Clinicopathologic Effects of a 21-Aminosteroid Compound (U74389G) and High-Dose Methylprednisolone on Spinal Cord Function After Simulated Spinal Cord Trauma

1995 ◽  
Vol 24 (2) ◽  
pp. 128-139 ◽  
Author(s):  
JOAN R. COATES ◽  
DONALD C. SORJONEN ◽  
STEPHEN T. SIMPSON ◽  
NANCY R. COX ◽  
JAMES C. WRIGHT ◽  
...  
2013 ◽  
Vol 179 (2) ◽  
pp. 345
Author(s):  
J.P. Pettiford ◽  
D. Juang ◽  
S. Shah ◽  
P. Thomas ◽  
N. Sharp ◽  
...  

2011 ◽  
Vol 28 (3) ◽  
pp. 287-294 ◽  
Author(s):  
Janine N. Pettiford ◽  
Jai Bikhchandani ◽  
Daniel J. Ostlie ◽  
Shawn D. St. Peter ◽  
Ronald J. Sharp ◽  
...  

Author(s):  
Saksith Smithason ◽  
Bryan S. Lee ◽  
Edward C. Benzel

Spinal cord injury (SCI), either traumatic or non-traumatic in aetiology, leads to temporary or permanent damage to the spinal cord function. Significant efforts have been directed towards the elucidation of the underlying pathophysiology of SCI. Both primary and secondary mechanisms of SCI exist, leading to immediate and often irreversible cell damage. Immediate treatment and adequate management in the setting of acute SCI are essential, preservation of even a small amount of functional neuronal tissue can permit ambulation. SCI is associated with a prolonged hospital stay, rehabilitation stay, and often associated with enormous monetary costs. Neurological recovery after SCI is largely dependent on the extent of injury. The management of SCI and the determination of the role and timing of surgical decompression remain crucial and yet controversial. Further epidemiological research and studies are warranted in order to enhance healthcare planning and cost-effectiveness.


Spinal Cord ◽  
2004 ◽  
Vol 43 (4) ◽  
pp. 199-203 ◽  
Author(s):  
T Qian ◽  
X Guo ◽  
A D Levi ◽  
S Vanni ◽  
R T Shebert ◽  
...  

2000 ◽  
Vol 55 (5) ◽  
pp. 452-453 ◽  
Author(s):  
T. Qian ◽  
D. Campagnolo ◽  
S. Kirshblum

Author(s):  
H. Hugenholtz ◽  
D.E. Cass ◽  
M.F. Dvorak ◽  
D.H. Fewer ◽  
R.J. Fox ◽  
...  

Background:A systematic review of the evidence pertaining to methylprednisolone infusion following acute spinal cord injury was conducted in order to address the persistent confusion about the utility of this treatment.Methods:A committee of neurosurgical and orthopedic spine specialists, emergency physicians and physiatrists engaged in active clinical practice conducted an electronic database search for articles about acute spinal cord injuries and steroids, from January 1, 1966 to April 2001, that was supplemented by a manual search of reference lists, requests for unpublished additional information, translations of foreign language references and study protocols from the author of a Cochrane systematic review and Pharmacia Inc. The evidence was graded and recommendations were developed by consensus.Results:One hundred and fifty-seven citations that specifically addressed spinal cord injuries and methylprednisolone were retrieved and 64 reviewed. Recommendations were based on one Cochrane systematic review, six Level I clinical studies and seven Level II clinical studies that addressed changes in neurological function and complications following methylprednisolone therapy.Conclusion:There is insufficient evidence to support the use of high-dose methylprednisolone within eight hours following an acute closed spinal cord injury as a treatment standard or as a guideline for treatment. Methylprednisolone, prescribed as a bolus intravenous infusion of 30 mg per kilogram of body weight over fifteen minutes within eight hours of closed spinal cord injury, followed 45 minutes later by an infusion of 5.4 mg per kilogram of bodyweight per hour for 23 hours, is only a treatment option for which there is weak clinical evidence (Level I- to II-1). There is insufficient evidence to support extending methylprednisolone infusion beyond 23 hours if chosen as a treatment option.


1972 ◽  
Vol 36 (4) ◽  
pp. 402-406 ◽  
Author(s):  
Thomas J. Croft ◽  
Jerald S. Brodkey ◽  
Frank E. Nulsen

✓ Cortical evoked potentials in anesthetized cats were recorded by a noninvasive averaging technique as a means of estimating spinal cord damage. Graded pressure on the spinal cord produced reversible blocking of these potentials. With this type of trauma, block of motor transmission through the cord paralleled the block of sensory transmission, and each seemed to be a sensitive indicator of spinal cord function. The possible use of such monitoring in anesthetized patients undergoing spinal operations is discussed.


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