NOTICE AVIS
The quality of this microform is heavilydependent upon the La qualité de celle microforme dépend grandement de la
quality of the original the sis submilled for microfilming. qualité de la thèse soumise au microfilmage. Nous avons
Every effort hasbeen made to ensure the highest quality of tout fait pour assurer une qualité supérieure de reproduc·
reproduction possible. tion.
If pages are missing, contact the university which granted S'il manque des pages, veuillez communiquer avec
the degree. l'université qui a conféré le grade.
Some pages may have indistinct print especially if the La qualité 'd'impression de certaines pages peul laisser il
original pages were typed with a poor typewriter ribbon or désirer, surtout si les pages originales ont été dactylogra·
if the university sent us an inferior photocopy. phiées à l'aide d'un ruban usé ou si l'université nous a fait
parvenir une photocopie de qualité inférieure.
Reproduction in full or in part of this microform is governed La reproduction, méme partielle, de cette microforme est
by the Canadian Copyright Act, R.S.C. 1970, c. C-30, and soumise à la Loi canadienne sur le droit d'auteur, SRC
subsequent amendments. 1970, c. C-30, et ses amendements subséquents.
Department of Psyehology
MeGill University
Montreal, Quebee, Canada
Mareh 1991
-7
, j
...
: .,
'
l
~Ialional Library Bibliothèque nationale
of Canada du Canada
The author has granted an irrevocable non- l'auteur a accordé une licence irrévocable et
exclusive licence allowing the National Ubrary non exclusive pennettant à la Bibliothèque
of Canada to r.,produce, Ioan, disbibute or sell nationale du Canada de reproduire, prêter,
copies of his/her thesis by any means and in distribuer ou vendre des copies de sa thèse
any form or format, mal<jng this thesis available de quelque manière et sous quelque forme
to interested persons. que ce soit pour mettre des exemplaires de
cette thèse à la disposition des personnes
intéressées.
The author retains ownership cf the copyright l'auteur conseNe la propriété du droit d'auteur
in his/her thesis. Neither the thesis nor qui protège sa thèse. Ni la thèse ni des extraits
substantial extracts from it may be printed or substantiels de celle·ci ne doivent être
otherwise reproduced without his/her per- imprimés ou autrement reproduits sans son
mission. autorisation.
ISBN 0-315-67484- 9
Canada
Abstract
Sons of male alcoholics (SOMAs) are at incLeased risk
for the development of alcoholism, and are apparently
characterized by other a~normalities. It is possible that one
or more of these abnormalities might ~êrVe as a marker for
the alcoholic predisposition. Research described in thls
thesls, conducted ln the hopes of Identlfylng such a marker,
was designed (1) to separate the relatlve pharmacologlcal and
psychologlcal effects of acute alcohol Intoxlcation upon
neuropsychologica! functlonlng; (2) to Investlgate the
neuropsychologlcal functlon of SOMAs wlth a multlgeneratlonal
family history of male alcoholism; (3) to examlne the
relatlonship between SOMAs' neuropsychological functlon and
their cardlovascular hyper-reactlvity to threat of and
aversive stimuli; and (4), to investlgate the relatlonship
between a number of cardiovascular response patterns and
voluntary weekly alcohol consumptlon. These studles are
linked conceptually, wlthin the context of a general the ory
of informatlon-processlng and actlon.
2
Résumé
l'information.
3
Acknowledgements
Dr. Robert O. Pihl supervised the research described in
this thesis. Dr. pihl took a calculated risk when he accepted
my original application to McGill. Biased perspective leads
me to much admire that calculation. His skepticism and
analytical ability helped me transform loose associations
into logically structured scientific arguments, and his
extensive knowledge of the general psychological literature
enabled me to place my theorizing within a proper, practical
context. Dr. pihl provided me with generous aggravation-free
financial support, and with time whenever l wanted it - which
was often. l believe that my association with him constituted
one of those fortunate working arrangements that everyone
wishes for, but seldom attains. l consider it a privilege to
have worked under his supervision.
l would also like to thank Dr. Peter Finn, with whom l
collaborated extensively. l believe that Dr. Finn, Dr. Pihl
and l formed a whole greater than the sum of its parts, and l
hope to continue working with both of them in the future.
The Douglas Hospital - McGill University Alcohol
Research Group provided me with financial support for five
years. A number of its members were of particular help. It
was a privilege to meet and to work with Dr. Frank Ervin, Dr.
Roberta Palmour and Dr. Maurice Oongier. It was a pleasure to
benefit from their collective experience and to make
acquaintance with their remarkable personalities.
4
A number of other people also helped me complete the
..
- Philip Zelazo, and Debble Ross, undergraduates at the time,
are all pursuing graduate degrees ln psychology now, and made
substantlal contributions to the first study described in
this thesis. Jean Seguin, graduate student under Dr. Pihl,
collaborated with me to complete the third study. Rhonda
Amsel contributed invaluable statistical advice whenev2r l
contacted her. r found her interesting personally and helpful
professionally. Judy Young, Dr. Plhl's secretary, was always
extremely decent to me as well, and aided me whenever she
could. l would also like to thank the members of my
committee, Dr. Barbara Sherwln and Dr. Blaine Dltto, and the
staff of the McGlll Psychology Department. The six years l
spent here were perhaps the best in rny life.
My wife, Tammy, helped keep me upright and disciplined
durlng some trylng tirnes, and deserves recognition for her
patience. My rnother and father have always supported my
ambitions, and the relatlonship l have with thern ls a source
of unceasing comfort. l hope that l will have the opportunity
to reward thelr falth and patience.
