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The Role of Cognitive Function in Substance Abuse Treatment

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Title: 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_at_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-Korsakoffs)

5
Background/History
  • Beyond thiamine-deficiency (i.e., Wernicke
    Korsakoffs), 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
  • Wernickes 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-IVAlcohol-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
Neurotoxicity
  • Why does neurodegeneration occur?
  • Cell loss
  • Volume loss
  • Synaptic plasticity changes

Nixon, 2006
23
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)

24
Reversibility
  • Recovery of function is supported in the
    neuropsychological and neuroradiological
    literature (Grant, 1987)
  • Some studies report only partial recovery (Oslin
    Cary, 2003)

25
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

26
Range of Impairment
No Impairment
Mild
Moderate
Severe
  • 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 Wernickes Encephalopathy (acute),
    Korsakoffs Disease, Alcohol-Induced Persisting
    Dementia (chronic)

27
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
28
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
29
Specific Neuropsychological Deficits and
Substance Abuse Treatment Process
  • Attention / Learning / Memory
  • Patients cant learn or remember new skills
    taught in treatment (Sanchez-Craig Walker,
    1982)

30
Specific Neuropsychological Deficits and
Substance Abuse Treatment Process
  • Executive function patients cant 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

31
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
32
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)

33
Treatment
34
Evidence-Based Treatments
  • Cognitive-Behavioral
  • Motivational Enhancement (MI)
  • Twelve Step Facilitation
  • Community Reinforcement
  • CRAFT
  • Behavioral Couples Therapy

35
Cognitive-Behavioral
  • Change thoughts, feelings, and behaviors
    associated with addiction
  • Relapse-Prevention Coping Skills Training
  • Communication Skills Training
  • Cue Exposure Treatment

36
Motivational Enhancement
  • Increase self-directed motivation to change
  • Increase self-efficacy for change
  • Be non-confrontational

37
Twelve Step
  • AA/NA/CA
  • Emergency planning
  • Sober social support

38
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.

39
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

40
Measures
  • Urge-Specific Strategies (USS 6 mo. a
    .91 12 mo. a .90)
  • 21 situation-specific strategies taught in cue
    exposure, communication skills, or
    relaxation/meditation
  • General Strategies for Alcoholics (GSA 6 mo. a
    .92 12 mo. a .90)
  • 21-item lifestyle change strategies taught in
    communication skills and in the general treatment
    program

41
Design
  • 6 and 12 mos post-Tx
  • USS
  • GSA
  • Measure of substance use

6 months
12 months
  • n 131
  • 55
  • n 117
  • 70

Sample size
Relapse rate
42
USS - Cognitive
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Positive consequence -.47 -.29
Negative consequence -.31 -.15
Mastery messages -.42 -.27
Distracting thoughts ns -.26 -.37
Challenge the thoughts -.24 -.32
Think about treatment ns -.13 -.28
p lt .01 p lt .001
43
USS Cognitive, Behavioral
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Alternative behavior -.33 -.33
Solve the problem -.30 -.34
Think through behavior chain -.21 -.37
Refuse the drink -.21 -.35
p lt .01 p lt .001
44
USS Behavioral, Other
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Escape ns -.25 -.32
Delay, wait it out ns -.25 -.23
Other social support -.21 -.31
Spiritual coping -.21 -.15
p lt .01 p lt .001
45
GSA - Cognitive
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Positive consequence -.50 -.46
Remind self sober -.43 -.49
Challenge thoughts -.34 -.41
Negative consequence ns -.27 -.24
Think about treatment -.25 -.30
Spiritual focus -.25 -.21
p lt .01 p lt .001
46
GSA - Behavioral
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Sober good time -.47 -.49
Work toward future goals -.40 -.45
Other social support -.36 -.26
Work on problems regularly -.30 -.18
Tell others sober -.29 -.17
p lt .01 p lt .001
47
GSA Behavioral, Other
Months 4-6 Months 7-12 Months 4-6 Months 7-12
Lapse Lapse pr pr
Keep busy ns -.40 -.39
Eat, sleep, healthy behavior ns -.39 -.30
Talk over feelings ns -.31 -.25
Avoid tempting situations ns ns -.27 -.32
Relax or meditate regularly ns -.16 -.26

p lt .01 p lt .001
48
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

49
Conclusions
  • Improve treatment by
  • Teaching situation-specific AND general lifestyle
    coping skills
  • Emphasizing strategies that are more effective
  • Eliminating skills that are ineffective

(Dolan et al., in preparation)
50
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

51
Hypothetical Patient - cont
  • He has started getting into trouble at work, and
    his grown children dont 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 isnt able to get his
    bills paid correctly

52
Hypothetical Patient - cont
  • He successfully completes detox
  • On Day 1 of Intensive Outpatient Treatment, he
    appears to have some difficulty comprehending the
    structure of the treatment program, and he asks
    repetitive questions

53
Hypothetical Patient - cont
  • A neuropsychological evaluation reveals that he
    has memory and executive dysfunction
  • Very typical profile for alcohol-related
    neuropsychological dysfunction
  • What do we do to maximize treatment benefit for
    this patient?

