Sections

Radiation Necrosis

Sections Radiation Necrosis
Overview
Presentation
- History
- Physical
- Causes
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DDx
Workup
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Medication
Follow-up
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References

Medication

Medication Summary

Medical therapy focuses on two mechanisms: controlling vasogenic edema and/or controlling vessel thrombosis.

Class Summary

Steroid therapy has only a temporary role in relieving neurologic decompensation and deficits. It relieves any symptomology related to vasogenic edema and disruption of the blood-brain barrier. While administering steroid therapy, the clinician must implement another medical or surgical therapy to treat radiation necrosis and to protect the patient from long-term complications.

Dexamethasone (Decadron, Dexasone)

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Glucocorticoids such as dexamethasone have potent anti-inflammatory effects in many disorders. In addition to metabolic effects, they modify immune system response. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV to PO regimen in a 1:1 ratio.

Class Summary

Because radiation necrosis pathophysiology involves vessel thrombosis and subsequent occlusion, anticoagulant use has been proposed.^[45]To date, few case studies have addressed use in this condition; the evidence for anticoagulation is very limited. Patients with radiation necrosis may also be at risk of intracranial hemorrhage, further limiting the presumptive benefits of this therapy. In most of these studies, histologic verification of radiation necrosis was present. Patients received 6 mo of IV heparin, then warfarin with aPTT and PT adjusted to 1.5 times the control. Patients had significant resolution of deficits. When anticoagulation was stopped, symptoms reemerged. Almost immediate resolution of symptoms occurred when anticoagulation was restarted. Before starting anticoagulation therapy, careful diagnostic evaluation and management are needed.

Heparin

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Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Check aPTT after the first 6 h, then periodically q4-6h in early treatment. Dosage is therapeutic when aPTT is adjusted to 1.5 times normal.

Warfarin (Coumadin)

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Inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and anticoagulants (proteins C and S). Vitamin K is a cofactor for postribosomal synthesis of vitamin K-dependent clotting factors, which promote synthesis of gamma-carboxyglutamic acid (necessary for proper coagulation). Reportedly interferes with vitamin K epoxide regeneration. Peak anticoagulant effect is 72-96 h. Like other anticoagulants, warfarin has no effect on a preexisting thrombus.

Individualize dose in response to PT/INR and therapeutic goal. Periodic determination of PT/INR is required.

Class Summary

Agents in this category are used to decrease blood supply to a tumor by inhibiting angiogenesis.^{[46, 47]}

Bevacizumab (Avastin)

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A recombinant, humanized antibody that inhibits vascular endothelial growth factor (VEGF). VEGF has a significant role in angiogenesis and maintenance of existing blood vessels. By inhibiting VEGF, the antibody would interfere with the blood supply to a tumor, which is thought to be critical to tumor metastasis. By preventing VEGF from reaching leaky capillaries that are associated with brain swelling, bevacizumab may also help in radiation necrosis.

Fifteen patients with malignant brain tumors were treated with bevacizumab or bevacizumab combination n in one study.

Follow-up

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Media Gallery

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.
T1-weighted contrast imaging shows left frontoparietal enhancing mass lesion with significant perilesional edema and midline shift. Peripheral wavy frond-like enhancement is typical of radiation necrosis.
T1-weighted contrast imaging after the corticosteroid administration showing a significant reduction in enhancement, swelling, and mass effect with reversal of midline shift.

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Author

Gaurav Gupta, MD, FAANS, FACS Associate Professor of Neurosurgery, System Co-Director, Cerebrovascular and Endovascular Neurosurgery, Fellowship Director, Endovascular Neurosurgery Fellowship (Site), Department of Surgery, Division of Neurosurgery, Rutgers RWJ Barnabas Healthcare, Rutgers Robert Wood Johnson Medical School

Gaurav Gupta, MD, FAANS, FACS is a member of the following medical societies: American Academy of Neurology, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, Congress of Neurological Surgeons, Facial Pain Association, Society for Neuroscience, Society of NeuroInterventional Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

Fareed R Jumah, MBBS Postdoctoral Research Fellow, Department of Neurosurgery, RWJ University Hospital, Rutgers Robert Wood Johnson Medical School

Disclosure: Nothing to disclose.

Bharath Raju, MBBS, MCh Postdoctoral Research Fellow, Department of Neurosurgery, RWJ University Hospital, Rutgers Robert Wood Johnson Medical School

Bharath Raju, MBBS, MCh is a member of the following medical societies: AOSpine, Bangalore Neurological Society, European Association of Neurosurgical Societies, Neurological Society of India, Neurotrauma Society of India

Disclosure: Nothing to disclose.

Sudipta Roychowdhury, MD Clinical Associate Professor of Radiology, Department of Radiology, Rutgers Robert Wood Johnson Medical School; Attending Radiologist/Neuroradiologist, University Radiology Group, PC

Sudipta Roychowdhury, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Neuroradiology, Medical Society of New Jersey, Radiological Society of New Jersey, Radiological Society of North America, Society of NeuroInterventional Surgery

Disclosure: Nothing to disclose.

Anil Nanda, MD, MPH, FACS Professor and Chairman, Department of Neurosurgery, Rutgers University Robert Wood Johnson Medical School and Rutgers New Jersey Medical School; Peter W Carmel, MD, Endowed Chair of Neurological Surgery, Senior Vice President of Neurosurgical Services, RWJBarnabas Health

Anil Nanda, MD, MPH, FACS is a member of the following medical societies: American Academy of Neurological Surgery, American Association of Neurological Surgeons, American Medical Association, Brain Attack Coalition, Congress of Neurological Surgeons, John C McDonald Surgical Society, Louisiana Neurosurgical Society, Louisiana State Medical Society, North American Skull Base Society, Shreveport Medical Society, Society of Neurological Surgeons, Society of University Neurosurgeons, Southern Neurosurgical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

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

Disclosure: Nothing to disclose.

Chief Editor

Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP, FANA Professor of Pediatrics, Neurology, Neurosurgery, and Psychiatry, Medical Director, Tulane Center for Autism and Related Disorders, Tulane University School of Medicine; Pediatric Neurologist and Epileptologist, Ochsner Hospital for Children; Professor of Neurology, Louisiana State University School of Medicine

Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP, FANA is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Medical Association, American Neurological Association, The Society of Federal Health Professionals (AMSUS), Child Neurology Society, Southern Pediatric Neurology Society

Disclosure: Nothing to disclose.

Additional Contributors

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

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

Disclosure: Nothing to disclose.

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 Institute, American College of Legal Medicine, American College of Physicians

Disclosure: Nothing to disclose.

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, International Association for the Study of Pain, Pennsylvania Medical Society, Society for Neuroscience, Children's Oncology Group, Society for Neuro-Oncology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Robert Wilson, MD to the development and writing of this article.

Sections Radiation Necrosis
Overview
Presentation
- History
- Physical
- Causes
- Show All
DDx
Workup
Treatment
Medication
Follow-up
Media Gallery
References

Radiation Necrosis Medication

Medication Summary

Corticosteroids