<b>BRAIN</b>

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Radiation therapy plays an integral part in managing intracranial tumors. <b>While the risk: benefit ratio is considered acceptable for treating malignant tumors</b>, risks of long-term complications of radiotherapy need thorough assessment in adults treated for benign tumors. In one study of post-irradiation effects for benign brain tumors, 38% had delayed side effects of radiotherapy [visual deterioration, pituitary dysfunction, brain tissue changes, new cancers].
 
Areas that have been irradiated should be regularly observed not only for recurrence of the initial tumor or its metastasis, and for late radiation effect, but also for the possibility of development of a New Cancer. <b>Additional or returning symptoms may indicate recurrence OR metastasis of original tumor, OR radiation damage, OR a New Cancer developing at that site</b>. Differentiation of radiation pathology from recurrent or metastatic tumor or new malignancy can be difficult.
 
<b>Fraction size, total dose, and treatment time are all important factors when considering the biological effects of radiation. A total dose of >40 Gy was frequently a major predictor of radiation damage. The combination of chemotherapy and radiation therapy seems to aggravate the course of radiation damage</b>.
 
<b>Intracranial Radiation Damage</b>

Essentially, the late effects of radiation are probably due to one of two processes: damage to the wall of the blood vessels, or damage directly to the chromosomes of the exposed cells. Chromosomal damage is likely the cause of the New Cancers that develop years later. Most of the other symptoms of late effects probably come from damage to the irradiated blood vessels that service the tissues, and subsequent tissue death and atrophy. Radiation necrosis is the death of normal tissue in small, localized areas, as a result of radiation exposure.

The steroid responsive neurological deterioration assumed to represent late radiation damage is radiation dose dependent. It might be useful for prevention of radiation damage to use split-course-method or shrinking-technique at doses of 40 Gy or more. Radiation damage may present in a CT scan as a multifocal, disseminated lesion, and misdiagnosed as tumor spread. There is a need for prevention, appropriate diagnosis, and subsequent life-saving management.

The long-term changes during late delayed radiation-induced brain damage: The radiation damage appeared as an enhanced lesion. The volume and number of enhanced lesions continued to increase for 3 to 23 months (mean 10.3 months). The lesions then stabilized, and in four long-term survivors, the lesions then decreased in size. The intervals from onset to regression were 12, 13, 17, and 35 months (mean 19.3 months). But two patients showed a relapse of the enhanced lesion. Finally, the radiation-damaged brain became atrophic. <b>Late delayed radiation-induced brain damage continues to progress for over a year and then regresses, but thereafter a relapse may occur</b>.

<b>Whole-Brain Irradiation.</b>

<b>Late effects of Whole Brain Irradiation can include abnormalities of cognition [thinking ability] as well as abnormalities of hormone production</b>. The hypothalamus is the part of the brain that controls pituitary function. The pituitary makes hormones that control production of sex hormones, thyroid hormone, and cortisol. Both the pituitary and the hypothalamus will be irradiated if whole-brain irradiation occurs. Damage to these structures can cause disturbances of personality, libido, thirst, appetite, or sleep, and other symptoms, as well. The CT scans show cortical atrophy and/or third ventricle dilation in approximately 1/2 of the patients so affected. Psychiatric symptoms can be a prominent part of the clinical picture presented when radiation necrosis occurs. Psychiatric consultation should be obtained in the diagnosis and management of such patients.
 
<b>Focal Irradiation.</b>
 
Late effects of Focal [specific site, rather than general] Irradiation, whether external beam or implant, could be seen in those tissues which were exposed to the radiation. Blindness or other focal symptoms can occur as a late effect.

Late radiation necroses and late delayed radiation damage occurred in 50% of patients after permanent implantation of Iodine-125 seeds. The occurrence of radiation necrosis was correlated with total radiation dose, amount of implanted radioactivity, and with velocity of tumour shrinkage. 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 could probably be minimized either by reduction of irradiation dose, or by using temporary implants of Iodine-125.
 
<b>There is a need for precision, high dose radiotherapy.</b>
 
<b>Stereotactic radiation therapy of intracranial lesions</b>. Fractionated Stereotactic RadioTherapy is a noninvasive form of localized radiation that may be a suitable alternative to interstitial therapy. It uses a linear accelerator (6 MV photons). Treatment relies on a fixation system permits a precise use of the coordinates estimated at stereotactic computed tomography. The field of treatment can be exactly outlined in the CT images during repeat examinations, thus facilitating the recognition of changes induced by radiation. A dose of 40 Gy or more was a major predictor of steroid responsive neurological deterioration assumed to represent late radiation damage. Hypofractionated SRT is a noninvasive, well-tolerated, outpatient-based method of delivering palliative, high-dose, focal irradiation.
 
<b>Boron neutron capture therapy</b>. It can be suggested that BNCT is a radiotherapy that can produce "cure" of both malignant and benign brain tumors while preserving a good quality of life if conducted without previous conventional radiotherapy. Out of 87 patients operated on before May 1987, 18 lived or have lived longer than 5 years. Nine of these 18 lived or have lived longer than 10 years out of 53 patients operated on before May 1982. Among more-than-10-year survivors, only two died at 17 and 12 years. All of the others are still alive. The two died of delayed radiation damage because BNCT was applied to glioblastomas that recurred after their conventional radiotherapy. They lacked evidence of tumors when they died. <b>Out of these nine more-than-10-year survivors, three had been previously treated by conventional external radiotherapy and they developed radiation damage that brought all patients ultimately to an incapacitated condition. Two of the three died</b>. All the other 6 who were free from previous radiation history are active in their jobs and have no evidence of tumors. 

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