In order to assess the clinical and
biological effects of
glucocorticoids in the
therapy of epidural
spinal cord compression, the T8-10 epidural space of 50 rats was implanted with Walker 256
tumor. The rats were studied 10 to 20 days later when they became paraparetic. The regional blood-spinal cord transport constant (K, a function of the blood-spinal cord barrier) of 14Carbon-labeled aminoisobutyric
acid was measured with quantitative autoradiography 6 hours after
intravenous injection of low-dose (0.1 mg/kg), intermediate dose (1 mg/kg), and high-dose (10 mg/kg)
dexamethasone. The effects of
dexamethasone in these doses on the clinical signs and water content of the compressed cord were also evaluated 40 hours
after treatment began. The K factor increased 730% in compressed compared with noncompressed spinal cords (p less than 0.001).
Dexamethasone induced a dose-related reduction of both K (p = 0.007) and water content of the compressed cord (p less than 0.0001). Stabilization or, more rarely, improvement of weakness at 24 and 40 hours posttreatment correlated with the dose of
dexamethasone (r = 0.88, p less than 0.001). This study demonstrates that
dexamethasone has a dose-related beneficial clinical effect associated with an improvement of blood-spinal cord barrier breakdown and a reduction of the water content of the compressed cord. This study supports the use of highdose
dexamethasone for the initial treatment of epidural
spinal cord compression.