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THE NEUROPSYCHOLOGICAL OUTCOME OF

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THE NEUROPSYCHOLOGICAL OUTCOME OF COMMUNITY ALCOHOLICS:
PSYCHIATRIC DISORDERS, NEUROMEDICAL PROBLEMS, AND DRINKING
HISTORY
By

Edwin Poon

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY
Department of Psychology
2002

ABSTRACT
THE NEUROPSYCHOLOGICAL OUTCOME OF COMMUNITY ALCOHOLICS:
PSYCHIATRIC DISORDERS, NEUROMEDICAL PROBLEMS, AND DRINKING
HISTORY
By

Edwin Poon

This study examined the validity of three different neuropsychological
models of alcohol abuse: the diffuse dysfunction model, the right hemisphere
deficits model, and the frontal dysfunction model. In addition, three potential
sources of variance that might influence the neuropsychological outcome of
alcoholics were explored: psychiatric disorders, neuromedical risk, and drinking
history. Participants were 327 adults drawn from the University of Michigan -—
Michigan State University Longitudinal Study. Neuropsychological functioning
was assessed using the Wechsler Adult Intelligence Test - Revised, the
MicroCog, and the Symbol Digit Modality Test. Results showed that alcoholics
performed poorly on a wide range of neuropsychological measures. Moreover,
perceptual motor functioning appears to be most sensitive to alcohol abuse.
Among all the drinking variables, chronic history of alcoholism was the most
reliable predictor for neuropsychological outcome. Path analysis revealed that
depression mediated the relationship between history of alcoholism and
perceptual motor functioning. In addition, higher level of current alcohol
problems predicted poorer perforrnanoe in visuospatial functioning. The current

study extended earlier research by Showing that poorer neuropsychological

performance previously documented among alcoholics in clinical populations is
present in a community-based population of alcoholics. Although the pattern of
deficits seems to be most consistent with the diffuse brain dysfunction model,
none of the three theoretical provided a definitive framework to describe the
effect of alcohol on brain functioning. Further, the results indicated that the direct
neurotoxic effect of alcohol is partially moderated by other alcohol-related factors
including depression and drinking pattern. In light of the current findings, it
appears that past approaches to studying the neuropsychological functioning of
alcoholics namely, comparing the three different theoretical models, may not
capture the full range of possible neuropsychological effects of sustained and/or
intensive alcohol consumption. Future research should focus on developing a
more comprehensive theory that incorporates the both the direct and indirect

effect of alcoholism on neuropsychological functioning.

To my mom and sister, your love and support are the foundation of my success.
To my dad, I will always miss you.

To Eric, my life is blessed with love and happiness because of you.

ACKNOWLEDGMENTS

I would like to express my utmost appreciation and gratitude to Dr. Hiram
Fitzgerald. I am grateful that he took me on as his student and guided me
throughout my graduate career. His unwavering support and encouragement
were invaluable to my professional and personal development. I would also like
to thank Dr. Robert Zucker for his mentoring and guidance. Without his
dedication to the research of alcoholism and his commitment to my work this
project would never have happened. A special thank you goes to Dr. Kenneth
Adams. His theoretical and empirical knowledge of neuropsychology and
alcoholism was invaluable to the completion of this work. I would also like to
extend my appreciation to Dr. Alex Von Eye for his statistical guidance, and Dr.
Robert Caldwell for his support throughout my graduate career. Finally, I would
like to thank all the families participating in the UM-MSU Longitudinal Study for
allowing us to enter their homes and provide us with valuable information about

their lives. Without their cooperation, none of this work would be possible.

This research was supported by a Student Award Program grant (grant #
04.SAP.OO) to Edwin Poon from the Blue Cross Blue Shield of Michigan
Foundation, and, in part, by grants to RA. Zucker and HE. Fitzgerald from the
National Institute of Alcohol Abuse and Alcoholism (NIAAA grant # R01 AA-

07065).

TABLE OF CONTENTS

LIST OF TABLES ........................................................................................ viii
LIST OF FIGURES ...................................................................................... ix
INTRODUCTION ......................................................................................... 1
REVIEW OF THE LITERATURE .................................................................. 4
Neuropsychological Functioning of Alcoholics ......................................... 4
Intellectual performance ................................................................... 5
Learning and Memory ...................................................................... 6
Visuospatial Ability ............................................................................ 8
Executive Functioning ...................................................................... 1O
Neuropsychological Models of Alcoholism ................................................ 12
Diffuse Dysfunction Model ............................................................... 12

Right Hemisphere Deficit Model ....................................................... 14
Frontal Lobe Dysfunction Model ....................................................... 15
Mediating Factors ..................................................................................... 16
Psychiatric Disorders ........................................................................ 16
Neuromedical Risk ........................................................................... 20
Drinking History ................................................................................ 21
PROPOSED STUDY ................................................................................... 24
HYPOTHESES ............................................................................................ 26
METHOD ..................................................................................................... 28
Participants ............................................................................................... 28
Data Collection ......................................................................................... 30
Measures .................................................................................................. 32
Alcoholism Diagnosis ....................................................................... 32
Alcoholism Subtype .......................................................................... 32
Drinking Variables .............................................................................. 33
Current Drinking .......................................................................... 33

History of Alcoholism .................................................................. 34
Neuropsychological Domains ........................................................... 34
General Cognitive Functioning .................................................. 34

Memory Functioning .................................................................. 36
Visuospatial Functioning ............................................................. 36
Perceptual Motor Functioning ................................................... 37

Executive Functioning ............................................................... 37
Neuromedical Risk ........................................................................... 38
Depression ....................................................................................... 38

vi

RESULTS .................................................................................................... 39

Missing Data ............................................................................................. 39
Descriptive Statistics .................................................................................. 39
Multivariate Analyses of Variance .............................................................. 40
Hypothesis 1 ...................................................................................... 40
General Cognitive Functioning .................................................... 42

Memory Functioning .................................................................... 42
Visuospatial Functioning ............................................................. 42
Perceptual Motor Functioning ..................................................... 45

Executive Functioning ................................................................. 45
Hypothesis 2 ...................................................................................... 48

Path Analysis ............................................................................................. 50
Hypothesis 3 ...................................................................................... 50
Hypothesis 4 ...................................................................................... 52
Hypothesis 5 ...................................................................................... 53
Hypothesis 6 ...................................................................................... 55
Hypothesis 7 ...................................................................................... 55
DISCUSSION .............................................................................................. 57
Limitation of Study .................................................................................... 66
Summary .................................................................................................... 67
APPENDICES .............................................................................................. 75
BIBLIOGRAPHY ........................................................................................... 86

vii

LIST OF TABLES

1. Background Characteristics of Participants ............................................. 31
2. Neuropsychological Tests for Memory, Perceptual Motor,

Visuospatial, Abstract Reasoning/Problem Solving and General

Cognitive Functioning ................................................................................... 35
3. Multivariate Analysis of Variance for Background Characteristics

based on Alcoholism Subtypes — Antisocial Alcoholics (AALS), Non-

antisocial Alcoholics (NAALs), and Non-alcoholics (controls) ...................... 41

4. Multivariate Analysis of Variance for General Cognitive Functioning
Measures ..................................................................................................... 43

5. Multivariate Analysis of Variance for Memory Functioning
Measures ..................................................................................................... 44

6. Multivariate Analysis of Variance for Visuospatial Functioning
Measures ..................................................................................................... 46

7. Multivariate Analysis of Covariance for Perceptual Motor
Functioning Measures .................................................................................. 47

8. Multivariate Analysis of Variance for Executive Functioning
Measures ..................................................................................................... 49

9. Relative Risk Significant Brain Impairment ............................................. 51

viii

LIST OF FIGURES

1. Multifactorial Etiology of Neuropsychological Functioning

of Alcoholics .................................................................................................. 69
2. Drinking Variables and Neuropsychological Outcome ............................... 70
3. Structural Equation Model for Memory Functioning .................................. 71
4. Structural Equation Model for Perceptual Functioning .............................. 72
5. Structural Equation Model for Visuospatial Functioning ............................ 73
6. Structural Equation Model for Executive Functioning ............................... 74

INTRODUCTION

In the 1992 National Household Survey on Drug Abuse, over 80 percent of
men between the ages of 18 and 25 reported some consumption of alcohol in the
past year (Substance Abuse and Mental Health Services Administration, 1993).
In Michigan, 51 percent of adolescent (9-12th grade) reported that they are
current drinkers (Michigan Department of Community Health, 1997). Moreover,
one in four men in the United States will meet the criteria for alcohol
abuse/dependence sometime in the course of their lifetime (Zucker & Fitzgerald,
1997). These statistics indicate that alcoholism is one of the major health
problems in the United States.

One of the adverse consequences of chronic alcoholism is brain
impairment‘. Neuroimaging and neuroradiological studies have shown that
cortical atrophy, ventricular dilation, and reduced brain weight are commonly
observed among chronic alcoholics (Rourke & Loberg, 1996). In addition,
alcoholics have been found to perform poorly on various neuropsychological
tests that are sensitive to brain damage (Charness, 1993). While the
neurotoxicity of alcohol is well established, the exact mechanism of such effects
is still relatively unknown. Three different theoretical models have been
proposed to describe the specific action of alcohol on the brain. First, the diffuse
dysfunction model suggests that alcohol abuse/dependence causes non-specific
neurological damage (Goldstein & Shelly, 1982). The second model proposes
that the right hemisphere of the brain is more prone to damage from alcohol

abuse/dependence than the left hemisphere (Jones & Parsons, 1972). Finally,

the frontal lobe dysfunction model suggests that alcohol-induced brain damage is
specifically concentrated in the anterior-basal region including the frontal, Iimbic
and diencephalic structures (Tarter, 1975).

Other factors that are associated with alcoholism might also mediate the
relationship between alcohol abuse and brain dysfunction. These factors include
head injuries (HillBom & Holm, 1986), antisocial personality disorder (Waldstein,
Malloy, Stout, & Longabaugh, 1996), depression (Shafer et al., 1991), and
drinking patterns (O’Donnell, De Soto, & De Soto, 1994). It is likely that the
etiology of neuropsychological deficits in alcoholics is multifactorial. Therefore, it
is important that these alcohol-related factors are taken into consideration when
evaluating the neuropsychological functioning of alcoholics.

The proposed study sought to examine the effects of chronic alcohol use
on neuropsychological outcome among community alcoholic and non-alcoholic
men. Specifically, the validity of three different theoretical models of alcohol
effects on brain functioning was evaluated: diffuse dysfunction model, right
hemisphere deficit model, and frontal lobe dysfunction model. It was
hypothesized that community alcoholic men would Show greater
neuropsychological deficits than controls. Moreover, deficits in executive
functioning would be most severe, supporting the frontal lobe dysfunction model.
The current study also investigated variables that might contribute to the
neuropsychological outcome in alcoholics. Three potential sources of variance

were explored: depression, neuromedical risk (i.e. problems with nervous

system), and drinking history (i.e. history of alcoholism, current alcohol problems,

and recent alcohol use).

REVIEW OF THE LITERATURE

Neuwolowunctionigq of Alcoholics

For many years, severe alcoholics were known to be at risk for one
specific kind of neurological impairment; namely, the Wemicke-Korsakoff
syndrome (WKS). This syndrome is believed to be caused by thiamin deficiency,
a result of malnutrition due to Chronic alcohol use. The early Clinical presentation
of WKS includes global confusion, abnormal eye movements, and gait ataxia.
Behavioral symptoms such as disorientation of time and place, apathy, and
emotional blandness are also prominent among alcoholics with Korsakost
psychosis. Alcoholics with WKS are also expected to suffer from severe memory
deficits (Lezak, 1995). Specifically, Korsakoff patients have great difficulties
teaming new verbal and nonverbal information (anteriograde amnesia). In
addition, they have trouble recalling historical events that occurred close to the
time of onset of the disorder (retrograde amnesia). However, semantic memory
(e.g. rules, general principle etc.) remains mostly intact, which may account for
the preservation of general intelligence (Bolden, 1994; Butters & Cerrnak, 1980).
Other neuropsychological deficits, including visual-spatial (Oscar-Berman, 1980),
conceptual (Kovner, Mattis, Goldmeier, & Davis, 1981), executive functioning
(Joyce & Robins, 1991), and psychomotor skills (Parsons & Nixon, 1993), have
also been noted among alcoholics with WKS.

