29 / 162
A4-07
AVAILABILITY OF OUTPATIENT REHABILITATION SER-
VICES AND BARRIERS TO CARE FOR VULNERABLE
POPULATIONS AFTER PEDIATRIC TBI
Megan Moore
1,2
, Nathalia Jimenez
5,2
, Ali Rowhani-Rahbar
6,2
,
Margaret Willis
3
, Kate Baron
1,2
, Jessica Giordano
4
, Deborah
Crawley
4
, Frederick Rivara
8,2
, Kenneth Jaffe
7,2
, Beth Ebel
8,2
1
University of Washington, Social work, Seattle, USA
2
Harborview Injury Prevention and Research Center, University of
Washington, Seattle, USA
3
Boston College, sociology, Boston, USA
4
BIAWA, N/A, Seattle, USA
5
University of Washington, 3Anesthesiology and Pain medicine,
Seattle, USA
6
University of Washington, Epidemiology, Seattle, USA
7
University of Washington, Rehabilitation Medicine, Seattle, USA
8
University of Washington, Pediatrics, Seattle, USA
Objective:
Aims were to explore associations between English pro-
ficiency, insurance status and outpatient rehabilitation service avail-
ability and travel time for children with traumatic brain injury (TBI).
Design:
This study used an ecologic cross-sectional design. Data
were analyzed from a cohort of 82 children (
<
18 years) treated for
moderate to severe TBI and rehabilitation providers in Washington
State. Main measures included availability and travel time to reha-
bilitation services.
Results:
Fewer than 20% of rehabilitation providers accepted
children with Medicaid and provided language interpretation services.
Mental health service provision was most limited. Adjusted for me-
dian household income, availability of multilingual services was
lowest in counties with greater language diversity; for every 10%
increase in persons over 5 years old speaking a language other than
English at home, there was a 34% decrease in availability of multi-
lingual pediatric services (Prevalence ratio
=
0.66; 95%; CI: 0.48–
0.90). Adjusted for education and Medicaid status, children from
Spanish-speaking families with limited English proficiency had sig-
nificantly longer travel times to all services: mean of 16 additional
minutes to mental health and 9 additional minutes to other therapies.
Conclusions:
Children in households with limited English profi-
ciency and Medicaid insurance faced significant barriers in availability
and proximity of outpatient rehabilitation services. There is a need for
innovative service strategies to equitably improve availability of services
for children with TBI. Studies in other regions utilizing similar methods
are needed to understand the scope of disparities noted in this study.
Keywords: TBI, rehabilitation, healthcare disparities, healthcare
accessibility, disability
A5 Poster Session II - Group A: Biomarker
A5-01
SINGLE MOLECULAR ARRAY GLIAL FIBRILLARY ACID
PROTEIN AND TOTAL TAU ARE INCREASED UP TO 90
DAYS AFTER TRAUMATIC BRAIN INJURY
Tanya Bogoslovsky
1
, David Wilson
3
, Yao Chen
3
, David Hanlon
3
,
Jessica Gill
2,1
, Andreas Jeromin
3
, Linan Song
3
, Yunhua Gong
1
,
Kimbra Kenney
1
, Carol Moore
1
, Ramon Diaz-Arrastia
1
1
Center for Neuroscience and Regenerative Medicine, Uniformed
Services University of the Health Sciences, Rockville, MD, USA
2
National Institute of Nursing Research, National Institutes of Health,
Bethesda, USA
3
Quanterix, Quanterix, Boston, USA
Background:
Glial fibrillary acid protein (GFAP) and tau are prom-
ising diagnostic and prognostic biomarkers in traumatic brain injury
(TBI). Single Molecule Array (Simoa) is a novel technology which
employs highly sensitive immunoassays for accurate measurements of
candidate biomarkers.
Design/Methods:
Plasma tau and GFAP were measured by Simoa
in serial samples from 33 TBI subjects (mean age 37; 73% male) at
days 1, 30 and 90 after TBI and compared to those of uninjured
controls (n
=
70).
Results:
GFAP was increased at days 1 (16.75 (3.84–100.6) pg/ml,
30 (1.330 (0.742–2.080)) pg/ml and 90 (1.350 (0.8870–2.280) pg/ml
after TBI compared to controls (0.5280 (0.216–1.220) pg/ml,
(p
<
0.0001 for all comparisons). Tau was similarly increased at days 1
(9.560 (5.895–17.10) pg/ml, 30 (6.665 (4.705–9.163) pg/ml, and 90
(5.720 (3.850–7.180) pg/ml compared to controls (4.340 (2.745–
5.128) (p
<
0.0001, p
<
0.0001 and p
=
0.0044, respectively). Receiver-
operator characteristic analysis found that the area under curve (AUC)
for tau at days 1 and 30 was 0.8973 (95% CI 0.8238 to 0.9709), and
0.8172 (95% CI 0.7254 to 0.9090) respectively. AUC for GFAP at day
1 was 0.9655 (95% CI 0.9212 – 1.010). There was a moderate cor-
relation (r
=
0.5256 (95% CI 0.1704 to 0.7600, p
=
0.0049) between
total tau and GFAP at day 1 after TBI and an inverse correlation
between day 1 GFAP and Glasgow Outcome Scale Extended-rated
recovery at day 180 (r
= -
0.4469 (95% CI
-
0.7316 to - 0.02953,
p
=
0.0325).
Conclusions:
Tau and GFAP are increased up to 90 days after TBI.
Tau and GFAP measured by Simoa may be useful as biomarkers of
TBI in the both acute and subacute phases.
Keywords: highly sensitive immunoassays, glial fibrillary acid
protein, total tau, diagnostic and prognostic biomarkers
A5-02
PERIPHERAL BLOOD MITOCHONDRIAL DNA AS A BIO-
MARKER OF CEREBRAL MITOCHONDRIAL DYSFUNC-
TION FOLLOWING TRAUMATIC BRAIN INJURY
Todd Kilbaugh
1
, Maria Lvova
2
, Michael Karlsson
3
, Zhe Zhang
2
,
Jeremy Leipzig
2
, Douglas Wallace
2
, Susan Margulies
4
1
Children’s Hospital of Philadelphia, Anesthesiology and CCM,
Philadelphia, USA
2
Children’s Hospital of Philadelphia, Mitochondrial and Epigenomic
Medicine, Philadelphia, USA
3
Lund University, Mitochondrial Medicine, Lund, Sweden
4
University of Pennsylvania, Bioengineering, Philadelphia, USA
Traumatic brain injury (TBI) has been shown to activate the peripheral
innate immune system and systemic inflammatory response, possibly
through the central release of damage associated molecular patterns
(DAMPs). We hypothesized TBI would increase peripheral whole
blood relative mtDNA copy number, and would be associated with
alterations in cerebral mitochondrial bioenergetics triggered by TBI.
Blood samples were obtained before, 6, and 25 hrs after focal (con-
trolled cortical impact injury: CCI) and diffuse (rapid non-impact ro-
tational injury: RNR) TBI. PCR primers, unique to mtDNA, were
identified by aligning segments of nuclear DNA (nDNA) to mtDNA,
normalizing values to nuclear 16S rRNA, for a relative mtDNA copy
number. Three unique mtDNA regions were selected, and PCR primers
where designed within those regions, limited to 25–30 base pairs to
ensure sequence specificity, and measured utilizing qRT-PCR. Mean
relative mtDNA copy numbers increased significantly following both
CCI and RNR. Specifically, the mean relative mtDNA copy number
from three mitochondrial specific regions pre-injury was 0.84
–
0.05.
After diffuse non-impact TBI at 6 and 25 hours, mean mtDNA copy
A-29