54
Factors that Might Influence Treatment Outcome
  • Treatment-specific variables
  • Length and type of treatment
  • Individual differences
  • Severity of dependence
  • Presence of comorbid psychiatric disorders
  • Personality factors
  • Anger level

(Project MATCH, 1997)
55
Patient-Treatment Matching
  • Comorbidity
  • Mood, anxiety disorders
  • PTSD
  • Medical conditions

56
Factors that May Influence Treatment Outcome
  • What about neuropsychological function?
  • Do these patients have the cognitive capacity to
    participate in treatment aimed at changing
    thoughts and behaviors related to their substance
    use disorder?
  • I.e., Are their brains intact enough to learn,
    process, and apply new relapse-prevention skills?

57
Methods
  • Participants
  • Substance dependent individuals (n20) from a
    local state-funded residential treatment program
  • Clean for gt 21 days
  • Procedures
  • Diagnostic interview (r/o psychotic disorder)
  • Questionnaires
  • Neuropsychological battery
  • Coping Skills assessment

58
Neuropsychological Battery
  • Baseline IQ
  • Verbal learning, memory
  • WAIS-III
  • Attention, working memory
  • Speeded information processing
  • Visuospatial functioning

59
Block Design(visuospatial function)
60
Neuropsychological Battery (cont)
  • Executive functioning
  • Wisconsin Card Sorting Test (Set-shifting,
    working memory, responsiveness to feedback,
    cognitive flexibility)
  • Trailmaking Test AB (Visual scanning, attention,
    cognitive flexibility)
  • Controlled Oral Word Association (verbal fluency)
  • Stroop Color Word Test

61
Trail Making Test Part B
62
Wisconsin Card Sorting Test
63
Stroop Color Word Test
64
Results
65
Results Coping Skills
66
Results Relationship Between Coping Skills and
NP Measures
67
Results NP Impairment Status
68
Study 2
  • More fine-grained analysis of executive
    functioning
  • N49
  • Neuropsychological Battery
  • Verbal Fluency
  • Trailmaking Test
  • Wisconsin Card Sorting Test
  • Color-Word Interference (Stroop)
  • Iowa Gambling Task
  • Tower of Hanoi

69
Iowa Gambling Task
70
Tower of Hanoi
71
Demographics
Mean / Frequency SD
Age 32.06 10.01
Gender 46 M
Education 12.17 2.03
Daily Alcohol Intake 7.23 23.97
Prior Treatment Attempts 2.33 2.89
Sobriety Length 54.53 53.71
Contemplation Ladder 9.21 1.75

SETOT 88.44 35.19
SOTOT 87.24 32.14
VF 9.4 3.4
VF Letter vs. Category 9.3 3.0
72
Verbal Fluency and Coping Skills
SETOT SOTOT Number of USC-E skills gt4 GETOT GOTOT
VF - Letter -.25 -.30 -.24 ns ns
VF Letter vs. Category -.33 -.31 -.23 -.25 -.27
73
Clinical Implications
  • Patient Treatment Matching
  • Pre-treatment neuropsychological assessment
  • Target skills to individual patients neuropsych
    profile
  • Reduction in number of skills taught in CBT
  • Behavioral possibly better than cognitive focus
  • Extensive repetition
  • Extra role-plays
  • Cognitive Rehabilitation
  • A la TBI, schizophrenia

74
Cognitive Rehabilitation
  • Computer-assisted cognitive stimulation exercises
    may increase speed of cognitive recovery
  • This may then improve treatment process and
    outcome
  • However, time- and cost-intensive

(Grohman et al., 2003)
75
Acknowledgements
  • Grant Support
  • Students
  • Baylor University Research Committee
  • NIAAA T32 (Brown University mentors Damaris
    Rohsenow, Ph.D. and Paul Malloy, Ph.D.)
  • Graduate Robyn Baldridge, Sarah Martindale,
    Laura Sejud, Sean McGowan, Anthony Giardina
  • Undergraduate Sanja Trtanj
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