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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 challenges

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 peripherallly 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

  • Conservative management:
    • Corticosteroids for oedema reduction
    • Anticonvulsants for seizure control
  • Bevacizumab:
    • VEGF inhibitor shown to reduce oedema and enhance quality of life
  • Hyperbaric oxygen therapy:
    • May promote angiogenesis and tissue healing
  • Surgical resection:
    • Reserved for large, symptomatic lesions or diagnostic uncertainty
  • Laser interstitial thermal therapy (LITT):
    • Minimally invasive option for selected cases

Differential diagnosis

Differential Diagnosis Differentiating Feature
Tumour recurrence Perfusion MRI shows lower relative cerebral blood volume in radiation necrosis compared to recurrent tumour
Tumour recurrence / pseudoprogression Radiation necrosis shows "soap bubble" or "Swiss cheese" enhancement; MR perfusion shows low rCBV; MR spectroscopy shows elevated lipid/lactate
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