The cerebrospinal fluid (CSF) in delayed progressive radiation transverse myelopathy is normal except for a slight elevation of protein content in some cases. MRI of the affected segments of cord demonstrates abnormal signal intensity, decreased in T1-weighted and increased in T2-weighted images. Early in the course of the myelopathy the cord may be swollen, and there is often heterogeneous enhancement with gadolinium infusion. The location of the lesion corresponds to the irradiated portal, which can be identified by the radiation effect on the marrow of the overlying vertebral bodies. The spinal cord lesion tends to be more extensive in rostral–caudal dimension than the usual vascular or demyelinative myelopathy. These are important points to establish, because a mistaken diagnosis of intraspinal tumor or of a dural arteriovenous fistula may lead to an unnecessary operation or further irradiation.
Pathologic findings Corresponding with the level of the radiated area and extending over several segments, there is an irregular zone of coagulation necrosis involving both white and gray matter, the former to a greater extent than the latter. Varying degrees of secondary degeneration are seen in the ascending and descending tracts. Vascular changes—necrosis of arterioles or hyaline thickening of their walls and thrombotic occlusion of their lumens—are prominent in the most severely damaged portions of the cord. Most neuropathologists have attributed the parenchymal lesion to the blood vessel changes; others believe that the degree of vascular change is insufficient to explain the necrosis (Malamud et al; Burns et al). Certainly, the most severe changes in the cord are consistent with infarction, but the insidious onset and slow, steady progression of the disorder and the coagulative nature of the necrosis would then have to be explained by a steady succession of vascular occlusions. Exceptional instances, in which a transverse myelopathy has developed within a few hours of radiation treatment (as described by Reagan et al), are more readily explained by thrombotic occlusion of a large spinal artery.
Neurologists associated with cancer treatment centers are sometimes confronted with a patient who exhibits the late development (up to 10 to 15 years after radiation) of a slowly progressive sensorimotor paralysis of only one limb (motor weakness predominates) or one region of the body. This usually represents damage in the peripheral nervous system. Examples that we have encountered are multiple cranial neuropathies after radiation of nasopharyngeal tumors, cervical and especially brachial neuropathies after laryngeal and breast cancers, and lumbosacral plexopathies and cauda equina damage with pelvic radiation. These are discussed further in Chap. 43, on diseases of the peripheral nerves.
Treatment and prevention Kagan and colleagues have determined the tolerance of the adult human spinal cord to radiation, taking into account the volume of tissue irradiated, the duration of the irradiation, and the total dose. They reviewed all of the cases in the literature up to 1980 and concluded that radiation injury could be avoided if the total dose was kept below 6,000 cGy and was given over a period of 30 to 70 days, provided that each daily fraction did not exceed 200 cGy and the weekly dose was not in excess of 900 cGy. It is noteworthy that in the cases reported by Sanyal and associates, the amount of radiation surpassed these limits. Forewarned with this knowledge, radiation specialists have the impression that the incidence of this complication is decreasing, especially as newer sterotactic methods of delivering radiation are introduced.If the underlying neoplasm is likely to be imminently fatal, palliative radiation can exceed these limits.