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  • This picture was taken when he was 106. He also served in WWII and was a POW. When asked about his secret for long life, he said, “When you start to die, don’t.”
  • Transcript

    • 1. Psychosocial Factors in Mild Traumatic Brain Injury (MTBI) Bradley J. Hufford, Ph.D., HSPP Clinical Neuropsychologist Rehabilitation Hospital of Indiana
    • 2. Mild Traumatic Brain Injury: Injury Description and Mechanisms
    • 3. 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
    • 4. 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
    • 5.  “Symptomatic (Possible) TBI”  One or more in the absence of Mod- Severe or Mild (Probable) criteria:  Blurred vision  Confusion  Dazed  Dizziness  Focal neurologic symptoms  Headache  Nausea
    • 6. MTBI-Pathophysiology  Diffuse Axonal Injury (Ylvisaker & Feeney, 1998)
    • 7. 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
    • 8. Mild TBI Incurred in Military Situations (Combat)
    • 9. 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
    • 10. 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
    • 11. Blast Injury As of 8/07, ~ 1,599 Coalition fatalities were due to IEDs
    • 12. 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
    • 13. Blast Causes  Improvised Explosive Device (IED)  Rocket Propelled Grenade (RPG)  Explosively-Formed Projectiles (EFP)  Mortar rounds  Grenades  Vehicle –Born Improvised Explosive Device (VBIED)
    • 14. Types of Blast-Related Injuries  Primary  Secondary*  Tertiary*  Quaternary
    • 15. 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
    • 16. Secondary Blast Injury  Blast puts objects into motion that collide with individual  Projectile injuries; often penetrating injuries  Most common injuries to those who survive
    • 17. 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
    • 18. 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)
    • 19. 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)
    • 20. Mild Traumatic Brain Injury: Effects
    • 21. 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).
    • 22. 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
    • 23. 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)
    • 24. 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 months  Other PCS symptoms commonly resolve within 12 months at the latest  True for 85-95% of veterans with MTBI  Majority of people recover from PCS in 3-6 months (Hall et al., 2005)
    • 25. …but Not All  Ponsford et al. (2000)  84 adults with MTBI  Pts had significantly greater PCS complaints than controls 1 week post  By 3 months, most symptoms had resolved  Subset of 24% of participants complained of marked symptoms  Significant psychopathology  Little evidence of cognitive impairment  No difference in injury severity
    • 26. 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)
    • 27. Physiogenesis vs. Psychogenesis “Mind Over Matter” by Bora Turkoglu
    • 28. What’s Causing PCS/PPCS? (Ruff, 2005)  Brain injury as the basis of persistent cognitive and emotional symptoms  More consistent with DSM-IV view — Versus—  Psychopathology is primary cause for persistent symptoms  More consonant with ICD-10 definition
    • 29. The argument of whether “brain injury” versus “psychological factors” cause PCS is nothing new Patient suffering from “shell shock” during WWI
    • 30. 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
    • 31. 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
    • 32. PTSD Symptom Triad 1) Re-experiencing  Dreams, flashbacks, intrusive recollections 2) 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
    • 33. MTBI and PTSD Symptom Overlap  Physiologic hyperactivity  Memory problems  Fatigue  Increased sensitivity to noise/light  Decreased concentration
    • 34. MTBI and PTSD (Civilian)  Prevalence varies considerably  13 – 84% of MTBI met criteria for PTSD  PTSD sx different for MTBI than non-BI  Dreams, nightmares, hyperarousal more common than intrusive thoughts  MTBI protects against intrusive sx, because pt cannot remember event
    • 35. MTBI and PTSD (Military) Surveyed 2525 soldiers 3-4 months after return home from Iraq  4.9% reported injuries with LOC  43.9% met criteria for PTSD  10.3% reported altered mental status  27.3 % met criteria for PTSD  17.2% reported other injuries  16.2% met criteria for PTSD Hoge et al., 2008
    • 36.  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 PTSD or depression.  Controlling for PTSD eliminated associations with PCS
    • 37. 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
    • 38. 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
    • 39. 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
    • 40. Psychological Factors in PCS
    • 41. 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
    • 42. 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)
    • 43. 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
    • 44. Strongest predictor for PPCS is litigation/compensation (Carroll et al., 2004)
    • 45. 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
    • 46. 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
    • 47. 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
    • 48. 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)
    • 49. 4) Psychological Maintenance (Mittenberg & Colleagues) MTBI Selective Attention to Internal States Attribute Sx to brain damage Symptoms Anxiety ANS Arousal
    • 50. Spiral of Deterioration Pre-injury Personality Injury Transient or Permanent Cognitive Impairments Awareness of Impairments (and Functional Limitations) Catastrophic Reaction Co-Morbities Emerge: Depression PTSD Anxiety Interpersonal and Social Withdrawal Modified from Trexler & Fordyce, 2000
    • 51. 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
    • 52. 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
    • 53. 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
    • 54. 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
    • 55. Case 1: Neuropsychological Test Results Mildly Imp. Moderate Imp Severely Imp Average IQ Verbal Memory Visual Memory Attn. EF Visual Spatial
    • 56.  Personality testing: Moderate concern over health and somatic functioning  Conclusions:  No sign of TBI  Results more consistent with anxiety d/o, likely PTSD
    • 57. Case Example 2 —Military  Age = 31; Education =15 years  No significant medical history  Seen 21 months after exposure to mortar fire  LOC = few seconds  Confused for “a couple of minutes”  Unsure about the duration of any retrograde or anterograde amnesia  Brain MRI was essentially unremarkable
    • 58. 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
    • 59. 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."
    • 60. Case 2: Neuropsychological Test Results Mildly Imp. Moderate Imp Severely Imp Average IQ Verbal Memory Visual Memory Attn. EF Visual Spatial
    • 61. 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
    • 62. 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)
    • 63. The Effect of Aging Frank Buckles, age 108, last known living US WWI Veteran
    • 64. 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
    • 65. 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
    • 66. 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 redundancy  Efficiency of cognitive functions and cognitive decline due to age highly heritable
    • 67. 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)
    • 68. PTSD and Aging  Older veterans  May show more somatic sx than psychiatric  More likely to attribute sx to aging  Frequently 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
    • 69. Treatment Sir John Pringle, (April 10, 1707- January 18, 1782) Considered the "father of military medicine"
    • 70. 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
    • 71. 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
    • 72. Education for Patients  Gave pts a 10-page manual, one hour discussion session (Mittenberg, 1996)  What happens to brain in MTBI  Typical symptoms, time to resolution  Effects of fatigue  Techniques to reduce symptoms during recovery period  Relaxation  Cognitive restructuring  Thought-stopping techniques
    • 73.  Clients using the manual showed:  Significantly shorter symptom duration  60% fewer symptoms at 6 months  Fewer symptomatic days  Lower average symptom severity levels  Levels of headache, fatigue, memory/ attention problems, anxiety, depression, dizziness decreased by up to 50% compared to controls
    • 74. 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
    • 75. 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
    • 76. Medications  Symptom relief  Antidepressants  Anxiety and depression  Avoid cognitively sedating agents  Pain, sleep, headache  Medications to enhance attention  Ritalin, amantadine
    • 77. 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