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A reproducible spinal cord injury model in the cat

Ronald W. J. Ford

D evelopment of a reproducible model of spinal cord injury has been the object of much research since Allen 4 first designed a technique for producing measurable experimental spinal cord trauma. He produced cord injuries by dropping a 30-gm weight from various heights onto the exposed dura of dog spinal cords. Other quantitative methods of injuring the spinal cord have been developed and include compressing the cord with epidural balloons, 29, 36, 48 circumferential cuffs, 30, 49 weights, 5, 6, 23, 41, 44 or aneurysm clips, 45 and by spinal distraction. 8

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The therapeutic window for spinal cord decompression in a rat spinal cord injury model

Christopher B. Shields, Y. Ping Zhang, Lisa B. E. Shields, Yingchun Han, Darlene A. Burke, and Norman W. Mayer

spinal cord compression. Although the relative contribution of each factor is unknown, we believe that the neurological deficit will be more pronounced as each component increases in severity either singly or combined. In our previous study of a rat stenosis—SCI model, mild spinal canal stenosis (< 35%) combined with a 12.5-g cm contusion injury at T-10 caused no additional locomotor dysfunction than that produced by the SCI itself. 6 Furthermore, severe stenosis (> 50%) and SCI resulted in irreversible damage and necrosis, presumably by direct severe spinal cord

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Methylprednisolone and neurological function 1 year after spinal cord injury

Results of the National Acute Spinal Cord Injury Study

Michael B. Bracken, Mary Jo Shepard, Karen G. Hellenbrand, William F. Collins, Linda S. Leo, Daniel F. Freeman, Franklin C. Wagner, Eugene S. Flamm, Howard M. Eisenberg, Joseph H. Goodman, Phanor L. Perot Jr., Barth A. Green, Robert G. Grossman, John N. Meagher, Wise Young, Boguslav Fischer, Guy L. Clifton, William E. Hunt, and Nathan Rifkinson

T he National Acute Spinal Cord Injury Study Group has conducted the first multi-center randomized clinical trial of a treatment modality for acute spinal cord injury. The study contrasted the efficacy of a 1-gm bolus dose of methylprednisolone sodium succinate (MPSS) followed by 1 gm daily for 10 days with results of an identical regimen using 0.1 gm of MPSS. We have previously reported the absence of any effect of the high-dose MPSS on neurological function 6 weeks and 6 months after injury. 2 This paper reports our analysis of the neurological function of

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Vascular mechanisms in the pathophysiology of human spinal cord injury

Charles H. Tator and Izumi Koyanagi

I ntensive studies of the pathophysiology of spinal cord injury have provided evidence that the primary mechanical trauma is followed by secondary injury mechanisms that contribute to the necrotizing process and that vascular injuries play a key role in both primary and secondary damage. 26, 38–40 For example, experimental studies have reported significant posttraumatic ischemia at the injured segment and adjacent areas after severe spinal cord injury. 9, 10, 13, 32, 33 Using microangiographic techniques, regions of severe ischemia were demonstrated in the

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Failure of tetracaine to reverse spinal cord injury in the cat

Ronald W. J. Ford and David N. Malm

pressure, heart rate, end-tidal CO 2 , and esophageal temperature were continuously recorded throughout the operative period on a six-channel Honeywell chart recorder. ‖ Injury Technique Spinal cord injuries were produced using a modified Allen technique. 22 Briefly, under general anesthesia, a partial laminectomy was performed at L-1, and the spine immobilized by clamping the spinous processes of T-13 and L-2 to the framework of the injury apparatus. A curved stainless steel plate, or anvil, was placed beneath the spinal cord and dura to center the cord and

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Dural closure, cord approximation, and clot removal: enhancement of tissue sparing in a novel laceration spinal cord injury model

Yi Ping Zhang, Christopher Iannotti, Lisa B. E. Shields, Yingchun Han, Darlene A. Burke, Xiao-Ming Xu, and Christopher B. Shields

S pinal cord injury is a devastating affliction that may produce lasting functional deficits due to irreversible damage to both descending and ascending axonal pathways. 43 Laceration of the spinal cord may be caused by bone fragments, gunshot wounds, and stab injuries. 2, 33, 35 Functional recovery after complete transection of the spinal cord can occur in mice if dural injury, retention of the ends of the spinal cord, and fibroblastic infiltration are minimized. 39 Several pathophysiological events occur following laceration-related SCI, including

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Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms

Charles H. Tator and Michael G. Fehlings

I n most countries, acute spinal cord injury occurs at an annual rate of 20 to 40 persons per million 85 and, although prevention programs have been initiated, there is no evidence that the incidence is declining. The main causes of spinal cord trauma are motor-vehicle accidents, sports and recreational activities, accidents at work, and falls at home. 122 Approximately half of the patients with spinal cord trauma have complete injuries of the spinal cord with no preservation of voluntary motor or sensory function below the level of the lesion, and almost

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Value of gas myelography in early management of acute cervical spinal cord injuries

Alain B. Rossier, Jean Berney, Arthur E. Rosenbaum, and Jurg Hachen

of radiographic evidence of bone defects. Myelographie absence of spinal cord compression should contraindicate surgical decompressive procedures. The present study was undertaken to assess the role of gas myelography in the diagnosis and treatment of acute cervical spine injuries with neurological involvement. Clinical Material and Methods Clinical Material Twenty-two patients with severe, acute injuries of the cervical spine were studied. Fourteen had a complete sensorimotor lesion from the very onset, three had an incomplete sensorimotor lesion, and

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Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data

Results of the second National Acute Spinal Cord Injury Study

Michael B. Bracken, Mary Jo Shepard, William F. Collins Jr., Theodore R. Holford, David S. Baskin, Howard M. Eisenberg, Eugene Flamm, Linda Leo-Summers, Joseph C. Maroon, Lawrence F. Marshall, Phanor L. Perot Jr., Joseph Piepmeier, Volker K. H. Sonntag, Franklin C. Wagner Jr., James L. Wilberger, H. Richard Winn, and Wise Young

A randomized double-blind clinical trial of the efficacy of very high doses of methylprednisolone or naloxone, compared with placebo, in the early treatment of acute spinal cord injury was conducted. In a previous report, 8 we have shown that neurological function is significantly improved 6 weeks and 6 months after injury among patients starting methylprednisolone treatment within 8 hours of injury. In this paper, we report the 1-year follow-up results of this trial: the second National Acute Spinal Cord Injury Study (NASCIS). We provide further details

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Therapeutic trial of hypercarbia and hypocarbia in acute experimental spinal cord injury

Ronald W. J. Ford and David N. Malm

M any studies have demonstrated that acute experimental spinal cord injuries sufficient to cause permanent paraplegia result in a marked reduction of blood flow in both the white and gray matter of the injured cord. 1, 3–12, 15, 19, 20, 22–24, 28–30 This ischemic process is thought to play a major role in the pathophysiology of spinal cord injuries. Improved spinal cord blood flow at the injury site has been observed following sympathectomy 28 and after administration of vasopressor drugs, 23, 25 mannitol, 19 aminophylline plus isoproterenol, 10