5
Table of Contents
TITLE PAGE 1
ABSTRACT 2
RESUME 3
ACKNOWLEDGEMENTS 4
TABLE OF CONTENTS 6
LIST OF FIGURES 9
LIST OF TABLES 10
INTRODUCTION 16
Alcoholism: Consequences 16
Alcoholism: Familial Transmission 16
Characteristics of SOMAs 20
Behavioural characteristics 20
Cognitive characteristics 24
Psychophysiological characteristics 27
Reaction to alcohol 31
Biochemical characteristics 34
STUDY 1 & 2 37
Introduction to Study 1 38
Method 40
Subjects 40
Design & procedure 40
Results 42
Blood alcohol level 42
Subjective intoxication 42
Effects of expectancy 42
6
Tests associated vitrr the 43
frontal cortex
Tests not directly associated 43
vith the frontal cortex
l Discussion 43
Table 1: Blood Alcohol Concentrations 42
Table 2: Subject Intoxication Measures 42
Table 3: Tests of Cognitive Function 44
References 45
Introduction: Study 2 48
Study 2: Cognitive Dysfunction and the Inherited 49
Predisposition to Alcoholism
Abstract 51
Introduction 52
Method 54
Subjects 54
Design and procedure 56
Results 63
Discussion 66
conclusion 70
References 71
Table 1: Tests of Cognitive Function 77
Table 2: Correlation Matrix 78
COMMENTS: STUDY 1 & 2 79
Conclusion 112
References 116
Table 1 134
Abstract 145
Introduction 146
Method 150
Subjects 151
Procedure 153
Results 155
Discussion 164
References 168
REFERENCES 186
8
List of Figures
Theoretical Discussion
t
~ Figure 1: Theoretical path 135
Figure 2: Neuropsychological path 137
Figure 3: Observable anomalies 139
Figure 4: Theoretical effect of alcohol 141
study 3
.~.
9
List of Tables
study 1
study 2
Table 1: Tests of Cognitive Function 77
Table 2: Correlation Matrix 78
Theoretical Discussion
Table 1 134
study 3
Table 1: Simple R(2) values 174
Table 2: Cross tabulation results 175
10
Note Regarding Manuscripts and Authorship
11
their original form. ln such instances, connecting texts are
mandat~ and supplementary explanatory material is almost
always necessary.
The inclusion of manuscripts co-authored by the candidate and
others is acceptable but the candidate is required to make an
explicit statement on who contributed to such work and to
what extent, and supervisors must attest to the accuracy of
the claims, e.g. before the Oral Committee. Since the task of
the Examiners is made more difficult in these cases, it is in
the candidate's interest to make the responsibilities of
authors perfectly clear. Candidates following this option
must inform the Department before it submits the thesis for
review."
:~
~-
12
Preface and statement of Originality
This thesis presents information unique in a number of
manners. The literature reviev is extensive, and originally
structured. study 1 is unique because of its methodology, and
in its findings. A balanced-placebo design has never been
applied to the problem of determining the cognitive effects
of expectancy of and acute-alcohol intoxication. In addition,
the application of tests standardized on populations vith
knovn forms of brain damage to acutely alcohol-intoxicated
normals has never been attempted. Study 2 is unique primarily
because it tests the relationship betveen a particular
pattern of abnormal cognitive functioning, and cardiovascular
reactivity to threat of and aversive stimulation, and because
it examines this relationship vithin the context of the
.T.-
predisposition to alcoholism. This contrlbution ls
significant because it links tvo general phenomena normally
considered in isolation, applies them to a common, serious
form of psychopathology, and provides for the possibillty of
attributing both to a single factor. study 3 presents the
flrst hard evidence that a putative marker for the
predisposition to alcoholism actually is related to voluntary
veekly alcohol consumption, among individuals theoretically
at risk for alcohol abuse, and among normals.
In addition, the thesls contains a unique application of
a general model of neuropsychological functlon to the problem
of the alcoholic predisposition. This model unites the
studies contained in the thesis vith the relevant general
13
literature, and contains numerous ideas for further
~.
investigation.
~
With regards to my specific contribution, and that of
others: the thesis introduction is based upon the latest
revis ion of a paper created during a intensive three-year
collaboration between Dr. Pihl, Dr. Finn and myself. Dr. Pihl
outlined the original structure of the pa,~=, published in
the Journal of Abnormal Psychology, wrote the introduction
and conclusion, and extensively edited each of perhaps twenty
successive drafts. Dr. Finn completed the review of
psychophysiological and biochemical characteristics of SOMAs,
and also edited each draft. l reviewed the relevant
literature on behaviour and cognitive function, edited each
draft, and attempted to stylistically unite the whole into
some form of literary unity.
study l, published in the Journal of Studies on Alcohol
(pages 114-122, volume 51(2), 1990), l designed, with Dr.
Pihl's guidance and direction. Jennifer Rothfleisch and
Philip Zelazo helped me select and organize the test battery,
and run aIl 72 subjects. l analyzed the data, and wrote the
paper. Study 2, in press in the Journal of Studies on
Alcohol, l designed and wrote, with Dr. Pihl's input, and
analyzed with Dr. Finn, who contributed data from hls earlier
studies on the cardiovascular reactivity of SOMAs. Study 3,
presently submitted for publication to Alcoholism: Clinical
and Experimental Research, l designed, analyzed and wrote,
with the help of Dr. Pihl, Jean Seguin, who set up the data
14
bank used in analysis, and Dr. Finn, who contributed data
from his earlier studies, referred to previously. The
theoretical discussion, which has been accepted for
publication in Neuropsychology Review, is the result of
extensive discussions between Dr. Pihl and 1, influenced by
Dr. Finn, written by me and edited by Dr. Pihl.
