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Ronald L. Hayes, Bruce G. Lyeth, Larry W. Jenkins, Richard Zimmerman, Tracy K. McIntosh, Guy L. Clifton, and Harold F. Young

P revious research has indicated that traumatic brain injury (TBI) increases levels of endogenous opioids. Naloxone, a nonspecific opioid antagonist, significantly reverses the hypotension and reduction in pulse pressure following fluid-percussion injury in cats. 26 There are also recent clinical reports of increased µ -endorphin levels in the cerebrospinal fluid of head-injured patients. 80 Other laboratory studies have indicated that dynorphin A-immunoreactivity (but not leucine-enkephalin or µ -endorphin immunoreactivity) increased in the brain regions

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Nam D. Tran, Stefan Kim, Heather K. Vincent, Anthony Rodriguez, David R. Hinton, M. Ross Bullock, and Harold F. Young

between salineand dexamethasone-treated animals at 24 hours (79.85 ± 0.14 [TBI-saline/24 hours] vs 79.60 ± 0.27 [TBI-Dex/24 hours], p = 0.98). Thus, dexamethasone was effective in reducing cerebral edema following TBI at 4 hours, but not at 24 hours. F ig . 5. Bar graph. Brain water content in TBI animals following acidosis and dexamethasone administration. Traumatic brain injury induced increasing cerebral edema at 4 hours (*p < 0.05, compared with uninjured controls) and 24 hours (**p < 0.03, compared with injured animals at 4 hours). This cerebral edema was

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Gerrit J. Bouma, J. Paul Muizelaar, Sung C. Choi, Pauline G. Newlon, and Harold F. Young

, measurements of CBF and AVDO 2 have been part of the routine management of severely head-injured patients since 1982. The purpose of the present study was to elucidate the role of ischemia in severe traumatic brain injury through analysis of the accumulated results of these measurements. We hypothesized that early after injury, CBF is reduced and is related to the severity of the injury, and that the presence of initial ischemia is associated with poor outcome. In addition, we speculated that the reversal of ischemia in these patients leads to improved outcome. Because of

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

, 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 2. Bergsneider M , Hovda DA , Shalmon E , et al : Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg 86 : 241 – 251 , 1997 Bergsneider M, Hovda DA, Shalmon E, et al: Cerebral hyperglycolysis following severe traumatic

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Gerrit J. Bouma, J. Paul Muizelaar, Warren A. Stringer, Sung C. Choi, Panos Fatouros, and Harold F. Young

E arly ischemic insults after severe traumatic brain injury may play a major role in determining clinical status and outcome, but the time-window in which ischemia occurs may be too narrow for its detection and possible treatment. Support for this hypothesis was recently found in a study of 186 severely head-injured patients among whom ischemia was present in one-third of the cases where cerebral blood flow (CBF) was measured between 4 and 6 hours postinjury. 2 In that series, the presence of ischemia was associated with poor outcome, while in a few cases

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Ross Bullock, Alois Zauner, John J. Woodward, John Myseros, Sung C. Choi, John D. Ward, Anthony Marmarou, and Harold F. Young

small numbers of patients by using the microdialysis technique. 9, 10, 15, 23, 44 We have therefore prospectively studied 80 patients by using intracerebral microdialysis to address the following hypotheses: 1) release of excitatory amino acids (EAAs) is a significant event after human traumatic brain injury (TBI); 2) the magnitude of EAA release in these patients is sufficient to account for neuronal damage in accordance with the excitotoxic hypothesis; and 3) the EAA release after trauma may be exacerbated by secondary ischemic events such as low cerebral perfusion

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J. Paul Muizelaar, Anthony Marmarou, Harold F. Young, Sung C. Choi, Aizik Wolf, Roberta L. Schneider, and Hermes A. Kontos

traumatic condition. In this context, multiple oxygen radical species may be involved. However, many investigators assume that the superoxide anion figures prominently. Not only is this oxygen radical damaging in itself, but it also contributes to the formation of other oxygen radicals which can even be more damaging. Accordingly, it would appear that any therapy targeted at scavenging the superoxide anion would prove beneficial in blunting some of the adverse consequences of traumatic brain injury. To date, the superoxide scavenger superoxide dismutase (SOD) has been