In a landmark paper, Courville (1955) reported that Chronic alcoholics

suffer widespread cortical atrophy and he argued that the damage is the result of

alcohol neurotoxicity rather than dietary deficiency. Since then, evidence from
neuroradiological and neuropathological studies have indicated that there is a
second kind of alcoholism-related brain impairment that is independent of the
Korsakoft‘s Amnesia (Bergman, Borg, Hindmarsh, ldestrom, & Mutzell, 1980;
Harper & Kril, 1990). Similarly, Butters and Salmon (1986) reported that
cognitive deficits associated with chronic alcohol use (i.e. visual-spatial
processing, abstraction, and problem solving) are independent of those related to
WKS (i.e. Amnesia).

The relationship between cognitive dysfunction and alcoholism was further
substantiated by studies that found alcoholics performed poorly on the Halstead-
Reitan Neuropsychological Battery (HRNB), a set of measures that is sensitive to
brain damage (Fitzhugh, Fitzhugh, & Reitan, 1965; Jones & Parsons, 1971;
Smith, Burt, & Chapman, 1973). More recently, Tuck and Jackson (1991)
reported that alcoholics with no neurological disorder performed significantly
worse on various neuropsychological tests than matched controls. These results
suggest that chronic alcoholism could cause cognitive impairment even before
the onset of any clinical signs of neurological disorder.

The following section reviews studies that examined the
neuropsychological functioning of alcoholics with no Clinical signs Of WKS.
Intellectual Performance

Typically, alcoholics with no signs of WKS are reported to have global
intellectual abilities within the normal range (Gordon, Kennedy, & McPeake,

1988; Page & Schaub, 1977). However, when being examined with a cognitive

test like the Wechsler Adult Intelligence Scale (WAIS), alcoholics often show
deficits in the performance subtests, which assess perceptual motor and
visuospatial skills while their verbal abilities remain mostly intact (Parsons & Farr,
1981; Parsons & Leber, 1981; Goldman, 1986). For example, Loberg (1980)
examined the neuropsychological functioning of male alcoholics and normal
drinkers and found that alcoholics obtained average general intelligence but they
had significantly lower scores than control subjects on several performance
subtests including Block Design and Digit Symbol.

More recently, Hambidge (1990) examined the intellectual functioning of
adult men ages 18 to 65 who were admitted to an inpatient psychiatric hospital
for alcohol related problems. Results showed that more than half of the
participants (58%) displayed visuospatial impairment on the WAIS. In contrast,
only 3% of the participants exhibited verbal deficits. Similarly, Mahony and
Doherty (1996) reported that detoxified alcoholics displayed impaired
performance on Block Design and Digit Symbol of the WAIS and WAIS-R,
whereas Vocabulary and Digit Span scores were within the normal range. These
findings further support the notion that chronic alcoholics are more likely to
display deficits in performance intelligence while their verbal intelligence is
relatively unimpaired.

Learning and Memom

Early studies on memory functioning of alcoholics without WKS have

yielded negative findings (Parsons & Prigatano, 1977; Ryan & Butters, 1980).

For instance, Loberg (1980) reported that alcoholic men performed within normal

limits on the Wechsler Memory Scale (WMS-R) and did not exhibit any signs of
gross memory deficits. More recent studies, however, have shown that
alcoholics might suffer mild deficits in learning and memory. In one study, Ryan
and Lewis (1988) investigated the validity of the WMS-R by comparing scores of
recently detoxified chronic alcoholics with matched controls. Results indicated
that alcoholics performed significantly worse on all five WMS-R index scores as
compared to controls. Moreover, the pattern of performance was comparable
between the two groups.

Other studies that looked at the different components of memory function
(learning, recall, retention etc.) have also found deficits among alcoholics. Using
a revised scoring method of the WMS, Nixon, Kujawski, Parsons, and Yohman
(1987) compared the semantic and figural memory abilities of detoxified male
alcoholics with control subjects. Findings indicated that both immediate and
delay recall of verbal and figural materials were significantly worse among
alcoholics than controls. Surprisingly, alcoholics did not Show greater deficits on
the recall of figural material than verbal material, suggesting that the levels of
impairment might be comparable across modalities. Alcoholics and controls also
did not differ significantly in rate of forgetting (retention ability), indicating that the
ability to retain learned materials was relatively intact among alcoholics. The
authors concluded that the memory deficit found in alcoholics might lie in the
initial acquisition process.

More recently, Sherer, Nixon, Parsons, and Adams (1992) reported that

alcoholics performed better on verbal memory functioning than brain damaged

patients. Moreover, alcoholics were significantly slower in acquiring verbal
information, suggesting that alcoholic memory deficits might be the result of
inferior acquisition processes rather than retrieval difficulties. Beatty, Hames,
Blanco, Nixon, and Tivis (1995) also found that alcoholics displayed deficits on
measures of anteriograde spatial memory (Figural Memory Test, Rey-Osterrieth
Figure, and New Map Test). Overall, alcoholics had greater difficulties learning
and remembering unfamiliar spatial objects than controls. The findings indicated
that these deficits were related to both the failure to acquire spatial information
and poor retention ability.

Some researchers have posited that alcoholism results in premature aging
of memory functioning. Kramer, Blusewicz, and Preston (1989) tested this
hypothesis by comparing the memory perforrnanoe of younger alcoholics and
older non-alcoholics. Using the California Verbal Learning Test (CVLT), the
authors showed that the effects of alcoholism and aging on memory functioning
were quite different. Although alcoholism and aging were found to be associated
with measures of immediate and delay recall, younger alcoholics performed more
poorly on recognition and produced more frequent intrusion and false positive
errors than older non-alcoholics.

Visuospatial Abilig

There is consistent evidence to support the finding that chronic alcoholics
have visuospatial deficits. For example, using a paired-associate learning
paradigm, Shelton, Parsons, and Leber (1984) examined the verbal and

visuospatial abilities of chronic alcoholic patients and matched controls. Results

showed that alcoholics performed significantly worse than non-alcoholics on
visuospatial learning. In contrast, no differences in verbal learning were found.
In another study, Kramer, Blusewicz, Robertson, and Preston (1989) assessed
the effect of chronic alcoholism on visuospatial processing ability using the Block
Design test from the WAIS-R. Male chronic alcoholics were found to have
greater difficulties completing the designs than controls. Analyses of the
configuration patterns showed that alcoholics were more likely to make errors on
the outer configuration of the design. These findings suggested that chronic
alcohol use might have a negative effect on visuospatial information processing.

Beatty, Hames, Blanco, Nixon, and Tivis (1995) also reported that
inpatient alcoholics performed poorly on several visuospatial measures including
Block Design, Rey-Osterrieth Complex Figure, and Benton Line Orientation Test.
Specifically, alcoholics made less accurate copies on the Rey-Osterrieth,
indicating difficulties in judging position of objects in space in relation to one
another. They also displayed poorer visuospatial scanning and construction
abilities as compared to controls. Further analyses revealed that alcoholics were
more likely to break configuration design on the Block Design test and made
more searching errors on the Letter/Symbol Cancellation Task.

More recently, Sher, Martin, Wood, and Rutledge (1997) studied the
relationship between alcohol use disorders and neuropsychological functioning in
young adults. Five neuropsychological factors were examined: language/verbal
memory, visuospatial ability, motor speed, Booklet Category performance, and

attention. Results indicated that subjects who met criteria for alcohol use

disorders performed more poorly on measures of visuospatial ability than those
with no alcohol diagnosis. Moreover, subjects with alcohol dependence showed
greater deficits in visuospatial ability and motor speed as compared to those with
alcohol abuse. Sher and his colleagues concluded that alcohol use disorders are
associated with deficits in visuospatial ability and the severity of the deficits may
depend on the type of diagnosis.
Executive Functioning

Detoxified alcoholics have been shown to exhibit problems in abstract
planning and reasoning abilities, which are thought to be mediated by the frontal
brain region (Grant, 1987, Rourke & Loberg, 1996). Using the California Card
Sorting Test, Beatty, Katzung, Nixon, and Moreland (1993) studied the
abstraction and concept formation abilities of a group of inpatient alcoholics and
matched controls. Subjects were presented with multiple sets of six cards each
and were asked to sort them into two groups with three cards in each group.
Each card had several different features (e.g. size, shape, color, nature of words)
and could be sorted into different groups based on the sorting principles. When
sorting was completed, subjects were asked to explain the principle they used to
sort the cards. Results showed that alcoholics identified fewer correct concepts
as compared to controls, suggesting deficits in abstraction abilities. Moreover,
alcoholics were unable to provide explanations of the concepts that they correctly
identified. These findings indicated that alcoholics have difficulties isolating
relevant information and eliminating non-relevant information. Beatty and his

colleagues also reported that alcoholics made more perseverative sorts and

10

perseverative verbalization. It appeared that these errors are independent of the
abstraction deficits and contributed to their overall difficulties in performing
problem-solving tasks. Other studies using the Wisconsin Card Sort Test and
Category Test have also shown that alcoholics exhibit deficits in abstract
reasoning and perseveration errors (Adams et al., 1993; Grant & Reed, 1985;
Ron, Acker, & Lishman, 1980; Steingass, Sartory, & Canavan, 1994; Sullivan et
aL,1993)

Another neuropsychological test many studies have used to measure
abstract planning is the Mazes test. This test provides a visuospatial
assessment of motor planning, organization and goal directed behavior.
Performance on Mazes is considered to depend on planning ability and foresight,
which are cognitive abilities thought to be mediated by the frontal brain system.
Bowden (1988) examined the performance of twenty male alcoholics using a test
of complex maze learning and found that alcoholics performed worse than
matched controls. Using the Porteus Maze Test, MacDonell, Skinner and Glen
(1987) also found that Chronic alcoholics had greater difficulties with planning
ability than controls.

In summary, chronic alcoholics have been found to exhibit deficits in
various neuropsychological functions including teaming and memory,
visuospatial ability, and executive functioning. While the poor cognitive outcome
of alcoholics is relatively well established, the exact mechanism of such effects is

still largely unknown.

11

Neuropsychological Models of Alcoholism

Acute alcohol intoxication has been shown to have a negative effect on
cognitive performance (Golby, 1989). In one study, Peterson, Rothfleisch,
Zelazo, and Pihl (1990) examined the hypothesis that acute alcohol intoxication
will produce cognitive change that is similar to the neuropsychological
impairment suffered by individuals with prefrontal damage. Seventy-two
moderate social drinkers were tested on tasks associated with frontal cortex (e.g.
Porteus Maze Test), temporal cortex (e.g. Logical Memory of the WMS-R), and
parietal-occipital cortex (e.g. Albert's Simple Test of Visual Neglect) after they
received one of three different doses of alcohol: high (1.32 mllkg), medium (0.66
mllkg), and low (0.132 mllkg). The results indicated that a high dose of alcohol
significantly impaired such cognitive functions as planning, verbal fluency,
memory, and complex motor control.

In cases of chronic alcohol abuse/dependence, three different theoretical
models have been proposed to describe the specific action of alcohol on the
brain.

Diffuse Dysfunction Model

First, the diffuse dysfunction model suggests that alcohol
abuse/dependence might cause non-specific neurological damage (Parsons &
Leber, 1981). Early evidence for this model has come from the results of
neuropathological studies that showed alcoholics suffer diffused brain damage
(Courville, 1955; Mancall, 1961). For instance, Lynch (1960) examined the brain

of eleven chronic alcoholics at postmortem and found that 20 to 40% of the

12

cortical cells were lost. However, since the majority of the subjects in these
studies were elderly, aging may have contributed to the neuronal damage
observed in some of these studies.

