Transcript Benfield - Mild Traumatic Brain Injury (mTBI): A Silent Epidemic

Mild Traumatic Brain Injury (mTBI)
– A Silent Epidemic –
Applications for Clinical Practice
Patricia S. Benfield, MHDL, CRT,
CBIS-CI, CCAA
North Carolina Biofeedback Society’s
2012 Conference
Greensboro, NC
November 2-4, 2012
Outline
 Brain development
 Overview of TBI-definitions &
epidemiology
 Mechanics of brain trauma
 Review study results
 Implications for treatment
 Better assessments & making referrals
Traumatic brain injury is the most
misunderstood, misdiagnosed,
underfunded
public health problem
our nation faces.”
Susan Connors, President
Brain Injury Association of America
With more than 100 billion neurons and billions of other
specialized cells, the human brain is a marvel of nature.
It is the organ that makes people unique.
Brain Development
Brain Development
Neuronal Networks
 Neurons
 form networks
 Networks
 hold data
 redesign often
 some are “carved in
stone”
 some are fleeting and
weak
Synapse
“Grand Central Communication”
 Allows a neuron to pass
electric or chemical signal
 Pre-synaptic neuron
releases a neurotransmitter
to bind to receptor neuron.
 The signal is passed
 Neurotransmitter is
uptaken
Glial Cells
Glial Cells
A glial cell (green) grows
among network of
cortical neurons (in red).
Studies using these
cultured cells have led to
discoveries on how
growth factors can
prevent neuronal death.
Glial Cells – Structural Support
Glial Cells – Brain’s Supervisors
Pax6 - Master Regulator of
Brain Development
Neurogenesis & Pruning
Making Connections
Making Connections
Making Connections
Making Connections
MacLean’s Model-Triune Brain
Reptilian-------survival
Limbic--------emotions
Neo-Cortex---thinking
Triune Brain-Reptilian
 Oldest part
 Survival or “Fight or
Flight”
 Acts without thinking
 Threats, real or
perceived, causes
“downshifting to occur
Triune Brain-Limbic
 Home of emotions
 Has visual memory
 Threat to our well-being
will cause “downshifting”
 Long-term memory
Triune Brain-Limbic System
Hypothalmus controls ANS
Cingulate Gyrus is conduit of
messages
Amygdala makes associations
across stimulus modalities
Hippocampus transitions
information from short to
long term memory
Basal Ganglia plans &
coordinates motor
movements & posture
Triune Brain-Cortex
 Thinking & new learning
 Processes 1,000s of bits of
information/minute
 Must be free from threat
for new learning or will
downshift into its more
primitive parts
Maslow’s Needs
Basic needs must be met in order to reach
the highest order of development
Brain Injury
Causes of BI
Risk by Age and Gender
Occurrence of Brain Injury
 1.7 million treated &
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released*
75% of those are mTBI
235,000 hospitalized
50,000 die
80,000 experience
long-term effects
5.3 million Americans
(2% of population) live
with a disability
*most current update from CDC
Image from www.biausa.org
Brain Injury
Congenital brain injury
Pre-birth
During birth
Acquired Brain Injury
After birth process
Traumatic Brain Injury
(external physical force)
Closed
Head
Injury
Open Head
Non-traumatic Brain
Injury
Injury
Savage, 1991
Acquired Brain Injury (ABI)
…is an injury to the brain that has occurred after
birth and is not related to congenital defect or
degenerative disease.
Causes of ABI include (but are not limited to) hypoxia,
illness, infection, stroke, substance abuse, toxic
exposure, trauma, and tumor.
…may cause temporary or permanent impairment in
such areas as cognitive, emotional, metabolic, motor,
perceptual motor and/or sensory brain function.
The Brain Injury Network
What is TBI?
As of February 6, 2011, BIAA adopts a new definition
TBI is defined as an alteration in brain
function, or other evidence of brain
pathology, caused by an external force.
2 Types of TBI
Two major types:
Penetrating brain injuries
2. Closed head injuries
1.
Type of TBI-Penetrating
 Foreign object enters brain (e.g. bullet)
 Damage occurs along path of injury
 Symptoms vary according to part of brain that is
damaged
Penetrating Wounds
 41 yr old man
 Attacked from behind
 Full recovery after removal
 No infection
 Left hospital 1 week after removal
 Epileptic medication and some
memory problems
 33 year old man
 12 nails in head/brain from nail gun
 Nails were not visible on initial exam
 X-rays revealed the nails
 Survived and released to psychiatry.
