patricia s. benfield , mhdl, crt, cbis-ci, ccaa north carolina biofeedback society’s

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.