1 certainly did not lack for help completing the
research described in this thesis. However, this help took
the form of collaboration and the work described herein can
accurately considered an original, personal contribution •
.'.-'"
.'>
15
Introduction
Alcoholism ~ Consequences
Alcohol causes more problems than any other drug, vith
the possible exception of nicotine. Most people in North
America drink upon occasion, and 5 to 10 per cent of adults
can be considered alcoholic (Kamerov, Pincus and MacDonald,
1986). The vast majority of these are men (Adrian, 1984).
Alcohol abuse has serious personal and social consequences.
Chronic ethanol consumption heightens individual risk for
heart and 1iver disease, brain degeneration, and cancer, and
often seriously interferes vith normal fetal development.
Alcohol intoxication predisposes otherwise normal people to
engage in acts of interpersonal aggression, both as
perpetrators and as victims. Suicide is more common among
~
~. drunken individuals. Intoxicated drivers are involved in a
significant proportion of fatal traffic accidents. Finally,
alcohol abuse is the leading cause of potentially productive
vork-years lost. In 1983 alone, the Americans spent fifteen
billion dollars on primary treatment of alcoho1 abuse, and an
additional $116.7 billion dealing vith its secondary effects
(Pihl, 1983; Adrian, 1984; Harvood, Napolitano and
Kristiansen, 1984).
Alcoholism ~ Familial Transmission
The familial nature of a1coholism was noted by
Aristotle, Plutarch, and the authors of the 01d Testament.
Prior to the time of Darwin and Mendel, this familial
predisposition vas assumed to be the consequence of
16
Lamarckian transmission of acquired traits. Researchers
working early in the post-Mendelian age, with an adequate
-1-
," ."
genetic model at hand, nonetheless generally attributed the
familial alcoholic pattern to learning (Goodwin, 1985). These
workers assumed that modelling, poor parenting, and various
additional environmental factors were responsible for the
development of alcoholism in children of alcoholic parents -
and indeed for the development of alcoholism in general. The
debate between nature and nurture continues to the present
day. While it is obvious that the effects of the environment
(most obviously, the availability of alcohol) help determine
the development of alcohol abuse, direct inheritance appears
to contribute as weIl.
A variety of adoption, family, twin and half-sibling
studies have investigated the degree to which familial
factors play a causal role in the etiology of alcoholism. The
adoption studies (Goodwin, Schulsinger, Hermansen, Guze and
Winokur, 1973; Cadoret and Gath, 1978; C1oninger, Bohman &
Sigvardsson, 1981j Cadoret, Cain and Grove, 1980) provided
support for the idea that genetic influences determine
predisposition to alcoholism, but have been subject, in
particular, to intense methodological criticism (Lester,
1988; Littrell, 1988; Murray, Clifford and Gurling, 1983;
Searles, 1968). These reviews have focused primarily on
criticizing the somewhat arbitrary criteria by which heavy
and moderate drinking by the experimental subjects were
distinguished from alcoholism, per se. Cotton (1979)
thoroughly reviewed the family studies, and concluded that
17
alcoholics were approximately 7 times more likely to have an
alcoholic parent than non-alcoholics. The relative
contribution of environmental and heritable factors could not
be determined in the course of this review. Researchers
involved in four twin studies (Kaij, 1960; Kaprio, Koskenvuo,
Langinvainio, Romanov, Sarna and Rose, 1987; Partanen, Bruun
and Markkanen, 1966; Pickens, Svikis, McGue, Lykken, Heston
and Clayton, 1991) concluded that pattern of alcohol
consumption, including normal social drinking, was
significantly affected by heritable factors. Two cited by
Gurling, Murray and Clifford (1981) did not support this
conclusion. Kaij (1960) and Hrubec and Omenn (1981) reported
that the twins in their studies were concordant for
alcoholism more often than would be dictated by chance, but
Gurling et al. (1981) and Partanen et al. (1966) did not
concur. It should be noted, however, that those twin studies
with the largest subject population produced evidence that
supported the supposition that heritable factors influence
transmission of alcoholism (Hrubec and Omenn, 1981) and
general pattern of alcohol consumption (Partanen et al.,
1966). Schuckit, Goodwin, and Winokur (1972) and Goodwin,
Schulsinger, Moller, Hermansen, Winokur and Guze (1974)
studied half-siblings raised with and without an alcoholic
parent. These researchers concluded that the environmental
effects of exposure to the alcoholic parent did net
additionally increase the heightened rate of alcohelism ameng
their subjects.
18
In toto, it appears that familial influences indeed
helps determine predisposition to alcoholism. Murray et al.
(1983), who offered a balanced review of the relevant
literature, suggested that genetic factors comprise one such
influence, modest but significant. Sons of alcoholics, in
particular, appear to be at elevated risk. This increased
risk has been estimated at three (Goodwin, 1985) to nine
times (Cloninger, Bohman and Sigvardsson, 1981) that of sons
of non-alcoholics. The precise nature of the inherited
predisposition remains unknown, in part because many who are
interested in its determination derive their conclusions from
the study of seasoned alcoholics. Pihl and Spiers (1978)
determined that 93% of 270 sampled studies examining the
"addictive personality" assessed subjects already in
treatment, for addiction. This approach cannot help
distinguish between those factors that might distinguish
individuals predisposed to drug or alcohol abuse, and those
that results as a consequence of that abuse.
Non-alcoholic sons of male alcoholics (SOMAs) appear to
be more suitable subjects than alcoholics for those
interested in studying the predisposition to alcoholism.
