[Actinic myelitis: diagnosis and treatment]

Spinal cord damage is one of the main dose limiting processes in radiation therapy. Radiation myelopathy was first observed in 1941, but it was only in the early 1980s that more clear information on tolerance was available. Animal experimentation in particular has thrown light on pathogenesis and factors playing a role in this pathology. Total dose, dose per fraction, age at irradiation, and interval between fractions are some of the main factors influencing this tolerance. From the literature the risk of progressive chronic radiation myelitis in man is estimated at less than 5%, with doses of 45-50 Gy in 1.8 to 2 Gy per fraction. The risk increases markedly with total dose and dose per fraction increase, and decreasing age. Cases of radiation myelitis are usually due to gross overdosage due to technical errors. More recently hyperfractionated accelerated schedules have occasioned major concern, with several unexpected myelopathies. Total cord dose using the alpha/beta model had appeared safe. Insufficient inter-fraction time (3-4 hours) is therefore likely to be the cause of the cases observed. Long half time for repair (underestimated in the LQ model) of sublethal damage resulting from slow tissue turnover is the most likely underlying mechanism. Morphological alterations are predominantly in white matter: lesions may be partial, focal or reaching total demyelinisation, with necrosis and malacia. Vascular damage may or may not be present. A dual pathogenesis is postulated. Oligodendrocytes and endothelial cells are the most likely target cells.(ABSTRACT TRUNCATED AT 250 WORDS)