Radiation Necrosis Clinical Presentation

  • Author: Michael J Schneck, MD; more...
 
Updated: Apr 19, 2011
 

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.[7]
  • 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.
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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.
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Causes

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 below 50 Gy in 25 fractions.[8]
  • Other predisposing factors include the following:
    • 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.
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Contributor Information and Disclosures
Author

Michael J Schneck, MD  Associate Professor, Departments of Neurology and Neurosurgery, Stritch School of Medicine, Loyola University; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center

Michael J Schneck, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, Neurocritical Care Society, and Stroke Council of the American Heart Association

Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching; Sanofi/BMS Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; UCB Pharma Honoraria Speaking and teaching; Talecris Consulting fee Other; NMT Medical Grant/research funds Independent contractor; NIH Independent contractor; Sanofi Grant/research funds Independent contractor; Boehringer-Ingelheim Grant/research funds Independent contractor; Baxter Labs Consulting fee Consulting

Coauthor(s)

Anna Janss, MD, PhD  Associate Professor of Pediatric Neuro-oncology, Emory University School of Medicine; Consulting Neuro-oncologist, Children's Healthcare of Atlanta

Anna Janss, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Association for Cancer Research, American Medical Association, Children's Oncology Group, International Association for the Study of Pain, Pennsylvania Medical Society, Society for Neuro-Oncology, and Society for Neuroscience

Disclosure: Nothing to disclose.

Specialty Editor Board

Frederick M Vincent Sr, MD  Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Jorge Kattah, MD  Head, Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, and New York Academy of Sciences

Disclosure: Biogen Honoraria Consulting; Bayer Corporation Honoraria Consulting

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MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to this MRI consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy.
Positron emission tomography with [18F]-labeled fluorodeoxyglucose (PET-FDG) performed following the MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to these studies consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy. PET-FDG demonstrates hypometabolism consistent with probable radiation necrosis. Four years later, the patient is stable and without evidence of tumor progression.
 
 
 
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