Examination of their youthful idiosyncracies, if any, in
evidence prior to chronic alcohol ingestion, might lead to
the discovery of markers associated with the alcoholic
tendency, or to the identification of underlying causal
psychological or physiological factors. The results of the
experimental research on subjects at high risk for alcohol
abuse, for various reasons, have been reviewed with varying
19
degrees of completeness by Tarter, Alterman and Edwards
(1985; 1988), Schuckit (1985), Zucker and Lisansky-Gomberg
(1986), El-Guebaly (1986) and Cloninger (1987). Relevant
experimental and theoretical analyses presented in these
reviews, and other pertInent and more recent studies that
focus specifically on SOHAs are summarized below. This brief
summary includes research classified according to commonality
of flnding into five subsections: behaviour, cognition,
psychophysl010gy, reaction to alcohol, and biochemistry. The
theoEetical overview presented later in the thesis contains a
more detaIled descriptIon of the meaning of these findings,
and an elaborated critical dIscussion.
Characteristics of Sons of Hale Aicoholics
Behavioural Characteristics
SOHAs have most consistently been described as conduct-
disordered and hyperactive (Alterman, Searles & Hall, 1989;
Cantwell, 1972; Horrison & Stewart, 1971, 1973; Nylander,
1960 (part 1); Stewart, deBlols & Singer, 1978; Tarter,
Hegedus, Goldsteln, Shelly & A1terman, 1984); sole1yas
conduct-disordered (Aronson & Gilbert, 1963; Cadoret & Gath,
1978; Harden & Pihl, 1988; Nylander, 1960 (part 2); Nylander
& Rydelius, 1982; Rydelius, 1978, 1981, 1983a, 1983b); and as
impulsive (Aronson & GIlbert, 1963; Knop, Teasda1e,
Schulsinger & Goodwin, 1985; Saunders & SchuckIt, 1981;
Schuisinger, Knop, Goodwin, Teasda1e, & Hikkelson, 1986).
These descriptors have been most frequently applied during
childhood, but often remain applIcable in adu1thood as we11.
20
They appear as valid even within those studies that provide
control for environmental influence (Cadoret & Gath, 1978;
1 Horrison & stewart, 1971, 1973; Nylander, 1960 (part 2);
stewart, deBlois, & Singer, 1978). This conduct-disordered/
hyperactive pattern of behaviour generally first presents a
serious problem in the early years of school, when it
disrupts the academic environment.
Children of alcoholics (male and female) have also been
frequently described as conduct-disordered (Chafetz, Blane &
Hill, 1971; Fine, Yudin, Holmes & Heinemann, 1976; Haberman,
1966). Such children frequently manifest behavioural patterns
associated with Attention Deficit Disorder and/or
hyperactivity (Fine et al., 1976; Sher & Alterman, 1988),
appear hypersensitive to auditory and visual stimulation
(Fine et al., 1976), and have difficulty in regulating
excitement and mood (Lund & Landesman-Dwyer, 1979).
Various longitudinal studies make the same points.
Children or adolescents who develop alcoholism later ln life,
as adults, are often antisocial and/or impulsive (Block,
1971; Hagnell, Lanke, Rorsman, & Ohman, 1986; Hechtman, Weiss
& Perlman, 1984; Hoffman, Loper & Kammeier, 1974; Jones,
1971; Loper, Kammeier & Hoffman, 1973; Hagnusson & Bergman,
1988; HcCord & HCCord, 1960; Nylander, 1979; Nylander &
Rydelius, 1973; Ricks & Berry, 1970; Robins, 1966; Vaillant,
1983), characterized by impoverished interpersonal ties
(Jones, 1968; HcCord & HCCord, 1962; Honely et al., 1983;
Robins, 1966), and hyperactive and/or aggressive (Hechtman et
al., 1984; Jones, 1968; Hagnusson & Bergman, 1988; HcCord &
21
HcCord, 1960; Ny1ander, 1979). A comparative1y high
proportion of these vulnerable individua1s have a1coho1ic
parents (Ny1ander & Ryde1ius, 1973; Vaillant, 1983).
The families of SOHAs are often overt1y unstable (Knop
et al., 1985; Nylander, 1960 (parts 1 and 2); Rydelius,
1983a; Schulsinger et al., 1986; Tarter et al., 1984).
Chi1dren of a1coho1ics are often raised in severe1y disrupted
fami1ies (Chafetz et al., 1971), and heightened conf1ict
among parents or between parents and chi1dren (Jones, 1968,
1971; Hechtman et al., 1984; HcCord & HcCord, 1960; Hone1y,
Hart1 & E1derkin, 1983; Ricks & Berry, 1970; Robins, 1966;
Vaillant, 1983) is common1y reported, in the longitudinal
studies of chi1dren who 1ater become a1coho1ic. The precise
effect of this genera1 instabi1ity is not known, but it is
not difficult to imagine that it may exacerbate any pre-
existing tendencies to disordered conduct and hyperactive
behaviour.
Familial alcoholism has a1so been associated with male
sociopathy (Guze, Tuason, Gatfield, stewart & Picken, 1962;
Guze, Wolfram, HcKinney, & Cantwe11, 1967; Latcham, 1985;
Winokur, Rimmer & Reich, 1971) and chi1dhood conduct disorder
(Cadoret, Cain & Grove, 1980; Goodwin, Schu1singer,
Hermansen, Guze & Winokur, 1975; Rosenberg, 1969), childhood
hyperactivity (A1terman, Petraru10, Tarter & HcGown, 1983;
Goodwin et al., 1975) and overt familial disruption
(Rosenberg, 1969). Ha1e-1imited Type II a1coho1ism,
22
von Knorring, von Knorring & Bohman, 1985; von Knorring,
Bohman, von Knorring & Oreland, 1985; von Knorring, Palm &
1 Andersson, 1985), early onset, and Increased heritability
(Cloninger, 1987), is often preceded by chi1dhood conduct
disorder (Cloninger, Sigvardsson & Bohrnan, 1988; Hasin, Grant
& Endicott, 1988; Schaeffer, Parsons & Errico, 1988; von
23
of the same long-term behaviour pattern.
