Psychosocial Factors in Mild Traumatic Brain Injury (MTBI)

Bradley J. Hufford, Ph.D., HSPPClinical Neuropsychologist

Rehabilitation Hospital of Indiana

Mild Traumatic Brain Injury: Injury Description and Mechanisms

Traumatic Brain Injury (TBI)

1.5 million TBIs annually, 90% survive 5.3 million persons in US living with TBI 500,000 individuals require hospitalization

due to TBI annually Third most common cause of death in US Accounts for more than 30% of all injury-

related deaths in the United States. TBI-associated costs estimated at $48.3

billion

Mild TBI

80% of all TBIs are “mild” Mayo Classification System for TBI Severity

“Mild (Probable) TBI” One or more of the following:

• Loss of consciousness < 30 minutes• Post-Traumatic Amnesia < 24 hours• Depressed, basilar, or linear skull

fracture• No neuroimaging abnormalities

“Symptomatic (Possible) TBI”One or more in the absence of Mod-

Severe or Mild (Probable) criteria:Blurred visionConfusionDazedDizzinessFocal neurologic symptomsHeadacheNausea

MTBI-Pathophysiology Diffuse Axonal Injury (Ylvisaker & Feeney, 1998)

Diffuse Axonal Disruption Most MTBI have no neuroimaging abnormalities Concussive injuries thought to be more metabolic

in nature (Collins, Stump, & Lovell, 2004)

Injured cells exposed to dramatic changes in intracellular/ extracellular environments

Energy demand and supply mismatched Cells become vulnerable to even minor changes

in blood flow, pressure, etc. This state lasts > 2 weeks in animal models,

perhaps longer in humans Problems worst in first 72 hours, rapid

improvement over first week

Mild TBI Incurred in Military Situations (Combat)

OEF/OIF

Nearly 1.6 million deployed through 7/07

Mortality rate for injuries (Jackson et al., 2008)

WWII = 30% Vietnam = 24% OEF/OIF = 10%

Improvements due to improved battlefield medicine and armor/protective devices Interceptor Body Armor Vest

OEF/OIF TBI Military TBI > Civilian, even in peacetime

Military females = civilian males TBI = “signature wound” of OEF/OIF Incidence of TBI among wounded ~ 22%

(Martin et al., 2008)

May be as high as 50% (Jackson, et al., 2008)

(Vietnam = 14-18% of casualties had TBI)

Blast injuries most common cause

Blast Injury

As of 8/07, ~ 1,599 Coalition fatalities were due to IEDs

Blast Injury “Any injury secondary

to explosive munitions” (Gaylord, et al., 2008)

43-50% of all injuries in modern warfare

~ 60% of blast injuries result in TBI

WRAMC 62% of pts had TBI

92% due to blast

Blast Causes Improvised Explosive

Device (IED) Rocket Propelled

Grenade (RPG) Explosively-Formed

Projectiles (EFP) Mortar rounds Grenades Vehicle –Born

Improvised Explosive Device (VBIED)

Types of Blast-Related Injuries

Primary Secondary* Tertiary* Quaternary

Primary Blast Injury Injury due solely to blast wave Explosion => rapid expansion of gas => shock

wave Shock wave travels supersonic speeds of 3,000-

8,000 meters/second Can be reflected off of solid surfaces Those close enough to blast generally die instantly Often results in polytrauma

Medical personnel may be overwhelmed with multiple injuries, may miss MTBI

Secondary Blast Injury Blast puts objects into motion that collide with

individual Projectile injuries; often penetrating injuries Most common injuries to those who survive

Tertiary Blast Injury The individual is

propelled by the force of the blast

Effects due to wind from blast Can collide with

object, walls, ground Abrasive, contusive,

blunt trauma injuries

Quaternary Blast Injury Injuries that occur from aftereffects of a blast

Burns Chemical, toxic dust inhalation Poisoning Radiation exposure Crush injuries due to building collapse

Of servicemen who sustained both burn and blast injuries, 1/3 had PTSD, 1/3 had MTBI, 1/5 had both (Gaylord et al., 2008)