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Anthony Marmarou, Harold F. Young, Gunes A. Aygok, Satoshi Sawauchi, Osamu Tsuji, Takuji Yamamoto, and Jana Dunbar

20. Marmarou A , Shulman K , Rosende RM : A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J Neurosurg 48 : 332 – 344 , 1978 Marmarou A, Shulman K, Rosende RM: A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J Neurosurg 48: 332–344, 1978 21. Mateer CA , Mapou RL : Understanding, evaluating and managing attention disorders following traumatic brain injury. J Head Trauma Rehabil 11 : 1 – 16 , 1996

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Ross Bullock, Alois Zauner, John J. Woodward, John Myseros, Sung C. Choi, John D. Ward, Anthony Marmarou, and Harold F. Young

Recent animal studies demonstrate that excitatory amino acids (EAAs) play a major role in neuronal damage after brain trauma and ischemia. However, the role of EAAs in patients who have suffered severe head injury is not understood. Excess quantities of glutamate in the extracellular space may lead to uncontrolled shifts of sodium, potassium, and calcium, disrupting ionic homeostasis, which may lead to severe cell swelling and cell death. The authors evaluated the role of EEAs in human traumatic brain injury.

In 80 consecutive severely head injured patients, a microdialysis probe was placed into the gray matter along with a ventriculostomy catheter or an intracranial pressure (ICP) monitor for 4 days. Levels of EAAs and structural amino acids were analyzed using high-performance liquid chromatography. Multifactorial analysis of the amino acid pattern was performed and its correlations with clinical parameters and outcome were tested. The levels of EAAs were increased up to 50 times normal in 30% of the patients and were significantly correlated to levels of structural amino acids both in each patient and across the whole group (p < 0.01). Secondary ischemic brain injury and focal contusions were most strongly associated with high EAA levels (27 ± 22 μmol/L). Sustained high ICP and poor outcome were significantly correlated to high levels of EAAs (glutamate > 20 μmol/L; p < 0.01).

The release of EAAs is closely linked to the release of structural amino acids and may thus reflect nonspecific development of membrane micropores, rather than presynaptic neuronal vesicular exocytosis. The magnitude of EAA release in patients with focal contusions and ischemic events may be sufficient to exacerbate neuronal damage, and these patients may be the best candidates for treatment with glutamate antagonists in the future.

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J. Paul Muizelaar, Anthony Marmarou, John D. Ward, Hermes A. Kontos, Sung C. Choi, Donald P. Becker, Hans Gruemer, and Harold F. Young

✓ There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO3 buffer from CSF. The latter disadvantage might be overcome by the addition of the buffer tromethamine (THAM), which has shown some promise in experimental and clinical use. Accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (PaCO2 35 ± 2 mm Hg (mean ± standard deviation): control group), hyperventilation (PaCO2 25 ± 2 mm Hg: HV group), or hyperventilation plus THAM (PaCO2 25 ± 2 mm Hg: HV + THAM group). Stratification into subgroups of patients with motor scores of 1–3 and 4–5 took place. Outcome was assessed according to the Glasgow Outcome Scale at 3, 6, and 12 months. There were 41 patients in the control group, 36 in the HV group, and 36 in the HV + THAM group. The mean Glasgow Coma Scale score for each group was 5.7 ± 1.7, 5.6 ± 1.7, and 5.9 ± 1.7, respectively; this score and other indicators of severity of injury were not significantly different. A 100% follow-up review was obtained. At 3 and 6 months after injury the number of patients with a favorable outcome (good or moderately disabled) was significantly (p < 0.05) lower in the hyperventilated patients than in the control and HV + THAM groups. This occurred only in patients with a motor score of 4–5. At 12 months posttrauma this difference was not significant (p = 0.13). Biochemical data indicated that hyperventilation could not sustain alkalinization in the CSF, although THAM could. Accordingly, cerebral blood flow (CBF) was lower in the HV + THAM group than in the control and HV groups, but neither CBF nor arteriovenous difference of oxygen data indicated the occurrence of cerebral ischemia in any of the three groups. Although mean ICP could be kept well below 25 mm Hg in all three groups, the course of ICP was most stable in the HV + THAM group. It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4–5. When sustained hyperventilation becomes necessary for ICP control, its deleterious effect may be overcome by the addition of THAM.