In the general literature, hyperactivity and conduct
disorder overlap, although subgroups of children within these
domains appear to differ in important ways (Hinshaw, 1987).
Low socioeconomic status, intrafamilial hostility, parental
alcoholism and/or drug abuse, antisocial personality, and/or
hysteria tend to characterize the families of conduct-
disordered children, while cognitive and achievement deficits
(which are also typical of SOMAs) are often associated with
hyperactivity (Hinshaw, 1987). It is of interest to note that
August ~nd Stewart (1983) and August, Stewart and Holmes
(1983) have described the relationship between alcoholism and
childhood hyperactivity as secondary to that which exists
between alcoholism and childhood conduct disorder. However,
children displaying a combination o~ hyperactivity and
aggression suffer from the worst consequences of both, in
terms of observed behaviour, peer status, and outcome
(Hinshaw, 1987; Magnusson & Bergman, 1988). It appears
possible that SOMAs are often characterized by such a
combination. The presence of these behavioural patterns in
childhood appears to be strongly associated with increased
risk for alcohol abuse later in life.
Cognitive Characteristics
SOMAs have been consistently characterized by
comparatively poor performance on tests of linguistic ability
(Drejer, Theilgaard, Teasdale, Schulsinger & Goodwin, 1985;
Gabrielli & Mednick, 1983; Harden & Pihl, 1988; Hegedus,
24
Alterman & Tarter, 1984; Knop et al., 1985; Noll & Zucker,
, .-
...~
1983; Schulsinger et al., 1986; Tarter et al., 1984; Whipple,
Parker & Noble, 1988). Reduced performance during tests
involving abstraction and/or problem solving are also
commonly reported (Drejer et al., 1985; Harden & Pihl, 1988;
Knop et al., 1985; Schaeffer, Parsons & Yohman, 1984;
schulsinger et al., 1986; Tarter, Jacob & Bremer, 1989).
comparative deficits in total Ia (Gabrielli & Mednick, 1983),
performance ra (Whipple et al., 1988), memory (Harden & Pihl,
1988; Hegedus et al., 1984; Tarter et al., 1984),
visuospatial ability (Hegedus et al., 1984; Tarter et al.,
1984), perceptual-motor capacity (Hegedus et al., 1984;
Schaeffer, Parsons & Yohman, 1984; Tarter et al., 1984) and
auditory/visual attention span (Hegedus et al., 1984; Tartcr
et al., 1984) llave been descr ibed ..,i th less consistency.
It is also important to note that SOMAs perform less
..,ell academically and have more trouble ..,ith school (Drejer
et al., 1985; Hegedus et al., 1984; Knop et al., 1985;
Rydelius, 1981; Schulsinger et al., 1986; Tarter et al.,
1984). Problems related to academic achiev.ment are also
reported in Many of the longitudinal studies, among children
and adolescents ..,ho later develop serious problems ..,ith
alcohol (see for example the revie.., by Zucker & Lisansky-
Gornberg, 1986). Such children are frequently characterized by
poorer school performance, more school truancy, and
completion of fe..,er years of schoel. The degree te ..,hich this
reduced performance can be attributed to impaired cognitive
ability per se is subject to debate. It could alse
25
conceivably arise as a consequence of the behavioural
-
, abnormalities discussed previously, or for other reasons,
such as poor family life, or because of frequent transfer
from school to school (Knop et al., 1985).
This literature is not as consistent as that describing
the behavioural characteristics of SOMAs. Those studies that
find a link betveen cognitive differences and the alcoholic
family history generally examine sons of severely alcoholic
fathers, vho often have additional alcoholic relatives. Those
that do not are characterized by one of tvo methodological
veakness: they either include a preponderance of females, as
subjects or as the alcoholic parent, and do not offer
breakdovn of results by sex (Hesselbrock, stabenau, &
Hesselbrock, 1985; Wilson & Nagoshi, 1988; Workman-Daniels &
Hesselbrock, 1987) or they look for cognitive deficits among
SOMAs dravn solely from a university population (Alterman,
Bridges, & Tarter, 1986a; Alterman, Bridges & Tarter, 1986b;
Alterman, Searles & Hall, 1989; Schuckit, Butters, Lyn &
Irvin, 1987), vhose familial alcoholism is limited to a
mildly affected (one symptom in four to six diagnostic
categories) alcoholic father. With regards to the inclusion
of vomen: offspring of alcoholic mothers might suffer the
residual effects of fetal alcohol exposure, vhich can be
dramatic. In addition, a1coholism tends to be a male problem.
These tvo facts combine to make the nature of alcoholism
among females, and its potential mode of transmission, very
resistant to comprehension. With regards to the use of
26
college students: SOMAs who attend university are those least
1··
likely to be characterized by cognitive deficits.
. -.'
Comparison of familial and no~-familial alcoholics
occasionally highlights weak group differences attributable
to family status (Schaeffer et al., 1984), vith the familial
alcoholics performing more poorly, particularly within
studies utilizing a large number of subjects (Schaeffer et
al., 1988), and sometimes fails to prcvide such
differentiation (Alterman, Gerstley, Goldstein & Tarter,
1987; Reed, Grant & Adams, 1987). Interpretation of these
studies in terms of predisposition is rendered difficult,
because the long-term effects of alcohol consumption upon
cognitive performance might vary according to family history.