Blast Injury--Pathophysiology Transfer of kinetic energy from blast wave to

brain, causing DAI, esp. with primary blast Direct and indirect

Unclear if blast injury is the same as MTBI from other causes Lack of good, systematic protocols Animal studies do not use standardized

protocols “There is no evidence that LOC from a blast is

clinically different from similar LOC from another mechanism” (Hoge et al., 2008)

Mild Traumatic Brain Injury: Effects

Post-Concussion Disorder (PCD)

DSM-IV (provisional): “Acquired impairment in cognitive functioning, accompanied by specific neurobehavioral symptoms, that occurs as a consequence of a CHI of sufficient severity…”

> 3 of the following persist for > 3 months: Fatigability; sleep disruption; headache;

vertigo/ dizziness; irritability/aggression; anxiety/ affective lability; apathy/lack of spontaneity; personality change (e.g., social/sexual inappropriateness).

Post-Concussion Syndrome (PCS) ICD-10 criteria: Head trauma with LOC

that precedes symptom onset by < 4 weeks >3 sx: somatic, emotional, subjective

cognitive deficits (with no neuropsych. evidence of marked impairment), insomnia, reduced alcohol tolerance

Preoccupation with above symptoms and fear of brain damage with hypochondriacal concern and adoption of sick role

Post-Concussion Syndrome

38% of pts with MTBI met ICD-10 criteria for PCS 6 weeks post injury (Mittenberg & Strauman, 2000)

PCS occurs in 38-80% of MTBI (Hall et al., 2005)

Good News for Most… Outcomes are generally positive

International Coma Data Bank: 83% of persons with PTA< 2 weeks had good outcome

Cognitive deficits resolve in 1-3 monthsOther PCS symptoms commonly resolve

within 12 months at the latestTrue for 85-95% of veterans with MTBI

Majority of people recover from PCS in 3-6 months (Hall et al., 2005)

…but Not All Ponsford et al. (2000)

84 adults with MTBI Pts had significantly greater PCS

complaints than controls 1 week postBy 3 months, most symptoms had

resolvedSubset of 24% of participants complained

of marked symptoms Significant psychopathologyLittle evidence of cognitive

impairmentNo difference in injury severity

Persistent PCS (PPCS) “Miserable Minority” Prevalence estimates vary:

< 5% by 6-12 months (Iverson, 2005)

7-15% have any symptoms one year postinjury (Hall et al., 2005)

10-20% of MTBI pts who have persistent symptoms at 6-12 months and beyond (Millis and Putnam, 1996)

Incidence of PPCS: ~ 27/100,000 Equal to annual incidence of Parkinson’s Disease,

Multiple Sclerosis, Guillain-Barre, motor neuron disease, myasthenia gravis combined (Satz, et al., 1999)

Physiogenesis vs. Psychogenesis

“Mind Over Matter” by

Bora Turkoglu

What’s Causing PCS/PPCS? (Ruff, 2005)

Brain injury as the basis of persistent cognitive and emotional symptomsMore consistent with DSM-IV view

— Versus—

Psychopathology is primary cause for persistent symptoms More consonant with ICD-10 definition

The argument of whether “brain injury” versus “psychological factors” cause PCS is

nothing new

Patient suffering from “shell shock” during WWI

Shell Shock (Jones et al., 2007)

Early in WWI, attributed to cerebral trauma 50-60% of SS pts claim concussion

Sx were non-specific, occurred in absence of obvious lesions Some thought must be psychological

Argument about brain injury vs. neuroses Huge expense (military pensions) Difficulty persists to this day

Post-Traumatic Stress Disorder (PTSD)

DSM-IV Anxiety disorder Person exposed to event that involved

actual/threatened death, serious injury to self or others

Person’s response involved intense fear, helplessness, or horror

PTSD Symptom Triad1) Re-experiencing

Dreams, flashbacks, intrusive recollections2) Avoidance and numbing of general responsiveness

Avoid thoughts, feelings, events associated with event; detachment; inability to recall part of trauma; sense of foreshortened future

