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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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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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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

= analysis of variance ; BBB = Basso-Beattie-Bresnahan ; SCI = spinal cord injury ; TTD = time to decompression . References 1. Arbit E , Galicich W , Galicich JH , Lau N : An animal model of epidural compression of the spinal cord. Neurosurgery 24 : 860 – 863 , 1989 Arbit E, Galicich W, Galicich JH, Lau N: An animal model of epidural compression of the spinal cord. Neurosurgery 24: 860–863, 1989 2747860 2. Astrup J , Siesjo BK , Symon L : Thresholds

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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

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Somatosensory evoked potentials and neurological grades as predictors of outcome in acute spinal cord injury

Chen Li, David A. Houlden, and David W. Rowed

A n accurate prognosis for recovery in patients with spinal cord injury is useful in planning acute management, rehabilitation, and counseling. Improved imaging techniques, such as computerized tomography, demonstrate spinal cord compression 2, 6, 31 but, in our experience, have failed to correlate well with either neurological deficit or prognosis for recovery. 11 Somatosensory evoked potential (SSEP) testing has been shown to have value in predicting recovery, 23, 24, 28–30, 38 but this has recently been questioned. 15, 21, 37 The present study attempts

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A therapeutic time window for anti-CD11d monoclonal antibody treatment yielding reduced secondary tissue damage and enhanced behavioral recovery following severe spinal cord injury

David S. Ditor, Feng Bao, Yuhua Chen, Gregory A. Dekaban, and Lynne C. Weaver

beginning at 2, 6, 12, or 24 hours following clip compression–induced SCI, and leukocyte infiltration and oxidative damage were assessed at 72 hours. In Study 2, rats were treated with either the anti-CD11d antibody or the 1B7 mAb starting at 6 hours after SCI (based on the findings obtained in Study 1) and then followed for 5 weeks to evaluate the effects of this delayed treatment on locomotor and autonomic function. Materials and Methods Spinal Cord Injury All protocols for these experiments were conducted in accordance with the policies established by the

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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

; CGRP = calcitonin gene—related protein ; CTB = cholera toxin subunit-B ; ECM = extracellular matrix ; GFAP = glial fibrillary acidic protein ; ML = mediolateral ; PBS = phosphate-buffered saline ; SCI = spinal cord injury . References 1. Benes V Jr , Rokyta R : Experimental spinal cord injury: lumbar vertebra resection to shorten the gap between spinal cord stumps. Acta Neurochir 90 : 152 – 156 , 1988 Benes V Jr, Rokyta R: Experimental spinal cord

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Magnetic resonance imaging versus histological assessment for estimation of lesion volume after experimental spinal cord injury

Laboratory investigation

David S. Ditor, Sunil John, Jason Cakiroglu, Colin Kittmer, Paula J. Foster, and Lynne C. Weaver

of lesion volume as obtained by MR imaging to those obtained using the Cavalieri method, 6 weeks after severe clip-compression injury (50 g) at the T-4 level in male Wistar rats. Methods Spinal Cord Injury All protocols for this experiment were carried out in accordance with the policies established by the Canadian Council on Animal Care and all protocols were reviewed and approved by the University of Western Ontario committee on animal experimentation. Male Wistar rats (Charles River Laboratories) weighing 200–250 g were used. The T-4 spinal cord

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The effect of nimodipine and dextran on axonal function and blood flow following experimental spinal cord injury

Michael G. Fehlings, Charles H. Tator, and R. Dean Linden

T here is evidence that spinal cord injury (SCI) in the acute phase is caused by two separate mechanisms: the initial mechanical damage and secondary changes due to vascular or biochemical effects. 2, 6, 36, 37 Indeed, measurements of spinal cord blood flow (SCBF) 2, 9, 12, 18, 19, 35, 47 as well as microangiographic studies 4, 14, 47 have shown ischemia at and extending away from the injury site. With recording of SCBF and motor and somatosensory evoked potentials (MEP's and SSEP's) from the cord with intraspinal microelectrodes, Fehlings, et al. , 9, 12

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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