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Section XIII. Neurologic Infectious Disease

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by Angi W.

A 57-year-old man who has been treated with a stable regimen

of highly active antiretroviral therapy (HAART) for 6 years is

referred for neurologic evaluation of subacute progressive cog-

nitive decline and personality changes. On examination, no

focal neurologic deficits are identified. Magnetic resonance

imaging of the brain shows faint symmetrical periventricular

white matter T2-signal abnormalities but is otherwise unre-

markable. His most recent CD4 count was normal, and a

plasma HIV RNA viral load is undetectable. Cerebrospinal fluid

(CSF) analysis shows a mildly elevated protein level (58 mg/dL)

and a cell count of 7/μL. What would be the best next step?

a. Polymerase chain reaction (PCR) for CSF JC virus

b. Brain biopsy

c. Measurement of CSF HIV RNA viral load

d. Empirical therapy for suspected central nervous system (CNS)

toxoplasmosis

e. PCR for Epstein-Barr virus

XIII.8. Answer c.

Patients with HIV infection who are receiving HAART can

present with neurologic symptoms with suppressed

peripheral viremia and normal CD4 counts but a discor-

dant elevation in CSF HIV RNA. This phenomenon is

caused by the disparate effects of antiretroviral therapy

between the CNS and the blood compartments, leading to

unchecked infection in the CNS (called CSF viral escape).

Changing the antiretroviral regimen to optimize CNS pen-

etrance usually leads to clinical and radiologic improve-

ment. On the basis of the clinical presentation, imaging

findings, and normal CD4 count, it is unlikely that the

patient has progressive multifocal leukoencephalopathy

or CNS toxoplasmosis.

Author

Angi W.

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