Psychophysiological Characteristics
..',......
Most of the psychophysiological research conducted to
date upon SOMAs has concentrated on their cortical evoked-
response to stimuli. The cortical event-related potential
(ERP) ls derived from the electroencephalogram (EEG) recorded
during the presentation of a brief stimulus in any sensory
modality. First, it might be noted that there are two studies
(Schmidt & Neville, 1984; Neville & Schmidt, 1985)
demonstrating that SOMAs are characterized by decreased
amplitude of the N430 ERP component, linked to semantic
processing, during the course of two verbal tasks. These
studies are important in their own right, and are in
concordance with the studies described previously
demonstrating that SOMAs may be deficient in verbal
abilities. However, it is the p300 ERP compone nt that has
27
been most commonly studied with respect to SOMAs. The
amplitude of P300 increases with the subjective motivational
relevance of stimuli (Begleiter, porjesz, Chou & Aunon,
19831; its latency varies with speed of identification and
processing (Donchin, Ritter & MCCallum, 1978). Eight studies
refer to SOMAs' production of P300 with reduced amplitude
(Begleiter, Porjesz, Bihari & Kissin, 1984; Beg1eiter,
Porj~sz, Rawlings, & Eckhardt, 1987; Elmasian, Neville,
Woods, Schuckit, & Bloom, 1982; O'Connor, Hesselbrock, &
Tasman, 1986; Steinhauer, Hill & Zubin, 1987; Whipple et al.,
1988) or increased latency (Hill, steinhauer, Zubin &
Baughman, 1988; Whipple & Noble, 1986) during the repeated
presentation of non-threatening, non-novel stimuli. This
pattern of p300 production also characterizes abstinent
....
j alcoholics (Begleiter, Porjesz & Tenner, 1980; Porjesz &
...
Begleiter, 1981). These abnormalities remain naticeable even
after periods of abstinence of up to 5 years, unlike deficits
in Brain Stem Auditory Response conduction velocity, which
characterize abstinent alcoholics (Porjesz & Beg1eiter, 1985)
but nat SOMAs (Begleiter, Porjesz, & Bihari, 1987).
It is important to note that these eight positive
studies are characterized by strl~t subject selection
procedures. Begleiter et al. (1984, 1987), Whipp1e and Noble
(1986), Whipple et al. (1988) examined non-drinking
adolescents or preadolescents and Hill et al. (1988),
O'Connor et al. (1986) and Steinhauer et al. (1987) young
adults whose fathers met Feighner criteria for alcoholism and
28
who often had additional alcoholic relatives. There are a
number of studies (Neville & Schmidt, 1985; Polich & Bloom,
1986, 1987, 1988; Polich, Burns & Bloom, 1988; Polich, Haier,
Buchsbaum & Bloom, 1988; Schuckit, Gold, Croot, Finn &
Polich, 1988) which report little or no differences in P300
production (amplitude and/or latency) between SOMAs and
matched controls. The majority of these (Neville & Schmidt,
1985; Polich & Bloom, 1986, 1987, 1988; Polich, Burns &
Bloom, 1988) report that such production is correlated vith
self-reported alcohol consumption, and/or by such alcohol
consumption in interaction with family history. Hovever,
these studies test university students, who are self-selected
for the absence of the kind of cognitive deficit that might
underlie P300 abnormalities (Begleiter, Porjesz & Tenner,
1980), and whose familial a1coholism is limited to a mildly
affected father (one symptom in four to six categories)
(Hill, Steinhauer, Park and Zubin, 1990). Given the
methodologica1 differences between the positive and negative
studies, it seems reasonable to conclude that SOMAs drawn
from the normal population, from families with extensive
histories of paternal alcoholism, may well be characterized
by abnormalities of the P300 ERP component. This pattern of
reaction might be considered an idiosyncratic cued
psychophysiological response.
There are four additional reports suggesting that
abnormalities in cued psychophysiological response might
characterize sober SOMAs. These studies differ
methodologically from the P300 studies described previously
29
in that they utilized stimuli whose motivational significance
might be described as inherent: Finn and Pihl (1987, 1988)
and Finn, Zeitouni and Pihl (1990) used 'countdown to shock,
electric shock, and presentation of novel tones; Harden and
Pihl (submitted) used mental arithmetic. These
investigations, conducted on individuals with extensive
multigenerational family histories of severe male-limited
alcohol abuse, demonstrated that SOMAs are characterized by
heightened cardiovascular reactivity to novel or avers ive
stimuli. Another study (Hennecke, 1984) notes that the
incidence of stimulus augmentation, characteristic of
alcoholics (Buchsbaum & Ludwig, 1978; Coger, Dymond,
Serafetenides, Lowenstam & Pearson, 1976; von Knorring,
1976), was significantly higher among children of alcoholics,
male and female, than among matched controls, while the
incidence of field-dependence, also characteristic of
alcoholics (Karp, Witkin & Goodenough, 1965), was not.
Stimulus augmentation might be considered a form of
perceptual hyper-reactivity.
