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Rachid Assina, Tejas Sankar, Nicholas Theodore, Sam P. Javedan, Alan R. Gibson, Kris M. Horn, Michael Berens, Volker K. H. Sonntag and Mark C. Preul

S pinal cord injury is a devastating clinical condition, with immense costs to both the individual and society. Current treatments for SCI are of limited therapeutic efficacy, which may be due to the poor capacity of axons in the mammalian CNS to regenerate. Over the past 2 decades, novel experimental therapeutic approaches have been developed to promote axonal regeneration and, by extension, functional recovery in animal models of SCI. Several of these strategies have used intraspinal cellular transplantation techniques in an attempt to overcome the

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Adib A. Abla, Timothy Uschold, Mark C. Preul and Joseph M. Zabramski

the use of live animal models provides the most realistic experience, their use requires strict adherence to institutional protocols regarding animal welfare, including appropriate housing and surgical management, and imposes significant time and location constraints on practice. These impediments exist aside the ethical issues raised by the use of live animal models for training. Prior reports have described the use of the turkey neck carotid artery 1 and the chicken wing brachial artery as models for practicing the microvascular anastomosis technique in the lab

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Celeste R. Brennecka, Mark C. Preul, Timothy A. Becker and Brent L. Vernon

Characteristics This 6-month pilot study was designed to investigate the potential effectiveness of using PPODA-QT as an embolic agent in experimental aneurysms. The study design included 3 groups: PPODA-QT alone, PPODA-QT delivered after placement of a single 3D framing coil, and standard embolization with coils only. Because this study was designed to be a “proof of concept” investigation in an appropriate animal model, only 3 subjects were included in each experimental group, and angiographic scoring was not blinded. In addition, the resulting tissue differences between

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Mark C. Preul, Patrick K. Campbell, David S. Garlick and Robert F. Spetzler

proceed judiciously when applying a hydrogel in tight anatomical areas or in situations in which there may be added instrumentation in association or contact with the hydrogel. Such materials added to the dura require rigorous testing and follow-up in large animal models to adequately mimic the gauge (size of the human spinal dural tube) and conditions of human anatomy and surgery. This further testing is particularly important for materials in which the inhibition of peridural scarring at the cost of dural healing is undesired. For example, initial excitement about

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Robert W. Ryan, Robert F. Spetzler and Mark C. Preul

needed to be low to avoid explosive damage to adjacent structures, no attempt was made to resect tumor tissue with the laser, and only minimal areas of tumor necrosis were induced, with no improvement in patient survival. Encouraged by their results in animal models, Stellar and colleagues 31 , 32 were, in 1969, the first to attempt the resection of a human brain tumor, a recurrent glioblastoma multiforme, by using the continuous-wave CO 2 laser ( Fig. 4 ). Given the location of the tumor in the left frontal area, gross-total resection was not attempted, but the

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Eric M. Horn, Nicholas Theodore, Rachid Assina, Robert F. Spetzler, Volker K. H. Sonntag and Mark C. Preul

the efficacy of lumbar CSF drainage in decreasing the amount of spinal cord ischemia both in animal models of spinal cord ischemia and in patients undergoing thoracic aorta cross-clamping for aneurysm surgery. 5 , 6 , 9 Based on these background studies, the objectives of the present study were first to determine the effects of CSF drainage on spinal cord tissue perfusion, and then test whether this treatment led to improvements in the electrophysiological, histological, and physiological outcomes in an animal model of acute SCI. Methods All methodologies

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Tejas Sankar, Rachid Assina, John P. Karis, Nicholas Theodore and Mark C. Preul

-described hazard of mannitol use in treating tumoral vasogenic edema, the so-called rebound phenomenon, in which ICP becomes elevated above pretreatment levels following several mannitol doses. 9 , 12 Rebound is believed to be caused by the penetration of mannitol into the brain parenchyma surrounding a tumor, which reverses the osmotic gradient between the blood and the extracellular space leading to a subsequent increase in edema. 9 , 16 , 17 To date there has been a paucity of evidence supporting this putative mechanism. Kaufmann and Cardoso 11 used an animal model of

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Mark C. Preul, Phillip B. Long, Jeffrey A. Brown, Manuel E. Velasco and Michael T. Weaver

which percutaneous compression injures or depletes primary afferent axons and cell bodies of the trigeminal ganglion and axons in the trigeminal root using the animal model. Materials and Methods Adult New Zealand White rabbits were selected for these experiments because of similarities of the autonomic response during trigeminal low-frequency electrical and mechanical stimulation to that seen in humans during percutaneous compression. 7, 19 In preliminary experiments, a modified No. 18 thin-wall needle * and a No. 2 Fogarty embolectomy catheter † were

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Editorial

Cavernous malformations

Issam A. Awad

antedating submission of the manuscript. While some articles on the basic biochemistry of CCM proteins or the CCM phenotype in nonmammalian species may be beyond the scope of a review targeting a neurosurgical readership, I wish to highlight other omissions that may inadvertently sideline cardinal discoveries and critical translational concepts relevant to our understanding of CCM as well as forthcoming translational strategies. While discussing animal models, for example, Cavalcanti and colleagues 3 do not mention the key article by Shenkar et al. 18 in the

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Daniel D. Cavalcanti, M. Yashar S. Kalani, Nikolay L. Martirosyan, Justin Eales, Robert F. Spetzler and Mark C. Preul

reduced expression of Notch 4 was seen in surgical specimens obtained from patients carrying mutations in CCM1, suggesting that mutations in the transforming growth factor β signaling pathway may cause the formation of CCMs. Lessons Learned From Various Animal Models of CCM Given the rare nature of CCMs, animal models have been the key source for studying CCM pathology. Animal models have helped to establish the role of CCM genes in vascular development and the pathobiology of CCM lesion development and to explain their focal nature. Zhang et al. 114 mapped