PTSD and TBI

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PTSD and TBI

• Tina M. Trudel, PhD
• President/COO,
• Lakeview Healthcare Systems, Inc.
• Principal Investigator/Site Director,
• Defense Veterans Brain Injury Center at VANC
• Assistant Clinical Professor of Psychiatry,
• University of Virginia School of Medicine
• ttrudel_at_lakeview.ws or 1-800-473-4221

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History of PTSD

• Evolution fight or flight and survival
• Increased pupil size
• Increased heart rate
• Rapidly contracting muscles
• Modern hard-wired stress response

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History of PTSD

• 19th century Railroad Spine
• WWI WWII
• Shell shock
• Battle fatigue
• Traumatic neurosis
• Concentration camp syndrome
• Sica, 1996

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History of PTSD

• 1970s Vietnam Syndrome
• 1970s Rape Trauma Syndrome
• 1980 PTSD recognized as a generalized anxiety
  disorder in the then DSM-III
• 1980s PTSD issues and controversy emerge in
  workers compensation, disability claims and
  medicolegal fronts
• 1990s PTSD becomes one of the most highly
  compensated psychological injury claims
  (Levy, 1995)

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PTSD Diagnosis

• Clinical experience research suggest shades of
  grey
• Medico-legal community issues
• Military TBI-PTSD overlap

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DSM-IV Diagnosis

• Exposure to a traumatic event in which both of
  the following were present
• Person experienced, or witnessed, or was
  confronted with an event or events that involved
  actual or threatened death or serious injury, or
  a threat to the physical integrity of self or
  others
• Persons response involved intense fear,
  helplessness or horror

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DSM-IV Diagnosis

• The traumatic event is persistently
  re-experienced in one or more ways
• Recurrent and intrusive recollections of the
  event including images/thoughts/perceptions
• Recurrent distressing dreams of the event
• Acting or feeling as if the event were recurring
  (flashbacks, reliving, illusions)
• Intense psychological distress on exposure to
  internal or external cues of event
• Physiological reactivity on exposure to internal
  or external cues of event

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DSM-IV Diagnosis

• Persistent avoidance of stimuli associated with
  trauma numbing of general responsiveness
  indicated by
• Avoidance of thoughts, feelings or conversations
  associated with trauma
• Avoidance of activities, places, people that
  arouse recollections of the trauma
• Inability to recall important aspect of trauma
• Diminished interest/participation in activities
• Feeling of detachment/estrangement
• Restricted range of affect
• Sense of foreshortened future

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DSM-IV Diagnosis

• Persistent symptom of increased arousal as
  indicated by (2)
• Difficulty falling or staying asleep
• Irritability or outbursts of anger
• Difficulty concentrating
• Hypervigilance
• Exaggerated startle response
• Duration more than one month
• Disturbance causes clinically significant
  distress or impairment in social/occupational/othe
  r fxn

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PTSD in the General Population

• 2-20 of civilians exposed to trauma
• Lifetime 5 males, 10 females
• Women 4x more likely if exposed
• PTSD beyond 3 months often becomes chronic

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Psychological Predictors of PTSD

• If exposed to trauma, most people experience
  stress reactions. The majority remit over a
  number of months after the event.
• What are the characteristics associated with
  developing PTSD?

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Predictors of PTSD

• Other anxiety disorders
• Depression
• Substance abuse
• Abuse/PTSD history
• Avoidant coping style
• Behavioral acting out style
• External attribution of blame
• Prior unemployment
• Loss of control during event
• Fear of death
• Chronic pain

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PTSD and Genetics

• PTSD is a polygenetic disorder
• Results of epidemiological studies have been
  contradictory
• Research problem for familial studies cannot
  assess in relatives without trauma

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PTSD and Genetics

• Refugee camp Holocaust studies demonstrate 5x
  PTSD in children of parent with PTSD
• Vietnam Era Twin (VET) registry genetic
  influences explained 47 of the variance re
  PTSD also supported in civilian twin studies
• Genes proposed are those influencing HPA axis
  dysregulation
• (Koenen, 2003)

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Brain Imaging Studies and PTSD

• Combat vets with PTSD 8 reduction in
  hippocampal volume
• Replicated with survivors of childhood abuse with
  PTSD correlated with level of abuse
• PET- low hippocampal activation
• Hippocampal reduction is specific to PTSD, not
  anxiety -Bremner, 2002

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Hippocampus and PTSD

• H has inhibitory effect on release of
  corticotropin releasing factor (CRF)
• CRF critical in stress response, mediating HPA
  axis activation, mediating fear behavior/chronic
  stress
• Leads to chronic CRF release
• Research notes elevated CRF in CSF of persons
  with PTSD
• Bremner, 2002

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Medial Prefrontal Cortex (MPC) in PTSD

• MPC modulates emotional responsiveness/conditioned
  fear responses through inhibition of amygdala
  function
• Believed to underlie pathological emotional
  responses in PTSD
• Connected to hippocampus
• PET dysfunction of both MPC and H regions
  during provocation of PTSD symptoms in Vets and
  women abused as children
• Bremner, 2002