Goldstein and Shelly (1982) compared the neuropsychological profile of
patients with various types of brain damage (frontal, right hemisphere, or diffuse)
with chronic alcoholic inpatients. The results indicated that neuropsychological
impairments exhibited in alcoholics resemble the deficits found in patients with
non-alcoholic diffuse brain damage rather than the deficits found in patients with
frontal lobe damage. Moreover, the authors noted that the measures used in
this study may not be selective enough to rule out specific damages to the brain
(e.g. frontal lobe). Despite the significant findings, Goldstein (1987) warned that
the diffuse dysfunction model is not sufficient to explain the pattern of
neuropsychological deficits found among all alcoholics. He further suggests that
genetic and antecedent cognitive functioning may play a role in the cognitive
functioning of different alcoholic subtypes.

More recently, Tivis and Parson (1995) argued that the reason that
chronic alcoholics do not show verbal deficits is because the tasks are often well
Ieamed and well rehearsed. The authors studied the verbal-spatial and visual-
spatial functioning of alcoholics to determine if damages are present in both
hemispheres. Results indicated that alcoholics performed worse on both verbal-
spatial and visual-spatial tasks, suggesting that chronic alcohol use might affect

brain functioning in a non-specific manner.

13

fight Hemisphere Deficit Model

The second model proposes that the right hemisphere of the brain is more
prone to damage from alcohol abuse/dependence than the left hemisphere
(Leber, Jenkins, and Parsons, 1981; Berglund, Hagstadius, Risberg, Johanson,
Bliding, & Mubrin, 1987). Early evidence for this model has come from
neuropsychological studies that showed alcoholics performed much worse on
task that are innervated by the right hemisphere. For example, Chandler and
Parsons (1977) reported that acute alcohol intoxication impaired recognition and
memory performance when material was presented to the left visual field, while
the performance was equal to controls when material was presented to the right
visual field. Moreover, several studies have indicated that chronic alcoholics
displayed impaired performance on visual spatial tasks, functions that are
thought to be mediated by the right hemisphere (Kramer, Blusewicz, Robertsons,
& Preston, 1989; Parsons & Leber, 1982; Wilkinson, 1987).

More recent studies have failed to validate this model (Ellis & Oscar—
Berman, 1985; Oscar-Berman & Weinstein, 1985). In one study, Akshoomoff,
Delis, and Kiefner (1989) administered the Block Design subtest of the WAIS-R
to four groups of subjects: detoxified chronic alcoholic men, right hemisphere
damaged men, left hemisphere damaged men, and normal male controls.
Analyses of block construction strategies and errors revealed that alcoholics did
not suffer visuospatial impairment which was seen in right hemisphere damaged
subjects. Moreover, their strategies and errors fell between the left and right

hemisphere damaged patients suggesting that both hemispheres might be

14

damaged as a result of Chronic alcohol abuse.
Frontal Lobe Deficit MOE

The frontal lobe deficit model suggests that alcohol-induced brain damage
is specifically concentrated in the anterior-basal region including the frontal,
Iimbic and diencephalic structures (T arter, 1975). According to Ron (1977),
autopsy reports of chronic alcoholics have shown that the frontal brain region is
more susceptible to damage and the damage is often more severe as compared
to the rest of the brain.

Results of neuropsychological investigations on alcoholics also concur
with the frontal lobe deficit model (Bergman, 1987; Gebhardt, Naeser, & Butters,
1984; Ron, 1987). For example, Steingass, Sartory, and Canavan (1994)
examined the cognitive functioning of 105 chronic alcoholics between the age of
28 and 69. Results showed that chronic alcoholics suffer a decline in IQ and
learning ability. Further analyses of the data revealed that alcoholics exhibit
perseveration and impaired ability to find semantic categories, both of which are
associated with frontal lobe dysfunction. Similarly, Gilman et al. (1998) examined
the neuropsychological functioning of chronic alcoholic patients and found that
they performed poorly on the Halstead Impairment Index, Halstead Category
Test, and Wisconsin Card Sort Test, all of which are known to be sensitive to
frontal lobe pathology. In addition, these researchers showed that the
neuropsychological performance of alcoholics was correlated with the metabolic

abnormality found in the frontal region of the cerebral cortex.

15

Most recently, Ratti et al. (1999) reported that heavy drinkers (daily
alcohol intake was more than 100 grams for at least the past 15 years) exhibited
deficits in attentional abilities. In contrast, no differences between alcoholics and
controls were noted on visuospatial measures. Neuroradiological data
(localization of morphological cerebral changes) showed that alcoholics suffered
widespread cortical and subcortical atrophy although the atrophy is more marked
in frontal lobes than in the other structures. Ratti and her colleagues concluded
that these findings were consistent with the frontal lobe deficit hypothesis.

Mediating Factors

Although there is evidence to support the claim that alcohol causes
neuropsychological deficits, the exact mechanism is still relatively unknown. In
addition, other factors might also have an influence on the neuropsychological
outcome of chronic alcoholics. The following section reviewed studies that have
examined the influence of comorbid psychiatric disorders, neuromedical
problems, and drinking history on neuropsychological differences in alcoholics.
Psvchiatric Disorders

The comorbidity of psychiatric disorders (e.g. personality disorders,
depression, anxiety) among chronic alcoholics is quite common. For example,
DeJong, Van den Brink, Harteveld, and Van der Wielen (1993) reported that 78%
of hospitalized alcoholics had received at least one personality disorder
diagnosis. More recently, Penick et al. (1994) investigated the lifetime
comorbidity of major psychiatric disorders in male alcoholics drawn from six

Veterans Administration Medical Centers. Results indicate that 62% of the

16

subjects met the Psychiatric Diagnostic Interview (PDI) criteria for alcoholism and
at least one additional psychiatric disorder. Moreover, depression and antisocial

personality were the most common co-occurring disorders reported by alcoholics
(36% and 24% respectively).

A number of researchers have studied the relationship between
depression and alcohol use disorders (Brown & Schuckit, 1988; Schuckit, Irwin,
& Smith, 1994). For instance, Brown, Inaba, Gillin, Schuckit, Stewart, and lrvvin
(1995) examined the level of depressive symptoms among hospitalized patients
who met diagnostic criteria for alcohol dependence and/or affective disorder.
Upon admission, 42% of alcoholics reported experiencing depressive symptoms
that reached Clinical significant levels (based on the Hamilton Rating Scale for
Depression). After 3 weeks of abstinence, only 6% of alcoholics continued to
present elevated levels of depressive symptoms.

Depression has also been shown to affect the neuropsychological
performance of alcoholics. For example, Loberg (1980) reported that depression
was significantly related to impaired scores on Performance ID in alcoholics. He
later suggested that the poor performance might be linked to the lack of
motivation and psychomotor retardation associated with depression (Loberg,
1986). Sinha, Parsons, and Glenn (1989) also studied the relationship between
depression and neuropsychological performance in alcoholics. Results showed
that depression, as measured by the Beck Depression Inventory, significantly
correlated with the overall impairment index regardless of the family history of

alcoholism. The authors concluded that depression could potentially be a

17

confounding factor in the relationship between alcohol use and cognitive
functioning.

More recently, Schafer et al. (1991) conducted a longitudinal study that
examined the role of depression on cognitive peIfom'Iance in detoxified male
alcoholics. A brief neuropsychological battery (Trail Making Test, Digit Symbol
and Vocabulary of WAIS, and Visual Search Test) was administered to all
subjects Upon admission to the hospital, before discharge, and 3 months
afterward. Results showed that depression was a significant factor in predicting
neuropsychological performance at admission. However, upon discharge
(several weeks later), only premorbid intelligence significantly predicted
neuropsychological scores. The authors concluded that levels of depression
have a negative impact on the cognitive functioning of alcoholics.

The relationship between antisocial personality and alcoholism has also
been studied extensively. In indeed, research has indicated that there are at
least two different types of male alcoholics: antisocial and non-antisocial
alcoholic (Cloninger, 1987; Zucker, Ellis, & Fitzgerald, 1993; Zucker, 1994).
Antisocial alcoholics are likely to drink more alcohol, have an earlier onset of
alcoholism, display more alcohol-related problems, and have more co-morbid
psychopathology such as depression and anxiety as compared to alcoholics
without antisocial personality (Hesselbrock, Meyer, & Keener, 1985; Zucker,
1987). Moreover, it has been hypothesized that among alcoholics with antisocial
personality (ASP), brain systems that modulate behavioral responses to the

effects of alcohol and other environmental stimuli may differ from those of other

18

alcoholics (Cloninger, 1987). Consistent with this hypothesis is the finding that
alcoholics with ASP exhibit a variety of neuropsychological impairments. In one
study, Malloy, Noel, Rogers, Longabaugh and Beattie (1989) examined how age,
gender, years of drinking, and ASP affected neuropsychological functioning of
alcoholics. Alcoholics with co-morbid ASP were found to be more impaired on a
variety of neuropsychological measures (WAIS, WMS, and the Halstead-Reitan
Neuropsychological Battery) than were alcoholics without co-morbid ASP. When
the effect of age, gender, and years of drinking were controlled, ASP still
contributed significantly to the cognitive impairment.

More recently, Glenn, Errico, Parsons, King, and Nixon (1993) examined
the role of antisocial, affective, and childhood behavioral Characteristics in the
neuropsychological performance of alcoholics. Although all subjects did not
meet a clinical diagnosis of anxiety, depression, or antisocial personality, all three
factors were found to be negatively related to cognitive performance in
alcoholics. In another study, Waldstein, Malloy, Stout, and Longabaugh (1996)
found that the path to neuropsychological impairment differed for antisocial and
non-antisocial alcoholics. For antisocial alcoholics, cognitive deficits were
predicted by less education, Childhood symptoms of conduct disorder, drinks per
day, and history of head injury. Conversely, cognitive performance of non-
antisocial alcoholics was predicted by self-reported history of diagnosed attention
deficit disorder, verbal learning disability, and symptoms of nonverbal teaming
disability. These findings suggest that neuropsychological functioning of

alcoholics may be mediated by co-occurring antisocial personality disorder.

19

Neuromedical Risk

Studies have indicated that poor physical health is associated with chronic
alcohol use. For example, Glenn, Parsons and Stevens (1989) reported that
alcoholics had significantly more health problems than community controls in four
physical health domains: medical problems, alcohol-related disorders, trauma
history, and drug use. Moreover, various medical problems including head injury
and liver disease might also contribute to the neuropsychological deficits found in
chronic alcoholics (Rourke and Loberg, 1996). In one study, Adams and Grant
(1986) investigated the influence of neuromedical risk factors on
neuropsychological functioning in recently detoxified alcoholics. Seven domains
of neuromedical risk were evaluated: early developmental, learning disability,
head injury, toxicity, neurological, anoxic, and sick risk. Subjects who endorsed
one or more risk items were Classified as “at risk”. Results indicated that recently
detoxified alcoholics with positive neuromedical risk performed worse than those
without on all neuropsychological measures. Moreover, the impairment exhibited
by recently detoxified alcoholics was beyond the additive effects of aging, alcohol
status and risk. The authors concluded that neuromedical risk negatively
affected the neuropsychological performance in the recently detoxified alcoholics
and suggested that history of neuromedical risk might predispose alcoholics to
neuropsychological deficits as a result of drinking.

Head injury is one of the neuromedical problems that might influence the
neuropsychological performance of alcoholics. For example, HillBom and Holm

(1986) reported that alcoholics who sustained traumatic brain injury performed

20

worse than those who did not admit to having suffered any brain injury on the
Halstead-Reitan Neuropsychological Battery (e.g. Finger Tapping, Tactual
Performance Test, Trails Making Test). No such differences were found in the
control group. The authors concluded that head injury might cause more
extensive damage to the brain in alcoholics than non-alcoholics.
Drinking Histom

Several studies have explored the relationship between drinking patterns
and neuropsychological functioning. For example, Svanum and Schladenhauffen
(1986) reported that increasing lifetime alcohol consumption was related to level
of impairment on the Category Test and Trails Making B, suggesting deficits in
higher cognitive functioning (i.e. set-shifting, concept formation). Further
regression analysis revealed that lifetime drinking total predicted the level of
impairment. In addition, increasing years of heavy drinking was found to be
related to an increasing frequency of impairment on Halstead-Reitan tests.
Eckardt, Stapleton, Rawlings, Davis, and Grodin (1995) also found that greater
lifetime alcohol consumption predicted poorer performance on the several
neuropsychological measures including the Boston Naming Test, Speech Sound
Perception Test, and Rey-Osterrieth Complex Figure. In addition, alcoholics with
longer period of abstinence (10 or more weeks) showed better
neuropsychological performance than those with shorter period of abstinence
(less than 2 weeks).

