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Injury to the CNS from radiation is appropriately discussed here, since it occurs mainly in relation to therapy of brain tumors Three syndromes of radiation damage have been delineated: acute, early delayed, and late delayed, although these stages often blend into one another The acute reaction may begin during the latter part of a series of fractionated treatments or soon thereafter There may be a seizure, a transitory worsening of the tumor symptoms, or signs of increased intracranial pressure The EEG reveals delta waves but with preserved background activity Although the condition has been attributed to brain edema, this is not visible in MRI scans and its basis is unknown The symptoms subside in days to weeks Corticosteroids are usually administered, but with the exception of cases with demonstrable edema, their effect is uncertain The early delayed syndrome has been more troublesome in our experience As with the acute syndrome, focal tumor symptoms may increase, and as seen on MRI (Fig 31-23), the tumor mass enlarges, raising the possibility of further tumor growth, but again the symptoms usually resolve within 6 to 8 weeks Postmortem examination discloses extensive demyelination, loss of oligodendrocytes beyond the con nes of the tumor, and varying degrees of tissue necrosis Possibly the administration of dexamethasone or a similar corticosteroid hastens resolution The late delayed injury is the most serious of the three complications Here one nds in structures adjacent to a cerebral neoplasm, the pituitary gland, or other structures of the head and neck a coagulation necrosis of the white matter of the brain and occasionally of the brainstem In some areas, the tissue undergoes
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Figure 31-23 MRI showing early delayed radiation change in white matter of both frontal lobes, particularly severe on the right in the region of the treated glioma
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softening and liquefaction, with cavitation With lesser degrees of injury, the process is predominantly a demyelinating one, with partial preservation of axons Later reactions are thought to be due to diffuse vascular changes as a result of radiation energy Endothelial cells frequently multiply and, since ionization injures dividing cells, the vessels are most vulnerable The result is hyaline thickening of vessels with brinoid necrosis and widespread micorthrombosis There is a lesser degree of damage to glial cells Neurons are relatively resistant The symptoms of delayed injury, coming on 3 months to many years after radiation therapy, are either those of a subacutely evolving mass, dif cult to separate from those of tumor growth, or of a subacute dementia The clinical pattern varies with the site of the lesion: focal or generalized seizures, impairment of mental function, and sometimes increased intracranial pressure Whole-brain radiation for metastatic tumor or acute lymphoblastic leukemia can lead to multifocal zones of necrosis and holohemispheric spongiform changes in the white matter, with diffuse cerebral atrophy and enlarged ventricles Progressive dementia, ataxia, and urinary incontinence are the main clinical features of this state (DeAngelis et al) In its mildest form there are no radiographic changes aside from the tumor, but the patient becomes mentally dull, slightly disinhibited, and often sleepy for large parts of the day Panhypopituitarism is another complication of whole-brain radiotherapy, particularly in children, who may also suffer growth retardation Radiation necrosis of the spinal cord is described on page 1055 In the production of radiation necrosis, the total and fractional doses of radiation and the time over which treatment is administered are obviously important factors, but the exact amounts that produce such damage cannot be stated Accepted levels of large eld radiation are tolerated in amounts approaching 6000 cGy, provided it is given in small daily doses (200 to 300 cGy) 5 days per
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week over a period of 6 weeks [1cGY 100 rads (radiation absorbed dose), or 100 ergs per gram of irradiated material] Other factors, still unde ned, must play a part, since similar courses of radiation treatment may damage one patient and leave another unaffected The severe necrotizing encephalopathy that has followed the combined use of methotrexate (intrathecally but also intravenously) was discussed earlier, under Involvement of the Nervous System in Leukemia, the condition in which it was rst described and formerly was most prevalent CT scans show a low-density contrast-enhancing lesion, and by angiography there is an avascular mass MRI is somewhat more sensitive in distinguishing radiation necrosis from tumor and peritumor products, but positron emission tomography (PET) is the most reliable way of making this distinction, perhaps obviating the need for biopsy (Glantz et al) Single-photon emission tomography (SPECT) can be equally useful for this purpose (Carvalho et al) Treatment has consisted of corticosteroids, which may cause regression of symptoms and of edema surrounding the lesion Very high doses may be necessary, 40 mg or more of dexamethasone (or its equivalent) Rarely, surgical resection has been attempted, with indifferent results It is also known that tumors, usually sarcomas, can be induced by radiation, as mentioned earlier (Cavin et al) While well documented, this occurs rarely and only after an interval of many years We have also seen two cases of brosacroma of the brachial plexus region in the radiation eld for breast tumors (Gorson et al) These lesions appeared more than 10 years after the initial treatment, and many cases of even longer latency are on record Tumors of the spinal cord and peripheral nerves are discussed in Chaps 44 and 46, respectively The various neurologic effects of chemotherapy for systemic tumors, especially polyneuropathy, are discussed in Chaps 43 and 46
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