Radiation Necrosis Clinical Presentation

Updated: Jul 20, 2021
  • Author: Gaurav Gupta, MD, FAANS, FACS; Chief Editor: Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP, FANA  more...
  • Print
Presentation

History

Radiation necrosis is a focal process that occurs at the initial tumor site.

  • The history generally reflects a subacute or chronic re-emergence of the initial tumor symptoms.

  • Occasional reports exist of patients developing diffuse areas of necrosis away from the initial tumor site.

  • When obtaining a history, include questions to exclude stroke and infection, which can cause a tumorlike appearance on MRI.

Breakthrough or new seizures may occur. These seizures may be partial, complex partial, or partial with secondary generalization (grand mal).

Depending on the tumor location and rate of growth, radiation necrosis can present with signs of mass effect, elevated intracranial pressure, obstructive hydrocephalus, or one of the herniation syndromes.

Hemorrhage in late radiation necrosis is a rare but described phenomenon. [8]

Radiation necrosis involving the frontal or temporal lobes may produce cognitive and personality changes.

  • In nasopharyngeal carcinoma, the anteromedial aspects of the temporal lobes are located in the radiation port.

  • A patient with radiation necrosis in this location may develop symptoms of personality change, memory loss, amnesia, and/or Klüver-Bucy syndrome.

  • Radiation necrosis resulting from radiotherapy for ocular and maxillary cancer can affect the frontal lobes. This can cause hemiparesis, apathy, and/or personality changes.

Next:

Physical

Evaluate mental status and cortical functioning in patients with radiation necrosis who have a supratentorial lesion or signs of increased intracranial pressure. In cortical testing, examine for aphasia, apraxia, attention, neglect, visuospatial skills, recognition, short-term recall, and calculation.

With the possibility of increased intracranial pressure, examine the fundus for possible papilledema and/or decreased or absent spontaneous venous pulsations.

Since radiation necrosis is a focal lesion, tailor the neurologic exam to look carefully for focality, lateralization, or asymmetry in motor, sensory, or coordination testing.

Since radiation necrosis occurs in the same region as the initial tumor bed, evaluate functions specific to that area of the CNS.

Previous
Next:

Causes

Multiple risk factors are thought to play a role in the development of radiation necrosis (RN). These include the cumulative radiation dose, fractionation size, treatment duration, treated volume, prior cranial radiation, and the use of adjuvant therapies. Additionally, probabilistic variables, such as the genetic profile of the radiated tumors or the host may also influence the risk of developing RN. [9]

Brain lesions > 1cm in diameter exhibit the greatest risk of developing RN. [9] Occurrence generally is related to total radiation doses and fractionation size. The risk increases with increasing doses and larger radiation fraction sizes.

  • Tolerable total radiation dose to the brain is 6500–7000 cGy.

  • Patients who have received a total dose of 5500 cGy have a 3–5% occurrence of radiation necrosis.

  • Fractionation daily dose exceeding 200 cGy also increases risk.

  • Cerebral necrosis is unlikely at doses less than 50 Gy in 25 fractions. [10]

  • Hypofractionation is an effective strategy for treating recurrent high-grade gliomas without increasing the risk of RN. [11]

  • A dose-dependent risk is also seen with stereotactic radiosurgery, where doses > 10 Gy to > 10.5 mL volume carry a 35% risk of RN, [12, 13] and up to 50% risk with 13 Gy to > 10 mL surface area. [13]

  • A systematic review showed no correlation between the duration from initial radiotherapy to re-irradiation and the risk of RN. [14]

Other predisposing factors include the following:

  • Adjunctive therapies such as the use of BRAF inhibitors with SRS, which in one study caused a 22% risk of RN compared to 11% in SRS alone. [15]

  • Other vasculopathic risk factors (eg, diabetes mellitus, hypercholesterolemia).

  • Chemotherapy: Chemotherapy increases the risks of necrosis even when adjusting for length of follow-up or initial radiation therapy dose.

  • A study of 5747 brain lesions by Miller et al. provided novel insight into the relationship between tumor biology and risk of RN. They found that metastatic renal and small-cell lung carcinomas were correlated with a greater likelihood of RN. Furthermore, HER2-amplification, BRAF V600+ mutational status, and ALK rearrangement appeared to be significantly associated with RN. [16]

  • Individual risk factors, such as variations in genetic radiosensitivity, also contribute to the risk of RN. Wang et al. identified the gene Cep128 as a radiation injury susceptibility gene. [17]

Previous