More recently, Homer, Waid, Johnson, Latham, and Anton (1999)

examined the relationship between neuropsychological functioning and alcohol

21

consumption in alcoholics. Findings indicated that recent amount of alcohol
consumption (last 3 months) was related to mild cognitive deficits in verbal
memory and reaction time. Specifically, recent alcohol consumption was
negatively correlated with verbal and visuospatial memory, executive functions,
and cognitive speed. In another study, Beatty, Tivis, Stott, Nixon, and Parsons
(2000) examined the relationship between neuropsychological functioning of
alcoholics and consumption variables. Results showed that long-term (10 or
more years) and short-term (4 to 9 years) alcoholics did not differ in the pattern of
neuropsychological deficits (SILS Vocabulary and Abstraction Scales and Digit
Symbol of WAIS-R) as both group performed more poorly than controls.
Moreover, measure of recent drinking history accounted for almost 5 percent of
the variance in neuropsychological performance of alcoholics. In contrast, no
relationship between length of drinking and neuropsychological impairment was
noted. Beatty and his colleagues cautioned that the neuropsychological
measures they used were not complete and other measures such as Block
Design and Object Assembly of the WAIS, which assess visuospatial information
processing, might be more sensitive to detecting deficits in chronic alcoholics.
Length of abstinence might also have an influence on the
neuropsychological functioning in alcoholics. Rourke and Grant (1999) reported
that recently detoxified alcoholics exhibited various neuropsychological deficits
including, abstract reasoning, learning, and complex perceptual-motor
integration. Moreover, those who resumed drinking in the two-year follow-Up

period continued to Show neuropsychological deficits in abstraction and cognitive

22

flexibility, complex perceptual-motor functioning, and simple motor skills. On the
other hand, those who continued to stay abstinent showed significant
improvement in abstraction and cognitive flexibility regardless of their age. Most
importantly, the study showed that the neuropsychological performance of long-
terrn abstinence alcoholics (average of 4.3 years of abstinence) was comparable
to matched controls, suggesting that long-term abstinence might lead to normal
neuropsychological status. The authors noted that the extent of the
neuropsychological recovery might depend on the age at which the alcoholic
stops drinking and the type of neuropsychological ability.

Based on the literature review, chronic alcohol use appears to have a
negative impact on cognitive functioning. However, the underlying mechanisms
mediating the relationship between alcoholism and neuropsychological deficits
offer many possibilities. Several theoretical models have been proposed to
explain the neuropsychological deficits observed in alcoholics, although none of
them are able to definitively capture the relationship. Furthermore, factors other
than the presumed direct neurotoxic effect of alcohol might influence the
neuropsychological consequences of alcoholism (see Figure 1). Alcoholism is a
multidimensional disorder with strong associations to other psychiatric disorders
and health problems. These alcohol-related factors could play an important role

in determining the neuropsychological functioning of alcoholics.

23

PROPOSED STUDY

The proposed study sought to examine the effects of alcohol on
neuropsychological outcome among community alcoholics and non-alcoholics.
The use of non-clinically accessed alcoholics made the sample more
representative of alcoholics and their families than is generally true of treatment
populations. Four domains of neuropsychological functioning (i.e. memory,
visuospatial, perceptual motor, and executive functioning) were assessed using
the MicroCog, the Wechsler Adult Intelligence Scale-Revised (WAIS-R), and the
Symbol Digit Modality Test (SMDT). In addition, Full Scale IQ score from the
WAIS-R and the General Cognitive Functioning Index from the MicroCog were
used to assess general cognitive ability (see Figure 1). These measures were
Chosen specifically to examine the validity of the three different
neuropsychological models of alcohol abuse as described in the literature review
section. The diffuse dysfunction model suggests that alcoholics would show
poorer general cognitive ability as well as relative deficits across all
neuropsychological measures. The right hemisphere model predicts that
alcoholics would perform worse on visuospatial tasks alone. In contrast, the
frontal lobe deficit model predicts that alcoholics would show selective deficits in
tasks that assess executive functioning.

The second goal of this study was to examine variables that might
influence the neuropsychological outcome of alcoholics. Three major sources of

variance were explored: psychiatric disorders, neuromedical risk, and drinking

24

history. The disorder that is of greatest interest is mood disorder, which was
estimated by the Hamilton Depression Scale. Neuromedical risk was determined
based on the number of nervous system related neuromedical problems subjects
endorsed on the Health History Questionnaire. Finally, drinking history was
assessed using the Drinking and Drug Use Questionnaire. Specifically, history of
alcoholism, current alcohol problems, and recent alcohol consumption were used

to assess subjects” drinking pattern.

25

HYPOTH ESES

. Neuropsychological deficits would be most severe among alcoholics who also
met the DSM-IV diagnostic criteria for antisocial personality disorder (i.e.
antisocial alcoholics). Moreover, executive functioning tasks would be most
impaired, supporting the frontal lobe deficit model. Non-antisocial alcoholics
would form an intermediate group that would show poorer neuropsychological
functioning across all measures than controls.

. Antisocial alcoholics would most likely be classified as suffering from “brain
impairment” as compared to non-antisocial alcoholics and controls. Non-
antisocial alcoholics would also more likely be classified as suffering from
“brain impairment” than controls.

. Drinking variables would mediate a poorer neuropsychological outcome.
Moreover, history of alcoholism would be the strongest predictor among all
drinking variables.

. A greater history of alcoholism would directly predict increased neuromedical
risks, higher current levels of depression and poorer memory functioning. In
addition, increased current neuromedical risks and higher current level of
depression would simultaneously predict poorer memory functioning.

A greater history of alcoholism would directly predict increased neuromedical
risks, higher current levels of depression and poorer perceptual motor

functioning. In addition, increased neuromedical risks and higher current

26

level of depression would simultaneously predict poorer perceptual motor
functioning.

. A greater history of alcoholism would directly predict increased neuromedical
risks and higher current alcohol consumption. In addition, increased
neuromedical risks and higher current alcohol consumption would
simultaneously predict poorer visuospatial functioning.

. A greater history of alcoholism would directly predict increased neuromedical
risk, higher levels of current alcohol consumption and poorer executive
functioning. In addition, increased neuromedical risk and current alcohol

consumption would simultaneously predict poorer executive functioning.

27

METHOD

Participants

Subjects for the present study were drawn from the University of Michigan
- Michigan State University Longitudinal Study (Zucker et al., 2000). This
ongoing longitudinal project utilizes population-based recruitment strategies to
access alcoholic men and their families and a contrast group of families with non-
substance abusing parents. During the initial contact, all families were invited to
participate in a long-term study of family and health and child development.
Families were assessed at three-year intervals beginning at Wave 1 when the
male target child (MTC) was age 3 to 5. All families received some payment for
participation in each data collection interval.

Alcoholic families were recruited by way of father’s drinking status.
Alcoholic fathers were identified in one of two ways. The first group was
recruited from the population of all convicted drunk drivers in a four county area
of mid-Michigan. Thereafter, all males meeting the family recruitment criteria
involving child age and coupling status who had a blood alcohol concentration
(BAC) of 0.15% (150 mg/100 ml) or higher when arrested, or a BAC of 0.12% if a
history of prior alcohol-related driving offenses existed, were asked for
permission to have their names released for contact by study staff. 79% agreed
to have their name released, and of those, 92% agree to participate. At initial
contact, a positive alcoholism diagnosis was established using the Short

Michigan Alcoholism Screening Test (SMAST; Selzer, 1975); this diagnosis was

28

subsequently verified by way of the NIMH Diagnostic Interview Schedule-Version
lll (DIS; Robins, Helzer, Croughan & Ratcliffe, 1980). All of these men met a
‘definite’ or ‘probable’ criterion for alcoholism using the Feighner Diagnostic
Criteria (Feighner, Robins, Guze, Woodruff, Winokur, & Munoz, 1972), with 92%
making a ‘definite’ diagnosis. Later, DSM-lll-R diagnoses were also established
although this was not a basis for study inclusion; 73% of the alcoholic men met
either moderate or severe alcohol dependence criteria.

The second strategy involved recruiting alcoholic fathers out of the same
neighborhoods where drunk driver alcoholic fathers resided. These families were
accessed during neighborhood canvasses for nonalcoholic (control) families.
Thus, they provided an ecologically comparable subset of high risk families
drawn out of the same social stratum as the drunk drivers, but where the
alcoholism was identified by way of community survey rather than by way of legal
difficulty. These alcoholic fathers also met Feighner criteria for probable or
definite alcoholism (85% made a definite diagnosis), had children and partners
who met the same inclusion criteria as the drunk driving group, but had no drunk
driving or drug involved arrest record occurring during the lifetime of the 3 to 5
year old target child.

In addition to alcoholic families, a group of community control families
were recruited via door-to-door community survey techniques. These families
were recruited out of the same neighborhoods as neither parent met Feighner
criteria for alcoholism or for other drug abuse/dependence. In addition, efforts

were made to match control families with alcoholic families on the basis of family

29

socioeconomic status by recruiting controls from the same neighborhood in
which the risk family lived. Canvassers initiated a door-to-door search a block
away from the alcoholic family, staying within the same census tract, and
screened for nonalcoholic families with a child of appropriate age. However, in
some cases locating a neighborhood control proved impossible due to high levels
of drug and/or alcohol abuse among potential control families living in
neighborhoods where the alcoholic families resided. In such cases, the
recruitment moved to an adjacent neighborhood and in some instances it was
necessary to go even more broadly afield in order to locate another socio-
demographically comparable community in which to continue the search. Ninety-
three percent of families who met eligibility criteria as controls agreed to
participate.

At the time this project was carried out, 332 adult from the UM-MSU
Longitudinal Study had completed the neuropsychological battery at Wave 4.
Five participants were omitted from the study due to their large percentages of
missing data (over 20 percent). Table 1 presents a summary of the demographic
information (gender, age, and years of education) for the sample.

Data Collection

Data were collected by trained project staffs who were blind to family risk
status. In most cases, the data were collected during a single campus visit. The
visit involved approximately four hours of contact time for each parent. Contacts
included questionnaires sessions, semi-structured interviews and interactive

tasks. The data used in this study came from Wave 1 to Wave 4.

30

Table 1.

