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literature has yielded different treatment modalities in acute spinal
cord injury with mixed results including surgical decompression and
neuroprotection methods but none evaluating the efficacy of hy-
pertonic saline administration. After a recent case of a young adult
male who presented with acute spinal cord injury at our institution,
neuroprotective methods and decompressive surgery were used in
addition to the administration of hypertonic saline with elevated
sodium goals. The patient’s discharge neurological function im-
proved with this multi-modal therapy and this is the first known case
in the English language literature in which hypertonic saline was
used in the treatment of acute spinal cord edema. Therefore, we
hereby provide a review of this case and the current literature ad-
dressing spinal cord edema in the setting of acute spinal cord injury
and the implications on neurological recovery.
Keywords: spinal cord injury, hypertonical saline, decompressive
surgery, multi-modal therapy, spinal cord edema
D8-08
PROTECTIVE EFFECT OF N-ACETYLCYSTEINE AMIDE
(NACA) AGAINST BRAIN DAMAGE AFTER EXPOSURE TO
BLAST IN A RAT MODEL
Mikulas Chavko
1
, Usmah Kawoos
1
, Ming Gu
1
, Jason Lankasky
1
,
Richard McCarron
1,2
1
Naval Medical Research Center, Neurotrauma, Silver Spring, USA
2
Uniformed Services University of the Health Sciences, Surgery, Be-
thesda, USA
Blast-induced traumatic brain injury (bTBI) has been a leading cause
of neurocognitive and psychological impairment in the military pop-
ulation. Brain edema and Blood Brain Barrier (BBB) function are
compromised in TBI including blast. In this study we determined if
blast induced changes in intracranial pressure (ICP), and BBB
breakdown, could be ameliorated by administration of the antioxidant
N-acetylcysteine amide (NACA).
Rats were exposed to either single or three blast overpressures
(BOP) (110 kPa) with animal’s head facing the blast wave. NACA
was administered either pre- or post-blast by single i.p injection
(500 mg/kg). ICP was monitored by a telemetric device over a
period of 7 days. BBB permeability and integrity were determined
by Evans Blue (EB) staining and occludin immunoreactivity, re-
spectively.
EB leakage into the brain was increased brain two hours after single
or multiple exposures of blast, indicating a compromise in the in-
tegrity and function of the BBB. Concomitantly, a significant eleva-
tion in ICP was observed after single or repetitive exposures to BOP.
In the single-blast group, ICP immediately returned to near pre-blast
levels after post-blast NACA administration. Also, in the repetitive-
blast group there was a significant amelioration in the ICP increase by
NACA. Immunoreactivity of occludin, a component of tight junctions
in BBB was significantly decreased after exposure to blast and this
was prevented by NACA administration. The protective effect of
NACA against blast-induced changes could be related to its anti-
oxidative effect as demonstrated by suppression of nitrotyrosine im-
munoreactivity increase after blast.
These results demonstrate that BBB breakdown may be an impor-
tant factor in the mechanism of bTBI. The subsequent ICP increase
can be used as one of the markers of brain damage and the antioxidant
NACA may be useful as a new therapeutic modality for ameliorating
BOP-induced brain damage.
Supported by ONR Work Unit 601152N.0000.0001.A1308
Keywords: Blast Brain Injury, N-acetyl cysteineamide, Antioxidant
D8-09
THE EFFECT OF INTERNAL JUGULAR VEIN COMPRES-
SION ON HEMORRHAGE IN A PORCINE CONTROLLED
CORTICAL INJURY MODEL
John Finan
1
, Vimal A. Patel
1
, James L. Stone
1
, John M. Lee
1
, Sydney
A. Sherman
1
, David W. Smith
2
, Julian E. Bailes
1
1
NorthShore University HealthSystem, Neurosurgery, Evanston, USA
2
Q30 Sports Science LLC., Research and Development, Wilton, USA
Internal jugular vein (IJV) compression reduced axonal injury in a rat
model of traumatic brain injury (TBI). However, IJV compression
also increases cerebral perfusion pressure. If this increases hemor-
rhage after TBI, the overall impact of IJV compression might become
harmful. We tested the hypothesis that IJV compression increases
hemorrhage after TBI in a porcine controlled cortical impact (CCI)
model.
Methods:
Yorkshire swine were anesthetized and prepared for
surgery with respiratory support, analgesia and vital signs monitoring.
An 18 mm wide burr hole was created over the right cortex. An In-
tegra Camino pressure sensor was placed in the left cortex. In IJV
compression animals, a custom-made collar was used to compress the
IJV until intracranial pressure rose by 1 mmHg. A beveled, cylindrical
indenter 15 mm in diameter was used with a Leica ImpactOne CCI
device to injure the exposed cortex (velocity
=
3.5 m/s; depth
=
9 mm;
dwell
=
400 ms). The collar was removed immediately after injury and
the burr hole was filled with bone wax. The animal was euthanized 5
hours later. The brain was fixed and sections were obtained from 10
predefined locations in the cortex of each animal. A blinded, clinical
neuropathologist assigned a score between 0 and 2 to the level of sub-
arachnoid hemorrhage (SAH) in each section. Scores for all 10 sec-
tions were totaled to measure the overall level of SAH in each animal.
Results:
4 pigs were injured, 2 with IJV compression and 2 without
(controls). SAH levels were 3.5 and 4.5 in the IJV compression ani-
mals and 9.5 and 10.25 in the control animals.
Conclusions:
Definitive conclusions cannot be drawn due to the
small sample size. In the animals tested, IJV compression did not
increase hemorrhage as hypothesized. In fact, it reduced hemorrhage.
This study was sponsored by Q30 Sports Science, LLC.
Keywords: protective device, hemorrhage, porcine, controlled
cortical impact
D8-10
THE EFFICACY OF PROGESTERONE DEPENDS ON THE
TRAUMATIC BRAIN INJURY MODEL
Anthony Choo
, Robert Komlo, Michael Manzano, Amidi Barboza,
Qing Chang, Taleen Hanania
PsychoGenics Inc., Behavioral Pharmacology, Tarrytown, USA
Progesterone was previously reported to improve outcomes in pre-
clinical studies of traumatic brain injury. Recent phase 3 clinical trials,
however, reported no clinical benefit of progesterone treatment for
moderate-to-severe as well as severe traumatic brain injuries. Given
the heterogeneity in human traumatic brain injuries, we aimed to
reassess the effectiveness of progesterone treatment in two preclinical
traumatic brain injury models. We compared progesterone treatment
(16 mg/kg for 5 days) in mechanically identical controlled cortical
impacts to the medial frontal cortex and the parasagittal cortex in rats.
During the first week following injury, progesterone improved motor
performance on the beam balance in both injury models. In the Morris
water maze test, progesterone improved learning and memory only in
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