160 / 198
Results:
Between July 1, 2005 and July 1, 2014 BCVI incidence
was 0.78% of total population (14,505) and 14.7% of those screened
(770). There were 113 patients with a BCVI diagnosis (three patients
with both); 37 carotid injuries (BCI), 79 vertebral injuries (BVI).
Injuries significant for BCVI include C2 fractures, fractures through
vertebral transverse foramina, cervical spine fracture dislocations,
fractures through the carotid canal, and proximal aortic artery injuries.
Stroke rate from injury was 5.3% (13.5% for carotid, 1.2% for ver-
tebral). Treatment practices for BCVI greatly varied with 39% of BVI
patients untreated.
Discussion:
Incidence of BCVI at a single institution is low.
Neurosurgical specific screening model is possible with BVI but
difficult with BCI due to low incidence and high stroke rate. Treat-
ment practices varied, however, no treatment of BVI without com-
plications raises question about needing to treat vertebral injuries.
Keywords: BCVI, Blunt Cerebrovascular Injury, Dissection, Stroke
D9-04
A COMPARISON OF THE CEREBRAL VASCULAR EFFECTS
OF VANDENBERG OR ADVANCED BLAST SIMULATOR
BLAST INJURY IN RATS
Ian Bolding
, Katherine Ruppert, Uylissa Rodriguez, Ya ping Zeng,
Don Prough, Doug Dewitt
University of Texas - Medical Branch, Anesthesiology, Galveston,
USA
Blast-induced neurotrauma (BINT) is one of the most common causes
of mortality and morbidity in military personnel. The development of
effective therapies for BINT requires experimental models that rep-
licate important features of BINT in humans. Although neuronal and
behavioral effects of BINT have been shown, little is known about its
effect on the cerebral vasculature. This study compared the effects of
two models of BINT on arterial blood pressure, relative cerebral
perfusion, righting reflex and middle cerebral arterial (MCA) diam-
eters during progressive reductions in intravascular pressure.
The Vandenberg model produces blast over/under pressures followed
by blunt impact, while the Advanced Blast Simulator (ABS) produces a
pure over/under pressure shock wave. We measured relative cerebral
perfusion (laser Doppler flowmetry) and arterial blood pressure in adult,
male rats that underwent either sham, Vandenberg BINT or ABS BINT.
In a separate group of animals, the duration of righting reflex (RR)
suppression was recorded following sham, Vandenberg BINT or ABS
BINT and the animals were reanesthetized for an additional 60 minutes
before being euthanized. The MCAs were then harvested from all an-
imals, mounted on an arteriograph and arterial diameters were measured
during progressive reductions in intravascular pressure.
Vandenberg BINT was associated with significant increases in the
duration of RR suppression (compared to ABS and Sham). Neither
model of BINT produced significant reductions in arterial blood
pressure, but both significantly reduced cerebral perfusion and dilator
responses to reduced intravascular pressure in isolated MCAs.
These results demonstrate that ABS BINT and Vandenberg BINT
significantly impaired dilator responses, specifically cerebral vasodi-
lation in response to reduced intravascular pressure, and suggest that
blast exposure, like impact TBI, compromises cerebral pressure au-
toregulation. These studies were completed as part of an interdisci-
plinary research team funded by The Moody Project for Translational
Traumatic Brain Injury Research.
Support:
Moody Project for Translational TBI Research & grant
W81XWH-08-2-0132 from the Department of Defense.
Keywords: Vasodilation, Blast Induced Neurotrauma, Advanced
Blast Simulator, Cerebral Vasculature, Blast Model
D9-05
THE EFFECTS OF BLAST-INDUCED NEUROTRAUMA ON
CEREBRAL VASCULAR, HISTOPATHOLOGICAL AND BE-
HAVIORAL OUTCOMES
Uylissa Rodriguez
, Maggie Parsley, Yaping Zeng, Donald S. Prough,
Douglas S. DeWitt
University of Texas Medical Branch, Anesthesiology, Galveston, USA
Introduction:
The effects of blast-induced neurotrauma (BINT) on
cerebral vascular responses to reduced intravascular pressure in isolated,
pressurized middle cerebral arterial (MCA) segments, relative cerebral
perfusion and mean arterial pressure (MAP), neuronal injury and cog-
nitive function were measured in rats subjected to BINT using an Ad-
vanced Blast Simulator (ABS), a compressed helium-driven shock tube.
Methods:
All rats were anesthetized and randomly subjected to
BINT or Sham BINT. To measure the effects of BINT on MCA
responses to reduced intravascular pressure, rats were anesthetized,
prepared for blast and subjected to Sham BINT or BINT (17 –
22 psi)(n
=
6/group). Immediately after BINT, righting reflexes (RR)
were assessed and MCAs harvested 30 or 60 min later. In a second set
of rats, MAP and laser Doppler (LDF) cerebral perfusion were mea-
sured before and for two hrs after Sham BINT (n
=
10) or BINT
(n
=
12). A third set of rats were subjected to Sham BINT or BINT
(n
=
6/group) and euthanized 24 or 48 hrs later for FluoroJade (FJ)
staining measurements. A fourth set were subjected to Sham BINT or
BINT (n
=
10/group) and beam balance and Morris water maze
(MWM) performances were tested.
Results:
RR suppression in the BINT group was significantly
(
P
<
0.05) higher than the Sham group. MAP did not differ signifi-
cantly between BINT and Sham groups. MCA dilator responses and
LDF were significantly reduced (
P
<
0.05) and cerebral vascular re-
sistance significantly increased (
P
<
0.0001) by BINT. BINT resulted
in significantly more FJ staining (
P
<
0.05) and significantly impaired
beam balance performance (
P
<
0.05). There was a trend (
P
=
0.063)
toward increased MWM latencies in the BINT group.
Summary:
These results suggest that mild BINT is associated with
cerebral arterial constriction and impaired cerebral vascular reactivity
that may contribute to impaired behavioral and cognitive function and
increased neuronal injury. Furthermore, blast-induced impairment of
cerebral dilator responses might contribute to further reductions in
cerebral perfusion in the presence of arterial hypotension.
These studies were completed as part of an interdisciplinary re-
search team funded by The Moody Project for Translational Trau-
matic Brain Injury Research and award W81XWH-08-2-0132 from
the Department of Defense.
Keywords: primary blast injury, blast induced neurotrauma, cere-
brovascular circulation, cerebral blood flow, behavior
D9-06
TREATMENT WITH DENDRO[60]FULLERENE PRESERVES
NEURONS AFTER TRAUMATIC BRAIN INJURY BUT DOES
NOT IMPROVE CEREBRAL VASCULAR RESPONSE
Bridget Hawkins
1
, Karon Wynne
1
, Ya Ping Zeng
2
, Donald Prough
2
,
Douglas DeWitt
2
1
University of Texas Medical Branch, Neuroscience, Galveston, USA
2
University of Texas Medical Branch, Anesthesiology, Galveston,
USA
Introduction:
TBI results in increased levels of reactive oxygen
species (ROS) that can cause cerebral vascular dysfunction. Reduction
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