73 / 198
C7 SCI from a type II odontoid fracture with extensive C1-2 liga-
mentous injury as well as very minimal frontal lobe contusions. On post
injury day 3, the patient became nonresponsive with a head CT dem-
onstrating new moderate hydrocephalus despite a negative CTA head/
neck. Emergent ventriculostomy revealed high pressure, but did not
produce neurologic improvement. Of note, c-spine MRI performed
approximately 12 hours prior to clinical decline demonstrated severe
edema of the spinal cord ascending from a focus at C5-6 to the cervico-
medullary junction. Literature search revealed 4 case reports of
hydrocephalus following SCI. Two mechanisms have been proposed
including a communicating hydrocephalus from traumatic blood
ascending in the subarachnoid space and non-communicating hydro-
cephalus from ascending edema causing a 4
th
ventricular outlet ob-
struction at the foramina of Lushcka and Magendie. The two suspected
mechanisms in the present cases: vertebral artery obstruction resulting
in cerebellar infarction, edema and herniation with 4
th
ventricular
obliteration; and ascending cord and brainstem edema resulting in 4
th
ventricular outlet obstruction.
Keywords: Acute hydrocephalus, Spinal cord injury, Vertebral
artery injury, Spinal cord edema
A6-02
CILOSTAZOL ATTENUATES BLOOD-BRAIN BARRIER
DISRUPTION AND SUBSEQUENT SECONDARY CELLULAR
DAMAGE FOLLOWING CORTICAL CONTUSION IN RATS
Takeshi Maeda
1
, Masamichi Fukushima
1
, Masahiro Tado
1
, Atsuo
Yoshino
1
, Yoichi Katayama
2
1
Nihon University School of Medicine, Neurological Surgery, Tokyo,
Japan
2
Nihon University, Research Center, Tokyo, Japan
Objective:
Cerebral contusion results in tissue damage from primary
(mechanical) and subsequent secondary (neurochemical) processes.
Our previous studies have demonstrated that regional cerebral blood
flow (rCBF) markedly decrease by microthrombosis formation that
underlie these secondary processes and represent potential targets for
therapeutic intervention. Meanwhile, the hemorrhagic lesion results in
cortical contusion often progresses during the several hours following
injury. Cilostazol has anti-plated aggregation effect, anti-thrombosis
effect, and vasoconstriction effect. The aim of the present study were
to examine whether cilostazol can attenuate secondary brain injury,
and whether cilostazol prevent hemorrhagic progression following
cortical contusion. The effect of cilostazol on the volume of the cavity
formation, and the influence of cilostazol on hemorrhagic progression
were tested employing a cortical contusion model in rats.
Methods:
Contusion injury was induced with a controlled cortical
impact (CCI) device in the parietal cortex of 30 male Wistar rats
under anesthesia. The animals were randomly divided into 3 group
and orally given cilostazol (30 mg/kg), aspirin (20 mg/kg) and vehicle
(control) 1 hour before CCI, and were sacrificed for making evalua-
tions of microthrombosis formation and extravasation of Evans Blue
dye (EBD) at 48 hours post injury and for the measurements cavity
formation at 14 days.
Results:
The cavity formation decreased in cilostazol
(5.918
–
1.269mm
3
) (mean
–
SD) relative to controls (7.083
–
2.052mm
3
),
whereas aspirin markedly increased (11.093
–
2.585mm3, P
<
0.05). He-
morrhagic progression and the measurement of EBD extravasation re-
duced in cilostazol (1.460
–
0.401mm3) relative to aspirin
(7.189
–
0.747mm3, P
<
0.05). The microthrombosis formation in the
peripheral areas of the contusion was significantly attenuated by cilostazol
(control: 757.2
–
46.0 pics/0.25mm
2
vs. cilostazol: 80.1
–
4.8 pics/
0.25mm
2
, P
<
0.05).
Conclusions:
Cilostazol may have a therapeutic potential to pre-
vent microthrombosis formation without hemorrhagic complication
and for attenuating changes vascular permeability within areas the
surrounding contusion.
Keywords: cerebral contusion, secondary cellular damage, micro-
thrombosis formation, cilostazol
A6-03
APOE GENOTYPE AND ACUTE EDEMA FORMATION FOL-
LOWING EXPERIMENTAL TRAUMATIC BRAIN INJURY
Patricia Washington
1,2
, Ahleum Kim
1
, Tzong-Shiue Yu
1
, Barclay
Morrison
2
, Steven Kernie
1
1
Columbia University Medical Center, Pediatrics and Critical Care
Medicine, New York, USA
2
Columbia University, Department of Biomedical Engineering, New
York, USA
APOE4 genotype has been associated with prolonged coma, increased
mortality and worsened outcome following traumatic brain injury (TBI).
Injury-induced edema and resulting increased intracranial pressure (ICP)
is one of the most serious complications of TBI and is associated with
adverse outcome. To determine whether Apolipoprotein E (ApoE) plays
a role in edema formation after injury and whether this is influence by
APOE genotype, we exposed ApoE wildtype (WT), ApoE knockout
(KO), and human APOE3 or APOE4 overexpression (GFAP-APOE3,
GFAP-APOE4) mice to the controlled cortical impact (CCI) model of
TBI or sham injury and assessed water content in the ipsilateral hippo-
campus and cortex 24h after injury using the wet weight/dry weight
method. Exposure to CCI increased water content in the ipsilateral cortex
of all genotypes 24h after injury (p
<
0.05 compared to sham, unpaired
t-test, within genotype comparison). However, water content in the ip-
silateral hippocampus was only increased after CCI in GFAP-APOE4
mice compared to sham (p
<
0.05, unpaired t-test, within genotype
comparison), suggesting an APOE-genotype effect on edema formation
in the hippocampus after injury. Further, while hippocampal water
content not differ in sham mice between genotypes, cortical water con-
tent was reduced in GFAP-APOE3 shammice compared to WT, KO, and
GFAP-APOE4 sham mice (p
<
0.01-p
<
0.05, one-way ANOVA w/Tu-
key post-hoc), suggesting that APOE genotype may have an effect on
inherent brain water content levels. Our preliminary data supports pre-
vious observations that ApoE status affects edema formation after brain
injury and, for the first time, shows an APOE genotype-specific effect on
injury-induced edema formation in the hippocampus.
Keywords: APOE, Transgenic mice, Hippocampus, Acute injury
A7 Poster Session II - Group A: Endocrine
A7-01
EXPERIMENTAL DIFFUSE BRAIN INJURY LEADS TO
CHRONIC CORTICOSTERONE DYSFUNCTION WITH EVI-
DENCE OF COMPROMISED NEURON MORPHOLOGY
Theresa Thomas
1–3
, Rachel Rowe
1–3
, Benjamin Rumney
1,3,5
, Hazel
May
1,3,5
, Cheryl Conrad
4
, P. David Adelson
1,3,4
, S. Mitchell Harman
2
,
Paska Permana
2
, Jonathan Lifshitz
1–3
1
University of Arizona College of Medicine-Phoenix, Phoenix, USA
2
Phoenix VA Health Care System, Phoenix, USA
3
BARROW Neurological Institute@Phoenix Children’s Hospital,
Phoenix, USA
4
Arizona State University, Tempe, USA
5
University of Bath, Bath, United Kingdom
A-37