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Glucocorticoids and PTSD

• High levels of stress released glucocorticoids
  (cortisol) are associated with damage to
  hippocampal neurons (esp. CA3 region)
• Glucocorticoids disrupt cellular metabolism
  increase vulnerability of H neurons to glutamate
  (excitatory amino acid)
• H regenerates neurons, stress inhibits this
• Animal studies support glucocorticoid-mediated
  hippocampal toxicity and memory dysfunction
• Bremner, 2002

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Challenges Reviewing the Research

• When data collected
• How data collected
• Interview vs. survey
• Control groups
• Scales
• Impact of Life Events
• PTSD Symptom Scale Interview
• Clinician Administered Post Traumatic Stress
  Disorder Scale

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PTSD and TBI Studies

• Mild versus Severe
• Mixed study of Cambodian refugees (n993) Those
  with TBI had highest rates of depression and PTSD
  only those with coercive trauma (AKA torture)
  were higher
• Mollica et. al., 2002

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Mild TBI Controlled Studies
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Severe TBI Studies (no controlled)
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Protective Amnesia

• Amnesia does not appear to protect entirely
  against PTSD, but there is some support that it
  may serve to lessen the probability, protect
  against severity, and decrease presence of
  specific intrusive symptoms.
• Ellenberg et. al., 1996
• Turnbull et. al., 2001
• Klein et. al., 2003

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Children, TBI PTSD

• Appears to be similar or slightly higher among
  children research weak
• Gerring et. al., 2002
• Levi et. al., 1999
• Some suggestion that lateralization of lesion
  location may influence expression of
  re-experiencing symptoms
• Herskovits et. al., 2002

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The Amnesia Controversy

• Debate PTSD and retrograde amnesia seen in TBI
  may not be diagnosed concurrently since memory
  for the trauma is assumed to be a necessary
  condition for PTSD.
• Primary foundation in retrospective, non-blind
  studies that relied on interview rather than more
  common survey format, however
• Sbordone, 1992
• Sbordone Leiter, 1995

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The Amnesia Controversy

• Research supports some protective aspects of
  amnesia as previously noted (weak)
• Rather than PTA as focus, those who had some
  memories were 5x more likely to develop PTSD
  (n120)
• Klein et. al., 2003
• Other means of memory may come into play other
  than specific direct memory of the event

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Some Proposed Mechanisms for Development of PTSD
with TBI

• People who are predisposed to anxiety may develop
  ruminations and fears from what they have been
  told about the event.
• Amnesia may be incomplete with fleeting islands
  of memory.
• Memory may be a narrative consistent with
  emotional state and reconstructed from other
  inputs
• Harvey Bryant, 2001 2002
• Swiercinsky, 2001
• Williams et. al., 2002

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Research on Reconstructed Memory

• 40 of individuals with mild TBI and significant
  memory loss at one month reported recall for the
  event when tested at two years (n50)
• Harvey Bryant, 2001
• Non-TBI accident survivors with PTSD usually
  experience a reduction of symptoms over time (1-6
  months) while those with TBI and PTSD displayed
  increased intrusive memories. The amnesic gap
  may itself be a cause for anxiety and rumination

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Memory as a Dual Construct

• Explicit/Declarative conscious awareness of
  facts requires focal attention for processing
  mediated by medial temporal lobe, hippocampus and
  related structures. Testable.
• Implicit/Procedural skills learning habit
  formation and classical conditioning knowledge
  expressed through action/performance rather than
  recollection believed inaccessible to
  consciousness. Not testable.
• Infantile Amnesia
• Example of HM from neurology literature

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PTSD and TBI

• Dispute as to whether TBI PTSD is caused by
  emotional reaction to brain injury or
  neurophysiological mechanisms can be put aside
  through recognition that complex changes are
  involved in all levels of TBI, including
  neurophysiological, psychological and other
  unknown factors. The absence of evidence is not
  evidence of absence.
• Sica, 1996

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The Role of the Neuropsychologist

• Use of standard PTSD assessment tools
• Evaluate cognitive processes affected
• Functioning before, during and after PTSD related
  arousal
• Cognitive and behavioral capacities for varying
  treatment options
• Monitoring efficacy of medications
• Validate individuals subjective complaints
• Discern TBI vs. PTSD related symptoms

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Treatment of TBI related PTSD

• Psychotherapy
• Group members
• CBT as foundation
• Education support
• Pharmacology
• SSRIs sertraline, paroxetine
• Antiandranergic agents
• Antiseizure medications (mood)
• Consensus Guidelines
• Family Support
• www.psychguides.com

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PTSD and the Military

• Insurgencies
• Blast Injury
• Complexities and interaction effects
• Roles and variety of personnel
• DoD and VA
• Returning home
• Need for additional psychologists

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Factors Affecting Long Term Outcomes for
Returning Military

• Premorbid Educational Level
• Attaining Successful Employment
• Lack of Generalization of Treatment Effects
• Need for Community Context for Interventions
• Psychosocial Context of War
• Availability of Rapid Expert Medical Care in the
  Field
• Positive Attitude of Civilian Populations
• References
• (Corkin et al. 1984) (Salazar et al. 2000)
  (Newcombe 1996)

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Thank You

• For Additional Info
• Tina M. Trudel, PhD
• ttrudel_at_lakeview.ws
• 800-473-4221