Neuro-lupus

Standard MRI findings in neurolupus

Diagnosis of inflammatory processes in the brain in systemic lupus erythematosus is highly variable. In some cases, structural imaging reveals no pathological abnormalities at all, rendering the diagnosis presumptive.

• Mild manifestations: axial T2-FLAIR slices show non-specific small punctate lesions. They are characterized by a hyperintense signal, localized in the deep white matter and periventricular regions. These lesions frequently tend to merge (confluent pattern).
• Severe manifestations: typical for the full-blown picture of neuropsychiatric SLE. They include cortical atrophy, ventricular enlargement, marked brain tissue edema, infarctions, as well as intracranial hemorrhages and specific signs of vasculitis.
• Spinal cord involvement: manifests as transverse myelitis. T2-weighted images show increased signal intensity, while contrast administration reveals patchy, uneven enhancement.

Advanced MR techniques

Since baseline MRI does not always reflect the true extent of damage, high-tech modalities come to the forefront to assess tissue metabolism and microstructure:

1. Proton MR spectroscopy (1H-MRS): demonstrates a decrease in N-acetylaspartate levels (indicating neuronal death) and an increase in the choline peak (Cho), reflecting accelerated cell membrane turnover. The most critical marker is myo-inositol—its elevation is considered the earliest predictor of NPSLE exacerbation, preceding structural changes.
2. Diffusion-weighted imaging (DWI) and magnetization transfer imaging (MTI): record an increase in overall brain diffusivity. These techniques verify microstructural degradation in both gray and white matter.
3. Resting-state functional MRI (rs-fMRI): reveals neural network abnormalities in the form of hyper- or hypoconnectivity.

Important clinical conclusion: demyelination and axonal loss in SLE are diffuse and occult, progressively worsening even in patients without overt neurological deficits.

Metabolic and toxic disorders in adults

Unlike pediatric practice, where congenital genetic defects predominate, metabolic encephalopathies in adults are acquired. They result from exogenous toxin exposure or the accumulation of endogenous metabolites.

The pathological process predominantly affects structures with maximal metabolic demand — the brainstem and basal ganglia. The cortex may be variably involved, and white matter damage is less pronounced than in hereditary forms. The key radiological pattern is strict bilaterality and symmetry of the lesions. Definitive diagnosis requires correlating MRI patterns (gray/white matter) with toxicological and laboratory screening.

Post-radiation central nervous system injuries

Radiation-induced brain tissue changes (Radiotherapy injuries) are classified according to the time of manifestation:

• Acute injuries: develop during radiotherapy or within the first few weeks after it. The pathogenesis is based on vascular endothelial damage leading to vasogenic edema. Clinically, this manifests as an acute encephalopathic syndrome.
• Early delayed injuries: occur months later, manifesting as diffuse progressive leukoencephalopathy. The main cause is direct radiation injury to oligodendrocytes and the microvasculature during whole-brain radiotherapy (whole-brain radiotherapy). This leads to myelin loss, atrophy, and severe neurocognitive disorders.
• Late delayed injuries: form months or years later. These include radiation necrosis (radiation necrosis), cerebral cavernous malformations, and SMART syndrome (stroke-like migraine attacks after radiation therapy). Combined chemotherapy significantly increases the risk of these complications.

Class and exam questions

What else to study on this topic

• Pathophysiological mechanisms of antibody-mediated neuronal injury
• Differential diagnosis of radiation necrosis and tumor recurrence
• Features of proton MR spectroscopy (1H-MRS) of the brain
• Resting-state fMRI (rs-fMRI): evaluation of neural network connectivity
• Cerebral cavernous malformation as a late post-radiation complication

Other topics in the Neuroimaging section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.