Experimental neoplastic spinal cord compression: evoked potentials, edema, prostaglandins, and light and electron microscopy.

Spinal cord compression was induced in Fischer rats by percutaneous inoculation of 10(6) cells of malignant fibrous histiocytoma anterior to the T13 vertebral body. Paraplegia and incontinence occurred in all animals after 14-27 days (median, 23 +/- 3.0 days). Autonomic dysfunction and a measurable increase in tumor volume were documented with the use of computer tomography. The tumor penetrated the vertebral bone, invaded the epidural space, and gradually compressed the lumbar spinal segments. Electron-microscopic examination revealed dilated intermyelin spaces containing exuded homogenous material and extravasated leukocytes and erythrocytes. Myelin breakdown was accompanied by the presence of lipid-laden macrophages. Sequential recording of somatosensory evoked potentials (SEP) revealed a progressive increase in the latency of the cervical responses, which preceded the onset of clinical signs. In the presence of paraplegia, spinal cord conductivity was abolished. The levels of the prostaglandins TXB2, 6-keto-PGF1 alpha, and PGE2 were measured in the compressed and remote spinal cord segments during the presymptomatic and symptomatic periods. Only PGE2 was significantly elevated (P less than 0.001) in the paraplegic rats, all along the spinal cord segments. A significant increase in water content was measured in the compressed lumbar segments in the presymptomatic period, and when paralysis set in it was increased in the adjacent low thoracic area as well. Tissue specific gravity was significantly increased only in paraplegic rats in the compressed (P less than 0.01) and the adjacent low thoracic areas (P less than 0.05) but no significant change occurred during the presymptomatic period. Multiple mechanisms play a role in the pathogenesis of neurologic symptoms in neoplastic spinal cord compression.(ABSTRACT TRUNCATED AT 250 WORDS)