± 11 168 ± 14 4.25 ± 2.75 3 140 ± 15 63 ± 33 143 ± 17 4.20 ± 1.64 4 147 ± 15 42 ± 12 — — * Values are presented as the means ± SDs. — = the [Na + ] e level could not be calculated; it was never restored postinjury. Traumatic Brain Injury Physiological Parameters Baseline MABP was 111 ± 1 mm Hg and exhibited a significant elevation to 124 ± 4 mm Hg (p < 0.05) during the first 30 minutes after TBI ( Fig. 3 ). Intracranial pressure was also significantly elevated (mean 15 ± 2 mm Hg) for 30 minutes
Michael F. Stiefel, Yoshiyuki Tomita, and Anthony Marmarou
Junki Ito, Anthony Marmarou, Pál Barzó, Panos Fatouros, and Frank Corwin
group (arrows) . H & E, original magnification × 300. Discussion One objective of these studies was to use ADCs to examine the temporal course and type of edema that occur with traumatic brain injury coupled with secondary insult. In this process, it was essential to determine if the ADCs were of sufficient sensitivity and specificity to detect different forms of edema. Importantly, our initial studies of models that produce purely extracellular and cytotoxic edemas indicated that ADCs increase with vasogenic and decrease with cytotoxic forms of edema
Pál Barzó, Anthony Marmarou, Panos Fatouros, Frank Corwin, and Jana Dunbar
disruption caused by traumatic brain injury, only very few investigations followed the early changes. 2, 4, 28, 30, 31 Our results are consistent with previous reports on the integrity of the BBB and the role of a permeability deficit in the formation of cerebral edema using other models of head injury. 2, 4, 20, 30, 35, 43 These studies analyzed permeability defect of short duration and reported increased permeability of BBB to trypan and Evans blue, phosphate ion, and different proteins (M r 44,000–820,000) following trauma. Moreover, they also showed that the peak of
Stefano Signoretti, Anthony Marmarou, Gunes A. Aygok, Panos P. Fatouros, Gina Portella, and Ross M. Bullock
be needed to confirm this view and to use 1 H-MR spectroscopy CS imaging both in evaluating prognosis and assessing patient response to novel therapies in the field of severe TBI. Acknowledgments We thank the NICU nurses, neurosurgical residents, and respiratory and radiology technicians for their invaluable assistance in the conduct of this study. References 1 Al-Samsam RH , Alessandri B , Bullock R : Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury
Brain edema resulting from traumatic brain injury (TBI) or ischemia if uncontrolled exhausts volume reserve and leads to raised intracranial pressure and brain herniation. The basic types of edema—vasogenic and cytotoxic—were classified 50 years ago, and their definitions remain intact.
In this paper the author provides a review of progress over the past several decades in understanding the pathophysiology of the edematous process and the success and failures of treatment. Recent progress focused on those manuscripts that were published within the past 5 years.
Perhaps the most exciting new findings that speak to both the control of production and resolution of edema in both trauma and ischemia are the recent studies that have focused on the newly described “water channels” or aquaporins. Other important findings relate to the predominance of cellular edema in TBI.
Significant new findings have been made in understanding the pathophysiology of brain edema; however, less progress has been made in treatment. Aquaporin water channels offer hope for modulating and abating the devastating effects of fulminating brain edema in trauma and stroke.
Pál Barzó, Anthony Marmarou, Panos Fatouros, Koji Hayasaki, and Frank Corwin
T he contribution of brain edema to brain swelling in cases of traumatic injury remains a critical problem. In head injury, the swelling and eventual rise in intracranial pressure (ICP) are frequent causes of death, and the poor prognosis in survivors with sustained ICP elevation has been well documented. 2, 30, 31 Vasogenic edema, secondary to blood-brain barrier (BBB) compromise following traumatic brain injury (TBI), has long been thought to be the major contributor to the swelling process and the subsequent rise in ICP. 22, 33, 35, 38 However
Andrea Kleindienst, Christos M. Tolias, Frank D. Corwin, Christian Müller, Anthony Marmarou, Panos Fatouros, and M. Ross Bullock
-specific enolase and S100B in cerebrospinal fluid after severe traumatic brain injury in infants and children. Pediatrics 109 : E31 , 2002 Berger RP, Pierce MC, Wisniewski SR, Adelson PD, Clark RS, Ruppel RA, et al: Neuron-specific enolase and S100B in cerebrospinal fluid after severe traumatic brain injury in infants and children. Pediatrics 109: E31, 2002 4. Ciccarelli R , Di Iorio P , Bruno V , Battaglia G , D'Alimonte I , D'Onofrio M , et al : Activation of A 1 adenosine or mGlu3 metabotropic glutamate
Part II: Morphological characterization
Montasser A. Abd-Elfattah Foda and Anthony Marmarou
glass knife and were stained with toluidine blue for LM studies. Next, 50-nm thin sections were cut with a diamond knife, double stained with uranyl acetate and lead citrate, and examined in a Zeiss EM 10 electron microscope. Immunocytochemical Procedure for Neurofilament Antibody Recently, antibodies to the 68-kD neurofilament subunit have been used for the detection of axonal change following traumatic brain injury. 48 We employed 68-kD immunoreactivity to confirm and map axonal injury in our model, in both respiratory-assisted and spontaneously breathing
Kazuo Yoshida and Anthony Marmarou
, 1961 Goetz RH, Selmonosky A, State D: Anuria of hypovolemic shock relieved by tris-(hydroxymethyl)aminomethane (THAM). Surg Gynecol Obstet 112: 724–728, 1961 14. Gordon E : Some correlations between the clinical outcome and the acid-base status of blood and cerebrospinal fluid in patients with traumatic brain injury. Acta Anaesthesiol Scand 15 : 209 – 228 , 1971 Gordon E: Some correlations between the clinical outcome and the acid-base status of blood and cerebrospinal fluid in patients with traumatic brain injury. Acta
Gerrit J. Bouma, J. Paul Muizelaar, Kuniaki Bandoh, and Anthony Marmarou
and with impaired autoregulation. J Neurosurg 73: 368–374, 1990 4. Bouma GJ , Muizelaar JP , Choi SC , et al : Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 75 : 685 – 693 , 1991 Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 75: 685–693, 1991 5. Gray WJ , Rosner MJ : Pressure-volume index as a function of cerebral