Radiation myelopathy: New perspective on an old problem

Abstract

This article discusses recent advances in basic research that alter the view of the pathogenesis of radiation myelopathy and summarizes the available data from developmental neurobiology and preclinical studies on demyelinating diseases. These studies have produced interesting insights into oligodendrocyte development, intercellular signaling pathways, and myelination processes. Current findings suggest that administration of cytokines as platelet‐derived growth factor and basic fibroblast growth factor could increase proliferation of oligodendrocyte progenitors, enhance their differentiation, upregulate synthesis of myelin constituents, and promote myelin regeneration in the adult central nervous system (CNS). Other compounds might also be able to modulate the progression of pathogenic processes that lead to myelopathy. In addition, several possible biological prevention or treatment strategies, for example stimulation of endogenous cellular regeneration and glial cell transplantation, are discussed. Rationally designed animal experiments pursuing such strategies could further elucidate the pathogenesis of radiation‐induced CNS damage. Radiat. Oncol. Invest. 7:193–203, 1999. © 1999 Wiley‐Liss, Inc.

Oral administration of melatonin modulates the expression of tumor necrosis factor-α (TNF-α) gene in irradiated rat cervical spinal cord

“…1 In the emergency treatment of a cancer pressing on the spinal cord, radiotherapy may be used to reduce the size of the tumor and prevent nerve damage. 2 The dose that can be administered without radiation myelopathy (RM) is, however, limited by the tolerance of the spinal cord to radiation. 3 Pathological features of radiation myelopathy (RM) are well-defined, but the molecular mechanisms of this injury remain uncertain.…”

Post-irradiation Skin Changes Associated with Lumbosacral Radiculopathy

“…Therefore, the proximal nerve roots were considered to be the site of the main pathological lesion, and the term post-irradiation lumbosacral radiculopathy was suggested (3). Microvascular damage in the cauda equina and the breakdown of the blood-nerve barrier, followed by the activation of cytokines, is considered to be a possible mechanism of motor axon damage (8)(9)(10). Because the symptoms associated with this condition are non-specific and affected patients occasionally experience long periods of incubation, making an appropriate diagnosis is often difficult.…”

Improvement of Motor, Sensory, and Functional Status of Post-Guillain-Barre Syndrome with the Use of 4-Aminopyridine

“…This is based on one animal study utilizing radiation myelopathy [101]. First, this study [101] acknowledges that it is conflict with the study by Shi and Blight [102,103]. In their animal model of demyelinated spinal cord injury there was an improvement in conduction at the level of the axon with 4-AP [103].…”

“…Indeed, it can also be argued that both models have little in common with autoimmune CNS lesions of demyelination such as MS. In a rodent model, radiation to the spinal cord induces a late myelopathy that not only has effects on the oligodendrocytes, but also has effects on vascular tissue and progenitor cells that may impede central nervous system recovery from injury [102]. In GBS there often is a small area of focal demyelination.…”