1. 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

2. Cognition and Emotion – Not just a journal title

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

4. Questions  Contraindications for CI?  Does CI influence treatment response?  What factors influence the answers above?  Do we use adequate measures of CI?

5. Contraindicates? Moderates response? Potential to augment? Severity of deficit Type of deficit Source of deficit Intervention Target of intervention Timing of deficit QuestionsConsiderations

6. Sources of Cognitive Impairment Cognitive Impairment Pain PTSD TBI Substance abuse

7. Sleep Disturbance Sleep Disturbance Distractions P3+ Cognitive Impairment Meds Neural/neurobiol Alterations Neural/neurobiol Alterations

8. Other Factors  Treatment type  Type of cognitive deficit  Severity of deficits

9. CI Threats to Treatment?: General Considerations  Adherence  Concentration/focus during sessions  Group behavior

10. 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

11. 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

12. Treatment Benefits for CI?  Structure of cognitive-behavioral interventions  Certain pharmacological therapies may enhance cognition

13. Case Studies  Mixed results Some successful At least 1 showed contraindication with patient with executive dysfunction

14. 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)

15. 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

16. PTSD and Depression (Chard cont.) VariablePre- treatmentM (SD) or % Post- treatment M (SD) or % Test statistic Cohen’s d CAPS78.21 (17.96) 40.14 (25.08) t(13) = 7.95, p <.001 4.41 PCL63.57 (10.09) 40.43 (16.63) t(13) = 5.07, p <.001 2.81 BDI-II34.71 (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 <.05

17. Cognitive prediction of post-treatment CAPS (Chard cont.)

18. Cognitive Prediction of Post-treatment PCL (Chard cont.)

19. Evidence  Wild & Gur (2008) (n = 23) Pre-tx verbal memory  poorer response to CBT (for PTSD)

20. Evidence Bryant et al. (2008 a & b) Smaller pre-tx posterior ACC; increased amygdala and ventral ACC activation  poorer response to CBT (for PTSD)