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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