Background Characteristics of Participants

 

 

M §Q
Alcoholics
Male (n=1 02)
Age 42.99 5.47
Years of Education 13.78 2.64
Female (n=66)
Age 39.77 4.59
Years of Education 13.85 2.38
Non-Alcoholics
Male (n=51)
Age 41.70 4.78
Years of Education 15.02 2.50
Female (n=108)
Age 40.81 3.86
Years of Education 13.57 1.86

 

31

Measures

Alcoholism Diagnosis

At the first wave of data collection, information on current and lifetime
prevalence of alcohol problems was gathered using the Short Michigan Alcohol
Screening Test (SMAST) and the Diagnostic Interview Schedule - Version Ill
(DIS; Robin, Helzer, Croughan, Ratcliffe, 1980). The SMAST (Selzer, 1975) is a
well validated inventory used extensively to assess alcohol problem. The DIS is
a structured interview that allows trained lay interviewers to gather extensive
physical, alcohol and drug related, and mental health (symptomatic) information
that can then be computer processed to yield diagnoses by way of the three
major nosological systems in use today (DSM-Ill; Feighner, RDC). At
subsequent waves, all subjects completed the SMAST and DIS again to obtain
information on their current alcoholic problems based on the past three-year
interval. The diagnosis of current or lifetime alcohol abuse/dependence was
made by a trained clinician for each wave of data collection using the DSM-IV
criteria based on the information provided on the SMAST and DIS. For the
present study, an alcoholic was defined as someone who met the DSM-IV criteria
for alcohol abuse and/or dependence during the his/her lifetime.
Alcoholic Subtype

Alcoholic subtype was determined based upon alcoholism diagnosis and
lifetime antisocial personality disorder (ASP) diagnosis. A diagnosis of antisocial
personality disorder (ASP) was made by a trained clinician using the DSM-IV

based on the information provided on the DIS at Wave 1. Unlike alcoholism,

32

which may remit, ASP, as an Axis II disorder, was presumed to be lifelong.
Alcoholics with co-morbid ASP were classified as antisocial alcoholics (AALs)
while those without ASP diagnosis were classified as non-antisocial alcoholics
(NAALs). Finally, those who did not meet criteria for alcoholism and ASP
diagnoses were classified as non-alcoholics. (controls).
Drinking Variables

Current Drinking. Two measures were used to assess subjects’ current
drinking problem: alcohol problems, and alcohol consumption. Both variables
were gathered using the Drinking and Other Drug Use Questionnaire (Zucker,
Fitzgerald, & Noll, 1990). This questionnaire incorporates already much tested
items from the 1978 NIDA Survey (Johnston et al., 1979), from the American
Drinking Practices Survey (Cahalan, Cisin, & Crossley, 1969) and from the VA.
Medical Center (University of California) San Diego, Research Questionnaire for
Alcoholics (Schuckit, 1978). All of the items have been extensively used in a
variety of survey and clinical settings. They provide data on drinking patterns
including age of first drunkenness, quantity, frequency and variability of alcohol
consumption, frequency of drug use, and multiple questions on consequences
and troubles related to the use of these substances. Items have been carefully
reviewed to yield information sufficient to provide diagnoses according to DSM-IV
diagnostic criteria. Alcohol problems were determined based on the total number
of drinking problems subjects endorsed on the instrument (31 items). Recent

alcohol consumption (last month) was calculated based on the average number

33

of days per month subjects had a drink and the number of drinks on a day when
they drank.

HistorLof Alpoholism. Alcoholism diagnosis was coded based on the
severity of the alcoholism (0 = no diagnosis, 1 = alcohol abuse, 2 = alcohol
dependence without physical dependence, and 4 = alcohol dependence with
physical dependence). History of alcoholism was created by adding each subject
lifetime alcoholism diagnosis at Wave 1 and the three-year diagnosis at each
subsequent Wave. This variable was designed to capture both the chronicity and
the severity of the subjects’ alcoholism.

Neuropsychological Domains

Table 2 presents a summary of the measures used in assessing
neuropsychological functioning at Wave 4.

General Cognitive F pnctioning, Two measures were chosen to assess
general cognitive ability: Full scale IQ from Wechsler Adult Intelligence Scale-
Revised (WAIS-R; Wechsler, 1981) and the General Cognitive Functioning Index
from the MicroCog (Powell, Kaplan, Whitla, Weintraub, Catlin, & Funkenstein,
1994). The short form of the WAIS-R was administered to each adult in the
study. This test has a composite reliability of .88 and has been demonstrated to
be a valid predictor of Full Scale IQ in normal adults (Reynolds et al., 1983) and
in neurologically impaired individuals (Ryan, 1985). Evidence generally supports
the use of the short form for research when characterizing group performance
(Silverstein, 1990; Schretlen, Benedict, & Bobholz, 1994). The short form of the

MicroCog is a computer administered and scored test that assesses global

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35

integrity of neurocognitive functions (Powell et al., 1994). The protocol utilizes 12
subtests covering the following five domains: a) mental control, b) memory, c)
calculation/reasoning, d) spatial processing, and e) processing speed. The
subtests administered in the Short Form version include Number Forward and
Reversed, Wordlist, Story 1 and 2 and Address, Analogies, Math Calculation,
Clocks, and Timers. An index score representing global functioning is formed
based on the subject’s overall performance. The average reliability coefficient for
this score is .94.

Memorv Fpnctioning; Two subtests from the MicroCog (Story Immediate
Recall and Story Delayed Recall) were used to assess memory functioning. The
two tests are analogous to those on the Wechsler Memory Scales. Green,
Green, Harrison, and Kutner (1994) reported that immediate and delayed stories
correlated moderately (.63) with immediate and delayed Logical Memory on the
WMS-R. The reliability coefficients for Story Immediate Recall and Story
Delayed Recall are .64 and .78 respectively.

Visuospatial Functioning. Three measures were selected to assess
visuospatial functioning: Clocks from the MicroCog, Picture Completion from the
WAIS-R, and Block Design from the WAIS-R. The Clocks subtest is similar to
the traditional Clock drawing task. Seven clock faces were presented in turn with
hands but no numbers. The subject had to choose the correct time from among
five Choices. Picture completion is a task that required the subject to identify a
missing portion of a picture. Block design is a task that required the subject to

replicate geometric designs using colored blocks. The reliability coefficients for

36

these measures are .69 (Clocks), .81 (Picture Completion), and .87 (Block
Design).

Perceptual Motor Fpnctioning Perceptual motor functioning was
assessed using the Symbol Digit Modality Test (SDMT, Smith, 1991). This test
was developed to evaluate cerebral dysfunction in children and adult. Numerous
studies with over 1000 subjects have demonstrated the sensitivity of this
neuropsychological screening test for detection of cerebral dysfunction.
According to Res (1979), scores 1.5 standard deviation below age norm means
are suggestive of cerebral dysfunction. Nevertheless, such scores must be
interpreted with caution since scores 1.0 standard deviation below age norm
means are associated with rather high rates of false positives (9-15%).
Significant impairment on both written and oral forms may indicate visual
perceptual, visual scanning, or oculomotor deficits and/or general information
processing impairment. Both the written and oral forms were given to each
subject independently.

Exepptive Fpnctioning; Three measures were used to assess executive
functioning: Wordlist 1, Wordlist 2, and Analogies. All of the measures were
drawn from the MicroCog. Wordlist 1 is task that required the subjects to press
the Enter key whenever a word appears that belongs to a category specified in
each of the four trials. Two categories are phonemic, and the other two are
semantic. Wordlist 2 required the subjects to press the Enter key whenever one
of the sixteen words from the first list appears on the screen. On the Analogies

subtest, the subject was presented a series of 11 relationships and had to

37

choose among the choices displayed. The reliability coefficients for these
measures are .91 (Wordlist 1), .92 (Wordlist 2), and .62 (Analogies).
Neuromedical Risk

The Health History Questionnaire (Carpenter & Lester, 1980) was used to
assess personal health and illness status in fifteen areas: hospitalization history;
current medication use; allergies; prior illnesses; skin and hair problems; eye,
ear, nose, and throat symptoms; heart and lung; G.l. tracts; skeleton and joints;
nervous system; alcohol and drug use; general health care patterns; diet and
weight control; physical fitness activities; pregnancy and delivery. Neuromedical
risk was determined based on the total number of endorsements for the following
items drawn from the nervous system section: frequent or severe headaches,
loss of balance or dizziness, loss of consciousness, head injury, and persistent
numbness or tingling of hands or feet.
Depression

The Hamilton Rating Scale for Depression (HRSD; Hamilton, 1960) was
used to assess level of depression. This rating covered a variety of behavioral,
affective, somatic, and psychological dimensions associated with depression,
and the score is based on the subject’s responses as well as the clinician’s
judgments. The clinician made both a current depression rating and a rating of
the level of the subject’s depression within the last three years when they were
most depressed. The current studied used the worst ever rating for the past

three year. lnterrater reliabilities are ranged from .80 to .90 (Hamilton, 1960).

38

RESULTS

Missing Data
Three hundred and thirty-two adults from the UM-MSU Longitudinal Study

had completed the neuropsychological assessment at Wave 4. Before beginning
analyses, all variables were screened for missing data. Five participants were
omitted from the analyses due to their large percentages of missing data (over 20
percent). In addition, two participants were excluded from the analysis due to
missing antisocial personality disorder diagnosis. Data imputation was
completed for all missing scores of the remaining 327 participants. A total of 293
(2.1%) data points out of the possible 14,147 were missing. All missing data
were imputed using the Expectation-Maximization (EM) method of maximum
likelihood (ML) estimation. The ML method was chosen because it is considered
to be less biased and more efficient than traditional methods such as pairwise
deletion and mean substitution (Arbuckle, 1996; Enders & Bandalos, 2001).
Descriptive Statistics

Thirty-eight percent of the female participants and sixty-six percent of the
male participants met DSM-IV diagnostic criteria for alcohol abuse and/or
dependence. A series of Multivariate Analysis of Variance (MANOVA) Tests
were conducted to determine whether there were differences in age and
education between groups based on alcoholism diagnosis (DIAGNOSIS). No
significant differences were found on these variables [F (2, 324) = 1.33, p = .27].
Conversely, when the sample was categorized based on alcoholism subtypes

(SUBTYPE), significant differences were noted [F (4, 646) = 3.68, p < .01].

39

Univariate Analyses of Variance (ANOVAs) revealed that the antisocial alcoholics
(AALs), non-antisocial alcoholics (NAALs), and non-alcoholics (controls) differed
significantly on both age [F (2,324) = 3.76, p < .05] and educational level [F
(2,324) = 4.48, p < .05]. Post-hoc comparisons between the three groups using
Tukey Test revealed that NAALs were significantly older than AALs. The results
also showed that AALs had significantly fewer years of education than NAALs
and controls (see Table 3). These results parallel earlier findings from the
longitudinal study (e.g. Zucker, Ellis, Fitzgerald, Bingham, & Sanford, 1996).
Multivariate Analysis of Va_r_igppe_

Hypothesis 1

Hypothesis 1 stated that neuropsychological deficits would be most severe
among AALs and that abstract reasoning tasks would be most impaired,
supporting the frontal lobe deficit model. NAALs would form an intermediate
group that would show poorer neuropsychological functioning across all
measures than controls. To test this hypothesis, a series of MANOVAs were
conducted for general cognitive functioning as well as measures for each of four
neuropsychological domains. Scaled scores were used in the analyses to
ensure that group differences were not attributable to age and educational level.
Means and standard deviations for all dependent variables are presented in
Table 3 — 7. Significance for all multivariate tests was determined using Wilks’
Lambda. In addition, Tukey Tests were used to conduct post-hoc comparisons in

cases where significant main effects were found.

40

Table 3.

Multivariate Analysis of Variance for Background Characteristics based on
Alcoholism Subtypes - Antisocial Alcoholics (AALs). Non-Antisocial Alcoholics

(NAALs), and Non-Alcoholic; (Controls) (N=3gz_)

 

Alcoholism Subtypes

 

 

AALs NAALs Controls
(n=24) (n=144) (n=159)
M(SD) MISD) MISD) F
Age 39.49 42.10 41.10 3.76“
(5.04) (5.34) (4.18)
Years of Education 12.54 14.02 14.04 4.48* a b
(1.53) (2.61) (2.18)

 

* p < .05
a AALs < NAALs, Tukey Test
” AALs < Controls, Tukey Test

41

MI Cognitive Fpnctioning; A MANOVA design was used to examine
the overall main effect of DIAGNOSIS on measures of general cognitive
functioning including Full Scale IQ score and the MicroCog’s General Cognitive
Functioning Index. The results did not yield a significant main effect [F (2,324) =
1.79, p = .17]. A second MANOVA was conducted to determine if general
cognitive functioning differed among alcoholism subtypes (SUBTYPE). The
results were also found to be non-significant [F (4,646) = 1.92, p = .11] (see
Table 4).

