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Radiation Necrosis

Summary

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  • Late complication of radiation therapy characterised by necrosis and oedema of brain tissue
  • Typically occurs 6 months to years after treatment
  • Imaging findings can mimic tumour recurrence, posing diagnostic challenges1

Pathophysiology

  • Radiation-induced vascular damage leading to:
    • Endothelial cell injury
    • Increased vascular permeability
    • Ischaemia and hypoxia
  • Subsequent tissue necrosis and oedema
  • Cytokine-mediated inflammatory response
  • White matter demyelination and axonal loss

Demographics

  • Incidence varies based on radiation dose and technique:
    • 3-24% after stereotactic radiosurgery
    • 5-15% after conventional fractionated radiotherapy
  • Risk factors:
    • Higher radiation dose
    • Larger treatment volume
    • Concurrent chemotherapy
    • Younger age at treatment

Diagnosis

  • Clinical presentation:
    • Focal neurological deficits
    • Cognitive decline
    • Seizures
    • Headaches
  • Differential diagnosis:
    • Tumour recurrence
    • Pseudoprogression
    • Infection
  • Diagnostic challenges:
    • Clinical and imaging overlap with tumour recurrence
    • Need for multimodal approach

Imaging

  • MRI:
    • T1-weighted: Variable enhancement patterns
    • T2/FLAIR: Oedema and mass effect
    • DWI: Variable diffusion restriction
    • Perfusion: Typically decreased relative cerebral blood volume (rCBV)
  • Advanced imaging techniques:
    • MR spectroscopy: Decreased Cho/Cr and NAA/Cr ratios
    • PET: Reduced FDG uptake or increased amino acid tracer uptake
  • Characteristic features:
    • 'Swiss cheese' or 'soap bubble' enhancement pattern
    • Lesion crossing white matter tracts
    • Corpus callosum involvement

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  • A 35-year-old patient presented following a seizure.
  • MRI showed an ill-defined left frontal lobe lesion with mild diffusion restriction and nodular enhancement.
  • Following a resection, a grade 3 astrocytoma was diagnosed.
  • The patient had 30 fractions of external beam image guided radiotherapy.
  • 6 months later, a heterogeneous and peripherally enhancing lesion developed around the resection cavity. The presence of only a lipid and lactate peaks with little NAA or choline on MR spectroscopy and the low CBV were consistent with treatment related changes, rather than disease progression.
  • The peripherally enhancing lesion was unchanged on further follow-up imaging at 1 year.

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  • A 30-year-old patient presented with headache and lethargy.
  • A diffuse non-enhancing lesion centred on the left insula that was ultimately diagnosed as a Grade 2 astrocytoma that was treated with debulking, radiation and chemotherapy.
  • On 1 year follow-up, the patient was clinically well after surgery but an area of enhancement developed in the left frontal white matter.
  • DSC perfusion showed no significant increase in CBV (ratio of ~1.2 relative to contralateral white matter) and a DCE Type 1 curve within the lesion, both of which were compatible with predominantly treatment related effects.
  • As expected with treatment related effects, the enhancement regressed over the following year.

Treatment

  • Corticosteroids and bevacizumab for symptomatic oedema; surgery for refractory or diagnostically uncertain lesions
  • Perfusion (low rCBV) and spectroscopy (lipid/lactate rather than choline) help distinguish it from tumour recurrence

Differential diagnosis

Imaging differential Differentiating feature
Tumour recurrence / pseudoprogression Recurrence shows high rCBV on perfusion; radiation necrosis gives "soap bubble"/"Swiss cheese" enhancement with low rCBV and a lipid/lactate-dominant spectrum
Abscess Thin smooth ring enhancement; restricted central DWI; satellite lesions; no prior radiation
Metastasis Located at grey-white junction; ring or nodular enhancement; multiple lesions; not confined to radiation field
Subacute infarct Follows a vascular territory; wedge-shaped; gyral enhancement; DWI restriction in acute/subacute phase
Progressive multifocal leukoencephalopathy Subcortical U-fibre involvement; restricted DWI at active edge; no enhancement; no prior radiation
Encephalitis Cortical and limbic T2 signal; temporal lobe predilection; not confined to radiation field
Demyelinating disease Ovoid periventricular lesions; incomplete ring enhancement; not confined to radiation field

  1. Furuse et al. Delayed brain radiation necrosis: pathological review and new molecular targets for treatment. 2015. Medical molecular morphology - Open in new tab. ↩