NNS 2015 Program & Abstract Book

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imaging, including image blurring, low resolution, radiation dose
limitation and the increased FDG accumulation, may cause false-
positive results in a longitudinal study. Here, we present an alternative
MRI-based molecular imaging, named chemical exchange saturation
transfer(CEST)-MRI, to detect the glucose metabolism without the
need for a radioisotope. Our results indicate that glucose CEST-
MRI(glucoCEST) could be another sensitive molecular imaging to
detect metabolism in brain trauma.
A phantom experiment was first conducted including five glucose
concentrations close to that of the living tissues(2 mM*10 mM).
Female SD rats(n = 6) were scanned for baseline, 1, 8, 16, 24 and 48
days-post-injury(DPI). glucoCEST were acquired using a Bruker 9.4T
scanner (TR 3.5 s, TE 11.5 ms, resolution 200l m, magnetiza-
tion transfer(MT) pulse 2l T/2s. MT-offset frequences(Dx) were
- 2 kHz* + 2 kHz with 100 Hz stepping(glucose at 1.2 ppm, 2.1 ppm,
2.9 ppm). MTR-asymmetry(MTRasym) derived from the glucoCEST
data was applied to detect the glucose concentration. One-way AN-
OVA with repeated measures was performed by Prism.
MTRasym generated clear contrast in the glucose phantom and
showed a linear relation to glucose concentrations. MTRasym maps
clearly distinguished levels of metabolism between cerebral structures
and exhibited temporospatial distributions of glucose in the injured
brains. The glucose metabolism significantly decreased 40%(p < 0.01)
in the injured cerebral cortex at 1DPI and progressive decreased to
16DPI. The glucose metabolism then slightly increased and reached
67% of that of the baseline in 48DPI.
Energy supply and consumption is crucial to salvage the trauma-
tized tissue. This study shows that glucose largely decreased after TBI
and persisted chronically. The widespread hypometabolic changes
affect the brain functions in learning and memory resulting in cerebral
atrophy. glucoCEST delivers results comparable to previous PET
studies yet delivers better image quality higher image resolution and
sensitivity. glucoCEST could provide the window for effective
treatments to increase the survival of traumatized tissue.
Keywords: glucose metabolic disorders, in vivo, glucoCEST
B6-11
MICROHEMORRHAGE IS NOT FOREVER: CROSS-
SECTIONAL ANALYSIS INDICATES RESOLUTION OVER
EXTENDED FOLLOW UP INTERVALS
John Butman1,2, Andre van der Merwe2, Christian Shenouda2, Chan
Leighton1,2, Latour Lawrence 3,2
1NIH, Clinical Center, Bethesda, USA
2CNRM, Core, Bethesda, USA
3NIH, NINDS, Bethesda, USA
Objective: To determine whether or not traumatic microhemorrhage
persists indefinitely, we evaluated microhemorrhage burden in two
cohorts of patients with severe brain injuries; i) within 1 year of injury
and ii) greater than 10 years post injury.
Methods: Traumatic brain injury (TBI) patients (n = 125) evaluated
and imaged at NIH for the CNRM (Center for Neuroscience and
Regenerative Medicine) were retrospectively reviewed to identify two
cohorts of patients with severe TBI: an ‘‘early’’ cohort (evaluated < 1 y
from injury), and a ‘‘late’’ cohort (evaluated > 10 y from injury. Be-
cause the distant time from injury in the ‘‘late’’ cohort precluded
accurate documentation of severity according to DOD/VA criteria, we
used loss of consciousness (LOC) of greater than 24 hours and a GCS
at presentation of less than 12 to qualify as severe.
Microhemorrhage burden (total lesion counts) were made by a
single neuroradiologist ( JAB) by marking microhemorrhages on
susceptibility weighted images (Carestream PACS v 12.0). Values for
age and microhemorrhage burden are reported as mean – standard
deviation, and statistical comparison was made using the Mann-
Whitney U-test (MedCalc).
Results: For the ‘‘early’’ cohort, 8 patients were identified (time
from injury 0.46 – 0.37 y) and for the ‘‘late’’ cohort, 6 patients were
identified (time from injury 28.0– 6.2 y). Similar to the ‘‘early’’
cohort, imaging findings in the late cohort confirmed significant
brain trauma, including non-hemorrhagic signs of traumatic/diffuse
axonal injury such as focal notching in the corpus callosum, en-
cephalomalacia from prior contusion, and hemorrhagic sequelae of
traumatic brain injury, such as superficial siderosis. However, sig-
nificantly fewer microhemorrhages were present in the ‘‘late’’ cohort
as compared with the ‘‘early’’ cohort (3 – 6 vs 167 – 133, p = 0.012).
Conclusion: In severe TBI, numerous microhemorrhages are often
identified shortly after injury, but are virtually absent in patients
evaluated many years after the injury. The precise time course of such
resolution is the subject for longitudinal imaging studies.
Keywords: susceptibility weighted imaging, microhemorrhage, severe
B6-12
IMPROVED VISUALIZATION OF SUPERFICIAL HEMOR-
RHAGE IN SUSCEPTIBILITY WEIGHTED IMAGES
Marcelo Castro2, Dzung Pham2, John Butman1,2
1NIH, Clinical Center, Bethesda, USA
2CNRM, Image Processing Core, Bethesda, USA
Objective: Minimum intensity projection (minIP) is used to display
susceptibility weighted images (SWI) - allowing the observer to dis-
tinguish microhemorrhage from vessel. Unfortunately, low signal in-
tensity of the skull projects into the thick slab of the minIP, masking
superficial tissues near the skull base and convexities. Because su-
perficial contusions are a common feature of TBI, we develop a
method to allow minIP projection to ‘‘see’’ superficial tissues adjacent
to the skull.
Methods: To prevent low intensity extraaxial voxels form pro-
jecting into the thick slab of the minIP, we develop a method to
precisely mask the brain and assign high signal intensity to voxels
outside the brain mask. First, the Brain Surface Extraction algorithm
(Shattuck,2001) is applied to generate two brain masks, one that is
slightly too small and one that is slightly too large. The rind of tissue
between these two masks is then a rind containing both high signal
intracranial tissues and low intensity voxels of the skull to be excluded
from the minIP process. Next, a clustering algorithm identifies tissues
within this rind to rejoins missing brain tissue into the mask.
SWI (0.65 mm isotropic) arbitrarily selected from our database of
patients with TBI were examined with minIP using the original data
and masked data using the new method.
Results: For the standard minIP, *1% of brain volume was lost
per 1 mm of slab thickness. So for a typical 15 mm minIP 15% of the
brain volume is completely hidden from the radiologist. For the new
method, the visible brain tissue in the minIP reconstruction was
complete and independent of slab thickness. Superficial micro-
hemorrhage and superficial veins could be visualized in all cases.
Conclusions: The proposed method represents a significant im-
provement in minIP visualization of SWI data, allowing for superficial
brain tissues to be assessed, surface venous anatomy to be visualized,
and larger slab thickness applied. This has the potential to facilitate
the detection of microhemorrhage, particularly in superficial cortex.
Keywords: susceptibility weighted imaging, microhemorrhage,
contusion
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