The Role of Cognitive Function in Substance Abuse Treatment

1. The Role of Cognitive Function in Substance Abuse Treatment Sara L. Dolan, Ph.D. Baylor University Department of Psychology and Neuroscience Baylor Addiction Research Center Baylor University One Bear Place #97334 Waco, TX 76798-7334 Sara_Dolan@baylor.edu (254) 710-2573 TIPSS 6/2010

2. Overview DSM-IV Alcohol-Related Disorders History and Background Review of neuropsychological, neuroimaging, and neuropathological correlates of alcohol related disorders Review of evidence-based treatments for alcohol dependence Neuropsychological function and treatment

3. DSM-IV Alcohol-Related Disorders - Temporary Alcohol Intoxication Delirium Alcohol Withdrawal Delirium (With Perceptual Disturbances)

4. DSM-IV Alcohol-Related Disorders – Persisting • Alcohol-Induced Persisting Dementia • Learning/memory impairment AND 1 +: • Aphasia, Apraxia, Agnosia, Executive dysfunction • Alcohol-Induced Persisting Amnestic Disorder • Learning/memory impairment (Wernicke-Korsakoff’s)

5. Background/History Beyond thiamine-deficiency (i.e., Wernicke – Korsakoff’s), alcoholism researchers have focused on models based on brain systems vulnerabilities Three predominant theories on the pattern of consequences of alcoholism on the brain Premature aging / whole brain Right brain Frontal lobes Parsons, Butters, and Nathan, 1987

6. The Human Brain

7. Targets of Alcohol and Other Drugs Cerebellum

8. Premature Aging / Whole Brain Alcoholism accelerates brain aging Findings only support premature aging in older alcoholics (i.e., age 50 +) (Oscar-Berman, 2000) Alcohol leads to mild generalized dysfunction of the brain (Parsons, 1996)

9. Right Brain Right hemisphere is more vulnerable to the effects of alcoholism than the left hemisphere Impairments in visuospatial functioning and emotional processing (Oscar-Berman, 2000) Emotional processing deficits also may be due to abnormalities in other brain regions (e.g., limbic system, frontal lobes; Colson & Dolan, 2010; Oscar-Berman & Schendan, 2000)

10. Frontal Lobes Frontal lobes show increased susceptibility to alcoholism-related damage Evidence from post-mortem neuropathological studies (Harper, 1998) and neuroimaging of living patients (Sullivan, 2000) Also behavioral and neuropsychological deficits in executive functioning seem to be prominent in both currently-drinking and recently-detoxified alcoholics (e.g., Bechara et al., 2001)

11. Neuropsychological Impairment in Substance Abusers • Approximately 33-75% of patients admitted to VA outpatient substance abuse treatment programs have measurable cognitive impairment • Mostly in the mild to moderate range (Eckardt & Martin, 1986; Meek et al., 1989; Parsons & Leber, 1981; Tabakoff & Petersen, 1988)

12. Neuropsychological Deficits in Substance Abusers • Alcoholics have deficits in: • Memory (anterograde worse than retrograde) • Visual worse than verbal • Visuospatial functions • Executive functions • Problem‑solving, abstraction • Cognitive efficiency • (Page, 1983; Page, 1987; Parsons et al., 1987; • Ratti et al., 2002; Wilson, 1987)

13. Executive Function • A disruption of processes thought to: • Monitor • Direct • Organize • Regulate behavior… …to enable persons effectively to achieve desired goals while minimizing adverse consequences • Mediated by the prefrontal cortex • (Lezak, 1995)

14. Neuropsychological Functioning Early studies suggested that sober alcoholics demonstrate impairment on neuropsychological tests that is similar to that of patients with diagnosed mild-to-moderate brain injury (Parsons, 1986).