Type of TBI-Closed Head Injury
 Results from blow to the head (e.g. car accident
or assault)
 Causes two type of brain injuries:
1.
Primary
2.
Secondary
2 Types of Closed Head Injury
 Primary
 Direct trauma to brain and vascular structures
 Examples: contusions, hemorrhages, and other direct mechanical
injury to brain contents (brain, CSF, blood).
 Secondary
 Ongoing pathophysiologic processes continue to injure brain for
weeks after TBI
 Primary focus in TBI management is to identify and limit or
stop secondary injury mechanisms
Primary Closed Head Injury
 Skull fracture: breaking of the bony skull
 Contusions/bruises: often occur right under the location of impact or at
points where the force of the blow has driven the brain against the bony
ridges inside the skull
 Hematomas/blood clots: occur between the skull and the brain or inside
the brain itself
 Lacerations: Tearing of the frontal (front) and temporal (on the side) lobes
or blood vessels of the brain ---(the force of the blow causes the brain to
rotate across the hard ridges of the skull, causing the tears)
 Nerve damage (diffuse axonal injury): Arises from a cutting, or shearing,
force from the blow that damages nerve cells in the brain's connecting nerve
fibers
(www.asha.org)
Primary Closed Head Injury
Coup
Contrecoup
Rotational
forces
Secondary Closed Head Injury
Evolves over time (after trauma has occurred)
 brain swelling (edema)
 increased pressure inside of the skull (intracranial
pressure)
 epilepsy
 intracranial infection
 fever
 hematoma (for more info visit: www.asha.org)
TBI – Signature Injury of War

Operation Iraqi Freedom (OIF) and Operation
Enduring Freedom (OEF)
 Most service related TBI caused by blast
injuries
 66% of service personnel in Iraq are exposed to
or injured by a blast injury
Blast Wound Mechanics - Primary
 Primary Blast Injury
An explosion generates a blast
wave traveling faster than sound
and creating a surge of high
pressure immediately followed
by a vacuum.
Studies show that the blast wave
shoots through armor and
soldiers' skulls and brains, even
if it doesn't draw blood.
While the exact mechanisms by
which it damages the brain's
cells and circuits are still being
studied, the blast wave's
pressure has been shown to
compress the torso, impacting
blood vessels, which then send
damaging energy pulses into the
brain.
Blast Wound Mechanics- Secondary
 Secondary Blast Injury
Shrapnel and debris propelled
by the blast can strike a
soldier's head, causing
either a closed-head injury
through blunt force or a
penetrating head injury that
damages brain tissue.
Blast Wound Mechanics-Tertiary
 Tertiary Blast Injury
Results from individuals
being thrown by the blast
wind.
Any body part may be
affected.
Causing
 fracture and traumatic
amputation
 Closed and open brain
injury
Blast Wound Mechanics-Quarternary
 Quarternary Blast Injury
All explosion-related injuries, illnesses, or diseases not due to primary,
secondary, or tertiary mechanisms.
Includes exacerbation or complications of existing conditions.
Any body part may be affected.
Includes
Burns (flash, partial, and full thickness)
Crush injuries
Closed and open brain injury
Asthma, COPD, or other breathing problems from dust, smoke, or toxic
fumes
 Angina
 Hyperglycemia, hypertension
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Review of Explosive-Related Injuries
 AUDITORY: TM rupture, ossicular disruption, cochlear damage, foreign body
 EYE, ORBIT, FACE: Perforated globe, foreign body, air embolism, fractures
 RESPIRATORY: Blast lung, hemothorax, pneumothorax, pulmonary contusion and
hemorrhage, A-V fistulas (source of air embolism), airway epithelial damage, aspiration
pneumonitis, sepsis
 DIGESTIVE: Bowel perforation, hemorrhage, ruptured liver or spleen, sepsis, mesenteric
ischemia from air embolism
 CIRCULATORY: Cardiac contusion, myocardial infarction from air embolism, shock,
vasovagal hypotension, peripheral vascular injury, air embolism-induced injury
 CNS INJURY: Concussion, closed and open brain injury, stroke, spinal cord injury, air
embolism-induced injury
 RENAL INJURY: Renal contusion, laceration, acute renal failure due to rhabdomyolysis,
hypotension, and hypovolemia
 CIRCULATORY: Traumatic amputation, fractures, crush injuries, compartment syndrome,
burns, cuts, lacerations, acute arterial occlusion, air embolism-induced injury
Statistics on Service Related Injuries
 40% of service personnel returning from OIF & OEF
show signs & symptoms of TBI due to a blast injury
 The large majority (80%) of combat head injuries
sustained in Operation Iraqi Freedom and Operation
Enduring Freedom are mild concussions as opposed to
severe, debilitating TBI.
