense on T2

Can see atypical enhancing lesions with immune reconstitution syndrome

Periventricular and subcortical white matter (rarely grey matter)

HIV Encephalitis (HIV)

Indistinct lesions in subcortical white matter

Symmetric; hyperintense on T2

CMV Encephalitis (CMV)

Scattered micronodules in the cortex, BG, brain stem, and cerebellum; or

Large ventricles with periventricular enhancement/hyperintensity on T2; or

Ring-enhancing lesions with edema

AIDS associated Lymphoma

HIV-associated CNS lymphoma is the second most common mass lesion after toxoplasmosis in patients with AIDS

Occurs in up to 5% of patients

The onset of CNS lymphoma is often more insidious than that of toxoplasmosis

Presenting symptoms may include lethargy, confusion, impaired memory, headache, seizures, or focal weakness

Fever is usually absent

Imaging Considerations

Thallium 201 single photon emission computed tomography (201Tl SPECT)

Increased 201Tl uptake co-localizing with the lesion on MRI is highly specific for primary CNS lymphoma

Positive results need to be confirmed by biopsy of the identified lesion

18-fluorodeoxyglucose positron emission tomography (18FDG-PET) has a predictive value similar to that of SPECT

Chest radiography and an abdominal CT or ultrasound may be of benefit to rule out systemic lymphoma as the underlying cause

Pathology

Prognosis

Survival duration

1 month without treatment

2-5 months with radiotherapy, which is of benefit in more than 75%

16-28 months with radiotherapy and systemic and intrathecal chemotherapy comprising methotrexate, thiotepa, and procarbazine (anecdotal reports)

Use of HAART leads to an increase in CD4+ T cells and increases survival to more than 18 months