Post-radiation neurotoxicity and necrosis
Radiotherapy neurotoxicity is particularly pronounced in children due to the vulnerability of developing brain tissue. A typical manifestation is post-radiation leukoencephalopathy, which appears on MRI as white matter hyperintensity. Notably, the pathological process spares (leaves intact) the subcortical U-fibers and the corpus callosum.
According to the National Cancer Institute classification, there are three grades of leukoencephalopathy severity:
- Grade I: Pronounced periventricular lesions.
- Grade II: Periventricular hyperintensity extending into the centrum semiovale.
- Grade III: Confluent (total) white matter involvement.
Radiation necrosis primarily affects the white matter. It is localized directly within the bed of the irradiated tumor, in adjacent tissues (during head and neck tumor irradiation), or within the treatment zone of arteriovenous malformations. Pathogenetically, necrosis is secondary to changes in small cerebral vessels, the walls of which become thickened.
Acute disseminated encephalomyelitis (ADEM)
ADEM is a diagnosis of exclusion. Its MRI pattern is characterized by large (greater than 1–2 cm) diffuse lesions with indistinct margins, located predominantly in the white matter. An important rule: MRI should not show T1-hypointense lesions. In children, the deep gray matter (thalami, basal ganglia) is frequently involved.
The disease typically has a monophasic course. The active phase lasts no more than 3 months. The diagnosis is confirmed retrospectively: a follow-up MRI at 3 months should show partial or complete resolution of lesions without the appearance of new ones. If new lesions appear within the first 6 months, a relapsing demyelinating disease should be suspected.
Multiple sclerosis (MS) and "black holes"
In clinically isolated syndrome (CIS) and MS, demyelinating lesions are clearly visible on T2-FLAIR imaging (e.g., in the periventricular white matter). For differential diagnosis, lesion localization in the posterior cranial fossa is crucial: the floor of the 4th ventricle, the surface of the pons, and the middle and superior cerebellar peduncles.
About 10–20% of T2-hyperintense lesions appear dark on T1-weighted images—these are the so-called "black holes":
- Acute ("wet"): caused by pronounced edema. Found in 80% of new lesions and become isointense after a few months as edema resolves and remyelination occurs.
- Chronic: a consequence of severe demyelination and axonal loss (irreversible damage). More common in progressive forms of MS within the supratentorial white matter.
Primary progressive MS is characterized by clinico-radiological dissociation: MRI shows few small lesions that rarely enhance with contrast, yet the patient's disability steadily increases due to cortical and spinal cord damage.
Features of traumatic injuries in children
When child abuse is suspected (e.g., shaken baby syndrome), a comprehensive evaluation is performed. It is necessary to differentiate traumatic subdural hematomas from fluid collections associated with coagulopathies, meningitis, or metabolic disorders (glutaric aciduria type I, Menkes disease).
- Intraventricular hemorrhages: associated with subependymal vein rupture. In the acute phase, they are visible on CT; in the chronic phase, on T2* or SWI MRI sequences. They can be complicated by obstructive hydrocephalus.
- Parenchymal contusions: hemorrhagic lesions located at the gray-white matter junction. They are easily recognized on MRI due to hemoglobin degradation products.
- "Tadpole" sign: visualization of a thrombus within a bridging vein on SWI images in infants with subdural hematomas.
Class and exam questions
How to distinguish acute "black holes" from chronic ones on MRI?
Acute "black holes" represent zones of pronounced edema and disappear after a few months, transitioning to an isointense signal. Chronic ones persist permanently, as their substrate is irreversible axonal loss.
What is the essence of the multiphasic form of ADEM?
This is the appearance of a new episode of encephalopathy with ADEM-typical features at least 3 months after the initial attack, which is not followed by further relapses.
How do multiple sclerosis lesions appear in the spinal cord?
They have a cigar-shaped appearance on sagittal projection, typically do not exceed 2 segments in length, and are located in the lateral and posterior white matter funiculi, involving the central gray matter.
What else to study on this topic
- ADEM diagnostic criteria (IPMSSG, 2012)
- Pathogenesis and stages of radiation necrosis formation
- The "central vein" sign in multiple sclerosis
- Clinico-radiological dissociation in primary progressive MS
- Optic neuritis: criteria for atypical course and indications for MRI
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