Specific Imaging Findings

Radiation-induced leukoencephalopathy presents with rapidly progressive, symmetric CT hypodensities and T2 hyperintensities in the periventricular and deep white matter, initially with sparing of the corpus callosum and subcortical arcuate fibers. Over time, lesions increase in size and coalesce leading to a confluent pattern with smooth peripheral margins. Concurrent cerebral atrophy may develop and rapidly progress. The affected white matter is of increased diffusivity on ADC maps and gradual decrease of rCBV on perfusion imaging may be observed. Pediatric patients may develop a mineralizing microangiopathy months or years following radiation or more commonly combined chemoradiation, with large calcifications within the affected white matter. Symptomatic reversible methotrexate toxicity shows T2 hyperintense areas in the supratentorial and cerebellar cortex and subcortical white matter in addition to deep white matter changes. Chemotherapy with or without radiotherapy, typically including intrathecal methotrexate, may lead to disseminated necrotizing leukoencephalopathy, characterized by rapidly progressive confluent white matter T2 hyperintensity and T1 hypointensity with internal hemorrhages and corresponding ill-defined areas of enhancement, which can evolve into circular necrotic lesions.

Pertinent Clinical Information

Radiation-induced delayed encephalopathy is a common and serious irreversible condition characterized by neurocognitive deterioration ranging from mild impairment to dementia. Known risk factors include combined radiation and chemotherapy, diabetes, hypertension, and advanced age. It is particularly common following whole-brain radiotherapy (WBRT), which can induce cognitive dysfunction in up to 50% of long-term survivors. Preexisting leukoaraiosis appears to be a predisposing factor for developing further leukoencephalopathy after WBRT.