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Internal Medicine

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A 42-year-old male with HIV (initial CD 4= 10, initial viral load -500,000 copies but current CD4 =50, VL <50 on darunavir/ritonavir, tenofovir alafenamide (TAF), emtricitabine started at another clinic 1 month ago) presents with 2 months of apathy, mild memory loss, bilateral hand tremors, but no fever.

Evaluation reveals negative serum IgGs for toxoplasma and CMV and negative RPR and FTA.

LP reveals 20wbc (100% lymphocytes), protein 11mg/dl, glucose 80g/dl) crypt antigen negative. VDRL negative.

MRI shown with dilated ventricles, cortical atrophy, but no other abnormalities.

The most like cause of this patient’s cognitive decline is:

  • HHV-6 encephalitis

  • Progressive multifocal leukoencephalopathy (JC encephalitis)

  • Syphilis

  • HIV encephalopathy

This patient has classic HAND (HIV-associated neurocognitive disease) with mild ventricular enlargement and periventricular enhancement. The triad of cognitive loss (memory, concentration, and executive function), behavioral issues (apathy) and motor abnormalities (tremor) are typical. This patient has HIV encephalopathy. HHV 8 does not cause encephalopathy.

HHV 6 has occasionally been associated with an acute or subacute encephalopathy, but this is uncommon.

JC encephalitis, also known as Progressive Multifocal leukoencephalopathy, usually manifests with multiple focal white matter lesions. A CSF JC PCR would confirm this diagnosis if the clinical history and MRI were compatible.

With negative serum RPR, CNS syphilis is not likely in a patient of this age. The negative CSF VDRL does not, however, rule out neurosyphilis.

The treatment of choice for HIV encephalopathy is antiretroviral therapy (ART).

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