60 / 162
Conclusion:
Leakage of contrast in TMI occurs on a time-scale
of
<
10 min, and persists for at least the next 45 minutes with minimal
change. Voxel-based mapping is needed to better describe spatial
variations in uptake rate.
Keywords: TBI, DCE FLAIR MRI, Meninges, Traumatic Me-
ningeal Injury, Kinetics, Blood Brain Barrier
B6-05
SHEAR SHOCK WAVE DEVELOPMENT IN NEUROLOGI-
CAL TISSUES
Caryn Urbanczyk
1
, Cameron Bass
1
, Gianmarco Pinton
2,3
1
Duke University, Biomedical Engineering, Durham, USA
2
University of North Carolina, Biomedical Engineering, Chapel Hill,
USA
3
NC State University, Biomedical Engineering, Raleigh, USA
Non-classical interactions of shock waves with biologicals underline
implications to traumatic brain injuries and diffuse axonal injuries. In-
jury patterns in blunt or blast induced neurotrauma are inconsistent with
commonly held etiologies, like those based on relative motion. In high
rate loading scenarios, where nonlinear effects dominate, interaction of
shear shocks with soft tissues presents a compelling alternative to
current hypotheses on injury mechanisms. When applied pressure is
sufficiently high, low shear elasticity of brain allows nonlinear wave-
form distortion to produce shock fronts and accumulate highly localized
stresses. Violent gradients in shear shock waves can tear and damage
neurons as well as change estimates of damage at the brain skull in-
terface. Nonlinear viscoelastic wave propagation in brain tissue was
studied experimentally using high frame rate ultrasound and high speed
video imaging. Parameters important to incipient shear shock formation
were characterized. Tissue phantoms were created to examine effects of
material properties (sound speed, nonlinearity, dispersion) and for
in vitro
cadaveric porcine brain imaging, layered construction allowed
embedding of whole brain samples in gelatin. 128-channel radio-
frequency data was collected at up to 10,000 fps, under shear loading
conditions delivered by a vibration generator. Frequency, strain, and
strain rate sweep tests were performed parametrically. B-mode image
stacks were compiled into full-field displacement films using an adap-
tive displacement estimation algorithm. We complimented ultrasound
data with high speed video which was used to capture external finite
deformation of the gelatin/brain phantom during shear shock loading, at
up to 20,000 fps with full resolution. External deformation was quan-
tified with edge tracking in image processing software. For linear shear
wave inputs, we showed shear shock wave behavior in the brain. In
realistic, physiological range, (50–500 Hz and 10–100Gs) we confirmed
cubic nonlinear distortion and shock formation by third order harmonics
in frequency content. We characterized the minimum requirements for
shock front development and showed with neuroimaging techniques,
the potential devastating cases of shock damage to brain tissue.
Keywords: Traumatic Brain Injury, Shear Shock, Ultrasound Ima-
ging, High Speed Video
B6-06
CLINICAL UTILITY OF OUTPATIENT FOLLOW-UP COM-
PUTED TOMOGRAPHY IN A TRAUMATIC SUBDURAL
HEMATOMA POPULATION
Thomas Gianaris, Shaheryar Ansari, Andrea Scherer,
Richard
Rodgers
Indiana University School of Medicine, Department of Neurological
Surgery, Indianapolis, USA
Introduction:
Following evaluation and/or treatment in a hospital
setting, many patients with diagnosed traumatic subdural hematomas
(SDH) are routinely seen in follow-up with a repeat computed to-
mography of the head (HCT) to assess for further progression of the
lesion, regardless of clinical exam findings. This study aims to de-
termine the clinical utility of additional routine HCT scans of brain
trauma patients presenting with SDH on initial HCT.
Methods:
A retrospective, single-center review of 319 traumatic
SDH patients was performed at IU Health Methodist Hospital in In-
dianapolis from February 2007 to May 2012.
Results:
Of 319 isolated traumatic SDH patients seen at a median
follow-up of 50 days, follow up HCT revealed worsened findings in 8
(2.5%). 69 patients underwent further follow-up with additional HCT
after the initial follow-up visit, with 11 of them suffering neurological
decline. However, none of those who declined neurologically had
worsened imaging findings. Surgical intervention was undertaken in
only one patient who suffered neurologic decline. One patient un-
derwent surgery based on worsened HCT without physical exam ev-
idence of neurologic decline.
Discussion:
Routine outpatient follow-up HCT poorly correlated
with clinical decline and was not predictive of further surgical inter-
vention. In our series, only one patient required surgical intervention
based on the results of the CT, and one patient underwent surgery
despite an unchanged CT. Additionally, there was no association
between neurologic decline and worsening head CT findings. Based
on these results, our institution now performs follow-up HCT on a
patient-by-patient basis, and not routinely.
Conclusions:
Routine outpatient follow-up HCT for traumatic SDH
is poorly predictive of neurological decline or need for surgical in-
tervention, and therefore should not be utilized.
Keywords: Computed Tomography, Subdural Hematoma, outpa-
tient follow-up
B6-07
PET IMAGING OF
a
7 NICOTINIC ACETYLCHOLINE
RECEPTORS IN A RAT MODEL OF TRAUMATIC BRAIN
INJURY
Courtney Robertson
1
, Masayoshi Nakano
2
, Heather Valentine
2
,
Manda Saraswati
1
, Daniel Holt
2
, Hiroto Kuwabara
2
, Robert F.
Dannals
2
, Ayon Nandi
2
, Dean Wong
2
, Ray Koehler
1
, Andrew Horti
2
1
Johns Hopkins School of Medicine, Dept. of Anesthesiology & Cri-
tical Care Medicine, Baltimore, USA
2
Johns Hopkins School of Medicine, Dept of Radiology and Radi-
ological Science, Baltimore, USA
There is evidence that the
a
7 subtype of nicotinic acetylcholine
receptors (
a
7-nAChR) plays a role in the physiology of acute brain
injury, with growing evidence for its role in traumatic brain injury
(TBI). We have developed a novel positron-emission tomography
(PET) radiotracer ([18F]ASEM) that is highly specific and selective
for distribution of
a
7-nAChR in brain. The main objective was to
evaluate [18F]ASEM for imaging of
a
7-nAChR binding in a rat
model of TBI. PET imaging and ex vivo biodistribution experi-
ments were performed in a controlled cortical impact (CCI) rat
model. The binding potential was calculated as BP
ND
=
(regional
uptake/cerebellum) - 1. The following times after TBI were eval-
uated: 1, 3, 7 and 26 days. Sham-operated animals and uninjured
control animals were compared with CCI animals (n
=
5/group).
Findings were correlated with staining of
a
7-nAChR’s (rabbit anti-
a
7-nAChR antibody) in brain tissue. In the biodistribution
A-60