Two studies have described EEG abnormalities as
characteristic of sober SOMAs. Gabrielli, Mednick, Volavka,
Pollock, Schulsinger and Itil (1982) demonstrated that the
EEGs of SOMAs were characterized by an significant excess of
high frequency beta activity. This pattern of response is
also typical of alcoholics (Mendelson & Mello, 1979). An
excess of fast beta activity has been associated with
psychological states of tension and anxiety (Kiloh &
30
Osselton, 1961). Begleiter et al. (1987) have also reported
that unspecified EEG abnormalities characterize SOHAs. It has
been commonly reported that alcoholics can be differentiated
from controls by their poorly synchronized brain wave pattern
(Begleiter & Platz, 1972), and Naitoh (1973) has argued as
weIl that individuals with such poorly synchronized EEGs are
predisposed to alcoholism. Propping, Kruger and Hark's (1981)
work, which showed that alcoholics and their first-degree
relatives shared EEG patterns, provides some support for this
notion, suggesting as it did that the EEG patterns
characteristic of alcoholics may be genetically determined.
However, the exact significance of these somewhat abnormal
patterns remains unspecified.
Finally, there are three studies (Hegedus, Tarter, Hill,
Jacob, & Winsten, 1984; Lipscomb, carpenter & Nathan, 1979;
Tarter et al., 1989) which suggest that sober static ataxia
characterizes SOHAs and three (O'Halley & Haisto, 1985;
Schuckit et al., 1987; Schuckit & Gold, 1988) that do not. It
is difficult to draw any final conclusions from these
studies. A pronounced lack of theory describing the
relationship between alcoholic predi:;position and increased
sober static ataxia complicates Interpretation and
Integration of these contradictory findings.
Reaction to Alcohol
SOHAs appear to be characterized most particularly by
increased susceptibility to what might be considered the
negatively and positively-reinforcing effects of alcohol
consumption. with regards ta putative negative reinforcement:
31
SOMAs appear hyper-sensitive to the dampening effect of
alcohol on cardiovascular and/or electrodermal reactivity to
aversive or novel stimulation (Finn & Pih1, 1987; Finn &
Pihl, 1988; Finn et al., 1990; Levenson, Oyama & Meek,
1987). A1coho1ics a1so seem to be characterized by some form
of susceptibi1ity to the stress-response dampening effect of
ethano1 intoxication. A1coho1ics manifest significant
reductions in e1ectroderma1 reactivity (Coopersmith &
Woodrov, 1967; Garfield & McBrearty, 1970) and to pain
reactivity (Brovn & cutter, 1977) after consuming alcohol. In
addition, alcoho1 consumption results in a shift from
stimulus augmentation to reduction in alcoholics (Buchsbaum &
Ludvig, 1978; Petrie, 1975), vhich might be considered a form
of dampening, and alcoholics vho are augmentors, like the
offspring of alcoho1ics (Hennecke, 1984), york harder for
alcohol than those vho are normalizers or reducers (Ludvig,
Cain & Wik1er, 1977).
With regards,to possible positive reinforcement: SOMAs
are characterized by significant1y increased baseline heart-
rate, vhen lntoxicated, during the ascending limb of the
b100d a1coho1 curve (Finn & Pihl, 1987; 1988; Finn et al.,
1990; Levenson et al., 1987). This increase appears of
importance, as Fov1es (1981; 1983) has described an
association betveen similar heart-rate elevations and revard.
More genera11y, a1coho1 intoxication appears to significant1y
reduce baseline muscle tension among SOMAs, (Schuckit,
Engstrom, A1pert & Duby, 1981), heightens their production of
32
EEG waveforms associated with states of well-being (Pollock,
Volavka, Goodwin, Mednick, Gabrielli, Knop & Schulslnger,
,....
_.~
33
SOMAs are more susceptible to alcohol's positive effects,
during the ascending limb of the blood alcohol curve, and
less susceptible to its negative effects, during the
descending limb. The potential consequences of this
differential sensitivity are obvious.
Finally, there have been two positive (Schuckit, 1980a;
Schuckit & Rayses, 1979) and one negative report (Behar,
Berg, Rappaport, Nelson, Linnoila, Cohen, Bozevich &
Marshall, 1983) that elevations in plasma acetaldehyde
characterize SOMAs after alcohol consumption. These results
may be unreliable due to difficulties in the accurate
measurement of blood acetaldehyde (Eriksson, 1980) although
elevated levels of blood acetaldehyde after alcohol
consumption are also characteristic of alcoholics (Korsten,
Matsuzaki, Feinman & Leiber, 1975).
Biochemical Functioning
Six studies describe what little is directly known about
the normal biochemistry of those with a positive-family-
history of alcoholism. Three studies of these 6 support the
most common finding, which is that family-history-positive
subjects are characterized by lower plate let monoamine
34
Murphy, 1978; Sullivan, Stanfield, Schanberg & Cavenar,
1978), generally associated with alcoholism (Alexopoulos et
al., 1983; Brown, 1977; Gottfries, 1980; Major & Murphy,
1978; von Knorring et al, 1985) and specifically linked to
Type 2 alcoholism, which is considered highly heritable (von
Knorring et al., 1985). However, relatively decreased
platelet MAO activity also characterizes those suffering from
other psychiatrie disorders (Buchsbaum, Coursey & Murphy,
1976) and may not provide accurate measure of central MAO
function (stahl & Kravitz, 1986). Its precise significance is
therefore difficult to determine.