3) Increased arousal Insomnia, irritability, hypervigilance, easily

startled Duration over one month

MTBI and PTSD Symptom Overlap Physiologic hyperactivity Memory problems Fatigue Increased sensitivity to noise/light Decreased concentration

MTBI and PTSD (Civilian) Prevalence varies considerably

13 – 84% of MTBI met criteria for PTSD

PTSD sx different for MTBI than non-BIDreams, nightmares, hyperarousal more

common than intrusive thoughts MTBI protects against intrusive sx, because

pt cannot remember event

MTBI and PTSD (Military)

Surveyed 2525 soldiers 3-4 months after return home from Iraq4.9% reported injuries with LOC

43.9% met criteria for PTSD10.3% reported altered mental status

27.3 % met criteria for PTSD17.2% reported other injuries

16.2% met criteria for PTSD

Hoge et al., 2008

Compared to soldiers with “other” injuries, those with LOC or altered mental status: Had significantly greater combat exposure More likely to have had blast injury More likely to report poor general health, more

missed work, higher number medical visits. Physical health problems

largely mediated by PTSDor depression.

Controlling for PTSD eliminated associations with PCS

Neuropathological Factors in PCS

“There is little doubt that abnormal neurophysiology is predominant cause of symptoms shortly after injury” (Iverson, 2005)

qEEG changes in combat veterans with history of blast concussion (Trudeau et al., 1998)

All veterans had chronic PTSD Substance abuse, prior TBI, ADHD did

not affect findings

Rat Studies (Cernak et al., 2000, 2001) Endocrine, plasma magnesium, blood oxidant

changes Both whole-body and local (chest) blast exposure

resulted in structural/chemical change in hippocampus, causing cognitive deficits Direct and indirect

Ratatouille, © 2007 Disney/Pixar

Hoge et al., 2008 No direct link between PTSD and injury to brain

(yet) Biological processes likely underlie onset of

PTSD and physical sx related to depression and PTSD Biological processes associated with exposure

to extreme stress Activation of the hypothalamic-pituitary-

adrenal axis Frontal, temporal, subcortical regions usually

implicated in TBI thought to underlie PTSD sx

Psychological Factors in PCS

Psychological Factors Suspected Because: 1) PCS symptoms: Non-specific and

subjective Brain injury not necessary for symptoms to

exist

2) Increased stressors associated with increased sx

3) Premorbid psychological factors Certain persons may be more vulnerable to

developing PCS

4) Psychological maintenance of symptoms Neuropathology may begin the process, but

emotional factors maintain PCS

1) Specificity of PCS Symptoms Iverson & McCracken (1997)

81% of chronic pain pts reported >3 PCS sx 39% could have been diagnosed with PCS

PCS symptoms also common in healthy persons, psychiatric outpatients (Fox et al., 1995), minor medical outpatients, and whiplash pts Non-TBI groups endorse more PCS symptoms

with increased life stressors (Mateer et al., 2005)

23% more forensic cases are symptomatic than are TBI patients not seeking compensation (Mittenberg and Strauman, 2000)

2) The Effect of Additional Stressors Millis and Putnam (1996) Having additional injuries (orthopedic, soft

tissue injuries) in same accident is related to psychosocial difficulties Only 18% of persons who sustained

MTBI and orthopedic injuries and/or soft tissue injuries returned to work at one month

88% of “pure” MTBI returned to work

Strongest predictor for PPCS is litigation/compensation (Carroll et al., 2004)

Social Factors Having a relative with TBI

changes everyone in family Role loss, caregiving

expectations, financial and other pressures

Can lead to increased depression, anxiety, frustration, stress for family members

Family stress influences pt behavior Pt’s psychiatric distress

determined by number of critical comments from family

When a Parent Has a TBI

Often has lowered self-control Responds to parenting situations with

bullying, threatening, other forms of maltreatment

Very common for children to have increased emotional, relationship, acting out, disobedience, temper outbursts, avoidance of injured parent

Fortunately, skill training can help

3) Premorbid Psychological Factors Fenton et al. (1993): 45 MTBI pts vs. controls

TBI group had significantly more adverse life events in past year than controls

At 6 weeks, symptomatic pts had 4 times the chronic social difficulties than asymptomatic

