Common data elements in radiologic imaging of traumatic brain injury.

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Mild Traumatic Brain Injuries were previously undiagnosable and therefore damages were
speculative
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Kim Armenta DO, Universitiy of California, Irvine Medical Center, Irvine, CA; Bianca Tribuzio DO, University of California, Irvine Medical Center, Irvine, CA; Robert A. Bitonte MD JD, University of California, Irvine Medical Center, Irvine, CA;
Julie K. Ho, Esq. Tustin, CA
.
Definition of Mild Traumatic Brain Injury (TBI)
Pathophysiology of Mild TBI
Advances in Biomarkers in Diagnosis of Mild TBI
WHO defines mild TBI as: “an acute brain injury resulting from
mechanical energy to the head from external physical forces.
Operational criteria for clinical identification include:
(i) one or more of the following: confusion or disorientation, loss
of consciousness for 30 minutes or less, post-traumatic amnesia
for less than 24 hours, and/or other transient neurological
abnormalities such as focal signs, seizure, and intra-cranial
lesion not requiring surgery;
(ii) Glasgow Coma Scale score of 13–15 after 30 minutes postinjury or later upon presentation for healthcare.
(iii)These manifestations of MTBI must not be due to drugs,
alcohol, medications, caused by other injuries or treatment for
other injuries (e.g. systemic injuries, facial injuries or intubation),
caused by other problems (e.g. psychological trauma, language
barrier or coexisting medical conditions) or caused by penetrating
craniocerebral injury”
(Iverson, 2006)
Diffuse Axonal Injury (DAI) is the most common cause of damage within
brain tissue in closed head trauma. It is due to sudden rotational
acceleration/deceleration motions resulting in shearing forces that change
the shape of the brain tissue. The change in alignment will produce
edema and leakage in axons in parts of the brain where there is a change
in density such as gray-white matter junction or in white matter tracts.
Common areas of brain affected by DAI included cerebral hemisphere
gray-white matter interface, subcortical white matter, corpus callosum,
basal ganglia, dorsalateral brainstem and cerebellem.
Mechanical and pathophysiological mechanisms of DAI. 1
Other new developments include advances in new biomarkers (specific
biological indicators of a disease state that can be measured using
samples from affected tissues or peripheral body fluid). S100B is a
serum protein that is transiently increased after mild TBI (Dash et al,
2010). It has been evaluated in six clinical trials with over 2000
participants and demonstrated 98% sensitivity in diagnosis of mild TBI,
but poor specificity (Dash et al, 2010). NSE is an additional biomarker
that has a high specificity. Furthermore, high initial levels of S100B, NSE,
and other biomarkers such as GFAP and tau are correlated with poor
outcomes six months after injury (Dash et al, 2010).
Compensation for Mild TBI
Epidemiology
Traumatic brain injury (TBI) affects more than 1.5 million people per year
(Center for Disease Control, 2003). Of those, approximately 75% have
mild TBI (Center for Disease Control, 2003).
Estimated Average Annual Numbers of Traumatic Brain InjuryRelated Emergency Department Visits, Hospitalizations, and
Deaths, by External Cause, United States, 2002–2006 4
Symptoms of Mild TBI
The term “mild” is potentially misleading because some individuals with
mild TBI may suffer long-term impairments and disabilities. It is also
an under-diagnosed issue for a variety of reasons. Some individuals
with mild TBI may appear ‘normal’, but may suffer from the inability to
concentrate, may develop headaches, or become more emotionally
labile.
TEMPLATE DESIGN © 2008
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(adapted from Andriessen et al,2010)
Diagnosis of Mild TBI
When individuals who have suffered from mild TBI actually seek medical
support for these symptoms, they are typically evaluated with medical
imaging. Unfortunately, the majority of head studies done through
computerized topograghy (CT) and magnetic resonance imaging (MRI) are
reported as normal. Currently mild TBI is best assessed through
neuropsychological testing. Although, conventional medical imaging
modalities do not generally recognize the damage sustained to the brain of
individuals with mild TBI’s, histological and animal studies have
demonstrated pathological changes consisting of wallerian degeneration,
diffuse axonal injury, release of excitatory neurotransmitters, and edema
(Smith et al, 2003 and Yi et al, 2006). The new advances in the diagnosis
of individuals with mild TBI should lead to improved treatment and
prevention of complications
Advances in Imaging in Diagnosis of Mild TBI
Advances in imaging and diagnostic studies provide improved methods of
diagnosing mild TBI. The most exciting developments are found in newer
MRI’s such as diffusion-tensor imaging (DTI) and susceptibility-weighted
imaging (SWI).
Diffusion Tensor Imaging (DTI)
DTI has a higher sensitivity to identify white matter damage typically
associated with diffuse axonal injury in mild TBI. It measures tissue
organization through measurements of random translation of water
molecules (Inglese et al, 2005). DTI uses fractional anisotropy as an
index of local coherence of fibers (Wei et al, 2008). Normally water
molecules in white matter tracts align along the direction of the tract, and
are therefore termed anisotropic. Decreased structural integrity of brain
tissue leads increase in random motion of water molecules in all directions
or otherwise described as a reduction in fractional anisotropy (Inglese et
al, 2005).