National Institute of Neurological Disorders and Stroke.
(http://www.americasheroesatwork.gov)
More on Occurrences of BI
 Traumatic brain injuries are among the top injuries of
soldiers serving in Iraq and Afghanistan, with military
estimates of over 200,000 affected soldiers. Most of these
injuries result in concussions, but repeated injuries can
result in permanent neurological problems.
 While a concussion means that the brain swells and heals,
those unseen breaks in the fiber pathways can cause
problems later in life. Current diagnostic equipment only
permits doctors to see swelling or bleeding.
Mild Traumatic Brain Injury (mTBI)
…defined as a loss or alteration of consciousness <30
minutes, post-traumatic amnesia < 24 hours, focal
neurologic deficits that may or may not be transient,
and/or Glasgow Coma Score (GCS) of 13-15.
…by definition, typically involves symptoms of brain
damage but no sign of damage based on a neurological
exam
Controversy over whether primary blast injuries damage
the brain. Animal models suggest they do.
Mild TBI
 In most cases of mTBI, the patient returns to their
previous level of function within 3-6 months.
 15% of patients may go on to develop chronic post-
concussive symptoms.
Chronic Post Concussive Symptoms
These symptoms can be grouped into 3 categories
1.
Somatic (headache, tinnitus, vertigo, insomnia, etc.)
2. Cognitive (memory, attention/concentration difficulties, etc. )
3. Emotional/behavioral (irritability, depression, anxiety,
behavioral dyscontrol)
Chronic Post Traumatic Concussions
“Concussions
can trigger a chemical
chain reaction in brain neurons that
leaves an athlete disoriented,
unconscious, or dead. They can also
impair learning over a period of
years.”
Chronic Post Concussive Symptoms
Comorbid Psychiatric Disorders-Patients who
have experienced mTBI are also at risk for psychiatric
disorders compared to the general population, including
depression and PTSD
Video-Mild TBI-Magnetoencephalography
http://www/youtube.com/watch?v=uhlANIGAJXA
PTSD and mTBI
Signs of BI
 Headaches or neck pain that do not go away
 Difficulty remembering, concentrating, or making
decisions
 Slowness in thinking, speaking, acting, or reading
 Getting lost or easily confused
 Increased sensitivity to lights, sounds, or distractions
 Blurred vision or eyes that tire easily
 Loss of sense of smell or taste
 Ringing in the ears
(http://www.cdc.gov/ncipc/factsheets/tbi.htm)
Signs of BI (cont’d)
 Feeling tired all of the time, having no energy or
motivation
 Mood changes (feeling sad or angry for no reason)
 Changes in sleep patterns (sleeping a lot more or having a
hard time sleeping)
 Light-headedness, dizziness, or loss of balance
 Urge to vomit (nausea)
TBI-The Silent Epidemic
Results of recent national survey:
 only 1 in 3 Americans are familiar with term "brain injury."
 Rarely associate TBI w/ most
common forms of BI-concussions.
Brain damage is not visible.
No way to assess extent of damage.
Clinical Implications
Studies Provides Evidence
for a
Need For New Standards
in
Competent Practice
Mounting Evidence-Studies
Links between head injury and mental illness, substance
abuse, and criminality (Helgeson, 2010).
Approximately 70% w/ co-occurring substance abuse and
mental health issues had a history—although not
necessarily a diagnosis—of TBI (Corrigan & Deutschle,
2008).
87% of a county jail population reported history of head
injury (Slaughter, Fann, & Ehde, 2003).
More Evidence-Comorbidity
Symptoms of clinical depression in 15-40% of
survivors (Teasdale & Engberg, 2001).
44% of soldiers returning from Iraq who had clear
evidence of mTBI also experienced PTSD,
compared w/ 9% having evidence of PTSD w/ no
BI (Hoge et al., 2008).
More Evidence-Comorbidity
Individuals w/ BI were 4 X more likely to attempt suicide
than their nonbrain-injured peers (Silver et al., 2001)
Suicide risk is even higher w/ mTBI group not dx’d or tx’d
(Teasdale & Engberg, 2001). These risks are compounded
by the co-occurring nature of mental health and substance
abuse.
