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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 200

l

m, magnetiza-

tion transfer(MT) pulse 2

l

T/2s. MT-offset frequences(

D

x

) 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 Butman

1,2

, Andre van der Merwe

2

, Christian Shenouda

2

, Chan

Leighton

1,2

, Latour Lawrence

3,2

1

NIH, Clinical Center, Bethesda, USA

2

CNRM, Core, Bethesda, USA

3

NIH, 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 Castro

2

, Dzung Pham

2

,

John Butman

1,2

1

NIH, Clinical Center, Bethesda, USA

2

CNRM, 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

A-62