NNS 2015 Program & Abstract Book

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Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative
disorder linked to repetitive TBI and diagnosed by autopsy. This
current study explores PET imaging with Pittsburgh Compound B
(PiB) to identify amyloid pathology in chronic TBI.
Methods: [11C]PiB PET data (8 male TBI subjects, mean age 47)
were compared to 15 healthy adults (7 males, mean age 59). PiB
SUVR images were calculated with cerebellar grey matter (GM) as
reference and aligned to diffusion data by registering to T1 MR se-
quences. High b-value diffusion imaging was processed in a High
Definition Fiber Tracking (HDFT) pipeline. Cortical segmentation
was performed using Freesurfer; labels were transferred to diffusion
space using FSL software. We performed two hierarchical regressions
to analyze diencephalic white matter (WM) regions: 1) regional cor-
pus callosum (CC) PiB SUVR treating TBI status (TBI/Control), age,
and region and their 2-way interactions as fixed effects; 2) voxel-level
WM PiB SUVR within TBI subjects, treating diffusion gFA, region,
and interaction as fixed effects.
Results: One participant was classified as PiB-positive (elevated
uptake in GM ROIs for Alzheimer’s Disease). PET PiB SUVR was
reduced in TBI subjects in Anterior and Mid-Anterior CC regions
( p = .03 & p< .01). Within TBI subjects, higher gFA significantly
predicted higher PiB SUVR at a voxel level in 3/5 CC regions and in
cerebral WM (all p < .01). PiB SUVR within TBI subjects was greatest
in Anterior and Mid-Anterior regions of CC (ß(anterior) = 0.45,
ß(mid-anterior) = 0.32).
Conclusion: Our preliminary analysis found changes in PiB uptake
in chronic TBI in the corpus callosum, a known area of vulnerability
to TBI damage, in the absence of the typical gray matter PiB depo-
sition seen in Alzheimer’s Disease. These are promising pilot results
in the search for an in vivo neuroimaging biomarker panel for CTE.
Keywords: Amyloid, White matter, Chronic TBI
B6-19
LONGITUDINAL CHANGES IN REGIONAL BRAIN VOL-
UME IN PEDIATRIC TBI: PRELIMINARY ANALYSES
Emily Dennis1, Xue Hua1, Julio Villalon-Reina1, Claudia Kernan2,
Talin Babikian2, Richard Mink3, Christopher Babbitt4, Jeffrey
Johnson5, Christopher Giza6, Paul Thompson1,7, Robert Asarnow2,8
1Keck SOM USC, IGC, NII, Los Angeles, USA
2UCLA, Dept Psychiatry Biobehav Sciences, Semel, Los Angeles, USA
3Harbor-UCLA Medical Center & LA BioMedical Research Institute,
Torrance, USA
4Miller Children’s Hospital, Long Beach, USA
5LAC + USC Medical Center, Dept Pediatrics, Los Angeles, USA
6Mattel Children’s Hospital, UCLA Brain Injury Research Center,
Dept. Neurosurg, Div. Ped Neurol, Los Angeles, USA
7USC, Dept. Neurology, Pediatrics, Psychiatry, Radiology, En-
gineering, and Ophthalmology, Los Angeles, USA
8UCLA, Dept Psychology, Los Angeles, USA
Traumatic brain injury (TBI) can cause widespread and prolonged brain
degeneration. This is especially damaging in young patients as it may delay
or alter brain present preliminary longitudinal analyses of
regional brain volume change, assessed by tensor-based morphometry
(TBM) in pediatric moderate/severe TBI. We assessed participants in the
post-acute phase (1–6 months post injury) and chronic phases (13–19
months post injury). We examined 40 participants: 15 with TBI (mean age
at T2 = 15.7, 4 female) and 25 controls (mean age at T2 = 16.3, 10 female).
We used the TBM protocol developed by our lab to generate Jacobian
determinant maps describing the displacement between T1 and T2 within
subject. We then ran a voxel-wise linear regression testing for group dif-
ferences in these longitudinal volume changes, covarying for age, sex,
scanner, and intracranial volume (ICV). Resultswere corrected for multiple
comparisons using searchlight FDR across the whole brain (q< 0.05). We
found significant differences in the genu, mid body, and splenium of the
corpus callosum – areas where the control group showed little to no change
over time, while the TBI group showed atrophy. We also found significant
differences in a large cluster between hemispheres spanning the frontal and
parietal cortices, indicating tissue contraction and CSF expansion. Our
results indicate continued, progressive tissue changes in the first year post-
injury. Whether these changes indicate progressive damage, or a natural
progression of injury and recovery is a topic for future investigation.
Keywords: traumatic brain injury, pediatric, tensor based mor-
phometry, MRI, volume, longitudinal
B6-20
AMYLOID PLAQUES ARE INCREASED IN THE BRAIN OF
TBI SURVIVORS AT 1, 12, AND 24 MONTHS AFTER INJURY
Joshua Gatson1, Christopher Madden1, Joseph Minei1, Ramon Diaz-
Arrastia2
1UT Southwestern Medical Center, Surgery, Dallas, USA
2Uniformed Services University of the Health Sciences, Center for
Neuroscience, Rockville, USA
Background: Traumatic brain injury (TBI) is a well recognized risk
factor for Alzheimer’s disease (AD). With respect to amyloid depo-
sition, there is little published data regarding the timing, location, and
deposition rate of amyloid in the brain after TBI, and no longitudinal
studies are available.
Objective: The primary objective of this study was to conduct
serial 18F-AV-45 (florbetapir F18) positron emission tomography
(PET) imaging in severe TBI subjects after injury.
Methods: Serial florbetapir F18 PET imaging was conducted in 2
individuals with a severe TBI at 1, 12, and 24 months after injury. A
total of 12 brain regions were surveyed for amyloid accumulation.
Results: Subject 1, was a 50 year old male who experienced a severe
TBI with moderate-to-good cognitive/functional outcomes (GOSE = 7).
An increase in amyloid (as indicated by standard uptake value ratios
[SUVR]) was observed in the hippocampus (+16%, left; + 12%, right) and
caudate nucleus (+14%, left; + 18%, right). At year 2, subject 1 complained
of severe memory deficits, which was captured on the Rivermead symp-
tom list. The lone affected brain region at year 2 was the right hippo-
campus (15% increase of amyloid). Subject 2 was a 37 year old male who
suffered a severe TBI and a poor outcome (GOSE = 6). An increase of
amyloid in the left anterior (+ 39%) and posterior (+ 20%) putamen was
observed at year 1. Also, a reduction of amyloid was observed in the
precuneus at the 12 (-19%) and 24 (-11%) month time-points.
Conclusions: Compared to SUVRs at 1 month, amyloid clearance
and accumulated was observed at all time-points. Longitudinal im-
aging conducted here suggests that florbetapir F18 PET imaging may
be useful in monitoring amyloid dynamics within brain regions fol-
lowing severe TBI and may be predictive of cognitive deficits.
Keywords: amyloid, TBI, florbetapir F18, PET imaging
B6-21
DIFFUSION TENSOR IMAGING ANALYSIS OF MILD
TRAUMATIC BRAIN INJURY
Juan Herrera, Kurt Bockhorst, Shakuntala Kondraganti, Ponnada
Narayana
UTHealth Medical School at Houston, Diagnostic and Interventional
Imaging, Houston, USA
A-65