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Neurosurgical Forum: Letters to the Editor To The Editor Carl-Henrik Nordström , M.D., Ph.D. Lund University Hospital Lund, Sweden 575 577 Abstract Object. Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid—base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia. Methods

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Asita Sarrafzadeh, Daniel Haux, Ingeborg Küchler, Wolfgang R. Lanksch, and Andreas W. Unterberg

levels compared with their levels in dialysates obtained in patients with favorable outcomes. 36 Microdialysis may help the physician select patients with poor-grade SAH in whom the prognosis after surgery is more favorable. The objectives of this study were as follows: 1) to evaluate whether cerebral metabolism measured by microdialysis differs in patients with high- and low-grade SAH; and 2) to determine if the microdialysis parameters are of prognostic value for the outcome in patients with SAH. Clinical Material and Methods This study was approved by the

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Alexandra Nagel, Daniela Graetz, Tania Schink, Katja Frieler, Oliver Sakowitz, Peter Vajkoczy, and Asita Sarrafzadeh

I ntracranial hypertension (ICP of ≥ 20 mm Hg) is common in patients with aSAH, even in those with low-grade aSAH. 9 , 13 Although this phenomenon has not been extensively studied, there is increasing evidence to support a relationship of high ICP and poor outcome after aSAH. 13 , 19 , 27 Many factors contribute to increased ICP, such as CSF outflow obstruction, hemorrhage volume, and cerebral edema. Elevated ICP has been associated with DIND, changes in CBF, and impaired cerebral metabolism with high levels of excitotoxic mediators. 3 , 8 , 11 , 26

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R. Tyler Frizzell, Yves J. Meyer, D. John Borchers, Bradley E. Weprin, Elizabeth C. Allen, W. Rene Pogue, John S. Reisch, Alan D. Cherrington, and H. Hunt Batjer

could be produced and to define the effects of etomidate on cerebral metabolism and CBF in this setting. Materials and Methods Animal Preparation Experiments were carried out on 29 mongrel dogs, weighing 19.0 to 36.2 kg each (mean ± standard error of the mean: 24.8 ± 1.9 kg), of either sex that were housed in an approved surgical facility. Laboratory protocol was approved by the University of Texas Southwestern Medical Center Investigational Review Board. All animals were fed at 3 p.m. on the day prior to the study and the food was not removed prior to the

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Sarah B. Rockswold, Gaylan L. Rockswold, Janet M. Vargo, Carla A. Erickson, Richard L. Sutton, Thomas A. Bergman, and Michelle H. Biros

treatments: the HBO chamber protocol in the earlier study was developed empirically, because there had been no specific recommendations in previous reports. Further investigation also was needed to elucidate the effect of HBO on cerebral metabolism, CBF, and ICP. The purpose of the present study, therefore, was to help determine the optimal HBO treatment paradigm as well as to elucidate potential metabolic effects of HBO in severely brain injured patients. Clinical Material and Methods Patient Population and Case Management Thirty-seven patients treated for

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Alois Zauner, Tobias Clausen, Oscar L. Alves, Ann Rice, Joseph Levasseur, Harold F. Young, and Ross Bullock

levels were markedly increased after TBI. This accords closely with the results in our human studies. 6, 7, 24 The highest glutamate levels in human studies were seen when intracranial hematomas or secondary ischemic insults were present, as in this animal study. 5, 7 Besides inducing ionic shifts and thus increasing cerebral metabolism, it is hypothesized that glutamate release after TBI is in part responsible for driving glycolysis. 1 An excessive glutamate release leads to an increase in lactate, although the exact mechanism for this increase is unknown and may

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Arthur Hosmann, Carmen Angelmayr, Andreas Hopf, Steffen Rauscher, Jonas Brugger, Lavinia Ritscher, Isabelle Bohl, Philipp Schnackenburg, Adrian Engel, Walter Plöchl, Markus Zeitlinger, Andrea Reinprecht, Karl Rössler, and Andreas Gruber

equipment failure. 4–8 In neurocritical care patients, an acute rise in intracranial pressure (ICP) and a critical drop of cerebral perfusion pressure are frequently observed, which might cause secondary brain injury. 4 , 7–9 However, a recent study using the microdialysis technique to monitor brain chemistry could not prove a significant effect of patient transportation on cerebral metabolism. 10 There were several important limitations of this study as it was retrospective, did not include data during the transport, and was performed in a mixed neurocritical care

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Michael N. Diringer, Kent Yundt, Tom O. Videen, Robert E. Adams, Allyson R. Zazulia, Ellen Deibert, Venkatesh Aiyagari, Ralph G. Dacey Jr., Robert L. Grubb Jr., and William J. Powers

substrate delivery is no longer adequate to meet metabolic needs. It is at this point that there is potential for tissue injury. Thus to assess whether hyperventilation leads to cerebral injury, its impact on CBF must be interpreted in relation to changes in OEF and CMRO 2 . Studies of hyperventilation during the first 24 hours after severe TBI have been limited and have not assessed its impact on cerebral metabolism. Given the potential for severe hyperventilation to produce cerebral injury, we chose first to study the impact of a moderate degree of hyperventilation on

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Sarah B. Rockswold, Gaylan L. Rockswold, David A. Zaun, Xuewei Zhang, Carla E. Cerra, Thomas A. Bergman, and Jiannong Liu

available. 47 , 66 Although severe TBI results in marked heterogeneous structural pathology, there are common metabolic pathways leading to cellular energy failure. 83 , 87 , 94 , 109 There is evidence of ischemia in the first 24 hours after injury, resulting in decreased O 2 delivery that is inadequate to maintain efficient oxidative cerebral metabolism. 8 , 9 , 102 This metabolic state appears to trigger a marked increase in the glycolytic metabolism of glucose. 6 , 7 , 37 This relatively inefficient anaerobic metabolism results in the depletion of cellular energy

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Sarah B. Rockswold, Gaylan L. Rockswold, David A. Zaun, and Jiannong Liu

combination of HBO 2 and NBH as a single treatment appeared compelling. The 2 treatments in tandem are potentially synergistic. The goal of this study was to evaluate cerebral metabolism, ICP, potential O 2 toxicity, and clinical outcome during a prospective, randomized Phase II clinical trial comparing a combined treatment of HBO 2 /NBH to standard care in patients with severe TBI. This study was a subsequent supplement to a larger prospective, randomized clinical trial. 45 This report differs from that previously published study in that O 2 delivery and cerebral