Acute injury to the spinal cord initiates a sequence of vascular, biochemic
al, and inflammatory events that result in the development of secondary tis
sue damage. Experimental studies and clinical trials in humans have demonst
rated that the extent of this secondary tissue damage can be limited by pha
rmacologic intervention at appropriate intervals after injury. High doses o
f methylprednisolone sodium succinate (MPSS) improve the outcome of acute s
pinal cord injury in humans if treatment is initiated within 8 hours of inj
ury. Starting therapy more than 8 hours after injury is detrimental to outc
ome. The clinical efficacy of methylprednisolone in improving the outcome o
f canine spinal cord injuries has not yet been demonstrated and its use by
veterinarians is controversial. Many dogs are not seen by a veterinarian wi
thin the 8-hour window after injury, and these dogs frequently are treated
with nonsteroidal anti-inflammatory drugs or large doses of dexamethasone o
r prednisone before methylprednisolone treatment can be initiated, thus inc
reasing the risk of severe adverse effects. Other drugs that may provide sa
fer and more effective alternatives to methylprednisolone include thyrotrop
in-releasing hormone (TRH), the 21-aminosteroids, and kappa opioid agonists
. Recent studies suggest that modulation of the influx of inflammatory cell
s and activation of endogenous microglial cells may provide another means o
f improving the outcome of acute spinal cord injuries. Many drugs being dev
eloped to treat acute spinal cord injury have shown promising results when
evaluated experimentally. However, any proposed therapeutic strategy should
be evaluated in prospective blinded clinical trials before being adopted i
n clinics.