patricia s. benfield , mhdl, crt, cbis-ci, ccaa north carolina biofeedback society’s
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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 - PowerPoint PPT PresentationTRANSCRIPT
Mild Traumatic Brain Injury (mTBI)– A Silent Epidemic –
Applications for Clinical Practice
Patricia S. Benfield, MHDL, CRT, CBIS-CI, CCAA
North Carolina Biofeedback Society’s2012 Conference Greensboro, NC
November 2-4, 2012
OutlineBrain development Overview of TBI-definitions & epidemiology
Mechanics of brain traumaReview study results Implications for treatment Better assessments & making referrals
Traumatic brain injury is the mostmisunderstood, 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 NetworksNeurons
form networks
Networks hold dataredesign oftensome 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 passedNeurotransmitter is
uptaken
Glial Cells
Glial CellsA 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-ReptilianOldest partSurvival or “Fight or
Flight” Acts without
thinkingThreats, 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 SystemHypothalmus controls ANSCingulate Gyrus is conduit
of messagesAmygdala makes
associations across stimulus modalities
Hippocampus transitions information from short to long term memory
Basal Ganglia plans & coordinates motor movements & posture
Triune Brain-CortexThinking & 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 NeedsBasic 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 & released*
75% of those are mTBI
235,000 hospitalized50,000 die80,000 experience
long-term effects5.3 million
Americans (2% of population) live with a disability
*most current update from CDC Image from www.biausa.org
Congenital brain injury
Pre-birth During birth
Acquired Brain Injury
After birth process
Traumatic Brain Injury(external physical force)
Closed Head Injury
Open Head
Injury
Non-traumatic Brain Injury
Savage, 1991
…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 TBITwo major types:
1. Penetrating brain injuries2. Closed head injuries
Type of TBI-PenetratingForeign 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 InjuryResults 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 InjurySkull fracture: breaking of the bony skullContusions/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 InjuryEvolves over time (after trauma has occurred) brain swelling (edema)increased pressure inside of the skull (intracranial
pressure)epilepsyintracranial infectionfeverhematoma (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
injuries66% of service personnel in Iraq are exposed
to or injured by a blast injury
Blast Wound Mechanics - Primary Primary Blast InjuryAn 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-TertiaryTertiary Blast InjuryResults from individuals
being thrown by the blast wind.
Any body part may be affected.
Causing fracture and traumatic
amputationClosed 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
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 Injuries40% of service personnel returning from OIF & OEF
show signs & symptoms of TBI due to a blast injuryThe 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 BITraumatic 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 TBIIn 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 SymptomsThese 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 SymptomsComorbid 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-Magnetoencephalographyhttp://www/youtube.com/watch?v=uhlANIGAJXA
PTSD and mTBI
Signs of BIHeadaches 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 EpidemicResults 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-ComorbiditySymptoms 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-ComorbidityIndividuals 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-Comorbidity68% 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 PracticeBoth client/patient and therapist are at
riskEthical responsibility to become better
educated about the realities of mTBIBetter and more thorough screening for
brain injuryRefer clients who report prior head
trauma for appropriate evaluation and treatment.
Recognizing Red FlagsVerbal skills far better than functional
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 abilityComplaints of low energy or easily fatiguedEasily overwhelmed and tendency to shut downLack of anger control or agitation
More Red FlagsDifficult patientPoor memoryPoor executive functions Failure to follow through w/o reason although
agreeable Failure to progress despite their reasons for attending
therapy Getting worse despite treatment especially
with prescribed medicationsFailure to participate in their own treatmentAppears to understand but fails to comply Inconsistencies
Some Questions to AskHave 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
Lack of awarenessCommunicationAttention/concentration impairmentEmotional lability ImpulsivityFatigue Judgement, problem-solving, decision
making, & organizational skills MemoryPersonality disturbance & social
isolationMasking
Some complexities facing practitioners working with TBI.
Brain RecoveryBrain 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 TBIAssessment & diagnosisAddress cognitive impairments through
retraining & compensatory strategiesBiofeedback & neurofeedbackSupport treatment
Education on the nature of their condition Counseling & family support
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.”
Dr. Walter Schneider University of Pittsburgh
Treating BI – Diagnosing
Extensive case historyScreening (BNCE) Formal neuropsychological evaluation by a
NeuropsychologistImaging 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 MisdiagnosisTraditional 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 TreatmentNational 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 Tool90-98% 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
Blue Brain Project
The Human Connectome Project
Human Brain Project
ReferencesBuck, 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): 87-121.
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.