NNS 2015 Program & Abstract Book

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B6-13
CHRONIC NEUROINFLAMMATION ANALYSIS AFTER
TRAUMATIC BRAIN INJURY USING TSPO-PET AND MRI IN
MICE
Sanae Hosomi1, Tadashi Watabe2, Yuki Mori3,4, Mituso Onishi1, Yuji
Ogura1, Yoshichika Yoshioka3,4 , Takeshi Shimazu1
1Osaka University Graduate School of Medicine, Department of
Traumatology and Acute Critical Medicine, Suita, Japan
2Osaka University Graduate School of Medicine, Department of Nu-
clear Medicine and Tracer Kinetics, Suita, Japan
3WPI Immunology Frontier Research Center (WPI IFReC), Osaka
University, Biofunctional Imaging, Suita, Japan
4National Institute of Information and Communications Technology
(NICT) and Osaka University, Center for Information and Neural
Networks (CiNet), Suita, Japan
Background: Traumatic brain injury (TBI) not only results in an
initial functional deficit, but also is frequently followed by chronic
cognitive impairment. The mechanism of this pathology has yet to be
fully understood and methods to accurately quantify of the progress of
these chronic traumatic encepalopathies are eagerly desired.
Objective: To detect neuronal inflammation in vivo in the chronic
phase after focal traumatic brain injury using positron emission to-
mography (PET) and 11.7T magnetic resonance imaging (MRI).
Methods: Adult male C57BL/6J mice (8–10 weeks-old) were in-
flicted with a single controlled cortical injury. At 1, 4, 7, 14, 21, 28,
42, 63 and 94 days after injury, translocator protein (TSPO)-PET
screening was performed. In addition, conventional MRI (T1, T2,
T2*) and magnetic resonance spectroscopy (MRS) were performed.
Results: TSPO uptake at the injured cortex almost vanished from
14 days post injury. In contrast, long-term TSPO uptake was ob-
served at the ipsilateral subcortex. T2-weighted MRI only detected
faint, low intensity areas of interest localized at the ipsilateral
thalamus. MRS in the associated area showed that peaks corre-
sponding to Choline, Myo-inositol, and Lactate were higher than
those in the contralateral thalamus. The peak corresponding to
N-acetyl Aspartate was lower. Together with histological findings,
these changes are thought to be chronically activated glial cells and
neuronal damage in the thalamus.
Conclusion: We first reported long-term neuroinflammation
spreading to the thalamus after TBI using in vivo imaging, TSPO-PET
and MRS. These noninvasive imaging device could prove useful in
determining the role of chronic inflammation.
Keywords: TSPO, PET, MRI, chronic phase
B6-14
ACUTE TRAUMATIC INTRACRANIAL LESIONS INCREASE
THE RISK OF CERVICAL SPINE INJURIES
Teemu Luoto, Tuomo Thesleff, Juha O¨ hman
Tampere University Hospital, Department of Neurosurgery, Tampere,
Finland
Objective: To study the concurrence of CT (computed tomography)-
detectible cervical spine injuries (CSI) and traumatic brain injury
(TBI). We hypothesized that CT-positive TBI patients would have a
significantly higher risk of having a concurrent CSI compared to CT-
negative TBIs.
Methods: This retrospective study included 3023 consecutive pa-
tients who underwent head CT due to an acute head injury (HI) at the
Emergency Department of Tampere University Hospital (August 2010–
July 2012), Tampere, Finland. The medical records of these patients
were reviewed to identify the individuals whose cervical spine was
CT-imaged due to a clinical suspicion of a CSI within one week post-
HI. Clinical data as well as CT findings (head and cervical spine) were
systematically collected.
Results: Of the whole sample (n = 3023), 19.2% (n= 579) had an
acute CT-positive TBI. Subdural hematomas (67.2%, n = 389) and
subarachnoid hemorrhages (48.7%, n = 282) were the most common
findings on head CT. The average age of the patients was 55.0 years
(SD = 24.0 years) and 56.4% (n = 1705) were male. Car accidents
9.7% (n = 294) and falls 63.5% (n = 1921) were the most frequent
injury mechanisms. Of the whole sample (n = 3023), 36.1% (n = 1091)
underwent cervical spine CT within one week post-HI. On cervical
CT, CSI (C0-CVII: fracture, dislocation, subluxation) was found in
2.5% (n = 77) of the patients. Altogether, 101 fractured vertebrae and
5 separate ligament injuries were detected. CII (0.8%, n = 23) was the
most commonly injured vertebra. The patients with acute traumatic
intracranial lesions had significantly (Pearson chi-square, p = 0.001;
OR = 2.206) more CSIs (4.5%, n= 26) compared to head CT-negative
patients (2.1%, n = 51). When the associations between CT-positive
TBIs, cervical spine fractures and dislocation/subluxation were ana-
lyzed separately, only fractures were related to intracranial lesions
(p = 0.001, OR = 2.206).
Conclusions: Head trauma patients with acute intracranial le-
sions on CT have a twofold risk of CSI in comparison to patients
with a CT-negative head injury. CSI should be always acknowl-
edged when treating CT-positive TBI patients. CT-imaging of the
cervical spine in case of CT-positive TBI is recommended based on
these findings.
Keywords: Traumatic brain injury, Cervical spine injury, Emer-
gency assessment, Computed tomography, Head injury
B6-15
DIFFUSION MR IMAGING REVEALS ABNORMALITIES IN
THE CORPUS CALLOSUM AFTER SINGLE TBI VERSUS
OVERLYING CORTEX AFTER REPETITIVE TBI
Bernard Dardzinski1, Fengshan Yu1, Dinesh Shukla1, Regina C.
Armstrong1, Reed Selwyn1,2
1Uniformed Services University of the Health Sciences, Center for
Neuroscience and Regenerative Medicine, Bethesda, USA
2University of New Mexico, Radiology, Albuquerque, USA
Non-invasive detection of brain abnormalities from single and re-
petitive mild traumatic brain injury (TBI) is important for evaluation
of the acute through chronic effects of impact-acceleration head in-
juries. Magnetic resonance imaging (MRI) is beginning to reveal
findings in mild TBI patients that are not detected with conventional
imaging. This MRI study used diffusion tensor imaging (DTI) to
evaluate longitudinal changes in both the corpus callosum and the
overlying cortical gray matter after single and repetitive impact in-
juries in adult male C57BL/6 mice. For single TBI (sTBI), mice had a
scalp incision to expose the skull and received a stereotaxically
controlled impact (3 mm tip) at bregma (1.5 mm depth; 4.0 m/sec;
100 msec dwell time). For repetitive TBI (rTBI), mice received a
milder impact (1.0 mm depth; 4.0 m/sec; 200 msec dwell time) onto
the scalp over bregma each day for 5 days. Sham mice were run in
parallel but without impact. T2-weighted MRI and DTI scans were
performed at baseline and at 3, 6, and 42 days post-TBI/sham. Frac-
tional anisotropy (FA) values were significantly decreased in the
corpus callosum after sTBI, but not rTBI. Histological analysis of
the corpus callosum confirmed less axon damage, astrogliosis, and
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