Post-radiation leukoencephalopathy
Post-radiation leukoencephalopathy is most pronounced in pediatric patients. The classic MRI picture is characterized by hyperintensity of the cerebral white matter.
A specific diagnostic sign — the pathological process affects the deep white matter, but always leaves the subcortical U-fibers and corpus callosum intact.
Severity grading (National Cancer Institute):
- Grade I: Pronounced focal periventricular hyperintensity.
- Grade II: Focal periventricular hyperintensity extending to the centrum semiovale (centrum semiovale).
- Grade III: Confluent total white matter hyperintensity.
Radiation necrosis and tumor recurrence
Radiation necrosis predominantly affects the cerebral white matter. It occurs as a secondary process against the background of small cerebral vessel damage (vessel wall thickening). Necrotic foci form directly at the site of the irradiated tumor, in the adjacent tissue, or in the treatment zone of arteriovenous malformations.
On standard MRI, radiation necrosis and tumor recurrence look identical: they are lesions with ring-like contrast enhancement and areas of hemorrhage, surrounded by a zone of perifocal edema. Advanced imaging techniques are used for differential diagnosis.
| Technique | Radiation necrosis | Tumor recurrence |
|---|---|---|
| DWI | Diffusion increased | Diffusion decreased (cytotoxicity) |
| Perfusion (CBV) | Blood flow decreased | Blood flow increased (neoangiogenesis) |
| MR spectroscopy | Low choline level | High choline level |
| PET | Metabolic activity decreased | Metabolic activity increased |
Vascular malformations and SMART syndrome
Brain irradiation can cause the delayed development of vascular malformations. Multiple cavernomas form most frequently, and telangiectasias less often.
On MRI, large cavernomas have a characteristic "popcorn" appearance — a hyperintense center on T1 and T2, surrounded by a hypointense rim. To detect small lesions, it is optimal to use modes sensitive to magnetic susceptibility and hemosiderin (Gradient echo T2* and SWI). They are usually asymptomatic.
Another delayed complication is SMART syndrome (stroke-like migraine attacks). It occurs years after treatment, manifesting as prolonged headache, neurological deficits, and sometimes seizures. MRI visualizes transient unilateral cortical hyperintensity (usually in the parieto-occipital region) with contrast enhancement, while the white matter remains intact.
Chemotherapy toxicity and PRES
During chemotherapy, conditions may arise that require differentiation from radiation injuries:
- Methotrexate toxicity: In the acute phase, it causes bilateral lesions with diffusion restriction in the centrum semiovale (usually reversible). Delayed toxicity manifests as confluent leukoencephalopathy.
- Posterior reversible encephalopathy syndrome (PRES): Develops against the background of chemotherapy, severe hypertension, or immunosuppression. Vascular autoregulation dysfunction leads to cerebral vasogenic edema. MRI shows bilateral cortico-subcortical confluent hyperintense lesions, predominantly in the parieto-occipital watershed zones. After withdrawal of the triggering factor, the lesions regress.
For differential diagnosis on MRI and PET, remember a simple rule: tumor recurrence is "alive and active" tissue (increased CBV blood flow, high choline, high metabolism), while radiation necrosis is a "dead" zone (all metabolic and perfusion parameters are reduced).
Class and exam questions
How to distinguish radiation leukoencephalopathy from other diffuse lesions?
Its key MRI sign is the complete preservation of the subcortical U-fibers and corpus callosum as absolutely intact against the background of pronounced damage to the rest of the white matter.
What MRI modes are needed to search for induced cavernomas?
It is necessary to use T2* gradient echo and susceptibility-weighted imaging (SWI), as they are most sensitive to microbleeds.
What is SMART syndrome?
This is a delayed side effect of radiation therapy, manifesting as stroke-like attacks. On MRI, it looks like a transient cerebral cortical lesion that does not affect the white matter.
What else to study on this topic
- Pathogenesis of mineralizing microangiopathy
- Differential diagnosis protocols for necrosis and recurrence
- Acute and delayed methotrexate toxicity
- Mechanisms of vasogenic edema formation in PRES
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