At 6 months, pts with persistent symptoms had twice as many chronic social difficulties

Psychological problems cannot be automatically attributed to TBI

Premorbid Psychological Factors

Lack of a documented psychiatric history does not eliminate the possibility of a premorbid emotional problem Less than 40% of persons who have a

lifetime psychiatric disorder receive any formal treatment (Millis and Putnam, 1996)

4) Psychological Maintenance (Mittenberg & Colleagues) MTBI

Selective Attention to

Internal States

Attribute Sx to brain

damage

Symptoms

Anxiety ANS Arousal

Spiral of DeteriorationPre-injury Personality

Injury

Transient orPermanent CognitiveImpairments

Awareness of Impairments(and Functional Limitations)

Catastrophic Reaction

Co-Morbities Emerge:DepressionPTSDAnxiety

Interpersonal andSocial Withdrawal

Modified from Trexler & Fordyce, 2000

Case Example 1 (Civilian) Age = 47, Education = 12 Restrained driver in a head-on collision 6

months previously No LOC, anterograde/ retrograde amnesia Felt “fuzzy” few minutes EEG, head CT normal Left hand, ribs broken; skin burns Legal action being pursued

Case 1: Cognitive and Pain Complaints

Poor memory, word-finding, and organization ability. Pt unsure if worsening over time

Continuing pain in broken hand Constant headaches starting 2-3 weeks

before assessment. Present upon awakening, worsened by

stress

Case 1: Emotional Complaints Poor sleep maintenance, tearfulness Pt reports “reliving accident,” seeing a mental

“documentary over and over” of the accident Discouraged over how his recent cognitive

difficulties interfere with his efficiency at “following through on business ideas”

Girlfriend feels he is more demanding and moody, she has threatened to end relationship

Case 1: Emotional Complaints No history of inpatient psychiatric

treatment. Received psychotherapy after accident to

help with intrusive thoughts. Had history of “heavy drinking;” treatment

at Alcoholics Anonymous. No alcohol whatsoever in the past 12-14 years

Case 1: Neuropsychological Test Results

Mildly Imp.

Moderate Imp

Severely Imp

Average

IQ VerbalMemory

VisualMemory

Attn. EF VisualSpatial

Personality testing: Moderate concern over health and somatic functioning

Conclusions:No sign of TBIResults more consistent with anxiety d/o,

likely PTSD

Case Example 2 —Military

Age = 31; Education =15 years No significant medical history Seen 21 months after exposure to mortar

fireLOC = few secondsConfused for “a couple of minutes”Unsure about the duration of any

retrograde or anterograde amnesia Brain MRI was essentially unremarkable

Case 2: Cognitive and Pain Complaints

Poor concentration, inability to multi-task, forgetful, slow processing speed

Constant, mild tinnitus Frequent headaches that vary in terms of

onset and severity. Intermittent blurriness of his vision Unsure if smell/taste has changed

Wife notes he is less interested in foods

Case 2: Emotional Complaints Rates sadness as a 5/10 (10 = worst). Poor sleep initiation and maintenance Denied crying, but "I feel like it on the inside." Irritability and frustration: 6-7/10. Intermittent worthlessness, lowered energy, and

hopelessness. Nightmares at least once nightly Multiple flashbacks per day. "I feel insecure...I make sure to check the kids

when they are asleep, I check twice to see if the doors are locked, and I jam the door closed."

Case 2: Neuropsychological Test Results

Mildly Imp.

Moderate Imp

Severely Imp

Average

IQ VerbalMemory

VisualMemory

Attn. EF VisualSpatial

Case 2: Neuropsychological Test Results

Good effort Significantly impaired olfaction, right-sided

touch, auditory, motor problems Significant anxious and depressive sx

Results consistent with both MTBI and PTSD

Organic vs. Psychological Revisited Hardly a simple distinction In any case, either/both could be present at

different points in healing MTBI & emotional distress each complicate

healing from and coping with the other Likely there are overlapping brain areas

involved Treatment needs to take both into account Outcomes similar between PCD and PCS

(McCauley et al., 2005)

