MAGNETIC-RESONANCE-IMAGING MONITORED ACUTE BLOOD-BRAIN-BARRIER CHANGES IN EXPERIMENTAL TRAUMATIC BRAIN INJURY

Citation
P. Barzo et al., MAGNETIC-RESONANCE-IMAGING MONITORED ACUTE BLOOD-BRAIN-BARRIER CHANGES IN EXPERIMENTAL TRAUMATIC BRAIN INJURY, Journal of neurosurgery, 85(6), 1996, pp. 1113-1121
Citations number
44
Categorie Soggetti
Neurosciences,"Clinical Neurology",Surgery
Journal title
ISSN journal
00223085
Volume
85
Issue
6
Year of publication
1996
Pages
1113 - 1121
Database
ISI
SICI code
0022-3085(1996)85:6<1113:MMABC>2.0.ZU;2-7
Abstract
The authors posit that cellular edema is the major contributor to brai n swelling in diffuse head injury and that the contribution of vasogen ic edema may be overemphasized. The objective of this study was to det ermine the early time course of blood-brain barrier (BBB) changes in d iffuse closed head injury and to what extent barrier permeability is a ffected by the secondary insults of hypoxia and hypotension. The BBB d isruption was quantified and visualized using T-1-weighted magnetic re sonance (MR) imaging following intravenous administration of the MR co ntrast agent gadolinium-diethylenetriamine pentaacetic acid. To avoid the effect of blood volume changes, the maximum signal intensity (SI) enhancement was used to calculate the difference in BBB disruption. A new impact-acceleration model was used to induce closed head injury. F orty-five adult Sprague-Dawley rats were separated into four groups: G roup T, sham operated (four animals), Group II, hypoxia and hypotensio n (four animals), Group III, trauma only (23 animals), and Group IV, t rauma coupled with hypoxia and hypotension (14 animals). After trauma was induced, a 30-minute insult of hypoxia (PaO2 40 mm Hg) and hypoten sion (mean arterial blood pressure sure 30 mm Hg) was imposed, after w hich the animals were resuscitated. In the trauma-induced animals, the SI increased dramatically immediately after impact. By 15 minutes per meability decreased exponentially and by 30 minutes it was equal to th at of control animals. When trauma was coupled with secondary insult, the SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically on reperfusion and was equal to that of control by 60 minutes after t he combined insult. In conclusion, the authors suggest that closed hea d injury is associated with a rapid and transient BBB opening that beg ins at the time of the trauma and lasts no more than 30 minutes. It ha s also been shown that addition of posttraumatic secondary insult-hypo xia and hypotension-prolongs the time of BBB breakdown after closed he ad injury. The authors further conclude that MR imaging is an excellen t technique to follow (time resolution 1-1.5 minutes) the evolution of trauma-induced BBB damage noninvasively from as early as a few minute s up to hours or even longer after the trauma occurs.