15. Neuropsychological Functioning 15 studies examining performance between alcoholic patients and control peers revealed poorer performance on a variety of tests (Parsons & Farr, 1981)

16. Neuropsychological Findings Compromised fronto-cortico-cerebellar circuits underlie cognitive deficits (Scheurich, 2005) Patterns of correlations between cortical and subcortical volume deficits To compensate for deficient task performance, alcohol-dependent patients require the use of additional and higher-order executive functions (Scheurich, 2005)

17. Structural Neuroimaging In recently detoxified alcoholics, CT findings show widened sulci, ventricular dilation, and cerebellar atrophy (Grant, 1987) MRI: Reductions in cortical and subcortical gray and white matter (Jernigan et al, 1992; Schmidt et al., 2005) Reduction in brain weight and volume associated with reduction in white matter volume (Harper et al., 2003) Reduction in total hippocampus volume(Arciniegas et al., 2006)

18. Functional Neuroimaging Functional MRI studies: Decreased prefrontal cortical function in chronic substance abusers (for a review, see London et al., 2000) Additional recruitment of brain areas (Scheurich, 2005) Cerebral glucose metabolism (PET studies): Decreased regional cerebral blood flow to frontal regions, ranging from a 75% (Nicolas et al., 1993) to 86% (Erbas et al., 1992) reduction in chronic alcoholics SPECT: decreased blood flow in frontal lobes and cerebellum (latter appears to persist even after a period of abstinence)

19. Functional Brain Changes in Problem Drinkers

20. Etiology of Progressive Cognitive Decline Wernicke’s Encephalopathy (B1 deficiency) Characterized by nystagmus, abducens and conjugate gaze palsies, ataxia, and mental disturbance (confusional state)

21. Etiology of Progressive Cognitive Decline • Wernicke-Korsakoff Syndrome (aka Korsakoff psychosis or Korsakoff amnesic state; DSM-IV=Alcohol-Induced Persisting Amnestic Disorder) • Retentive memory impaired out of proportion to other cognitive functions (chronic manifestation of Wernicke disease) • With treatment, recovery occurs in less than 20% of patients

22. Alcohol and Dementia Association between alcohol use (especially heavy use or dependence) and the development of dementia (Oslin et al., 1998) Heavy alcohol use contributes to the emergence of dementia in more than 20% of patients diagnosed with dementia (cited in Kapaki et al., 2005) May be most apparent among men and those with ApoE4 allele (Mukamal et al., 2003) Cortical and subcortical pathology (Schmidt et al, 2005)

23. Reversibility Recovery of function is supported in the neuropsychological and neuroradiological literature (Grant, 1987) Some studies report only partial recovery (Oslin & Cary, 2003)

24. Reversibility • Cognitive functioning improves with extended abstinence • Much improvement over first 21-30 days of abstinence • Can take as long as 1 year • How does recovery occur? • Glial regeneration • Synaptic plasticity

25. Range of Impairment Mild (subtle) = may or may not evidence impairment in daily life “Social” drinkers (6+ drinks per day; Parsons, 1998) Moderate = more likely show some impairment in daily life Severe = Wernicke’s Encephalopathy (acute), Korsakoff’s Disease, Alcohol-Induced Persisting Dementia (chronic) No Impairment Mild Moderate Severe

26. Prevalence of Impairment • 33 – 75% of alcoholics entering treatment display neuropsychological deficits, most in the mild to moderate range • Problem-solving • Abstract thinking • Concept shifting • Learning / Memory Eckardt & Martin, 1986; Meek et al., 1989; Parsons & Leber, 1981; Tabakoff & Petersen, 1988

27. Prevalence of Impairment • Categories = 50% • Abstract thinking • COWA = 50% • Verbal fluency • Trails-B = 17% • Cognitive flexibility • Stroop = 12% • Response inhibition • Shipley Vocabulary = 13% • Verbal skills • Morgenstern & Bates, 1999

28. Specific Neuropsychological Deficits and Substance Abuse Treatment Process Attention / Learning / Memory Patients can’t learn or remember new skills taught in treatment (Sanchez-Craig & Walker, 1982)

