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
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.