HIV Encephalitis: A Comprehensive Clinical and Imaging Overview

Keywords: HIV encephalitis, HIV dementia, vacuolar myelopathy, neuroHIV, brain atrophy in HIV, white matter T2 signal, CNS HIV, AIDS-related dementia

Introduction

HIV encephalitis (HIVE), also known as HIV-associated neurocognitive disorder (HAND), is a progressive neurological disorder seen in HIV-positive individuals, particularly in those with advanced immunosuppression. As combination antiretroviral therapy (cART) has evolved, the incidence of full-blown AIDS dementia complex (ADC) has decreased, yet milder neurocognitive impairments persist in many.

This column explores the pathophysiology, imaging features, and clinical manifestations of HIV encephalitis through the lens of a real clinical case involving a 35-year-old HIV-positive male, presenting with subacute behavioral changes and cognitive decline.

Case Summary

Patient: 35-year-old male
Clinical presentation: HIV-positive, with subacute behavioral changes and dementia
Diagnosis: HIV encephalitis with vacuolar myelopathy

Etiology and Pathogenesis

HIV encephalitis results from direct viral infection of the central nervous system (CNS) by HIV-1. The virus does not infect neurons directly; instead, it targets macrophages and microglial cells, leading to:

Neuroinflammation
Cytokine-mediated neuronal damage
Demyelination
White matter degradation
Neuronal loss

HIV enters the CNS early in infection, but encephalitic manifestations occur more frequently in late-stage disease or in cases with poor viral suppression.

Epidemiology

Up to 30–50% of untreated HIV patients develop some form of neurocognitive disorder.
With ART, the incidence of severe HIV dementia has decreased; however, HIV-associated neurocognitive disorders (HAND) still affect 20–30% of patients.
Risk increases with:
- Low CD4 counts (<200 cells/mm³)
- High viral load
- Prolonged infection duration
- ART nonadherence

Clinical Presentation

Symptoms of HIV encephalitis may vary based on the stage and severity:

Early Signs

Subtle cognitive dysfunction
Memory lapses
Attention difficulties

Advanced Signs

Dementia-like symptoms (impaired memory, language, motor skills)
Apathy and social withdrawal
Gait disturbance
Behavioral changes
Urinary incontinence

In our case, the 35-year-old patient exhibited subacute behavioral change and cognitive decline consistent with HIV-associated dementia (HAD).

Imaging Features

Brain MRI Findings

MRI remains the modality of choice in evaluating HIV encephalitis.

Common Findings:

Diffuse white matter hyperintensity on T2 and FLAIR
No contrast enhancement
No mass effect
Global cerebral atrophy, especially in younger patients

Case-Specific Observations:

[Figure 1] Sagittal T2 Weighted Image

Global cerebral atrophy with visible sulcal enlargement and white matter signal changes.

[Figure 2] Axial T1 Weighted Image

Marked volume loss disproportionate to age with cortical thinning.

[Figure 3] Axial FLAIR

Diffuse bilateral white matter hyperintensities without mass effect, suggesting demyelination.

[Figure 4] Axial T2 Weighted Image

Extensive T2 hyperintensities in the periventricular white matter.

[Figure 5] Axial C+ T1 Weighted Image

No significant contrast enhancement, ruling out active opportunistic infection or neoplasm.

[Figure 6] Coronal C+ T1 Weighted Image

Again shows no enhancement; confirms absence of focal mass or breakdown of blood-brain barrier.

Spine MRI Findings

[Figure 7] Sagittal T2 Weighted Image (Spine)

High T2 signal in bilateral dorsolateral columns; pattern consistent with vacuolar myelopathy.

[Figure 8] Axial T2 Weighted Image (Spine)

Symmetrical dorsolateral T2 hyperintensities typical for HIV-related myelopathy.

Interpretation:

No contrast enhancement differentiates HIV encephalitis from infectious or neoplastic processes.
Volume loss in a 35-year-old raises strong suspicion for HIV-related neurodegeneration.
White matter T2 hyperintensity without enhancement supports a diagnosis of chronic demyelination due to HIV encephalitis.