29. Specific Neuropsychological Deficits and Substance Abuse Treatment Process • Executive function – patients can’t apply new skills after treatment (Morgenstern & Bates, 1999) • Abstract thinking • Generalizability of skills outside of treatment • Cognitive flexibility • Switching tracks • Verbal Fluency • Producing alternative strategies • Response Inhibition • Inhibiting pre-potent responses

30. Neuropsychological Deficits and Substance Abuse Treatment Process Failure to acquire strategies taught during treatment The cognitive and behavioral strategies taught in treatment may be less effective in preventing relapse Impaired individuals have different change processes than unimpaired individuals Block, Bates, & Hall, 2003; Morgenstern & Bates, 1999

31. Neuropsychological Function and Treatment Process / Outcome • Clinicians’ misattributions of patients’ behaviors • Verbal skills (previously learned information) remain relatively preserved, so patients appear unimpaired • Clinicians fail to identify cognitive impairment in at least 40% of patients (Fals-Stewart et al., 1993; 1994) • Neuropsychological dysfunction may result in more rule violations in treatment (Fals-Stewart et al., 1994)

32. Treatment

33. Evidence-Based Treatments • Cognitive-Behavioral • Motivational Enhancement (MI) • Twelve Step Facilitation • Community Reinforcement • CRAFT • Behavioral Couples Therapy

34. Cognitive-Behavioral Change thoughts, feelings, and behaviors associated with addiction Relapse-Prevention Coping Skills Training Communication Skills Training Cue Exposure Treatment

35. Motivational Enhancement Increase self-directed motivation to change Increase self-efficacy for change Be non-confrontational

36. Twelve Step • AA/NA/CA • Emergency planning • Sober social support

37. Common Themes • Empirically-supported psychosocial treatments for SUDs (Finney, Willbourne, and Moos, 2007): • Enhance/maintain motivation to change. • Involve teaching/learning of coping skills. • Restructure the social environment. • Can involve conditioning-based interventions. • Change perceptions of social norms. • Enhance self-efficacy for robust behavioral change.

38. Participants • 187 Alcohol-Dependent patients in residential treatment • Clinical trial of naltrexone and coping skills training • 31% female • 39.0 ± 9.4 years of age • 13.4 ± 2.3 years of education • 66.1 ± 28.3 % alcohol use days during the 6 months pre-treatment

39. Measures • Urge-Specific Strategies (USS; 6 mo. α = .91; 12 mo. α = .90) • 21 situation-specific strategies taught in cue exposure, communication skills, or relaxation/meditation • General Strategies for Alcoholics (GSA; 6 mo. α = .92; 12 mo. α = .90) • 21-item lifestyle change strategies taught in communication skills and in the general treatment program

40. Design • 6 and 12 mos post-Tx: • USS • GSA • Measure of substance use n = 131 55% n = 117 70% 6 months 12 months Sample size Relapse rate

41. USS - Cognitive *p < .01; **p < .001

42. USS – Cognitive, Behavioral *p < .01; **p < .001

43. USS – Behavioral, Other *p < .01; **p < .001

44. GSA - Cognitive *p < .01; **p < .001

45. GSA - Behavioral *p < .01; **p < .001

46. GSA – Behavioral, Other *p < .01; **p < .001

47. Summary • Top 5 situation-specific coping strategies • Positive consequence thoughts, mastery messages, alternative behaviors, problem solving, think through a behavior chain • Top 5 general lifestyle coping strategies • Positive consequence thoughts, remind self that you are sober, challenge thoughts about drinking, sober good time, work toward future goals

48. Conclusions (Dolan et al., in preparation) • Improve treatment by: • Teaching situation-specific AND general lifestyle coping skills • Emphasizing strategies that are more effective • Eliminating skills that are ineffective

49. Hypothetical Patient Bill is a 50 year-old male veteran who presents for treatment of his “excessive drinking” Self-reported alcohol consumption escalated to a fifth of vodka per night for 7 months, following his divorce

50. Hypothetical Patient - cont • He has started getting into trouble at work, and his grown children “don’t seem to know who he is anymore” because of his behavior • He used to be a very organized person and now his apartment is a mess and he isn’t able to get his bills paid correctly