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Case Reports
. 2021 Oct 5;13(10):e18494.
doi: 10.7759/cureus.18494. eCollection 2021 Oct.

HIV Encephalopathy Mimicking Acute Demyelinating Processes

Affiliations
Case Reports

HIV Encephalopathy Mimicking Acute Demyelinating Processes

Wasey Ali Yadullahi Mir et al. Cureus. .

Abstract

Human immunodeficiency virus (HIV) encephalopathy lies in the severe spectrum of HIV-associated neurological disorder (HAND) and ranges from asymptomatic condition to minor neurological features to severe dementia. Cerebrospinal fluid (CSF) analysis helps to rule out the presence of other opportunistic infections. Neuroimaging helps establish the diagnosis. We report a case of a 39-year-old African American female who presented with signs and symptoms suggestive of acute multiple sclerosis (MS) flares in the setting of advanced acute immunodeficiency syndrome (AIDS) encephalopathy. She presented with bilateral lower extremity muscle weakness and pain with apparent cognitive decline. Notable laboratory findings included leukopenia with normal neutrophils and positive serology for HIV-1. The MRI showed mild post-contrast enhancement suggestive of demyelinating disease, favoring MS over progressive multifocal leukoencephalopathy (PML). Cerebrospinal fluid analysis was significant for positive oligoclonal bands and negative serology. She was started on antiretroviral therapy (ART) for AIDS while holding steroids due to the possibility of worsening AIDS. After treatment for HIV, she showed immunologic and functional status improvement. HIV encephalopathy must be diagnosed by ruling out other similar presenting neurological illnesses for tactful patient management.

Keywords: acquired immunodeficiency syndrome; antiretroviral therapy; human immunodeficiency virus; leukoencephalopathy; multiple sclerosis.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Diffusion-weighted MRI when the patient presented. Arrows show both brachium (left>right) of pons with extensive hyperintense T2-signal abnormality (also present over pericallosal and periventricular white matter suggesting demyelination).
Figure 2
Figure 2. Post-contrast diffusion-weighted MRI when the patient presented. The arrows show brachium pontis.
Figure 3
Figure 3. FLAIR image with an arrow showing hyperintense signal abnormality over left brachium pontis
FLAIR: Fluid-attenuated inversion recovery
Figure 4
Figure 4. Post-contrast FLAIR imaging with the arrow showing equivocal contrast with mild enhancement.
FLAIR: Fluid-attenuated inversion recovery
Figure 5
Figure 5. Diffusion-weighted MRI. The arrows show marked improvement in the brachium pontis lesion.
Figure 6
Figure 6. Diffusion-weighted MRI, post-contrast phase. The arrows show marked improvement in the brachium pontis lesion.
Figure 7
Figure 7. FLAIR imaging. The arrow shows the resolution of the hyperintense lesion in the left brachium pontis.
FLAIR: Fluid-attenuated inversion recovery
Figure 8
Figure 8. FLAIR imaging post-enhancement. The arrow points at the resolution of the prior enhancement.
FLAIR: Fluid-attenuated inversion recovery

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