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Jin-Young Hwang, Seong-Won Min, Young-Tae Jeon, Jung-Won Hwang, Sang-Heon Park, Jin-Hee Kim and Sung-Hee Han

P araparesis or paraplegia is a serious complication following thoracoabdominal aortic aneurysm surgery and is a consequence of spinal cord ischemia-reperfusion injury secondary to aortic clamping and declamping. 9 A series of processes, including the glutamate-mediated excitotoxicity, inflammation, and apoptosis involved in spinal cord ischemia-reperfusion and oxidative stress, have emerged as key mechanisms of neuronal ischemia-reperfusion injury. 14 Ischemia-induced malfunction of the oxidative respiratory chain in mitochondria results in a burst of

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Claudia S. Robertson and Robert G. Grossman

to the right of the midline. The probe was perfused with buffered Ringer's solution at a rate of 10 µ l/min. The perfusate was collected at 5- to 15-minute intervals. Lactate concentration was measured in the dialysate samples by an enzymatic method. 6 Approximately 7% recovery of lactate was obtained with this probe construction and flow rate in in vitro studies. To produce spinal cord ischemia, a No. 4 French pediatric Swan-Ganz catheter § was inserted into the right femoral artery and was positioned in the aorta with the aid of fluoroscopic arteriography

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Edward H. Oldfield, Robert J. Plunkett, William A. Nylander Jr. and William F. Meacham

vascular occlusion is required. Although there are several clinical circumstances in which focal spinal cord ischemic injury occurs, 2–4, 8, 10, 11, 13, 38, 41, 46 the potential influence of barbiturates on spinal cord ischemia has received scant attention. Pentobarbital and thiopental have been the agents most frequently employed for experimental and clinical cerebral protection. Thiopental was chosen in this study because its lipid solubility is greater by 15- to 20-fold than that of pentobarbital and because of its relative ease in penetrating the central nervous

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Gokhan Kurt, Zuhal Yildirim, Berker Cemil, Emrah Celtikci and Gulnur Take Kaplanoglu

C urcumin , a polyphenol derived from the herbal remedy and dietary spice turmeric, possesses diverse antiinflammatory and anticancer properties following oral or topical administration. 29 , 40 Extensive research within the past decade has established curcumin as a pleotropic molecule, which is useful for neurodegenerative, cardiovascular, pulmonary, metabolic, arthritic, and autoimmune diseases. 24 Cemil et al. 6 showed neuroprotective effects of curcumin in an experimental spinal cord ischemia model. During surgery of abdominal aortic aneurysms

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Ivo Vanický, Martin Maršala, Ján Gálik and Jozef MarŠala

in this case are limited to secondary pathomechanisms, the highly effective spinal cord cooling achieved and the almost complete avoidance of systemic complications support a wide use of this technique. Extravascular perfusion cooling in spinal cord ischemia was reported by Negrin, 25 who used a heat-exchange device to induce deep hypothermia and observed complete neurological recovery after 90 minutes of aortic cross-clamping in dogs. Similarly, we recently tested the efficacy of a simple cold fluid infusion into the epidural space in a canine model, and a

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Aydemir Kale, Alp Özgün Börcek, Hakan Emmez, Zuhal Yildirim, Emre Durdağ, Neşe Lortlar, Gökhan Kurt, Fikret Doğulu and Nedret Kılıç

N eurological deficits that arise in connection with spinal cord ischemia after thoracoabdominal vascular procedures are not uncommon and may lead to catastrophic problems despite the advances in vascular operations. The pathophysiological mechanism of the ischemic/hypoxic damage to the spinal cord is still not completely understood. The physical damage occurring after trauma in the trauma zone results in tissue necrosis and loss of function due to mechanisms such as compression, distraction, and laceration; this is referred to as primary injury. The

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Man-Kai Cheng, Claudia Robertson, Robert G. Grossman, Richard Foltz and Vick Williams

direct information about the function of motor neurons, during the global ischemia produced by complete aortic occlusion the survival of motor neurons might correlate with survival of the dorsal interneurons. The purpose of our present study was to refine a classical model of spinal cord ischemia to include the following features: 1) rapid, simple preparation using a relatively noninvasive balloon catheter occlusion; 2) the ability to control or at least measure systemic factors that might contribute to ischemic injury; and 3) the capability of predicting

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Edward D. Hall

tested. The SCBF at 4 hours postinjury was increased from a mean of 4.5 ml/100 gm/min to 7.4 ml/100 gm/min after the administration of U74006F (p < 0.05, an increase of 64.4%). On the other hand, the MABP was not significantly altered. TABLE 3 Partial reversal of posttraumatic spinal cord ischemia by a 3-mg/kg intravenous dose of U74006F * Variable & Experiment No. Preinjury 4 Hrs Postinjury 4.5 Hrs Postinjury: After U74006F SCBF (ml/100 gm/min)  47D 14.6 4.3 9.3  47E 13.7 2.1 5.2  47F

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Edward D. Hall, Daniel L. Wolf and J. Mark Braughler

✓ The ability of a single large intravenous dose of methylprednisolone sodium succinate (MPSS: 15, 30, or 60 mg/kg) to modify the evolution of lumbar spinal cord ischemia in cats undergoing a contusion injury of 500 gm-cm is examined. Repeated measurements of spinal cord blood flow (SCBF) in the dorsolateral funiculus were made via the hydrogen clearance technique before and for 4 to 5 hours after injury. The mean preinjury SCBF for all animals was 12.29 ± 0.77 ml/100 gm/min. Following injury, SCBF began to decrease progressively in vehicle-treated animals to a level of 7.71 ml/100 gm/min, a fall of 37.3%. In contrast, cats that received a 30-mg/kg intravenous dose of MPSS at 30 minutes after injury maintained SCBF within normal limits (p < 0.05 at 3 and 4 hours after contusion). A 15-mg/kg MPSS dose was less effective at preventing posttraumatic white matter ischemia, and a 60-mg/kg dose was essentially ineffective.

It was determined that the 30-mg/kg MPSS dose was optimal for supporting SCBF when the drug was given at 30 minutes after spinal trauma, and a second series of experiments was carried out to examine the ability of this dose, when given at longer latencies, to improve decreased flow. Methylprednisolone given at 1½ hours after injury in four cats produced a slight (12.7%) but transient improvement in SCBF, and when administered at 4½ hours in another three animals was totally ineffective. These results show that MPSS in a 30-mg/kg dose can prevent posttraumatic spinal cord ischemia. However, it would appear that the ability of the steroid to reverse the ischemia once it has developed is limited, and probably lost, within a few hours of onset. This further suggests that the ischemic process is irreversible and underscores the need for early treatment with a large MPSS dose in order to prevent full development of ischemia and to promote neurological recovery.

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Gillian Shasby

T o T he R eadership : An error occurred during preparation of the paper “Neuroprotective effects of gabapentin on spinal cord ischemia-reperfusion injury in rabbits. Laboratory investigation” ( J Neurosurg Spine: published online May 20, 2011; DOI: 10.3171/2011.4.SPINE10583 ). The degree held by one of the authors, Nedret Kılıç, was incorrectly listed as M.D. The degree should have been listed as Ph.D. The list of authors now appears as the following: A ydemir K ale , M.D., A lp Ö zgün B örcek , M.D., H akan E mmez , M.D., Z uhal Y