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delivery exceeds metabolic requirements by a factor of two to three, there is a considerable reserve in place before available O 2 is reduced below the minimum needed to maintain cerebral metabolism. It is only when available O 2 falls below this minimum level that the brain can no longer produce sufficient high-energy phosphate molecules to maintain its functions (energy failure). Energy failure must occur before ischemic damage is possible. Thus, the question that needs to be addressed is whether hyperventilation in patients with TBI reduces CBF to the point of

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Wilson P. Daugherty, Joseph E. Levasseur, Dong Sun, Gaylan L. Rockswold, and M. Ross Bullock

, Doppenberg E, Bullock R, et al: Glucose and lactate metabolism after severe human head injury: influence of excitatory neurotransmitters and injury type. Acta Neurochir Suppl 75: 21–24, 1999 3. Andersen BJ , Marmarou A : Post-traumatic selective stimulation of glycolysis. Brain Res 585 : 184 – 189 , 1992 Andersen BJ, Marmarou A: Post-traumatic selective stimulation of glycolysis. Brain Res 585: 184–189, 1992 4. Artru F , Philippon B , Gau F , et al : Cerebral blood flow, cerebral metabolism and

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Peter A. Winkler, Walter Stummer, Rainer Linke, Kartik G. Krishnan, and Klaus Tatsch

issue has not been previously addressed, our prospective study was designed to investigate the influence of cranioplasty on indices of CBF as determined by TCD ultrasonography during postural maneuvers. From the TCD findings the CVR capacity (as a percentage value) was calculated. Furthermore, the effect of cranioplasty on cerebral metabolism was investigated using 18 FDG-PET, which also served as an indicator of functional improvement. Clinical Material and Methods This study was approved by the ethics committee of the Ludwig Maximilian University, Munich, Germany

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Martin M. Tisdall, Ilias Tachtsidis, Terence S. Leung, Clare E. Elwell, and Martin Smith

shown to improve cerebral metabolism and outcome, but studies of NBH have produced variable results. In a fluid percussion injury model in rats, HBH alleviated injury-induced reduction in mitochondrial redox and increased cerebral O 2 consumption. 9 In a randomized controlled clinical trial, Rockswold et al. 34 found that HBH reduced mortality rates after TBI without increasing the number of patients with favorable outcome. In a further study by the same group, HBH reduced the lactate concentration in the cerebrospinal fluid, and this effect lasted for 6 hours

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outcome after head injury. J Neurol Neurosurg Psychiatry 57 : 717 – 723 , 1994 Gopinath SP, Robertson CS, Contant CF, et al: Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psychiatry 57: 717–723, 1994 3. McHenry LC Jr , Slocum HC , Bivens HE , et al : Hyperventilation in awake and anesthetized man. Effects on cerebral blood flow and cerebral metabolism. Arch Neurol 12 : 270 – 277 , 1965 McHenry LC Jr, Slocum HC, Bivens HE, et al: Hyperventilation in awake and

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Delbert E. Evans, Philip W. Catron, James J. McDermott, Linda B. Thomas, Arthur I. Kobrine, and Edward T. Flynn

neural function when given immediately after the ischemic event. The mechanisms by which lidocaine was effective is unknown. Two separate actions seem possible: an action on cerebral blood vessels or an action on neural membranes and cerebral metabolism. With regard to the first possibility, lidocaine has been shown to cause both vasodilation and vasoconstriction depending upon the dose, the method of administration, and the vascular bed being studied. 1, 32, 38 However, intravenous lidocaine has been found to sharply decrease the elevated intracranial pressure

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Nathan Beucler, Aurore Sellier, and Arnaud Dagain

3 different intracerebral monitoring devices (intracerebral pressure probe, oxygen pressure probe, and microdialysis probe). Invasive cerebral monitoring is known to be possibly associated with numerous complications, among which are hematoma, infection, device misplacement, and seizures. 11 Could the authors provide data concerning the complications if encountered and the induced morbidity? This study preaches toward high SBP targets to optimize cerebral metabolism in the acute phase after ICH. Nevertheless, the choice of the primary endpoint and its

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Roberto Imberti, Marinella Fuardo, Guido Bellinzona, Michele Pagani, and Martin Langer

, Frederiksen R , Pless S : Effects of perioperative indomethacin on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients subjected to craniotomy for cerebral tumors. J Neurosurg Anesthesiol 8 : 273 – 279 , 1996 Bundgaard H, Jensen K, Cold GE, Bargholt B, Frederiksen R, Pless S: Effects of perioperative indomethacin on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients subjected to craniotomy for cerebral tumors. J Neurosurg Anesthesiol 8: 273–279, 1996 3 Cruz J

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Setti S. Rengachery, David A. Roth, Norman W. Andrew, and Vernon H. Mark

. , Cooper , D. Y. , Emmel , G. L. , Loeschcke , H. H. , and Schmidt , C. F. Oxygen toxicity. Effects in man of oxygen inhalation at 1 and 3.5 atmospheres upon blood gas transport, cerebral circulation and cerebral metabolism. J. appl. Physiol. , 1953 , 5 : 471 – 486 . Lambertsen , C. J., Kough , R. H., Cooper , D. Y., Emmel , G. L., Loeschcke, H. H., and Schmidt , C. F. Oxygen toxicity. Effects in man of oxygen inhalation at 1 and 3.5 atmospheres upon blood gas transport, cerebral circulation and cerebral metabolism. J. appl

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: Effects of perioperative indomethacin in intracranial pressure, cerebral blood flow, and cerebral metabolism in patients subjected to craniotomy for cerebral tumors. J Neurosurg Anesthesiol 8 : 273 – 279 , 1996 Bundgaard H, Jensen K, Cold GE, Bergholt B, Frederiksen R, Pless S: Effects of perioperative indomethacin in intracranial pressure, cerebral blood flow, and cerebral metabolism in patients subjected to craniotomy for cerebral tumors. J Neurosurg Anesthesiol 8: 273–279, 1996 3. Cold GE : Does acute hyperventilation provoke