Neurol Med Chir (Tokyo) 1996 Dec;36(12):870-5; discussion 876 
<b>Long-term evaluation of radiation-induced brain damage by serial magnetic resonance imaging.</b> 
Kato T, Sawamura Y, Tada M, Abe H, Shirato H. 
Department of Neurosurgery, University of Hokkaido School of Medicine, Sapporo. 
&&url PMID: 9002715 


Strahlenther Onkol 1996 Oct;172(10):559-66 
<b>[Blood volume changes after the radiotherapy of the central nervous system].</b> [Article in German] 
Wenz F, Fuss M, Scholdei R, Essig M, Lohr F, Rempp K, Brix G, Knopp MV, Engenhart R, Wannenmacher M. Radiologische Universitatsklinik Heidelberg. 
BACKGROUND: <b>The pathogenesis of late delayed radiation damage in normal brain tissue is most likely due to damage to the vascular endothelium. The mitotic activity of gliomas was shown to correlate with the tumor induced angiogenesis. Dynamic susceptibility contrast MR imaging (DSC MRI) allows the measurement of the cerebral hemodynamics based on the indicator dilution theory. We describe theory and technique of the method and present our experience with blood volume measurements after irradiation of the CNS.</b>
&&url PMID: 8966673 


Int J Radiat Oncol Biol Phys 1994 Oct 15;30(3):557-65 
<b>Radiation therapy for pituitary adenoma: treatment outcome and prognostic factors.</b> 
Tsang RW, Brierley JD, Panzarella T, Gospodarowicz MK, Sutcliffe SB, Simpson WJ. Department of Radiation Oncology, Princess Margaret Hospital, Toronto, Ontario, Canada. 
...<b>Radiation was the contributing cause of the hypopituitarism in only 23%, 16%, and 13%, respectively. There were no cases of brain necrosis or radiation damage to the optic pathways. Two patients developed a fatal in-field glioma of the brain stem at 10 and 15 years following radiation. CONCLUSION: Postoperative external beam radiation therapy is highly effective in preventing recurrence of hormonally inactive pituitary adenomas. Hypopituitarism is commonly observed, but radiation can only be incriminated as the contributing cause in approximately one-fifth of the cases. Treatment of patients at the time of recurrence gave comparable local control rates to those irradiated initially. Favorable patients (age < or = 50, with small tumors removed totally) probably can be safely observed postoperatively with radiation reserved for recurrence.</b> 
&&url PMID: 7928486 


J Endocrinol Invest 1994 Sep;17(8):615-23 
<b>A prospective study of hypothalamus pituitary function after cranial irradiation with or without radiosensitizing chemotherapy.</b> 
Huang TS, Huang SC, Hsu MM. Department of Medicine, National Taiwan University Hospital, Taipei, Republic of China. 
<b>Hypopituitarism can occur after cranial irradiation.... In conclusion, cranial irradiation caused a progressive impairment of the hypothalamus-pituitary-endocrine axes. Combined CT may mask the radiation damage to GnRH neuron by inducing primary hypogonadism. There may be hippocampal damage in addition to hypothalamo-pituitary damage after cranial irradiation. Publication Types: Clinical trial Randomized controlled trial</b> 
&&url PMID: 7868799 


J Neurosurg 1990 Oct;73(4):502-12 Comment in: J Neurosurg. 1991 Jun;74(6):1026-7 
<b>The long-term side effects of radiation therapy for benign brain tumors in adults.</b> 
al-Mefty O, Kersh JE, Routh A, Smith RR. Department of Neurosurgery, University of Mississippi Medical Center, Jackson. 
...Findings related to tumor recurrence or surgery were excluded. Twenty-two patients had complications considered to be delayed side effects of radiotherapy. Two patients had visual deterioration developing 3 and 6 years after treatment; six had pituitary dysfunction; and 17 had varying degrees of parenchymal changes of the brain, occurring mostly in the temporal lobes and relating to the frequent presentation of pituitary tumors (two of these also had pituitary dysfunction). One clival tumor with the radiographic appearance of a meningioma, developed 30 years post-irradiation for acromegaly. This study unveils considerable delayed sequelae of radiotherapy in a series of adult patients receiving what is considered "safe" treatment for benign brain tumors. 
&&url PMID: 2204689


