Page 153 - NNS 2014 Program & Abstract Book

1Medical College of Wisconsin, Milwaukee, USA
2Milwaukee School of Engineering, Milwaukee, USA
3Zablocki VA Medical Center, Milwaukee, USA
A new experimental model was developed to induce TBI in rats
through pure coronal plane angular acceleration to aid in the under-
standing of injury biomechanics and tolerance. Devices of this type can
be large and have high maintenance costs. This project designed and
characterized a compact rotational acceleration model to induce TBI in
rodents through coronal plane rotational acceleration at specific mag-
nitudes and durations. The design was based on the existing MCW
Rotational Injury Device, consisting of an energy delivery device
(EDD) and rodent helmet. The new EDD pneumatically propelled an
impactor rod through a barrel using compressed air, towards the lateral
extension of the existing helmet fixture. The helmet rotational axis was
aligned with the cervical spine of the rat. When the impactor contacted
the moment arm, the animal’s head and helmet rotated in the coronal
plane. The acceleration phase was designed to be much higher mag-
nitude than the deceleration phase, so rodent TBI was attributed to the
initial acceleration. The compact device delivered impactor exit ve-
locities from the launcher of 8.1 – 0.1m/s at input pressures of 12psi,
and showed the potential for exit velocities as high as 14.7m/s at 35psi.
These exit velocities, along with mass of the rod, allowed for a large
amount of energy to be transferred to the helmet with only a
1.00x0.75x2.25-meter footprint (LxWxH). This will permit a wide
range of rotational accelerations while maintaining consistent durations
using the existing elastomer interface. These rotational accelerations
were 560 – 57krad/s2, with a duration of 1.69 – 0.24msec at input
pressures of 12psi. The experimental methodology remains flexible,
permitting adjustment of model parameters to continually expand the
range of acceleration pulses to produce different TBI outcomes.
Key words
brain mass scaling, mild TBI, rodent model, rotational acceleration
D2-23
IN VS. OUT: CONTROVERSIES IN SHOCK TUBE BLAST
EXPERIMENTS
Yu, A.W.1 , Bigler, B.R.1, Wood, G.W.1, Panzer, M.B.2, Meaney, D.F.3,
Morrison III, B.4, Bass, C.R.1
1Duke University, Department of Biomedical Engineering, Durham,
NC, USA
2University of Virginia, Center for Applied Biomechanics, Charlot-
tesville, VA, USA
3University of Pennsylvania, Department of Bioengineering, Phila-
delphia, PA, USA
4Columbia University, Department of Biomedical Engineering, New
York, NY, USA
Inconsistencies in blast experiment methodologies confound the proper
characterization of primary blast exposure. Comparisons across models
of blast injury are virtually impossible due to non-standardized proto-
cols. A major ambiguity is the placement of test subjects relative to
the shock tube exit, interior vs exterior. This study characterizes
overpressure waveform at potential test locations to determine ideal
placements.
A cylindrical 305 mm diameter shock tube was used to generate
blasts replicating those in the free field. Wave profiles and blast pa-
rameter measurements were acquired using specialized pressure
transducer housing fixtures at various tube diameter (DT) lengths from
the exit. Finite element (FE) numerical simulations were used to
validate experimentally derived blast parameter results.
FE simulations showed good comparison against experimental re-
sults. Shock waves were planar 8DT lengths past the driver until ½DT
exterior. Significant decline of overpressure was found after 1DT
outside the shock tube. No significant differences in peak overpres-
sure, duration, and impulse were found at the exit and DT/12 past the
shock tube exit.
Both inside and outside the shock tube are appropriate specimen
placements depending on desired overpressure/duration parameters.
Specimens should be placed at least 8–10 tube diameters downstream
from the driver. Test subjects placed outside the shock tube should
minimize standoff distance, ideally to less than half a tube diameter
length. Findings can be scaled to cylindrical shock tubes of all sizes.
Key words
animal models, blast, numerical simulation, pressure profiles, shock
tube, traumatic brain injury
D2-24
INFLUENCE OF HEAD ROTATIONAL ACCELERATION
PULSE SHAPE ON BRAIN TISSUE STRAINS
Baumgartner, D.3, Shah, A.1,2, Umale, S.1,2, Budde, M.D.1,2, Ren, L.4,
Yang, J.5, Willinger, R.3, Stemper, B.D.1,2
1Medical College of Wisconsin, Milwaukee, USA
2Zablocki VA Medical Center, Milwaukee, USA
3Strasbourg University, Strasbourg, France
4Hunan University, Changsha, China
5Chalmers University, Goteborg, Sweden
Brain tolerance to rotational acceleration is relevant for understanding
injury thresholds and development of injury mitigation techniques for
automobiles and sporting events. This computational-modeling study
outlined effects of head rotational acceleration pulse shape on strains
within brain tissues. A detailed finite element model of the human
skull and brain was developed and validated previously. The model
was exercised using realistic rotational accelerations with different
magnitude and duration characteristics, and the principal strain re-
sponse was extracted for parietal cortex, hippocampus, thalamus, and
hypothalamus. Rotational acceleration magnitude was varied to three
levels: 3.6krad/s2 (M1), 5.3krad/s2 (M2), and 6.6krad/s 2 (M3).
Duration was varied to 9msec (D1), 18msec (D2), and 27msec (D3).
Hippocampus and hypothalamus sustained more strain than cortex and
thalamus. With increasing acceleration magnitude from M1 to M2 and
M2 to M3, strain in all brain regions was uniformly increased by 42%
and 80%. However, strains demonstrated regionally dependent chan-
ges with increasing duration (D1 to D3): 68%, 37%, 33% and 14% in
parietal cortex, hippocampus, thalamus and hypothalamus, respec-
tively. The trend was consistent for all acceleration magnitudes. This
study demonstrated differing and independent effects of rotational
acceleration magnitude and duration on strains within brain tissues
during rotational acceleration. Magnitude has long been a correlate of
injury severity and this study supports that finding in that increased
acceleration magnitudes led to uniformly higher brain tissue strains
(higher injury risk). However, rotational acceleration duration chan-
ged the strain distribution within the brain, resulting in different injury
risks in different brain regions. This finding is significant as changing
strain distribution with different durations can manifest as different
injury distributions within the brain and different neuropsychological
outcomes following exposure to head rotational acceleration.
Key words
finite element model, rotational acceleration, tissue strain, traumatic
brain injury
A-121