The Effect of Aging

Frank Buckles, age 108, last known living US WWI Veteran

Later Effects of MTBI Most persons recover well and quickly

Moderate/severe TBI have more persistent effects

Need more research--studies vary in terms of quality—many not carefully controlled

Multiple concussions in athletes often associated with higher rate of memory and cognitive problems over time (Guskiewicz et al., 2005; Moser et al., 2005)

Link b/t MTBI and Alzheimer’s not consistently demonstrated

MTBI Sustained Later in Life

Elderly have worse outcomes after severe TBI After MTBI, outcomes may not differ

Older MTBI had better GOS scores than younger at 1 month (Rapoport et al., 2001)

Older MTBI not different from younger cognitively at 2 weeks (Stapert et al., 2006)

Functional outcome after 6 months good to excellent for old and young (Mosenthal et al., 2004)

Having multiple injuries +TBI more detrimental to older patients

Brain Reserve Capacity

Biological, genetic, or behavioral factors that can increase brain’s ability to recover from an injury and/or resistance to the effects of aging/cognitive decline.Neuronal redundancyEfficiency of cognitive functions and

cognitive decline due to age highly heritable

Behavioral BRC (Valenzuela and Sachdev, 2006)

Meta-analysis of 22 studies Education reduced risk of dementia 47% High occupational status reduced risk 44%

Managerial status may be important High premorbid IQ reduced risk ~ 42% Mentally stimulating leisure lessened risk 50% Overall high brain reserve decreased risk 46% Findings persist after controlling for other

predictors of dementia (e.g., age, health, CVD)

PTSD and Aging Older veterans

May show more somatic sx than psychiatric

More likely to attribute sx to agingFrequently misdiagnosed

Sx often occur after trauma, decline, then resurge in later life

Combat-related PTSD sx can occur 50 years later (triggered by other losses?)

May have less social support, worse health

Treatment

Sir John Pringle, (April 10, 1707- January 18, 1782) Considered the "father of military medicine"

First and Foremost…

Need standardized definitions, improved and standardized diagnostic criteria

Improved screening and more timely identification of MTBI Military has made advances

in this area Thorough medical eval Neuropsychological eval Thorough history

Education for PCS Patients Normalize, but don’t minimize, symptoms Assure pts that symptoms common after

MTBI, and generally get better Not that symptoms are “nothing.”

In meantime, help pts regulate their lifestyle and environment to avoid problems and to recognize and reduce stress

Education for Patients Gave pts a 10-page manual, one hour

discussion session (Mittenberg, 1996)

What happens to brain in MTBITypical symptoms, time to resolutionEffects of fatigueTechniques to reduce symptoms during

recovery periodRelaxationCognitive restructuringThought-stopping techniques

Clients using the manual showed:Significantly shorter symptom duration 60% fewer symptoms at 6 months Fewer symptomatic days Lower average symptom severity levelsLevels of headache, fatigue, memory/

attention problems, anxiety, depression, dizziness decreased by up to 50% compared to controls

Education for Practitioners (Fann et al., 2002)

Educate medical practitioners, pts, families about increased risk for TBI in psych populations

Discuss ways to decrease behaviors that can put one at risk for TBI, preventative measures

Recognize complex interplay of factors initiating/maintaining PCS Cannot automatically assume psychiatric

deficits are/are not secondary to MTBI

Cognitive Behavioral Treatments for PPCS

12 week CBT program How to gradually resume activities to minimize

PCS-prolonging stress, maximizing reinforcement of positive behaviors

Adequate rest Cognitive restructuring: replace negative beliefs

re: symptoms with accurate ones Taught to recognize selective attention tendencies,

misattribution, etc. Recognize early signs of stress response (body,

thought cues, etc.) Relaxation to control initial response to stress

Medications Symptom relief Antidepressants

Anxiety and depression

Avoid cognitively sedating agents

Pain, sleep, headache

Medications to enhance attention Ritalin, amantadine

Supports Rehabilitation therapies

Strategies and compensations for attention, memory, and organizational problems

Psychiatric/psychotherapy support No age limit

Family education and support

Parenting training Thankfulness