Neurol Med Chir (Tokyo) 1990 Jan;30(1):36-42Related Articles, Books, LinkOut 
<b>Radiation-induced brain damage in children--histological analysis of sequential tissue changes in 34 autopsy cases.</b> 
Oi S, Kokunai T, Ijichi A, Matsumoto S, Raimondi AJ. Department of Neurosurgery, Kobe University School of Medicine. 
.... The histological features of irradiated brains were compared with those of non-irradiated brains. Microscopic findings included demyelination (seven cases), focal necrosis (six cases), cortical atrophy (four cases), endothelial proliferation (four cases), and telangiectatic vascular proliferation with vascular thickening and oozing of a thick fluid (one case). Such findings were rare in non-irradiated patients. Demyelination was observed earliest in a patient who died 5 months after radiation therapy and was more common after 9 months. Focal necrosis was first observed 9 months post-irradiation but was more advanced and extensive after 1 year. Calcified foci were found only after 60 months. Various vascular changes such as vascular thickening and thrombosis suggested ischemic insult to the brain as a late effect of radiation injury. ... the manifestations of radiation-induced injury depend on the time elapsed after irradiation. 
&&url PMID: 1694271 


Acta Neurochir (Wien) 1989;99(3-4):104-8 
<b>Incidence of late radiation necrosis with transient mass effect after interstitial low dose rate radiotherapy for cerebral gliomas.</b> 
Wowra B, Schmitt HP, Sturm V. Clinic of Neurosurgery, University of Heidelberg, Federal Republic of Germany. 
Late radiation necroses constitute a hazard in low dose rate interstitial irradiation for inoperable gliomas. An incidence of 40% (8/20 patients) was found after permanent implantation of Iodine-125 seeds. This finding may even underestimate the real frequency...The occurrence of radiation necrosis was correlated with total radiation dose, amount of implanted radioactivity, and with velocity of tumour shrinkage. A mechanism underlying the development of radiation necrosis is proposed: A rapid shrinkage of tumour after interstitial Iodine-125 implantation may cause a significant irradiation of surrounding brain tissue, which was initially lying outside the target volume... the risk of radiation damage should be minimized. This could probably be achieved either by reduction of irradiation dose, or by using temporary implants of Iodine-125. 
&&url PMID: 2549766 


Gen Hosp Psychiatry 1986 Nov;8(6):437-41 
<b>Radiation damage to the brain: neuropsychiatric aspects.</b> 
McMahon T, Vahora S. 
Although radiation necrosis of the brain is a recognized complication of irradiation of the central nervous system, the psychiatric aspects of this phenomenon are less well defined. Two cases of radiation necrosis in which psychiatric symptoms were a prominent part of the clinical picture are presented. Factors that determine the evolution and clinical presentation of radiation necrosis are reviewed. In particular, the role of the consultation psychiatrist in the diagnosis and management of such patients is discussed. 
&&url PMID: 3792834 


J Neurosurg 1986 Oct;65(4):490-4 
<b>Hypothalamic dysfunction following whole-brain irradiation.</b> 
Mechanick JI, Hochberg FH, LaRocque A. 
The authors describe 15 cases with evidence of hypothalamic dysfunction 2 to 9 years following megavoltage whole-brain x-irradiation .... Fourteen patients displayed symptoms reflecting disturbances of personality, libido, thirst, appetite, or sleep. .... Seven patients developed cognitive abnormalities. .... Cortical atrophy was present in 50% of cases and third ventricular dilatation in 58%. Hypothalamic dysfunction, heralded by endocrine, behavioral, and cognitive impairment, represents a common, subtle form of radiation damage. 
&&url PMID: 3760958 


