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Abstract

Hemorrhage in late cerebral radiation necrosis is a rare complication after radiotherapy for intracranial and extracranial neoplasms. We report 5 cases of acute hemorrhage in late radiation necrosis of the temporal lobe following radiation therapy for nasopharyngeal carcinoma. In a review of the literature, the authors identified a total of 27 such cases. The interval period between the onset of hemorrhage and cranial irradiation is long (mean = 7.8 years). The most prominent histological feature was the proliferation of large, dilated and thin-walled new blood vessels in a background of gliosis and fibrinoid necrosis of vessels. Rupture of these thin-walled new blood vessels is the proposed mechanism of hemorrhage in this condition.

Changes in Protein Level in the Cerebrospinal Fluid of a Patient with Cerebral Radiation Necrosis Treated with Bevacizumab

“… 3 , 4 The etiology of RN is not well known; however, endothelial cell dysfunction is thought to contribute to the pathogenesis that increases capillary permeability and extracellular edema. 5 It has been reported that resected RN lesions overexpress VEGF, which potentiates capillary permeability, contributing to RN pathogenesis. 6 , 7 von Baumgarten studied the bevacizumab effect on the morphologic and functional vascular changes using U87 mouse model.…”

Radiation induced temporal lobe necrosis in patients with nasopharyngeal carcinoma: a review of new avenues in its management

“…It may also be indicated in cases of TLN complicated by hemorrhage or brain abscess formation [8,64]. Previously, conflicting outcomes have been obtained with neurosurgery, with good outcomes in some [65] while poor in others [9].…”

“…Classical histological findings of TLN include various degrees of coagulative necrosis of brain parenchyma associated with fibrinoid changes of blood vessels while demyelination without blood vessel changes may be observed in less severely affected areas [6]. Other histological features include oligodendrocyte dropping out, axonal swelling, reactive gliosis, and disruption of the blood brain barrier [7,8]. …”

Blood-brain barrier permeability following conventional photon radiotherapy – A systematic review and meta-analysis of clinical and preclinical studies

“…It is assumed that cellular and vascular responses of the BBB upon RT are mediated by astrogliosis and endothelial ultrastructural changes [12] . These changes to the BBB can eventually lead to seizures, brain inflammation and leaky vessels causing haemorrhage and/or stroke [13] , [14] , [15] . Furthermore, it has been postulated that mostly RT with cumulative doses between 20 and 30 Gy increases BBB permeability [16] , however the actual impact of RT protocols (fractions, frequency) on BBB integrity remains to be elucidated, in order to support decision-making with regard to the prevention of toxicity and the use of concomitant chemotherapeutic therapies.…”