Susceptibility Weighted Imaging (SWI)
SWI has enhanced recognition of microhemorrhages (Haacke et al,
2010). SWI is able to detect blood at the level of iron and blood products
(Haacke et al, 2010).
Legal Perspective of Mild TBI
Previously, individuals suffering from mild TBI frequently were difficult to
diagnose because their symptoms and impairments could not be identified
through traditional CT, MRI scans or biomarkers. An individual instituting a
lawsuit cannot be compensated for damages he expects to incur in the
future unless he can prove such damages with reasonable certainty. CA
Civil Code section 3282 provides that “damages may be awarded, in a
judicial proceeding, for detriment resulting after the commencement
thereof, or certain to result in the future.” In Scognamillo v. Herrick, 106
Cal. App. 4th 1139, the court reversed a portion of the damage award
because it was not supported by sufficient evidence and therefore
speculative. In Scognamillo, the treating physician testified that it was
possible that one surgery might sufficiently alleviate plaintiff's problems, or
that a second surgery might be deemed to not be worth the risk. The court
found that the second surgery was speculative and therefore, not
reasonably certain to occur in the future. With advances in diagnostic
modalities such as DTI, SWI and new biomarkers to detect mild TBI,
calculating damages for a typical client can be done with more reasonable
certainty and are not speculative
Complications of Mild TBI
Individuals with mild TBIs can have a multitude of complications ranging
from medical, employment, social, and cognitive. Many will complain of
post-concussive symptoms such as headache, photophobia, nausea,
dizziness, fatigue, and sleep disturbances (CDC, 2003). They will have a
pattern of responses with neuropsychological assessment that
demonstrate difficulty with executive functions such as organization, logic
and reasoning, comprehension, visual perception, and balance (Dr.
Texiera of UCI Neuropsychology, personal communication Nov 2010).
Mild TBI patients will take an average of two years to reach highest
potential cognitive function when receiving maximum treatment. During
this time, patients will incur costs for medications needed for mood
disorders and pain, for visits with physicians, therapists, day treatment
programs and other measures such as environmental modifications. If
treatment is delayed or inadequate, individuals with mild TBI could
possibly develop other psychological and emotional issues due to the
inability to function at their previous level. They will need compensation
for their damages if legally entitled
References
1.Andriessen TM, Jacobs B, Vos PE. Clinical characteristics and pathophysiological mechanisms of focal and diffuse
traumatic brain injury.J Cell Mol Med. 2010 Oct;14(10):2381-92. doi: 10.1111/j.1582-4934.2010.01164.x.
2.National Center for Injury Prevention and Control. Heads up: Facts for Physicians about Mild Traumatic Brain
Injury (MTBI). Centers for Disease Control and Prevention. Accessed from:
http://www.cdc.gov/concussion/headsup/pdf/Facts_for_Physicians_booklet-a.pdf
3.National Center for Injury Prevention and Control. Report to Congress on Mild Traumatic Brain Injury in the United
States: Steps to Prevent a Serious Public Health Problem. Atlanta, GA: Centers for Disease Control and Prevention;
2003.
4.Dash PK, Zhao J, Hergenroeder G, Moore AN. Biomarkers for the diagnosis, prognosis, and evaluation of
treatment efficacy for traumatic brain injury. Neurotherapeutics. 2010 Jan;7(1):100-14. Review.
5.Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits,
Hospitalizations and Deaths 2002–2006. Atlanta (GA): Centers for Disease Control and Prevention, National Center
for Injury Prevention and Control; 2010.
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Elovic E, Hurley R, Latour L, Smirniotopoulos JG, Smith DH. Common data elements in radiologic imaging of
traumatic brain injury. J Magn Reson Imaging. 2010 Sep;32(3):516-43.
7.Inglese M, Makani S, Johnson G, Cohen BA, Silver JA, Gonen O, Grossman RI. Diffuse axonal injury in mild
traumatic brain injury: a diffusion tensor imaging study. J Neurosurg. 2005;103(2):298–303.
8.Smith DH, Meaney DF, Shull WH. Diffuse axonal injury in head trauma. J Head Trauma Rehabil. 2003;18(4):307–
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9.Scognamillo v. Herrick (2003)106 Cal.App.4th 1139 , 131 Cal.Rptr.2d 393
10.Dr. Jerry Texiera of UCI Neuropsychology, personal communication Nov 10, 2010
11.Wei CW, Tharmakulasingam J, Crawley A, Kideckel DM, Mikulis DJ, Bradbury CL, Green RE. Use of diffusiontensor imaging in traumatic spinal cord injury to identify concomitant traumatic brain injury. Arch Phys Med Rehabil.
2008 Dec;89 (12 Suppl):S85-91.
12.Yi JH, Hazell AS. Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain
injury. Neurochem Int. 2006;48:394–403.
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