suggestive of traumatic vasospasm are unlikely to improve the patients' cerebral metabolism and clinical outcomes, unless cerebral oxygen extraction is abnormally high (which has not been found 4 ). References 1. Cruz J : An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J Neurosurg 82 : 379 – 385 , 1995 Cruz J: An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J
Daniel F. Kelly, Neil A. Martin, Rouzbeh Kordestani, George Counelis, David A. Hovda, Marvin Bergsneider, Duncan Q. McBride, Ehud Shalmon, Dena Herman, and Donald P. Becker
surprising given the decline in blood flow that normally occurs with aging, presumably as a result of reduced cerebral metabolic demands. 27, 32 The strong correlation between age and outcome seen in this and other studies, although likely to be multifactorial, may be related to a global reduction in cerebral metabolism. 46 Regarding the increased incidence of evacuated subdural or intracerebral hematomas in Groups 1 and 2, a similar correlation between evacuated intradural hematomas and low blood flow has been reported by Bouma, et al. 6 Salvant and Muizelaar 42 also
Daniel F. Kelly, Neil A. Martin, Rouzbeh Kordestani, George Counelis, David A. Hovda, Marvin Bergsneider, Ehud Shalmon, Duncan Q. McBride, Dena Herman, and Donald P. Becker
As part of a prospective study of the cerebrovascular effects of head injury, 54 moderate and severely injured patients underwent 184 133Xe-cerebral blood flow (CBF) studies to determine the relationship between the period of maximum blood flow and outcome. The lowest blood flows were observed on the day of injury (Day 0) and the highest CBFs were documented on postinjury Days 1 to 5. Patients were divided into three groups based on CBF values obtained during this period of maximum flow: Group 1 (seven patients), CBF less than 33 ml/100 g/minute on all determinations; Group 2 (13 patients), CBF both less than and greater than or equal to 33 ml/100 g/minute; and Group 3 (34 patients), CBF greater than or equal to 33 ml/100 g/minute on all measurements. For Groups 1, 2, and 3, mean CBF during Days 1 to 5 postinjury was 25.7 ± 4, 36.5 ± 4.2, and 49.4 ± 9.3 ml/100 g/minute, respectively, and PaCO2 at the time of the CBF study was 31.4 ± 6, 32.7 ± 2.9, and 33.4 ± 4.7 mm Hg, respectively.
There were significant differences across Groups 1, 2, and 3 regarding mean age, percentage of individuals younger than 35 years of age (42.9%, 23.1%, and 76.5%, respectively), incidence of patients requiring evacuation of intradural hematomas (57.1%, 38.5%, and 17.6%, respectively) and incidence of abnormal pupils (57.1%, 61.5%, and 32.4%, respectively). Favorable neurological outcome at 6 months postinjury in Groups 1, 2, and 3 was 0%, 46.2%, and 58.8%, respectively (p < 0.05). Further analysis of patients in Group 3 revealed that of 14 with poor outcomes, six had one or more episodes of hyperemia-associated intracranial hypertension (simultaneous CBF > 55 ml/100 g/minute and ICP > 20 mm Hg). These six patients were unique in having the highest CBFs for postinjury Days 1 to 5 (mean 59.8 ml/100 g/minute) and the most severe degree of intracranial hypertension and reduced cerebral perfusion pressure (p < 0.0001).
These results indicate that a phasic elevation in CBF acutely after head injury is a necessary condition for achieving functional recovery. It is postulated that for the majority of patients, this rise in blood flow results from an increase in metabolic demands in the setting of intact vasoreactivity. In a minority of individuals, however, the constellation of supranormal CBF, severe intracranial hypertension, and poor outcome indicates a state of grossly impaired vasoreactivity with uncoupling between blood flow and metabolism.
Paul M. Vespa, Marc R. Nuwer, Valeriy Nenov, Elisabeth Ronne-Engstrom, David A. Hovda, Marvin Bergsneider, Daniel F. Kelly, Neil A. Martin, and Donald P. Becker
mild hemorrhage in cats. J Neurosurg 76: 812–821, 1992 14. Eisenberg HM , Gary HE Jr , Aldrich EF , et al : Initial CT findings in 753 patients with severe head injury. A report from the NIH Traumatic Coma Data Bank. J Neurosurg 73 : 688 – 698 , 1990 Eisenberg HM, Gary HE Jr, Aldrich EF, et al: Initial CT findings in 753 patients with severe head injury. A report from the NIH Traumatic Coma Data Bank. J Neurosurg 73: 688–698, 1990 15. Engel J Jr , Kuhl DE , Phelps ME , et al : Local cerebral metabolism during partial seizures
Daniel F. Kelly, Rouzbeh K. Kordestani, Neil A. Martin, Tien Nguyen, David A. Hovda, Marvin Bergsneider, David L. McArthur, and Donald P. Becker
the six patients in whom metabolic suppressive therapy failed, the presence of hyperemia and intracranial hypertension in the setting of metabolic suppressive therapy and vasopressor support in five of these patients substantiate this concept. Metabolic suppressive therapy appears destined to fail in the great majority of these patients, given the severity of injury and the fact that cerebral metabolism may already be profoundly depressed. Whether there are viable treatment options for these patients is unclear. One approach advocated to control marked
Marvin Bergsneider, David A. Hovda, Ehud Shalmon, Daniel F. Kelly, Paul M. Vespa, Neil A. Martin, Michael E. Phelps, David L. McArthur, Michael J. Caron, Jess F. Kraus, and Donald P. Becker
“normal” cerebral metabolism is primarily oxidative in nature, it has been assumed that total cerebral metabolism is depressed after severe head injury based on studies demonstrating an approximate 50% reduction in the cerebral metabolic rate of oxygen (CMRO 2 ). 10, 11, 48, 53, 67 As such, the interpretation of related clinical data has been made with the presumption that glycolytic metabolism maintains the normal, resting-state stoichiometric relationship to oxidative metabolism. Several lines of evidence indirectly suggest a pathogenesis and existence of
Michael A. Williams, James P. McAllister, Marion L. Walker, Dory A. Kranz, Marvin Bergsneider, Marc R. Del Bigio, Laurel Fleming, David M. Frim, Katrina Gwinn, John R. W. Kestle, Mark G. Luciano, Joseph R. Madsen, Mary Lou Oster-Granite, and Giovanna Spinella
outflow of CSF in normal pressure hydrocephalus . Acta Neurochir (Wien) 71 : 1 – 45 , 1984 21 Borgesen SE , Gjerris F : The predictive value of conductance to outflow of CSF in normal pressure hydrocephalus . Brain 105 : 65 – 86 , 1982 22 Bradley WG : Cerebrospinal fluid dynamics and shunt responsiveness in patients with normal-pressure hydrocephalus . Mayo Clin Proc 77 : 507 – 508 , 2002 23 Braun KPJ , Vandertop WP , Gooskens RH , Tulleken KA , Nicolay K : NMR spectroscopic evaluation of cerebral metabolism in hydrocephalus: a