• D A Nelson.
• Section of Neurology in Medicine, Medical Center of Delaware, Wilmington.
• Arch Neurol Chicago. 1988 Jul 1;45(7):804-6.

AbstractClinical trials first began in 1960 with methylprednisolone acetate (Depo-Medrol) administered intrathecally, in an attempt to treat both disk disease and multiple sclerosis. After a few reports of salubrious results, there began an outpouring of contradictory data, which continues in 1988. During this time span, researchers who cautiously tested the different theses of improvement began to publish serious warnings of many complications. For ten years prior to the intraspinal use of methylprednisolone acetate, basic scientists in anesthesiology and neurochemistry had published the following facts: (1) Methylprednisolone acetate's content of polyethylene glycol raises the risks of using it near the central nervous system. (2) Deleterious effects follow the use of glycols when they are placed into or near the neuraxis. (3) Methylprednisolone acetate contains approximately 30 mg of polyethylene glycol per milliliter. (4) When that glycol, which is both alcohol and detergent, is injected intraspinally, sterile meningitis, arachnoiditis, or pachymeningitis will occur. It has also been recognized since the 1960s that the epidural space is not wholly separate from the subdural and/or subarachnoid space. Many thousands of arachnoid villi subtend all the membranes from the intrathecal space, and many of these end in the large epidural veins. Therefore, the various spaces and membranes are not only contiguous, but continuous. It follows that an injection of methylprednisolone acetate into the epidural space does not guarantee that it will remain isolated there. Finally, the inadvertency of injections by the epidural route occurs with the following frequency: 40% of injections can be inadvertently made into interspinous ligaments, and 2.5% into the subarachnoid space.

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