Differential Diagnosis

Progressive Multifocal Leukoencephalopathy (PML)
- Asymmetric lesions, often with mass effect, JC virus-related.
CNS lymphoma
- Enhancing mass-like lesions, periventricular involvement.
Cytomegalovirus (CMV) encephalitis
- Enhancing ventriculitis, ependymal involvement.
Multiple sclerosis (rare in HIV patients)
- Discrete, enhancing white matter plaques.

Treatment

1. Antiretroviral Therapy (ART)

Primary and most effective treatment
Reduces viral load in CNS and improves cognitive outcomes
Medications with high CNS penetration (e.g., zidovudine, abacavir) are preferred

2. Supportive Care

Cognitive rehabilitation
Occupational therapy
Psychosocial support

3. Treatment of Opportunistic Infections

If concurrent CNS infections are present, targeted antimicrobial therapy is essential.

Prognosis

Prognosis has improved dramatically with the advent of ART.
Reversible symptoms are possible if ART is started early.
Delayed treatment can result in irreversible neuronal loss and persistent dementia.
Vacuolar myelopathy is often less responsive to therapy but may stabilize with ART.

Quiz

1. Which imaging finding is most characteristic of HIV encephalitis?

A) Ring-enhancing lesion in the basal ganglia

B) Diffuse bilateral T2 hyperintensity without enhancement

C) Periventricular hemorrhage

D) Midline shift and mass effect

2. Which of the following cells are most involved in HIV-associated CNS injury?

A) Neurons

B) Astrocytes

C) Microglia and macrophages

D) Oligodendrocytes

3. What spinal cord finding is associated with HIV-related vacuolar myelopathy?

A) Ventral horn atrophy

B) Central cord edema

C) Dorsolateral column T2 hyperintensity

D) Cauda equina enhancement

4. Which treatment offers the best outcome for patients with HIV encephalitis?

A) Corticosteroids

B) Antibiotics

C) Antiretroviral therapy

D) Chemotherapy

Answer & Explanation

1. Answer: B. Explanation: HIV encephalitis typically presents with diffuse white matter T2 hyperintensity without enhancement or mass effect.

2. Answer: C. Explanation: HIV infects microglia and macrophages, not neurons, leading to inflammation and neurotoxicity.

3. Answer: C. Explanation: Symmetric T2 hyperintensity in the dorsolateral spinal cord columns is characteristic of vacuolar myelopathy in HIV.

4. Answer: C. Explanation: Combination antiretroviral therapy is the mainstay treatment, reducing viral replication and inflammation in the CNS.

Conclusion

HIV encephalitis remains a significant neurological complication of HIV infection, particularly in patients with poor viral control or delayed ART initiation. MRI plays a pivotal role in diagnosis, often revealing widespread white matter abnormalities and cerebral atrophy. Prompt ART initiation can reverse or stabilize symptoms, emphasizing the importance of early detection and treatment.

This case not only exemplifies classic imaging findings of HIVE but also highlights the importance of recognizing spinal involvement, such as vacuolar myelopathy. Understanding the neuroimaging, clinical spectrum, and evolving treatment options is vital for improving outcomes in these patients.

References

[1] L. M. McArthur, et al., "HIV-associated neurocognitive disorders: Pathogenesis and prospects for treatment," Nature Reviews Neurology, vol. 6, pp. 543–552, 2010.
[2] C. A. Sacktor, et al., "HIV-associated cognitive impairment before and after the advent of combination therapy," J Neurovirol., vol. 8, pp. 136–142, 2002.
[3] M. J. Brew, et al., "HIV, AIDS and the nervous system," J Neurol Neurosurg Psychiatry, vol. 75, no. 4, pp. S29–S33, 2004.
[4] A. T. Gisslen, et al., "HIV-related neurocognitive disorders: Recent advances," Lancet Neurol, vol. 10, pp. 877–887, 2011.
[5] R. Navia, et al., "The AIDS dementia complex: I. Clinical features," Ann Neurol., vol. 19, pp. 517–524, 1986.
[6] P. B. Rosenbloom, et al., "Vacuolar myelopathy in AIDS: Magnetic resonance imaging and pathologic correlation," Neurology, vol. 37, pp. 1470–1474, 1987.
[7] C. Joseph, et al., "Neuroimaging of HIV-associated neurocognitive disorders," Neuroimaging Clin N Am, vol. 26, no. 4, pp. 419–431, 2016.

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