Cognitive deficits as a treatment moderator?

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Cognitive Deficits as a Treatment Moderator?
Jennifer J. Vasterling, Ph.D. VA Boston
Healthcare System VA National Center for
PTSD P3 Research Summit September, 2009
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• Cognition and Emotion
• Not just a journal title

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What do we mean by cognitive impairment (CI)?
Pre-defined threshold? Relative
weakness? Intra-individual change?
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Questions

• Contraindications for CI?
• Does CI influence treatment response?
• What factors influence the answers above?
• Do we use adequate measures of CI?

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Questions
Considerations
Severity of deficit
Contraindicates? Moderates response? Potential
to augment?
Type of deficit
Timing of deficit
Source of deficit
Intervention
Target of intervention
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Sources of Cognitive Impairment
PTSD
Pain
Cognitive Impairment
Substance abuse
TBI
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P3
Sleep Disturbance
Distractions
Neural/neurobiol Alterations
Meds
Cognitive Impairment
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Other Factors

• Treatment type
• Type of cognitive deficit
• Severity of deficits

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CI Threats to Treatment? General Considerations

• Adherence
• Concentration/focus during sessions
• Group behavior

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CI Threats to Treatment?Exposure Based
Interventions (Memory)

• Require controlled retrieval of the trauma memory
  assoc. emotions
• Require modification of the memory assoc.
  emotions/formation of new associations

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CI Threats to Treatment? Cognitive
Interventions (Inhibition and Flexibility)

• Target distorted thoughts with goal of
  reappraisal
• Require inhibition of maladaptive thoughts
• Require sufficient flexibility to re-appraise

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Treatment Benefits for CI?

• Structure of cognitive-behavioral interventions
• Certain pharmacological therapies may enhance
  cognition

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Case Studies

• Mixed results
• Some successful
• At least 1 showed contraindication with
  patient with executive dysfunction

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Evidence

• Bryant et al. (2003) (n 24)
• RCT showed that CBT for acute stress
  disorder after mTBI was assoc with reduced PTSD
  at 6 mo. follow-up
• CBT beneficial following mTBI for range of
  emotional concerns (Soo Tate, 2007 review)

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Evidence from Kate Chard CPT to Treat PTSD
with TBI

• Cincinnati mTBI/PTSD Residential Program
• n 20 male vets 10 bed cohort
• 33 mild, 66 mod, 1 severe TBI
• CPT-Cognitive Only paradigm
• Combined group and individual tx
• Avg of 15 sessions
• Augmented with group psychoeducation

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PTSD and Depression (Chard cont.)
Variable Pre-treatmentM(SD) or Post-treatment M (SD) or Test statistic Cohens d
CAPS 78.21 (17.96) 40.14 (25.08) t(13) 7.95, p lt .001 4.41
PCL 63.57 (10.09) 40.43 (16.63) t(13) 5.07, p lt .001 2.81
BDI-II 34.71 (8.80) 20.64 (13.15) t(13) 4.06, p .001 2.25
PTSD diagnosis present 100 43 ?2(1) 6.13, p .01
MDD diagnosis present 86 36 ?2(1) 5.14, p lt .05
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Cognitive prediction of post-treatment CAPS
(Chard cont.)
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Cognitive Prediction of Post-treatment PCL
(Chard cont.)
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Evidence

• Wild Gur (2008) (n 23)
• Pre-tx verbal memory ? poorer response to CBT
  (for PTSD)

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Evidence

• Bryant et al. (2008 a b)
• Smaller pre-tx posterior ACC increased
  amygdala and ventral ACC activation ?
• poorer response to CBT (for PTSD)