70% of dually-diagnosed reported a hx of TBI—although not
necessarily were diagnosed (Corrigan & Deutschle, 2008).
More Evidence-Comorbidity
68% incarcerated for substance-related offenses reported
previous head trauma. (Walker, Staton, and Leukefeld,
2001).
As high as 87% prevalence of TBI among the populations
incarcerated for a range of offenses (Slaughter et al., 2003).
High correlation of TBI to violent criminal behavior,
including sexual assault and homicide (Leon-Carrion &
Ramos, 2003).
Implications for Clinical Practice
 Both client/patient and therapist are at risk
 Ethical responsibility to become better educated
about the realities of mTBI
 Better and more thorough screening for brain
injury
 Refer clients who report prior head trauma for
appropriate evaluation and treatment.
Recognizing Red Flags
 Verbal skills far better than functional
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skills.
Depression and other secondary
issues do not seem to improve with
traditional therapies and often get worse over time.
Impulsive behavior often creating unsafe situations
Personal hygiene and the way a person is dressed is often
an initial indicator of self care ability
Complaints of low energy or easily fatigued
Easily overwhelmed and tendency to shut down
Lack of anger control or agitation
More Red Flags
 Difficult patient
 Poor memory
 Poor executive functions
 Failure to follow through w/o reason although agreeable
 Failure to progress despite their reasons for attending
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therapy
Getting worse despite treatment especially
with prescribed medications
Failure to participate in their own treatment
Appears to understand but fails to comply
Inconsistencies
Some Questions to Ask
Have you ever hurt your head or had a head injury that
caused you to “see stars” or feel dazed?
Have you ever lost consciousness, even momentarily, after
hurting your head?
After hurting your head, have you ever had headaches,
dizziness, or been irritable?
Have you ever been diagnosed with a concussion or whiplash,
or seen a doctor for a head or neck injury?
(Schwab et al., 2006)
So let’s
recap………..
So Let’s recap…mTBI…
…is a major public health concern,
…is difficult to diagnose,
…has symptoms that are nearly indistinguishable
from other conditions,
…has survivors who are often unaware or unwilling
to report symptoms, and
…is highly correlated with mental health, substance
abuse, and criminality.
Rehabilitation Specialists & Counsellors
The importance of attending to basic needs,
re-training for employment, and
social re-involvement
must be aligned with
the needs of the self,
working through the losses,
integrating a new sense of purpose and
accomplishment.
Possible Barriers to Change
Some complexities facing practitioners working with TBI.
 Lack of awareness
 Communication
 Attention/concentration impairment
 Emotional lability
 Impulsivity
 Fatigue
 Judgement, problem-solving, decision
making, & organizational skills
 Memory
 Personality disturbance & social isolation
 Masking
Brain Recovery
 Brain recovery follows patterns of brain
development. Gross or large-scale systems must
develop (or be retrained) before fine systems.
 Attention, focus, and perceptual skills develop (or
are retrained) before complex intellectual activity
can be successful.
 Source: NIH Pub. No. 98-4315
Treating TBI
 Assessment & diagnosis
 Address cognitive impairments through retraining &
compensatory strategies
 Biofeedback & neurofeedback
 Support treatment
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Education on the nature of their condition
Counseling & family support
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address adjustment issues
resolve emotional issues no matter how old the issues are
Sleep hygiene for more restorative sleep
Brain Perfect Nutrition
Daily exercise
Medication for symptomatic relief
TBI-The Silent Epidemic
“If you cannot see or quantify
the damage, it is hard to treat
it.”
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
Dr. Walter Schneider
University of Pittsburgh
Treating BI – Diagnosing
 Extensive case history
 Screening (BNCE)
 Formal neuropsychological evaluation by a
Neuropsychologist
 Imaging can be helpful as well as deceptive
a normal CT scan can mean “no brain bleeding”
 a normal MRI can mean “no brain parts shifted in
skull”

Missed Diagnosis or Misdiagnosis
Traditional methods for diagnosing mHI, i.e.
medical history, CAT scan and MRI, often show
normal test results even though patients complain of
significant neurocognitive dysfunctions.
Diagnosis and Treatment of Head Injury by Hoffman DA
M.D., Stockdale S Ph.D., Hicks LL B.A., Schwaninger JE B.A.
TBI
Using EEG Technology for Treatment
 National Library of Medicine lists 1,672 peer reviewed
journal articles on the subject of EEG and TBI
 The vast majority of these studies involved
quantitative analyses and, in general, the scientific
literature presents a consistent and common
quantitative EEG pattern correlated with TBI.
