Neuroimaging and Cognitive Disorders
To detect subtle changes in the brain parenchyma, advanced MRI methods are used: perfusion MRI, MR spectroscopy, and diffusion tensor imaging (DTI). A striking sign of pronounced HIV encephalopathy is the loss of brain volume (atrophy), primarily affecting the frontal lobes, corpus callosum, thalamus, and basal ganglia. This was especially relevant before the introduction of combination antiretroviral therapy (cART).
Brain function disorders are grouped under the term HIV-associated neurocognitive disorders (HAND), which are divided into three categories:
- Asymptomatic neurocognitive impairment (ANI) — detected only by tests, the patient is independent in daily life.
- Mild neurocognitive disorder (MND) — there is a mild decline in functions.
- HIV-associated dementia (HAD) — a severe form (formerly "AIDS dementia"). In the cART era, it is rare, but mild forms are detected in nearly 50% of HIV-infected individuals.
Progressive Multifocal Leukoencephalopathy (PML)
PML is a progressive demyelination resulting from the reactivation of latent John Cunningham polyomavirus (JC virus). It is characteristic of profound immunodeficiency (CD4 count less than 100 cells/mm³). Patients complain of a progressive decline in cognitive functions, personality changes, and occasionally experience seizures and focal neurological symptoms.
MRI findings in PML:
- Lesions are localized in the white matter (subcortical or cerebellar) and have indistinct margins.
- Involvement of subcortical U-fibers is typical.
- The signal from the lesions is hyperintense on T2 and FLAIR, and hypointense on T1.
- Diffusion-weighted imaging (DWI) reveals a peripheral hyperintense rim around the central necrotic zone, indicating active demyelination.
Immune Reconstitution Inflammatory Syndrome (IRIS)
CNS-IRIS is a paradoxical worsening of an HIV patient's condition that occurs a few days or months after starting antiretroviral therapy (cART). The cause lies in the robust inflammatory response of the recovering immune system to existing antigens (dead or latent microorganisms).
On MRI, the syndrome manifests as new areas of hyperintensity on T2/FLAIR sequences, contrast enhancement, and occasionally restricted diffusion and mass effect. If IRIS develops in the setting of PML (PML-IRIS), peripheral, ill-defined contrast enhancement appears around the demyelination zones, reflecting inflammation. Timely recognition of IRIS is critical for adjusting treatment and saving the patient's life.
Cerebral Toxoplasmosis
The most common opportunistic CNS infection in severe immunodeficiency (CD4 < 100 cells/mm³). Caused by the intracellular parasite Toxoplasma gondii.
MRI findings:
- The formation of abscesses with ring enhancement is typical.
- Localization: basal ganglia, thalamus, and the gray-white matter junction.
- T2-weighted images often demonstrate the "target sign": a bright center (fluid), a dark rim (blood), and a bright outer ring (edema).
The diagnosis is often established based on the clinical response (ex juvantibus) to therapy (pyrimethamine-sulfadiazine): lesion sizes should decrease within 10 days. The main differential diagnosis is with primary CNS lymphoma.
HIV and Vascular Diseases
HIV infection increases the risk of ischemic stroke. Several mechanisms contribute to this:
- Chronic inflammation causes endothelial dysfunction.
- Coagulopathies (e.g., thrombocytopenia).
- Accelerated atherosclerosis and vasculitis of intracranial and extracorporeal vessels.
- Atherogenic side effects of antiretroviral drugs.
Furthermore, immune-mediated damage to the vessel wall can lead to aneurysm formation (fusiform dilatations), especially in young men.
Briefly: answers to topical questions
How does the MRI appearance of CNS lymphoma differ from cerebral toxoplasmosis?
The MRI appearance of primary CNS lymphoma and cerebral toxoplasmosis differs in the pattern of contrast enhancement, signal intensity, and diffusion characteristics.
| Sign | Primary CNS lymphoma | Cerebral toxoplasmosis (Toxoplasma gondii) |
|---|---|---|
| Contrast enhancement | Usually homogeneous; atypical ring enhancement may occur in AIDS | Usually ring-enhancing; in severe immunodeficiency, enhancement may be nodular or absent |
| Signal intensity | Usually isointense on T1- and T2-weighted images | Hyperintense on T2/FLAIR, hypointense on T1 |
| Diffusion characteristics | Typically demonstrate restricted diffusion on DWI | Diffusion characteristics vary and may overlap with lymphoma |
| Specific features | — | Target sign on T2-weighted images |
| Edema and mass effect | Vasogenic edema and mass effect are relatively mild | Variable perifocal edema and mass effect are possible |
Class and exam questions
What is the main MRI distinction of PML from other lesions?
A typical sign of PML is the involvement of subcortical white matter U-fibers. On DWI, a hyperintense rim corresponding to the zone of active demyelination is identified around the lesions.
When should the development of IRIS be suspected?
If a HIV-positive patient develops new neurological symptoms or progressive cognitive dysfunction within 8 weeks of starting cART (with good viral control).
How to distinguish cerebral toxoplasmosis from lymphoma?
Toxoplasmosis has a broader spectrum of diffusion characteristics, whereas lymphoma typically demonstrates restricted diffusion on DWI and high tracer uptake on 18F-FDG PET or thallium-201 SPECT. Additionally, the diagnosis of toxoplasmosis is confirmed by the response to empirical therapy.
What else to study on this topic
- Mechanisms of MR signal generation in cerebral toxoplasmosis
- Differential diagnosis of primary CNS lymphoma
- Neuroimaging patterns in CNS-IRIS
- Pathogenesis of HIV vasculitis and aneurysm formation
- CNS cysticercosis: etiology and transmission routes
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