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
Alois Zauner, Tobias Clausen, Oscar L. Alves, Ann Rice, Joseph Levasseur, Harold F. Young, and Ross Bullock
Gerrit J. Bouma, J. Paul Muizelaar, Sung C. Choi, Pauline G. Newlon, and Harold F. Young
CBF, which leaves some doubt about the interpretation of these data. Another factor to be taken into account in determining whether CBF is sufficient to meet the metabolic demands of the injured brain, is that cerebral metabolism is often decreased after severe brain trauma. Consequently, reduced flow does not necessarily mean ischemia in these patients. Therefore, determinations of arteriovenous oxygen difference (AVDO 2 ) are necessary for the proper evaluation of CBF data following head injury, as this parameter reflects the link between flow and metabolism
Part 1: Relationship with GCS score, outcome, ICP, and PVI
J. Paul Muizelaar, Anthony Marmarou, Antonio A. F. DeSalles, John D. Ward, Richard S. Zimmerman, Zhongchao Li, Sung C. Choi, and Harold F. Young
✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI.
Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.
Egon M. R. Doppenberg, Joe C. Watson, William C. Broaddus, Kathryn L. Holloway, Harold F. Young, and Ross Bullock
T emporary vessel occlusion during aneurysm surgery and intracranial mass lesions are examples of conditions in which cerebral metabolism is compromised as a result of decreased availability of glucose and O 2 to the brain tissue. Temporary occlusion of a parent vessel during aneurysm surgery is an accepted method of facilitating dissection and clipping of both ruptured and unruptured aneurysms. 5, 13, 20 Many authors assert that this method reduces the risk of intraoperative bleeding from the aneurysm, which decreases the morbidity and mortality rates
Nam D. Tran, Stefan Kim, Heather K. Vincent, Anthony Rodriguez, David R. Hinton, M. Ross Bullock, and Harold F. Young
, Clausen T , Alves OL , Rice A , Levasseur J , Young HF , : Cerebral metabolism after fluid percussion injury and hypoxia in a feline model . J Neurosurg 97 : 643 – 649 , 2002