QEEG
qEEG as a Diagnostic Tool
 90-98% reliability –use of qEEG for diagnostic
purposes (Thatcher et al, 1999; 2003)
 Strong correlations exist betw/ qEEG & performance
on neuropsychological tests (Thatcher et al, 1998a;
1998b; 2001a; 2001b)
BI Research - EEG & NF Studies for
Treatment
 Memory, attention and response accuracy during
problem solving tasks (Tinius & Tinius, 2000)
 88% of mHI had 50% improvement in EEG coherence
scores & all who were employed pre-injury reported
RTW following tx (Walker, Norman, & Weber, 2002)
 Improved cognitive functioning & self-reports of
depression & fatigue (Schoenberger, Shif, Esty, Ochs,
& Matheis, 2001)
 Beta feedback improved attention deficits compared to
controls (Keller, 2001)
Treating
Comorbid
and
Other Conditions
Typical ADD Signature
Anxiety
Depression
Chronic Lyme Encephalopathy
ADD-Without & With Ritalin
ADD & Effects of Marijuana
Neurofeedback
…has been proven so effective in treating TBI that
the Texas Legislature recently passed a law
preventing insurance companies from denying
coverage for it if the patient is being treating for
TBI.
Another effort is currently under way to lobby
the State to mandate the same coverage for
those being treated autism spectrum disorders.
Broken Fiber Tracks
Human Brain Projects
The Human Connectome Project
Human Brain Project
Blue Brain Project
References
Buck, P.W. (2011). Mild traumatic brain injury: A silent
epidemic in our practices. Health & Social Work, 36(4),
299-302.
Corrigan, J.D., & Deutschle, J.J. (2008). The presence and
impact of traumatic brain injury among clients in
treatment for co-occurring mental illness and
substance abuse. Brain Injury, 22, 223-231.
Helgeson, S.R. (2010). Identifying brain injury in state
juvenile justice, corrections, and homeless
populations: Challenges and promising practices.
Brain Injury Professional, 7(4), 18-20.
References (cont’d)
Hoge, C.W., McGurk, D., Thomas, J. L., Cox, A.L., Engel,
C.C., & Castro, C.A. (2008). Mild traumatic brain
injury in US soldiers returning from Iraq. New England
Journal of Medicine, 358, 453-463.
Leon-Carrion, J., & Ramos, F.J. (2003). Blows to the head
during development can predispose to violent criminal
behaviour: Rehabilitation of consequences of head
injury is a measure for crime prevention. Brain Injury,
17, 207-216.
References (cont’d)
Silver, J.M., Kramer, R., Greenwald, S., & Weissman, M.
(2001). The association between head injuries and
psychiatric disorders: Findings from the new Haven
NIMH Epidemiologic Catchment Area Study. Brain
Injury, 15, 935-945.
Slaughter, B., Fann, J.R., & Ehde, D. (2003). Traumatic
brain injury in a county jail population: Prevalence,
neuropsychological functioning and psychiatric
disorders. Brain Injury, 17, 731-741.
Teasdale, T.W., & Engberg, A.W. (2001). Suicide after
traumatic brain injury: A population study. Journal of
Neurology, Neurosurgery & Psychiatry, 71, 436-440.
References (cont’d)
Thatcher, R., Walker, B., Biver, C., North, M., Curtin,
R. (2003). Sensitivity and specificity of an EEG
normative data base: Validation and clinical
correlation. Journal of Neurotherapy, 7 (3/4): 87121.
Walker, R., Staton, M., & Leukefeld, C.G. (2001). History
of head injury among substance users: Preliminary
findings. Substance Use & Misuse, 36, 757-770.
References (cont’d)
Thatcher, R., Lubar, J. (2009). History of the scientific standards of QEEG
normative databases. In Budzynski, T., Budzynzki, H., Evans, R.,
Abarbanel, A. (Eds). Introduction to Quantitative EEG and
Neurofeedback: Advanced Theory and Applications, 2nd Edition. (pp.
29-62). New York, NY: Academic Press.
Thatcher, R., Walker, B., Biver, C., North, M., Curtin, R. (2003). Sensitivity
and specificity of an EEG normative data base: Validation and clinical
correlation. Journal of Neurotherapy, 7 (3/4): 87-121.
Tramontano, G. (2006). QEEG testing can discern reason for cognitive
disorder: Digital EEG recordings of brainwaves can determine TBI
etiology. Connecticut Lawyer, March 2006, pp.14-16.