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Each year more than 150,000 new cases of secondary brain tumors
are diagnosed, along with 16,500 new cases of primary brain tumors
and more than 2500 new cases of arteriovenous malformations
(AVM).3,36,115
Radiation therapy is a vital component of tumor management, with
the goal being to eradicate the malignancy or abnormality without
damage to healthy tissue. This objective is difficult to achieve
and in practice there is always some degree of residual
injury.37,44,50,72
Brain radionecrosis is the most serious complication associated
with radiation therapy for these conditions and it can result in
significant morbidity and mortality. It is a progressive spectrum
of injury ranging from early edema to total tissue necrosis. It
is currently thought that early radiation injury results from a
vascular insult causing edema in the neural tissue. The symptoms
of brain radionecrosis are dependent on the location of the injury.
Individuals may experience focal motor or sensory deficits, seizures,
aphasia, headaches, hypothalamic and pituitary insufficiency, neuropsychiatric
deficits and dementia, among others.34,47,65,77 In those
patients it does not kill, it can be devastating with significant
morbidity associated.6 The incidence of brain radionecrosis
is unknown, but has been reported to be as high as 40-50% in patients
exposed to certain types of radiation therapy.64 Its
development is dependent on the type, dose and fraction size of
radiation received.8,40,98
The incidence is greater in individuals who receive combined forms
of radiation, repeated radiation or concomitant or sequential
chemotherapy.7,10,91,102
The incidence of injury for intra-axial tumors such as gliomas and
metastases will most likely increase given the recent emphasis on
aggressive localized radiation therapy.37
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Existing therapies for brain radionecrosis are not evidence-based
and possess significant side effects. There is no proven treatment
modality that can mitigate the injury for all brain radionecrosis
patients. Once a patient becomes symptomatic, they are usually treated
with corticosteroids to control edema. The steroid regimen is often
extreme and can result in significant morbidity if continued
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over
several months. In one study, 65% of patients had their steroid
levels continually increased in a failing attempt to alleviate deteriorating
clinical status and progressive neurologic deficit.58
The failure of steroids to control or even stabilize the neurologic
deficit is problematic. Steroids cannot be increased indefinitely
and their failure is usually an indication for surgical resection
of the affected neural tissue18, an outcome yielding
high risk and increased cost. In cases where steroids fail and surgery
is not possible there ensues a fatal progression of the necrotic
process18 and the patient has little or no chance of
survival.6
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