Clinical use of spinal or epidural steroids

Steroids, drugs with potent antiinflammatory properties on the damaged nervous roots, have been especially used as adjuvants of local anesthetics, by spinal route, in the treatments of low-back pain. Spinal route was chosen to obtain a higher local concentration of drug, with few systemic side effects and to improve drug's action mechanism. Steroids seem to interact with GABA receptors and thus control neural excitability through a stabilising effect on membranes, modification of nervous conduction and membrane hyperpolarization, in supraspinal and spinal site. Epidural steroids are especially used in the treatment of low back pain due to irritation of nervous roots. They have been administered alone or in association with local anesthetics and/or saline solution. Slow release formulations have been generally used (methylprednisolone acetate, and triamcinolone diacetate). Other indications of epidural steroids are: postoperative hemilaminectomy pain, prevention of post herpetic neuralgia, degenerative ostheoartrithis. Intra-thecal steroids have been frequently used in the treatment of lumbar radiculopathy due to discopathy, as an alternative treatment when epidural administration is ineffective. Positive results have been obtained with methylprednisolone acetate, alone or in association with local anesthetics. Complications related to intraspinal steroids injections are due to execution of the block and side effects of drugs. Complications associated with intrathecal steroids are more frequent and severe than epidural injections and include: adhesive arachnoiditis, aseptic meningitis, cauda equina syndrome. Steroidal toxicity seems to be related to the polyethylenic glycole vehicle. Anyway, slow release formulations contain less concentrated polyethylenic glycole. The epidural administration, a correct dilution of steroid with local anesthetics solution and/or saline solution, and a limited number of injections (no more than three) allows a significant reduction of steroid neurotoxicity.