Transcript Alcohol and Cognition - The Association of Substance Abuse

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
[email protected]
(254) 710-2573
TIPSS 6/2010
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
DSM-IV Alcohol-Related
Disorders - Temporary
 Alcohol Intoxication Delirium
 Alcohol Withdrawal Delirium (With
Perceptual Disturbances)
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 (WernickeKorsakoff’s)
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
1. Premature aging / whole brain
2. Right brain
3. Frontal lobes
Parsons, Butters, and Nathan, 1987
The Human Brain
Targets of Alcohol and
Other Drugs
Cerebellum
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)
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)
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)
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)
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)
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)
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).
Neuropsychological
Functioning
 15 studies examining performance
between alcoholic patients and control
peers revealed poorer performance on a
variety of tests (Parsons & Farr, 1981)
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)
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)
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)
Functional Brain Changes
in Problem Drinkers
Etiology of Progressive Cognitive
Decline
 Wernicke’s Encephalopathy (B1
deficiency)
 Characterized by nystagmus, abducens and
conjugate gaze palsies, ataxia, and mental
disturbance (confusional state)
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
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)
Reversibility
 Recovery of function is supported in the
neuropsychological and neuroradiological
literature (Grant, 1987)
 Some studies report only partial recovery
(Oslin & Cary, 2003)
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
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 = Wernicke’s Encephalopathy (acute),
Korsakoff’s Disease, Alcohol-Induced Persisting
Dementia (chronic)
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
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
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)
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
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
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 (FalsStewart et al., 1993; 1994)

Neuropsychological dysfunction may
result in more rule violations in treatment
(Fals-Stewart et al., 1994)
Treatment
Evidence-Based
Treatments




Cognitive-Behavioral
Motivational Enhancement (MI)
Twelve Step Facilitation
Community Reinforcement
 CRAFT
 Behavioral Couples Therapy
Cognitive-Behavioral
 Change thoughts, feelings, and
behaviors associated with addiction
 Relapse-Prevention Coping Skills
Training
 Communication Skills Training
 Cue Exposure Treatment
Motivational Enhancement
 Increase self-directed motivation to
change
 Increase self-efficacy for change
 Be non-confrontational
Twelve Step
 AA/NA/CA
 Emergency planning
 Sober social support
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.
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
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
Design
6 and 12 mos post-Tx:
1.USS
2.GSA
3.Measure of substance use
6 months
12 months
Sample size
n = 131
n = 117
Relapse rate
55%
70%
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**
*
*
-.24*
-.32**
ns
*
-.13
-.28*
Challenge the
thoughts
Think about treatment
*p < .01;
**p < .001
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 < .01;
**p < .001
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 < .01;
**p < .001
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 < .01;
**p < .001
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 < .01;
**p < .001
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**
*
ns
-.16
-.26*
*p < .01;
**p < .001
Relax or meditate
regularly
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
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)
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
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
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
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?
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)
Patient-Treatment
Matching
 Comorbidity
 Mood, anxiety disorders
 PTSD
 Medical conditions
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?
Methods
 Participants
 Substance dependent individuals (n=20) from
a local state-funded residential treatment
program
 Clean for > 21 days
 Procedures




Diagnostic interview (r/o psychotic disorder)
Questionnaires
Neuropsychological battery
Coping Skills assessment
57
Neuropsychological
Battery
 Baseline IQ
 Verbal learning, memory
 WAIS-III
 Attention, working memory
 Speeded information processing
 Visuospatial functioning
58
Block Design
(visuospatial function)
59
Neuropsychological
Battery (con’t)
 Executive functioning
 Wisconsin Card Sorting Test (Set-shifting,
working memory, responsiveness to
feedback, cognitive flexibility)
 Trailmaking Test A&B (Visual scanning,
attention, cognitive flexibility)
 Controlled Oral Word Association (verbal
fluency)
 Stroop Color Word Test
60
Trail Making Test Part B
Wisconsin Card Sorting Test
Stroop Color Word Test
63
Results
64
Results – Coping Skills
65
Results – Relationship
Between Coping Skills and
NP Measures
66
Results – NP Impairment
Status
67
Study #2
 More fine-grained analysis of executive
functioning
 N=49
 Neuropsychological Battery:






Verbal Fluency
Trailmaking Test
Wisconsin Card Sorting Test
Color-Word Interference (Stroop)
Iowa Gambling Task
Tower of Hanoi
68
Iowa Gambling Task
69
Tower of Hanoi
70
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
71
Verbal Fluency and Coping
Skills
SETOT
SOTOT
Number of
USC-E
skills >4
GETOT
GOTOT
VF - Letter
-.25*
-.30**
-.24*
ns
ns
VF – Letter vs.
Category
-.33**
-.31**
-.23*
-.25*
-.27*
72
Clinical Implications

Patient – Treatment Matching

Pre-treatment neuropsychological
assessment


Target skills to individual patient’s neuropsych
profile
Reduction in number of skills taught in CBT

Behavioral possibly better than cognitive focus
 Extensive repetition
 Extra role-plays
 Cognitive Rehabilitation
73
Cognitive Rehabilitation
 Computer-assisted cognitive stimulation
exercises may increase speed of
cognitive recovery (Grohman et al., 2003)
 This may then improve treatment process
and outcome
 However, time- and cost-intensive
Acknowledgements
Grant Support
 Baylor University
Research Committee
 NIAAA T32 (Brown
University; mentors:
Damaris Rohsenow,
Ph.D. and Paul Malloy,
Ph.D.)
Students
 Graduate: Robyn
Baldridge, Sarah
Martindale, Laura Sejud,
Sean McGowan, Anthony
Giardina
 Undergraduate: Sanja
Trtanj
75