Meflgrv Fpnctioning, Two subtests from the MicroCog, Story Immediate
Recall and Story Delay Recall, were used to assess memory functioning.
MANOVA results showed a significant main effect of DIAGNOSIS [F (2,324) =
4.39, p < .05]. Univariate ANOVAS revealed that alcoholics performed
significantly worse than non-alcoholics on Story Immediate Recall and Story
Delay Recall. A second MANOVA was conducted to examine the effect Of
SUBTYPE on memory functioning. The overall main effect was marginally non-
significant [F (4,646) = 2.20, p = .07]. Because of a trend effect, univariate
ANOVAS were conducted and revealed a main effect of SUBTYPE on Story
Immediate Recall. Post-hoc comparisons indicated that NAALs performed
significantly worse than controls on Story Immediate Recall (see Table 5).

Visuospatial Functioning. Three measures were used to assess
visuospatial functioning: Clocks, Picture Completion, and Block Design.
MANOVA results revealed a Significant main effect of DIAGNOSIS [F (3,323) =

2.85, p < .05]. Univariate ANOVAS indicated that alcoholics performed

42

Table 4.

Multivariate Analysis of Variance for General Cognitive Functioning Measures

(N=327)

 

 

Alcoholism Diagnosis

 

 

Alcoholics Non-Alcoholics
(n=168) (n=159)
M (SD) M (SD) F
MicroCog General Cognitive 94.79 97.01
Functioning (13.9) (13.6) 2.14
WAIS Full Scale IQ 104.94 107.10
(10.6) (11.6) 3.10

 

 

Alcoholism Subtypes

 

 

AALS NAALs Controls
(n=24) (n=144) (n=159)
M (SD) M (SD) M (SD) F
MicroCog General 90.04 95.58 97.01 2.76
Cognitive Functioning (15.5) (13.57) (13.6)
WAIS Full Scale IQ 101.51 105.51 107.10 2.90
(9.7) (10.71) (11.6)

 

43

Table 5.

Multivariate Analysis of Vapignce for Memory F pnctionipg Measures (N=3gZ)

 

Alcoholism Diagnosis

 

 

 

 

 

 

Alcoholics Non-Alcoholics
(n=168) (n=159)
M (SD) M (SD) F
Story Immediate Recall 8.64 9.86 8.51**
(3.77) (3.78)
Story Delay Recall 8.56 9.37 5.54*
(3.12) (3.11)
Alcoholism Subtypes
AALS NAALs Controls
(n=24) (n=144) (n=159)
M (SD) M (SD) M (SD) F
Story Immediate Recall 8.83 8.60 9.86 4.28"“I
(4.09) (3.73) (3.78)
Story Delay Recall 8.58 8.56 9.37 2.76
(3.02) (3.15) (3.11)

 

*p <05, ** p < .01

a NAALs < Controls

44

significantly worse than non-alcoholics on Picture Completion and Block Design.
A second MANOVA was conducted to examine the effect of SUBTYPE on
visuospatial functioning. The overall main effect was non-significant [F (6,644) =
1.63, p = .14] (see Table 6).

Perceptual Motor Fpnctioning The SMDT was used to assess perceptual
motor functioning. Only raw scores were available for this measure. Thus, to
determine whether group differences existed after variability in age and
educational level had been accounted for, a multivariate analysis of covariance
(MANOVA) was conducted on the scores with age and years of education as the
covariates. The results showed a significant main effect of DIAGNOSIS [F
(2,322) = 4.47, p < .01]. Univariate ANOVAS indicated that alcoholics performed
significantly worse than non-alcoholics on both the written and oral version of the
SDMT. A second MANCOVA was conducted to examine the main effect of
SUBTYPE on perceptual motor functioning. The results yield a significant main
effect [F (4,642) = 4.60, p < .01]. Univariate ANOVAS revealed that the three
groups differed significantly on both the written and oral scores. Post-hoc
comparisons using Tukey Tests showed AALS performed significantly worse than
NAALS and controls on both the written and oral SDMT. In addition, NAALS
performed significantly worse than controls on oral SDMT (see Table 7).

Executive Fpnctioniryq, Three measures from the MicroCog were used to

 

assess executive functioning: Wordlist 1, Wordlist 2, and Analogies. Results of a
MANOVA did not show a significant main effect of DIAGNOSIS [F (3,323) = 1.77,

p = .15]. However, univariate ANOVAS indicated that alcoholics performed

45

Table 6.

Multivariate Analysis of Variance for Visuospatial Functioning Measures (N=327)

 

Alcoholism Diagnosis

 

 

 

 

 

 

 

Alcoholics Non-Alcoholics
(n=168) (n=159)
M. (S_D) M (E) F
Clocks 11.64 11.52 1.23
(0.91) (1.16)
Picture Completion 11.84 12.50 5.31 *
(2.65) (2.48)
Block Design 11.34 12.03 5.18*
(2.42) (3.03)
Alcoholism Subtypes
AALS NAALs Controls
(n=24) (n=144) (n=159)
M (SD) M (SD) M (SD) F
Clocks 11.58 11.65 11.52 1.18
(1.02) (0.90) (1.16)
Picture Completion 11.31 11.93 12.50 3.26
(2.71) (2.64) (2.48)
Block Design 10.99 11.40 12.03 2.82
(2.30) (2.44) (3.03)
*p < .05

46

Table 7.

Multivariate Analysis of Covariance for Perceptual Motpr Functioning Measures
with Age and Education as Covariance (N=327)

 

 

Alcoholism Diagnosis

 

Alcoholics Non-Alcoholics

 

(n=168) (n=159)
M (SD) M (SD) F
SDMT — Written 55.33 58.54 8.48**
(10.36) (10.25)
SDMT — Oral 63.67 67.27 7.85**
(10.64) (12.54)

 

 

Alcoholism Subtypes

 

 

 

AALS NAALS Controls
(n=24) (n=144) (n=159)
M (SD) M (SD) M (SD) F
SDMT — Written 49.75 56.26 56.53 6.71 ** a b
(9.74) (10.11) (10.25)
SDMT — Oral 59.38 64.38 67.27 5.83“ a b °
(14.56) (10.88) (12.54)
**p < .01
“AALS < NAALS

bAALS < controls
°NAALs < controls

47

significantly worse than non-alcoholics on Wordlist 2. A second MANOVA was
conducted to examine the effect of SUBTYPE on executive functioning. The
main effect was significant [F (6,644) = 2.15, p < .05]. Univariate ANOVAS
indicated a significant effect of SUBTYPE on Wordlist 2. Post-hoc comparisons
using Tukey Test revealed that NAALS performed significantly worse than
controls on Wordlist 2. Univariate also revealed a marginal effect of SUBTYPE
on Analogies. Post-hoc comparisons indicated that AALS performed marginally
worse than controls on Analogies (see Table 8).
Hypothesis 2

Hypothesis 2 stated that AALs would most likely be classified as suffering
from brain impairment as compared to NAALS and controls. NAALS would also
more likely be classified as suffering from brain impairment than controls. It was
originally proposed that Clinical rating of each individual’s neuropsychological
profile would be obtained to determine the likelihood of brain dysfunction.
However, due to difficulties in developing a guideline and finding suitable
clinicians to complete the rating, an alternative approach was developed to test
the hypothesis. Any neuropsychological score that fell below the 8th percentile,
i.e. in the borderline to impaired range, was coded as a positive indicator for
brain impairment. All 12 measures were coded based on the above criteria.
Subjects with three or more positive indicators were classified as having “brain
impairment.”

In order to evaluate the relationship between alcoholism subtypes and

brain impairment, percentages of subjects from each group having three or more

48

Table 8.

Multivariate Analysis of Vflignce forjixecutive Fpnctioning Measures (N=327)

 

Alcoholism Diagnosis

 

 

 

 

 

 

 

Alcoholics Non-Alcoholics
(n=168) (n=159)
M (SD) M (SD) F
Wordlist l 9.95 10.18 0.68
(2.54) (2.65)
Wordlist ll 10.17 10.73 4.05*
(2.63) (2.41)
Analogy 9.96 10.04 0.07
(3.16) (2.75)
Alcoholism Subtypes
AALs NAALS Controls
(n=24) (n=144) (n=159)
M (SD) M (SD) M (SD) F
Wordlist l 9.33 9.94 10.45 1.76
(3.82) (3.22) (3.13)
Wordlist II 10.67 9.79 10.51 3.21"“al
(2.82) (2.75) (2.49)
Analogy 7.75 8.99 9.24 2.39
(3.27) (3.09) (3. 12)
*p < .05.

a NAALS < Controls

positive indictors of neuropsychological impairment were calculated. Results
showed that 20.8% of AALS, 5.6% of NAALS, and 6.3% of controls were
categorized with having significant brain impairment. Odds ratios were
calculated to estimate the relative risk for significant brain impairment. Ratios
that are greater than or equal to three are typically considered as strong effects
(Chassin, Rogosch, Barrera, 1991). Chi-square statistics were used to assess
the degree of association in each 2 x 2 contingency table from which the odds
ratio was calculated. The odds ratio for AALS was calculated to be 3.10 ( x2 =
5.86, p < .05), indicating that AALS were more than three times more likely than
controls to have significant brain impairment. In contrast, the chi-square for
NAALS showed that they did not vary significantly from controls (Odds ratio =
0.89; x2 = 0.07, n.s.) (see Table 9).
Path Analysis

For hypotheses 3 to 7, path analyses were conducted using LISREL 8.3
(JOreskog & SOrbom, 1999). The maximum likelihood procedure was used to
estimate model coefficients and a covariance matrix was analyzed.
Standardized parameters were presented to facilitate interpretation. One tailed
tests (p = .05) was used to determine whether or not each parameter was
significant.
Hypothesis 3

Hypothesis 3 stated that drinking variables would mediate a poorer
neuropsychological outcome. Moreover, history of alcoholism would be the

strongest predictor among all drinking variables. A MIMIC (Multiple Indicators

5O

Table 9.

Relative Risk for Significant Brain lmgirment (N=32_7_)

 

Alcoholism Subtypes

 

 

Antisocial
Alcoholics Controls
(n=24) (n=159)
Number of Positive Impairment
lndictors
0 — 2 19 (79.2%) 149 (93.7%)
3 and above 5 (20.8%) 10 (6.3%)

 

Odds Ratio = 3.10; Pearson Chi-Square = 5.86, p < .05

 

Alcoholism Subtypes

 

Non-Antisocial

 

Alcoholics Controls
(n=144) (n=159)
Number of Positive Impairment
lndictors
0 — 2 136 (94.4%) 149 (93.7%)
3 and above 8 (5.6%) 10 (6.3%)

 

Odds ratio = 0.89; Pearson Chi-Square = 0.07, n.s.

51

and Multiple Causes) model design was used to examine the relationship
between drinking variables and neuropsychological outcome. The three drinking
variables used in the analyses were current alcohol problems, current alcohol
consumption, and history of alcoholism diagnosis. One measure from each
neuropsychological domain (Wordlist 2, Story Immediate Recall, Block Design,
and Hand SDMT) was selected as indictors for the latent variable
“neuropsychological outcome.”

The overall MIMIC model showing the significant standardized coefficients
is presented in Figure 2. The overall goodness of fit for the model was good.
Although the resulting Chi-Square showed significant model-data discrepancies
[X2 (11, M = 329) = 21.12, p < .05], the GFI and CFI were acceptably large (0.98
and 0.98 respectively) and root mean square error of approximation (RMSEA)
was at an acceptable level (.05). Examination of the factor estimates showed
that indicator loadings were statistically significant for the latent construct, i.e.
neuropsychological outcome. Errors of the terms were not allowed to be freely
correlated. Regarding the mediating effect of drinking variables, only history of
alcoholism diagnosis significantly predicted neuropsychological outcome. See
Appendix A for the Lisrel program and the covariance matrix analysis.
Hypothesis 4

Hypothesis 4 stated that a greater history of alcoholism would directly
predict increased neuromedical risks, higher current levels of depression and
poorer memory functioning. In addition, increased neuromedical risks and higher

current level of depression would simultaneously predict poorer memory

52

functioning. Story Immediate Recall was chosen as measure of memory
functioning. Path analysis was conducted to test the validity of the model. The
overall goodness of fit for the model was poor. The Chi-Square indicated
significant model-data discrepancies [x2 (2, M = 329) = 36.35, p < .01]. In
addition, the CF I was smaller than .90 (.19) and RMSEA was above the .05 level
(.23).

