MRS, perfusion MRI separate radiation necrosis from tumor

Radiation plays an important role in the treatment of primary and secondary central nervous system neoplasms. External-beam radiotherapy and gamma knife radiosurgery have become essential tools for managing these tumors.

Increasingly aggressive treatment protocols are being used in the hope of improving patient survival rates. These regimens, however, can lead to a wide spectrum of complications owing to the overlap between “effective” and “neurotoxic” doses of radiation. Differentiating tumor recurrence from treatmentinduced change is a clinical and radiological challenge.

Researchers have suggested three mechanisms to explain radiationinduced neurotoxic effects in the brain:

• Direct cellular damage. Radiation generates reactive oxygen species that damage cellular DNA, eventually leading to the induction of cellular apoptosis. Tumor cells with a high mitotic rate are affected the most because they are less able than normal cells to instigate DNA repair.

Healthy cells can undergo radiation-induced apoptosis too, the most sensitive being oligodendrocytes, endothelial cells, and subependymal cells. Neurons are relatively insensitive to radiation-induced damage.^1-3

• Vascular damage. Hyalinization, wall thickening, and fibrosis of irradiated vessels result in accelerated atherosclerosis with potential vascular obstruction and thrombosis. The endothelial damage and increased vascular permeability can also disrupt the blood-brain barrier.^1,4

• Inflammatory and immunologic phenomena. Cellular death and tissue destruction induces an immunologic response that results in reactive gliosis, endothelial proliferation, and other inflammatory changes. A complex scenario is generated and a vicious destructive cycle is set up.⁵

DIAGNOSTIC DILEMMA

Normal parenchyma close to target neoplasms can receive highs doses of radiation, resulting in edema, demyelination, and radiation necrosis. Radiation necrosis is the most severe of these radiation-induced injuries. This complication, which is secondary to coagulative necrosis of the brain, generally affects white matter at the site of the primary tumor. It is irreversible, often progressive, and fatal.^5-7

Distinguishing between radiation necrosis and tumoral recurrence presents clinicians and radiologists with an important diagnostic challenge. Both conditions occur within two years of radiation therapy, and morphological features are often unspecific. Symptoms associated with radiation necrosis are also unspecific. These include seizures, focal neurologic deficits, personality changes, memory loss, dementia, and/or reemergence of the initial tumor symptoms. Radionecrosis at the resected tumor bed may consequently mimic recurrence, while any radiation-induced lesions detected distant to the primary tumor site may be misinterpreted as multifocal glioma.⁶