23 / 162
motor recovery (n
=
16, p
<
0.05) following injury. These results shed
light on the importance of mitoNEET as a novel target for the treat-
ment of TBI and as a necessary protein in pioglitazone mediated
neuroprotection.
Keywords: mitochondria, mitoNEET, pioglitazone, NL-1, Con-
trolled Cortical Impact (CCI)
A2-12
DANTE: DEFORMITY, ANKYLOSIS, NEUROLOGIC DEFI-
CIT, TRANSLATION, EXTENSIVE TRAUMA. A MNEMONIC
PREDICTING SPINAL INSTABILITY
Ryan Nazar
1
, Richard Holt
1
, Michael Kim
2
1
University of Louisville, Neurosurgery, Louisville, USA
2
University of Indiana, Neurosurgery, Indianapolis, USA
Clinical evaluation of thoracolumbar trauma requires a complex under-
standing of spinal anatomy and mechanism of injury in order to determine
stability. Numerous classification systems exist; however, each has lim-
itations that risk potential missed diagnoses, progressive instability, and
neurologic compromise. The limitations include poor reliability and re-
peatability, non-inclusion of comprehensive bodily survey, oversimpli-
fication, and failure to consider late mechanical and neurologic instability.
Thus; a comprehensive system that is relatively simple to recall and
apply which incorporates basic modalities of patient evaluation in-
cluding history, physical examination, and imaging is needed to help
surgeons and non-surgeons in the decision making process.
A review of the literature revealed a core set of elements that may
predict and determine thoracolumbar spinal stability. These elements
can be summarized by the mnemonic
DANTE:
D: Deformity
– Radiographic criteria that can be observed on plain
films; CT, or MRI. Greater than 15 to 25 degrees of kyphosis or 14
degrees of scoliosis is associated with discoligamentous instability.
(McAfee)
A: Ankylosis, Age
– Preexisting osseous disorders, such as anky-
losing spondylitis, diffuse idiopathic skeletal hyperostosis, or osteo-
porosis may also affect treatment decisions and initiate further
imaging studies. Younger patients have ligamentous laxity; whereas,
older patients bones are brittle.
N: Neurologic Injury
– New neurologic deficit, even despite
normal plain films or computerized tomography, should be evaluated
further for discoligamentous instability. (Bradford, McBride)
T: Translation
– Subluxation of adjacent segments of 10% or
4 mm in either the sagittal or coronal plane is associated with dis-
coligamentous instability. (White, Panjabi)
E: Extensive Trauma
–Traumatic injuries other than those involving
the TL spine such as cervical spine fractures, multiple limb fractures,
closed head injury, internal organ injuries are typically associated with
high-velocity mechanisms and potential spinal instability.
In summary, DANTE is designed only as a guideline and teaching
tool for physicians to increase clinical suspicion of potential early and
late mechanical and neurological spinal instability.
Keywords: Spinal Instability, Thoracolumbar Trauma, Thor-
acolumbar Fracture
A2-13
INCREASES IN INFLAMMATION-ASSOCIATED MIRNAS
AND CHARACTERIZATION OF LONG-TERM OUTCOMES
IN A CCI MODEL OF TBI
Emily Harrison
1
, Sowmya Yelamanchili
1
, Brenda Morsey
1
, Mary
Banoub
1
, Tammy Chaudoin
2
, Matthew Kelso
3
, Stephen Bonasera
2
,
Howard Fox
1
1
University of Nebraska Medical Center, Pharmacology and Experi-
mental Neuroscience, Omaha, USA
2
University of Nebraska Medical Center, Internal Medicine Ger-
iatrics, Omaha, USA
3
University of Nebraska Medical Center, Department of Pharmacy
Practice, Omaha, USA
Traumatic brain injury causes life-long changes in the brain that can lead
to neuropsychiatric symptoms, cognitive deficits, metabolic dysfunction,
and dementia, but how molecular events contribute to long-term dys-
function is largely unknown. The controlled cortical impact (CCI) mouse
model of traumatic brain injury is a useful tool for examining the mo-
lecular cascades following TBI. One important class of regulatory mol-
ecules in the brain, responsible for CNS development, function, and
disease are miRNAs. We have identified 3 inflammation-associated
miRNAs with increased expression following TBI. Although these
miRNAs are involved in immune cell development, we found that they
were highly expressed in neurons of both the injured cortex and hippo-
campus. Genetic knock-out mice are being used to determine the role that
these miRNAs may have in neuronal survival and function after TBI.
Although there are many approaches to characterizing the acute
damage after CCI, the long-term phenotype of this model is still
lacking. To address this deficit, we have characterized the phenotype
of mice after mild (0.5 mm), and moderate (1.0 mm) CCI compared to
craniotomy only as well as naı¨ve mice controls using a multifactorial
approach. Activity and feeding were monitored continuously for 21
days using a home cage system, allowing for non-biased collection of
behavioral data. In addition, oxygen consumption rate was measured
as an indicator of metabolic changes. To examine neuropsychological
alterations, tail suspension, open field, and elevated zero maze texts
were performed. Using this approach we have identified quantitative
methods for measuring long-term deficits following CCI. These data
will inform our characterization of knock-out mice and allow us to
link acute molecular changes with meaningful outcomes.
Keywords: inflammation, microRNAs, animal models, molecular
mechanisms
A2-14
ENHANCING HIPPOCAMPAL NEURON SURVIVAL AFTER
MULTIPLE BRAIN INJURIES BY HUMAN NEURAL STEM
CELL-SECRETED GLIAL CELL LINE-DERIVED NEU
Junling Gao, Margaret Parsley, Tiffany Dunn, Douglas DeWitt,
Donald Prough,
Ping Wu
University of Texas Medical Branch, Neuroscience & Cell Biology,
Galveston, USA
Peoples with traumatic brain injury (TBI) often suffer from bleeding and
hypotension. We hypothesize that neural stem cell grafting will attenuate
cognitive impairments in TBI plus hemorrhagic ischemia, which is me-
diated by NSC-secreted glial cell-derived neurotrophic factor (GDNF) to
protect host hippocampal neurons from secondary damage. A rat fluid
percussion injury (FPI) followed by induced hemorrhagic shock is applied
in this study. Rats received a 2.0-atm parasagittal FPI, followed 40-min
later by withdrawing blood from the right common jugular vein to lower
the mean arterial pressure to 40mmHg. One day after injury, animals
received either vehicle injection or hNSC transplantation near the injured
hippocampus. To determine the role of GDNF, GDNF neutralizing or IgG
control antibody was given through Alzet pumps immediately after cell
transplantation. Morris water maze (MWM) tests were performed on all
animals starting on days 7 or 28 post injury, followed by brain tissue
collection. Rats with hNSC transplantation showed improved spatial
learning and memory at a later time point. Histological analyses of rat
brains indicated that hNSC transplantation improved hippocampal neuron
A-23