To increase model fit, a fifth variable, current alcohol problems was added
to the model. The results indicated improvement in goodness of fit: )8 (4, M =
329) = 40.01, p = .001, GFI = 0.95, CFI = 0.85, and RMSEA = 0.17. To further
refine the model, neuromedical risk was allowed to directly predict current
depression. The modification produced a model that fit the data well: X2 (3, M =
329) = 2.89, p = .41, GFI = 1.00, CFI = 1.00, and RMSEA = 0.00. The final
model showing the significant standardized coefficients is presented in Figure 3.
The structural paths showed that greater history of alcoholism predicted lower
perforrnanoe on memory functioning, higher current level of depression, and
higher level of current alcohol problems. In contrast, none of the immediate
measures, i.e. current depression, current alcohol problems, and neuromedical
risks significantly predicted memory functioning. See Appendix B for the Lisrel
program and the covariance matrix analyzed.

Hypothesis 5

Hypothesis 5 stated that a greater history of alcoholism increased level of

lifetime alcohol use would directly predict increased lifetime neuromedical risks,

higher current levels of depression and poorer perceptual motor functioning. In

53

addition, increased lifetime neuromedical risks and higher current level of
depression would simultaneously predict poorer perceptual motor functioning.
Written score of the SDMT was chosen as measure of perceptual motor
functioning. Path analysis was conducted to test the validity of the model. The
results indicated a poor fit of data. The Chi-Square showed significant model-
data discrepancies [X2 (2, M = 329) = 36.62, p < .001]. In addition, the CFI (0.29)
was unacceptably small and RMSEA (.23) was above the .05 level.

To increase model fit, a fifth variable, current alcohol problems was added
to the model. The revised model showed improvement in goodness of fit: X2 (4,
M = 329) = 40.01, p = .001, GFI = 0.95, CFI = 0.86, and RMSEA = 0.17. To
further refine the model, neuromedical risk was allowed to directly predict current
depression. The modification produced a model that fit the data well: )8 (3, M =
329) = 2.89, p = .41, GFI = 1.00, CFI = 1.00, and root mean square error of
approximation (RMSEA) = 0.01. The final model showing the significant
standardized coefficients is presented in Figure 4. The structural paths showed
that greater history of alcoholism predicted lower performance on perceptual
motor function, higher current level of depression, and higher level of current
alcohol problems. In addition, higher current level of depression predicted poorer
perceptual motor functioning. Neither current alcohol problems nor neuromedical
risks significantly predicted perceptual motor performance. See Appendix C for

the Lisrel program and the covariance matrix analyzed.

Hypothesis 6

Hypothesis 6 stated that a greater history of alcoholism would directly
predict increased neuromedical risks and higher current alcohol problems. In
addition, increased neuromedical risks and higher current alcohol problems
would simultaneously predict poorer visuospatial functioning. Block Design was
selected as a measure of visuospatial functioning. Path analysis was conducted
to test the validity of the model. The model resulted in a good fit of data: X2 (3, M
= 329) = 1.19, p = .76, GFI = 1.00, CFI = 1.00, and RMSEA = .001. The model
showing the significant standardized coefficients is presented in Figure 5. The
structural paths showed that greater history of alcoholism predicted higher level
of current alcohol problems, which in turn predicted lower level of performance
on visuospatial processing. Conversely, greater history of alcoholism did not
predict higher neuromedical risk. Further, neuromedical risk did not predict
poorer performance on visuospatial processing. See Appendix D for the Lisrel
program and the covariance matrix analyzed.

Hypothesis 7

Hypothesis 7 stated that greater history of alcoholism would predict higher
levels of neuromedical risk and current alcohol problems. In addition, increased
neuromedical risk and current alcohol problems would simultaneously predict
poorer executive functioning. Path analysis was conducted to test the validity of
the model. The model resulted in a good fit of data: X2 (2, M = 329) = 1.01, p =
.60 and RMSEA = .000. In addition, the GFT (1.00) and CFI (1.00) were both

exceptionally high. The model showing the significant standardized coefficients

55

is presented in Figure 6. The structural paths showed that greater history of
alcoholism predicted higher level of current alcohol problems and poorer
executive functioning. Conversely, greater history of alcoholism did not predict
higher neuromedical risk. Further, neuromedical risk and current alcohol
problems did not predict poorer performance on executive functioning. See

Appendix E for the Lisrel program and the covariance matrix analyzed.

56

DISCUSSION

Research has shown that alcoholism can lead to neuropsychological
impairment. However, the underlying mechanisms mediating the relationship
between alcoholism and neuropsychological deficits are many in terms of
possibilities. By focusing on the neuropsychological functioning of community
alcoholics, the current study sought to investigate the validity of the three
theoretical models: the diffuse dysfunction model, the right hemisphere deficit
model, and the frontal lobe dysfunction model.

The diffuse dysfunction model holds that alcoholics are more likely to
show poorer general cognitive ability as well as relative deficits across all
neuropsychological domains. Results of the present study showed that
alcoholics and non-alcoholics did not differ on measures of general cognitive
ability. Similarly, no difference in general cognitive ability was observed among
alcoholism subtypes. These findings are inconsistent with the diffuse dysfunction
model. Other studies have also shown that alcoholics do not have lower level of
intelligence. It appears that standard intelligence tests have limited value when it
comes to detecting cognitive deficits among alcoholics.

Although scores on general cognitive functioning did not yield significant
finding, alcoholics were found to have a wide range of relative
neuropsychological deficits. This was evident in three of the four
neuropsychological domains: visuospatial, memory, and perceptual motor

functioning. In addition, AALS were found to perform significantly worse than

57

NAALS and controls on perceptual motor functioning. These results showed that
alcoholics suffer generalized neuropsychological deficits, which are indicative of
diffuse brain dysfunction. More importantly, perceptual motor functioning was
found to be the most significant deficit among AALS and NAALS. SDMT, which
was used to assess perceptual motor ability in the present study, is known to be
a sensitive measure to brain dysfunction (Lezak, 1995). Thus, the poor
performance on SDMT among alcoholics could be interpreted as evidence for the
diffuse dysfunction model.

The right hemisphere model suggests that chronic alcoholism affects
predominantly functions of the right hemisphere. One of the major functions of
the right hemisphere is processing visuospatial information. Therefore, poor
performances in visuospatial tasks could be indications of right hemisphere
damage. Indeed, the current study revealed that alcoholics performed
significantly worse than non-alcoholics on two of the visuospatial measures (i.e.
Picture Completion and Block Design). Conversely, no differences were found
among AALS , NAALS, and controls on visuospatial ability. One of the
visuospatial tasks, Clocks, was proven to be a weak measure due to a marked
ceiling effect. This was likely attributed to the fact that the measure has only a
few items. Overall, these results suggest that alcoholics suffer visuospatial
deficits that might be linked to right hemisphere dysfunction; however, the deficits
are unrelated to alcoholism subtypes.

Although visuospatial deficits were evident among alcoholics, other

deficits including memory and perceptual motor functioning that are not dominant

58

functions of the right hemisphere were also noted in the present study. These
findings are inconsistent with the idea that the right hemisphere is most
vulnerable to damage due to alcoholism. Moreover, some researchers have
argued that visuospatial processing is not an exclusive function of the right
hemisphere. In a recent study, Beatty, Hames, Blanco, Nixon, and Tivis (1995)
examined alcoholics’ performances on two different types of visuospatial tasks:
featural and configural. The authors noted that visuospatial tasks that require
featural analysis (e.g. Picture Completion) are primarily measures of left
hemisphere function, whereas those that require configural analysis (e.g. Block
Design) are mostly measures of right hemisphere function. Results showed that
alcoholics were impaired on both types of visuospatial tasks. A similar
conclusion could be drawn from the results of the current study. It is likely that
the right hemisphere is not specifically more vulnerable to the effect of alcoholism
than the left hemisphere.

The frontal lobe deficit model suggests that frontal lobe functioning is most
susceptible to the effect of alcoholism. Many cognitive functions are associated
with the frontal lobe including selective attention, abstract reasoning, and
planning. In the current study, alcoholics were found to perform significantly
worse than non-alcoholics on only one of the three frontal lobe measures, i.e.
Wordlist 2, suggesting difficulty in selective attention. Similar results were also
observed among alcoholism subtypes. These findings are somewhat surprising
given that research has consistently reported frontal lobe deficits in alcoholics.

One possible explanation is that the measures chosen to assess executive

59

functions in this study might not be sensitive to alcohol abuse. In fact, there are
a number of abilities involved in executive functioning: selective attention,
planning, reasoning, purposive action, and effective performance. Of the all the
various abilities of executive functions, only selective attention (Wordlist) and
abstract reasoning (Analogies) were assessed in the current study. It is possible
that selective attention and abstract reasoning are less affected by alcoholism
than other components of executive functions. Future studies should compare
the performances of alcoholics on these different components.

There is yet another alternative explanation to the current finding. Some
researchers have posited that deficits in Block Design might be related to
problem-solving difficulty, a function that is associated with the frontal lobe. For
instance, alcoholics have been found to perform adequately on visuospatial tasks
that require little or no synthesizing, organizing, or orienting activity (Oscar-
Ben'nan & Weinstein, 1985; Tarter, 1975). Moreover, research has
demonstrated a frontal constructional difficulty that involves the disruption of one
or more of the steps in problem-solving, i.e. intention, programming, regulation or
verification (Lezak, 1995). Further, neuroimaging studies have shown that
performance on Block Design is correlated with frontal regional blood flow
(Rourke and Loberg, 1996). These findings suggest that the poor performance
by alcoholics on Block Design alcoholics in the current study might be associated
with frontal lobe dysfunction.

The current study showed that alcoholics had poorer memory functioning

than non-alcoholics. This finding was extended to alcoholism subtypes by

60

Showing that poor memory functioning is also present in NAALS. Although
memory deficits are generally considered to be associated with temporal lobe
dysfunction, some researchers have postulated that the frontal lobe is involved in
modulating memory functioning. Specifically, the prefrontal cortex is thought be
part of the limbic structures that mediate explicit memories. Memory difficulties
can occur due to poor execution of the mental strategies that bring recall and
memorization into play during memory tasks. Moreover, distraction could also
affect memory performance. A person who has poor ability to withstand
interference is likely going to have difficulty performing memory tasks. This type
of memory difficulty might be relevant to the current findings. As mentioned
earlier, alcoholics were found to have poor selective attention. Unlike the Logical
Memory in WMS, the Stories subtest in MicroCog required subjects to read the
stories on their own, which demand focused attention and concentration. Thus,
the current finding of memory difficulty in alcoholics is supportive of frontal lobe
dysfunction.

Overall, results of the present study lend support to the diffuse brain
dysfunction with the frontal lobe being more susceptible to damage. Among the
four neuropsychological domains, perceptual motor functioning appears to be
most sensitive to alcohol abuse. As mentioned before, SDMT is sensitive to
damage in many areas of the brain. If alcohol does cause mild to moderate
damage throughout the brain, it would be expected that alcoholics would perform
worse on this task. Notably, perceptual motor functioning was the only

neuropsychological domain that AALS performed significantly worse than NAALS

61

and controls. One of the main features of antisocial alcoholics is that their
alcoholism is likely to be more Chronic and severe. Perhaps the deficit in
perceptual motor functioning is a reflection of such differences.

Although the mean scores on all neuropsychological measures were
within normal limits, the proportion of subjects that were classified as having
significant brain impairment were much higher among AALS than NAALS and
controls. This finding suggests that AALS might be most susceptible to
neuropsychological impairment as a result of drinking. One possible explanation
is that AALS might have a premorbid cognitive dysfunction before the
development of alcoholism. Studies have shown that antisocial personality
disorder is related to frontal lobe dysfunction (Deckel, Hesselbrock, 8. Bauer,
1996; Dinn & Harris, 2000). In addition, AALS are more likely to have a positive
family history of alcoholism, which is also linked to cognitive deficits. For
instance, studies have shown that certain cognitive deficits are present in
children of alcoholics who are at risk for developing alcohol abuse/dependence
(Noll, Zucker, Fitzgerald, & Curtis, 1992; Poon, Ellis, Fitzgerald, & Zucker, 2000;
Tarter, Hegedus, Goldstein, Shelly, & Alterrnan, 1984).