Surg Neurol 1984 Jan;21(1):35-41 
<b>Multifocal brain radionecrosis masquerading as tumor dissemination.</b> 
Safdari H, Boluix B, Gros C. 
The authors report on an autopsy-proven case of multifocal widespread radionecrosis involving both cerebral hemispheres and masquerading as tumor dissemination on a CT scan done 13 months after complete resection of an oligodendroglioma followed by radiation therapy. This case demonstrates that radiation damage may be present in a CT scan as a multifocal, disseminated lesion. Since the survival of brain-tumor patients who have undergone radiation therapy is prolonged by aggressive therapy, the incidence and variability of radiation-induced complications in such cases is likely to increase. For similar reasons, the radionecrosis in such cases should be taken into consideration. A short review of the CT scan findings and diagnostic and therapeutic considerations in a case of widespread radionecrosis is presented. The need for appropriate diagnosis and subsequent life-saving management is emphasized. 
&&url PMID: 6689807 


Q J Med 1982 Summer;51(203):279-91 
<b>Cerebral embolism in cancer patients.</b> 
Kearsley JH, Tattersall MH. 
Sudden neurological deterioration suggesting embolism in a patient with a history of cancer should alert the physician to the possibility of a non-metastatic, and therefore potentially reversible, cause of cerebral embolism before cerebral metastasis is implicated. During a four year period, we have observed eight cases of acute cerebral embolism among 3000 cancer patients seen in a department of medical oncology. Five patients had features post mortem of non-bacterial thrombotic endocarditis, and in one, the diagnosis had been made antemortem, but treatment with heparin did not prevent further emboli. Two patients had radiation related carotid vascular disease, and one patient post lymphangiographic embolism. The literature reporting these uncommon causes of cerebral embolism is reviewed. Post-lymphangiographic embolism carries a uniformly good prognosis. In selected cases of post-irradiation cerebral embolism, surgical intervention may prevent a neurological catastrophe. Non-bacterial thrombotic endocarditis and mucin embolism are of uncertain aetiology and natural history; long-term survival is uncommon, and treatment does not appear to influence the clinical course or outcome. 
&&url PMID: 7146312 


Neurosurgery 1981 Mar;8(3):329-33 
<b>Radiation necrosis after treatment of solitary intracranial metastases.</b> 
Sundaresan N, Galicich JH, Deck MD, Tomita T. 
During the period from July 1977 to June 1980, 75 patients underwent the surgical excision of solitary brain metastases, and 61 of these patients received whole brain radiation. Three patients developed chronic radiation necrosis. In the 3 patients with necrosis, computed tomography suggested recurrent tumor; the histological diagnosis of necrosis only was obtained at operation in 2 of these patients and by autopsy in the third. Radiation damage resulted in the death of 1 patient, a chronic vegetative state in another, and severe neurological deficit in the third. An additional 4 patients had neurological complications probably related to radiation therapy. As the survival of such patients is prolonged by aggressive treatment, the incidence of radiation-induced complications is likely to increase. The optimal dose of radiation necessary to destroy microscopic foci of tumor after the surgical resection of a single brain metastasis is unknown. Because of the significant incidence of damage after radiation as currently delivered, studies using graded, lower doses are indicated. 
&&url PMID: 7242882 


Morphol Igazsagugyi Orv Sz 1980 Apr;20(2):130-4 
<b>[Post-irradiation brain necrosis causing apoplexy and death 33 years after irradiation].</b>[Article in Hungarian] 
Frohlich A. 
A case of post-irradiation brain-necrosis resulting in apoplexia of the cerebellum after 33 years of irradiation (19 984 r.) of a presumptive cerebellar tumour in childhood is reported. The pathohistologic study revealed symptoms of the "late" damage and vascular changes appeared to be the most prominent. Thickening of the vessel walls, hyperplasia of collagen fibres and deposition of calcium in the media, were the most characteristic lesions revealed. In some of the small vessels isolated calcification of the media was observed. It seems most probable, that in the development of apoplexia vascular alterations could play an important part. In the available literature author has not found report on a similarly long interval elapsing between the irradiation and death. 
&&url PMID: 7266501