Magnetic Resonance Imaging in Early Diagnosis
MRI has significantly higher sensitivity compared to CT in detecting viral CNS infections. Standard T2 and FLAIR sequences can demonstrate hyperintense signals and the development of edema (swelling) within the first two days from symptom onset.
The pathological process typically begins in the cerebral cortex, with subsequent secondary involvement of the underlying white matter (subjacent white matter). Diffusion-weighted imaging (DWI) is used for maximum sensitivity to early cortical changes. If inflammation is accompanied by microhemorrhages, gradient echo T2* (gradient echo) or susceptibility-weighted imaging (SWI — susceptibility-weighted imaging) sequences become the method of choice.
Neuroimaging patterns of various types of encephalitis
The MRI appearance in viral CNS infections is often non-specific, which does not always allow for the immediate identification of the specific pathogen. However, certain viruses exhibit characteristic lesion topography:
- Herpes simplex encephalitis (herpes simplex encephalitis): causes asymmetric edema and signal hyperintensity predominantly in the anteromedial temporal lobes.
- Japanese encephalitis (Japanese encephalitis): caused by a flavivirus (flavivirus). On T2 and FLAIR, lesions are typically localized in the thalamus, basal ganglia, and brainstem (with the substantia nigra being particularly affected — substantia nigra).
- West Nile virus and tick-borne encephalitis: also demonstrate tropism for brainstem structures, the thalamus, and the basal ganglia.
CNS involvement in HIV infection
With the introduction of combination antiretroviral therapy (кАРТ / cART), AIDS-related mortality has dropped sharply (by 43% since 2003), and the incidence of opportunistic infections has decreased. Currently, neurocognitive and vascular complications have come to the forefront.
The spectrum of CNS pathologies in HIV includes:
- Direct viral effects on brain tissue.
- Progressive multifocal leukoencephalopathy (PML — PML).
- Immune reconstitution inflammatory syndrome (IRIS — IRIS).
- Opportunistic infections (OIs — OIs) developing in untreated individuals (e.g., toxoplasmosis or cryptococcosis).
HIV Encephalopathy (HIVE)
HIV encephalopathy (Human Immunodeficiency Virus Encephalopathy) develops as a result of viral invasion into peripheral macrophages, astrocytes, and microglial cells. Direct neuronal invasion is extremely rare. Neuronal damage is mediated by pro-inflammatory cytokines (tumor necrosis factor [TNF], quinolinic acid, platelet-activating factor) and viral proteins.
MRI correlates of HIVE: T2-weighted and FLAIR images show areas of hyperintense signal. These may be poorly defined, diffuse, and symmetrical, or focal. The deep grey matter is involved in the process.
Typical topography includes involvement of:
- The white matter of the centrum semiovale (centrum semiovale) and periventricular zones.
- The thalami (thalami) and caudate nuclei (nuclei caudati).
- The optic radiation (radiatio optica) and internal capsules (capsulae internae).
- The middle cerebellar peduncles (pedunculi cerebellares medii).
Pathophysiologically, these changes are driven by increased vascular permeability, edema, and partial demyelination. With antiretroviral therapy, such white matter and subcortical structural damage is potentially reversible.
Clinical examples of opportunistic infections
In immunosuppressed patients (e.g., transplant recipients), CNS infections exhibit specific features:
- Cryptococcus neoformans infection: can cause meningitis and cerebellar inflammation (cerebellitis). FLAIR shows a high signal from the subarachnoid spaces of the cerebellar vermis (cerebellar vermis). The T2 sequence reveals a hyperintense signal in the parenchyma. Following contrast administration (T1), marked leptomeningeal enhancement is observed (strong leptomeningeal enhancement).
- Multiple fungal abscesses (Multiple Fungal Abscesses): visualized on post-contrast T1-weighted images as focal lesions (e.g., in the parietal lobe and cerebellar hemisphere) with characteristic ring enhancement.
Briefly: answers to topical questions
What opportunistic CNS infections develop in HIV patients at the AIDS stage?
HIV patients can develop opportunistic central nervous system infections, including:
- Cryptococcal infection (Cryptococcus).
- Toxoplasmosis (Toxoplasma gondii).
- Progressive multifocal leukoencephalopathy (PML — PML) associated with the JC virus.
- Cytomegalovirus infection (CMV), which develops when the CD4+ count is below 50 cells/µL.
What cerebrospinal fluid changes are characteristic of viral encephalitis?
Viral encephalitis is characterized by the following cerebrospinal fluid changes:
- Appearance — clear, colorless fluid.
- Pandy's test — weakly positive or negative.
- Cytosis — normal cell count or mononuclear (lymphocytic) pleocytosis.
- Biochemistry — albumin quotient exceeds 10 × 10⁻³.
- Immunological parameters — elevated levels of IgG, IgM, and IgA; specific antibodies may be detected.
- In herpes simplex encephalitis, PCR testing may detect the herpes simplex virus.
What clinical symptoms are part of the classic presentation of viral encephalitis?
The classic clinical presentation of viral encephalitis includes general infectious and neurological manifestations. The disease typically begins gradually with prodromal symptoms:
- General infectious symptoms — malaise, headache, fever (irregular or remittent fever).
- Cranial nerve palsies — partial oculomotor disorders (most commonly involving the III cranial nerve nuclei), as well as involvement of cranial nerves I, V, VII, and XII.
- Specific manifestations — somnolence or persistent insomnia, hyperkinesia of various types.
Tick-borne encephalitis is also characterized by nausea, vomiting, dizziness, autonomic dysfunction, meningeal signs, and focal CNS deficits.
To remember the tropism of herpes simplex encephalitis: "Herpes hits the TEMPLES" — the anteromedial temporal lobes are affected.
Class and exam questions
Which MRI sequences are best for detecting early signs of viral encephalitis?
The optimal sequences are T2 and FLAIR, which visualize brain tissue edema within the first two days. DWI has even greater sensitivity to cortical changes.
Which brain structures are most commonly affected in Japanese encephalitis?
The infection demonstrates tropism for the thalamus, basal ganglia, and brainstem, with pathological signal abnormalities specifically detected in the substantia nigra.
Does the human immunodeficiency virus directly infect neurons in HIV encephalopathy?
No, direct neuronal invasion is extremely rare. The virus infects macrophages, microglia, and astrocytes, while neuronal damage occurs indirectly due to the release of cytokines (e.g., tumor necrosis factor).
What does central nervous system cryptococcal infection look like on contrast-enhanced MRI?
Contrast-enhanced T1-weighted images clearly demonstrate marked enhancement of the pia mater and arachnoid mater (leptomeningeal enhancement).
What else to study on this topic
- Pathogenesis of progressive multifocal leukoencephalopathy (PML) in HIV patients
- Differential diagnosis of microhemorrhage foci using SWI and T2* sequences
- Mechanisms of immune reconstitution inflammatory syndrome (IRIS)
- Role of cytokines and quinolinic acid in neurite-mediated neuronal damage
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