A second major goal of the present study was to examine variables that
might influence the neuropsychological outcome of alcoholics. Three potential
sources of variance were studied: depression, neuromedical risk, and drinking
history. Path analyses were conducted on each of the four neuropsychological

domains to determine factors that mediate neuropsychological outcome.

62

Results of the present study showed that history of alcoholism, in terms of
length and severity, was the most reliable predictor for neuropsychological
outcome among all the drinking variables. Interestingly, none of the current
drinking variables were significant predictors of neuropsychological outcome.
Further, path analyses showed that current alcohol problem was a significant
mediating factor for visuospatial processing only. This finding is somewhat
surprising given that current alcohol consumption had been found to predict
neuropsychological performance (Beatty et al., 2000; Horner et al., 1999). One
could possibly argue that current alcohol problem and current alcohol
consumption are two variables that measure different constructs. Specifically,
current alcohol problem is more related to symptomatology of alcohol use while
recent alcohol consumption measures quantity of alcohol use. However, many
alcohol symptoms assessed in this study were closely related to frequency and
quantity of use. Thus, it is difficult to conceive that this is the reason for the
negative findings. An alternative explanation is that the effect of current alcohol
problem on neuropsychological functioning is domain specific whereas the effect
of chronic and severe use of alcohol is more global in nature. In fact, the present
study supports this argument by showing that increased current alcohol problem
is related to poor performance in a specific area, i.e. visuospatial processing. On
the other hand, history of alcoholism has a direct effect on various cognitive
functions.

Path analysis revealed that length and severity of alcoholism significantly

predicted poor performances on three of the four neuropsychological domains:

63

memory functioning, perceptual motor functioning, and executive functioning (i.e.
selective attention). Moreover, for memory functioning and selective attention,
no other significant predictors emerged from the path models. These results
suggest that length and severity of alcoholism is the main factor that mediates
these functions. This finding is consistent with previous research that has shown
a strong relationship between Chronic alcohol consumption and
neuropsychological deficits. In one of the studies, Eckardt, Stapleton, Rawlings,
Davis, and Grodin (1995) reported that greater lifetime estimate of alcohol
consumption predicted worse performance on Halstead lmpairrnent Index,
Speech Sounds Perception, Benton Naming Test, Tactual Performance Test for
memory, and the delayed recall portion of the Rey-Osterrieth Complex figure. In
contrast, recent alcohol consumption did not have any predictive importance on
these measures.

The fact that only history of alcoholism predicted memory functioning is
particularly interesting. Studies have shown that alcoholics tend to
underestimate and minimize their memory problems (Ryan & Lewis, 1988).
Further, the memory deficits observed among alcoholics are often subtle and
only apparent when the memory tasks become more difficult. Undiagnosed
memory impairment could potentially have a negative impact on treatment
efficacy. Thus, it is important to assess the extent of memory deficits in treating
chronic alcoholics.

As predicted, path analysis revealed that history of alcoholism strongly

predicted current alcohol problem in all four models. In contrast, history of

64

alcoholism was found to be unrelated to neuromedical risk. This finding is rather
disappointing but not entirely inconsistent with the literature. Several studies
have failed to document a relationship between head injury, alcoholism, and
neuropsychological dysfunction. In one particular study, Alterman, Goldstein,
Shelly, Bober, and Tarter (1985) reported that the neuropsychological
performance of alcoholics with histories of mild head injury is comparable to
those without histories of mild head injury. More recently, Dikmen, Donovan,
Loberg, and Machamer (1993) examined the relationship between
neuropsychological outcome and alcohol use problem among patients with
various level of head injury. Specifically, the study sought to determine whether
alcohol abuse prior to any head injury would negatively affect the
neuropsychological outcome. Results showed that poor neuropsychological
outcome was related to several factors including limited education,
neuropsychological impairments, and a lifestyle concurrent with heavy drinking,
including an increased risk for head injuries. Contrary to expectation, there was
no evidence for a greater head-injury effect in those with more severe alcohol
problems. Alternatively, the negative finding could be attributed to the limited
scope of the measure. Items that were included in the measures were mostly
related to the nervous system. If other alcohol related diseases (e.g. liver
cirrhosis) were to be included in the measure, the results might show a stronger
predictive power on cognitive functioning.

Depression is another mediating factor that was of interest to this study.

Results of the current study showed that chronic alcoholism predicted higher

65

level of depression, which in turn predicted poorer performance on perceptual
motor functioning. This finding is consistent with research and clinical data that
indicate depressive individuals are more likely to exhibit psychomotor retardation
(Brebion, Amador, Smith, Malaspina, Sharif, & Gonnan, 2000; Berndt & Berndt,
1980; Hart & Kwentus, 1987). In one study, Austin (1992) examined the
neuropsychological functioning of individuals with a major depressive episode.
Results showed that depression is associated with impaired performance on
Auditory Verbal Learning Test, Digit Symbol Substitution and the Trail-Making
Test. These findings might have significant implications on treatment of
alcoholics. In particular, successful treatment of depression in alcoholics could
result in significant alleviation of cognitive impairments, which may improve their

chance of succeeding in alcohol rehabilitation.

Limitation of the Study

The current study showed that alcoholics exhibit generalized
neuropsychological impairment. Moreover, executive deficits appear to be most
prominent, suggesting that the frontal lobe might be more susceptible to damage.
Results of the present study also showed that AALs are more likely to be
classified as neuropsychologically impaired as compared to NAALS and controls.
Path analyses revealed that history of alcoholism is the strongest predictor for
neuropsychological impairment. Although these are significant findings, it is
important to note that there are several limitations to the present work. First, the

neuropsychological measures used in this study to assess executive functioning

66

were somewhat limited in scope and focused mainly on selective attention and
abstract reasoning. It is possible that other types of executive functions deficit
might exist among alcoholics but were not detected in this study. Using other
executive function measures may help clarify the exact nature of such deficits as
well as provide additional information regarding brain-behavior linkage.

The current study only examined three potential mediating factors that
might contribute to the neuropsychological outcome of alcoholics. Future studies
should explore other potential sources of variance such as family history of
alcoholism, nutrition, length of abstinence, and age. As mentioned earlier, the
measure used in this study to assess neuromedical risk only focused on
problems with the nervous system. Other diseases such as liver cirrhosis, HIV,
or hypertension might play a significant role in mediating the relationship

between alcoholism and neuropsychological functioning.

Summam

The current study showed that community alcoholics performed poorly on
a wide range of neuropsychological measures. Moreover, perceptual motor
functioning appears to be most sensitive to alcohol abuse. Among all the
drinking measures, history of alcoholism was the most reliable predictor for
neuropsychological outcome. Path analysis revealed that depression mediated
the relationship between history of alcoholism and perceptual motor functioning.
In addition, higher current level of alcohol problems predicted poorer

performance in visuospatial functioning.

67

The current study extended earlier research by showing that poorer
neuropsychological performance previously documented among alcoholics in
clinical populations is present in a community-based population of alcoholics.
Although the pattern of deficits seems to be most consistent with the diffuse brain
dysfunction model, none of the three theoretical models provided a definitive
framework to describe the effect of alcohol on brain functioning. Further, the
results indicate that the direct neurotoxic effect of alcohol was partially
moderated by other alcohol-related factors including depression and drinking
pattern.

In light of the current findings, it appears that the past approaches to
studying the neuropsychological functioning of alcoholics namely, comparing the
three different theoretical models, may not capture the full range of possible
neuropsychological effects of sustained and/or intensive alcohol consumption.
Future research should focus on developing a more comprehensive theory that
incorporates the both the direct and indirect effect of alcoholism on

neuropsychological functioning.

68

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APPENDICES

75

APPENDIX A

Lisrel Prggram — MIMIQ Mog_el for Drinking Variables and Neuropsychological
Outcome

DA Nl=7 NO=327

RA FI=C:\L|SREL83\DISSERT\RAWDATA\MIMIC.DAT
LA

WORDZ STORY1 WAISBLCK SDMTHAND ALPROB NUMDRINK ALCHRON
SE

1 2 3 4 5 6 7

MO NY=4 NE=1 NX=3 LY=FR

LE

NEUROPSY

PD

OU SE TV EF RS MI

76

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77

APPENDIX B
Lisrel Program — Path Analysis for Mimcm Functioning

DA N|=5 NO=327

RA FI=C:\L|SREL83\D|SSERT\RAWDATA\MEM2.DAT
LA

STORY1 HAMILTON NRISK ALPROB ALCHRON
SE

1 2 3 4 5

MO NY=4 NX=1 BE=FI GA=F| PH=F|
FRGA11GA21GA31GA41
FRBE128E138E14BE23

PD

OU ME=ML RS Ml SE TV EF

78

APPENDIX B

Covariance Matrix Analyzed — Path Analysis for Memorv Functioning

 

STORY1 HAMILTON NRISK ALPROB ALCHRON
STORY1 14.57
HAMILTON -1.83 87.38
NRISK 0.08 2.38 0.60
ALPROB -0.41 5.67 0.11 12.85
ALCHRON -1.44 5.01 0.00 8.64 12.36

 

79

 

APPENDIX C

Lisrel Program — Path Analysis for Perceptual Motgr Functioning

DA Nl=5 NO=327

RA FI=C:\L|SREL83\DISSERT\RAWDATA\SPEED.DAT
LA

SDMTHAND HAMILTON NRISK ALPROB ALCHRON
SE

1 2 3 4 5

MO NY=4 NX=1 BE=F| GA=FI PH=F|
FRGA11GA21GA31GA41
FRBE12BE13BE14BE23

PD

OU ME=ML RS Ml SE TV EF

80

 

APPENDIX C

Covariance Matrix A_nalyzed — Path Ana_lvsis for Perceptual Motor anctioning

SDMTHAND HAMILTON NRISK ALPROB ALCHRON

 

SDMTHAND 1 08.62

 

HAMILTON -15.14 87.38

NRISK -0.26 2.38 0.60

ALPROB 2.92 5.67 0.11 12.85

ALCHRON -5.14 5.01 0.00 8.64 12.36

81

 

APPENDIX D

Lisrel Program - Path Analysis for Visuospatial flunctioning

DA Nl=5 NO=327

RA FI=C:\LISREL83\DISSERT\RAWDATA\SPATIAL.DAT
LA

WAISBLCK NRISK ALPROB ALCHRON
SE

1 2 3 4

MO NY=3 NX=1 BE=F| GA=F| PH=F|
FR GA 2 1 GA 3 1

FR BE 1 2 BE 1 3

PD

OU ME=ML RS Ml SE TV EF

82

APPENDIX D

Covariance Matrix Anayzed — Path Analvsis for \fisuosgatial Functioning

WAISBLCK NRISK ALPROB ALCHRON

 

WAISBLCK 7.55

 

NRISK -0.19 0.60
ALPROB -1.69 0.11 12.85
ALCHRON -1.27 0.00 8.64 12.36

83

APPENDIX E

Lisrel Program - Pafth Analysis for Executive chtioning

DA NI=5 NO=327

RA Fl=C:\L|SREL83\DISSERT\RAWDATA\EXEC.DAT
LA

WORD2 NRISK ALPROB ALCHRON
SE

1 2 3 4

MO NY=3 NX=1 BE=F| GA=FI PH=FI
FRGA11GA21GA31

FR BE 1 2 BE 1 3

PD

OU ME=ML RS MI SE TV EF

 

‘1
.L

APPENDIX E

Covariance Matrix Analyzed - Palh Analvsimrgxecflve anctioning

WORD2 NRISK ALPROB ALCHRON

 

WORD2 7.24
NRISK 0.12 0.60

ALPROB 0.01 0.11 12.85

 

ALCHRON -0.65 0.00 8.64 12.36

85

I»
:—
.0

 

”I

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86

 

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