The three remaining studies variously describe the
biochemistry of individuals with alcoholic relatives. Moss,
Guthrie and Linnoila (1986) offered evidence that adolescent
SOMAs manifest an enhanced thyrotropin response to
thyrotropin releasing hormone. Swartz, Drews, and Cadoret
(1987) demonstrated that nonalcoholic adoptees with alcoholic
biological first or second degree relatives were
characterized by significantly reduced mental stress-induced
epinephrine release. This pattern is apparently also
characteristic of those with aggressive or hyperactive traits
(Swartz et al., 1987). Rosenthal, Davenport, Cowdry, Webster
& Goodwin, (1980) demonstrated that depressed first-degree
relatives of alcoholics are characterized by lower
cerebrospinal fluid levels of the serotonin metabolite 5-
hydroxyindoleacetic acid. Although the full significance of
these findings is not yet clear, the latter study may be of
particular interest, given the wealth of indirect evidence
35
suggesting that the dysfunctions of the serotonergic system
Conclusion
Non-alcoholic sons of male alcoholics have been most
consistently described as eonduct-disordered and as
hyperactive. They have difficulty in maintaining
concentratl'Jn and focus of attention, and can not or do not
regulate their overt behaviour in accordance with age-
approprlate structured social norms. They appear heir ta a
number of mild cognitive deficits, and manifest decrements ln
performance durlng tests of llngulstlc ability, abstract
thlnklng, and problem solving. Their academic performance is
often reduced. It has been demonstrated, with less
consistency, that SOMAs are characterized by abnormal
patterns of cued psychophysiological response. They appe~r to
hypo-react ta stimuli that require the allocation of
36
Study 1 and 2
The pattern of behaviour, cognition and psycho-
...;,
physio1ogica1 response typica1 of SOMAs appears reminiscent
of that manifested by individua1s who have suffered sorne form
of mi1d pre frontal cortical trauma, in adulthood (Tarter,
Alterman and Edwards, 1985; 1988; Gorenstein, 1987). Sons of
male a1coho1ics and individua1s with minimal pre frontal
damage are characterized by increased impu1sivity,
attentiona1 deficit, impairments in the vo1untary regulation
of social behaviour, heightened levels of activity, poor
,~.
37
Introduction to study l
study 1 (Peter~on, Rothf1eisch, Zelazo and Pihl, 1990)
examined the effects of three different levels of alcohol
intoxication the neuropsychological functioning of 72 (6 X
12) undergraduate males, in the context of a ba1anced-placebo
design. This study was designed to examine the relative
contributions of expectancy and pharmaco1ogy to normal, but
alcohol-intoxicated neuropsychological functioning. The study
additiona11y allowed for the determination of the alcohol
dose sufficient to serious1y impair inte11ectual function.
This is a critically important point, as the use of many
different alcohol-dosing procedures in the relevant
literature excessively complicates comprehension of alcohol's
effects.
38
Journal of Siudin 011 A/collot, Vol. JI .•,"'0. ]. /990
,.~
Department of Psycholov. McGiII University. 120S Docteur Penfield Avenue., Montreal, Quebec H3A IBI, Canada
ABSTRACT. Acute a1cohol intoxication produces chanaes in the widely different doses of alcohol. Analysis of the rC3ulu of the
coanitive functionina of normal individuals. Thc:sc chaniC3 appear coJOitive test b&ncry clemonsuatcd that a h.iIh dose of alcobol
simiIar prima fade to those e:thibitcd by indhidu.ils who sustain deuimenl&11y arfccu a numba' of funaions wociated with the
prd'ronl&1 lobe damaae durina adulthood. In order to test the prefronl&1 and temporal lobes. includina pLannina. verbal Ouency,
validity of this observation. and to conuol for the confoundina memory and compla motor control. Espcctancy does not appear
effccu of ~tancy. 72 male subjeeu were adminiuered a to play a sianificant role in àeterminina this effcet. The impü·
battery of neuropsycholoiÎcaJ tau. within the context of a cations of this panem of impairment ue ana.lyz.ed and disctwed.
balaDced·placebo desisn. Eacb subjec:t rcecived one of three (J. Stud. Alcohol 51: 114-122. 1990)
39
.r PETERSON ET AL. 115
,:",
(Lezak, 1976). W..hbume (1956) poSlulated that al· Ross and Pihl (1989). The present Sludy was addi·
cohol intoxication simiIarly reduces people's aware- tionally predicated upon the hypothesis that expec·
ncss of thcir own actions, making them unable to tancy detrimentally affects performance. This
modify these actions in r~sponse ta environmentaJ secondary hypothesis was based on the assumption
demands. Hull (19SI) has also proposed that alcohol that alcohol intoxication provides an excuse for in·
intoxication imcrferes with encoding processcs fun· appropriate or substandard behavior (Graham. 1980:
damentaJ to the state of self·awareness. These proc- Hull and Bond. 1986).
esses inc1ude the evaluation of self-relevant
information. including eues about appropriate forros Metbod
of conduct and evaJuation of behavior in the recent
pasto S"bjects
Deficits in verbal ability have also been associated Seventy·two male university students between the
with alcohol intoxication and with prefrontal impair- agto of 18 and 34 were reeruited as paid subjects by
ment. AJthouSh patients with left frontal lobe lesions adverti:·;~r.1ent at McGiIl University. Moderate social
often appear 10 possess intact speech upon superficial ùrinkers « 15 drinks/week) in good physical and
examination (Walsh, I97S). closer analysis reveals mental heaJtn were selected for panicipation. The use
impoverishment (Lezak. 1976), adynamia and persev. of experienced drinke" in the sample ensured that
eration (Walsh, 1978). Prefrontal patients often offer ail ,ubjects were farniliar with the effeets of alcohol
cxtraneous associations during verbal tests (Luria et consumption. Exclusion criteria also included famil·
al., 1967). Clinical studies show that patients with iarity with psychological experimentation, and medical
left frontal dan",.e perform significantly worse than trcatment that contraindicated alcohol consumption.
controls on word-fluency tests (Bentan, 1968; Miller, Subjeets were asked to refrain from consumption of
1988; Milner, 1964; Ramier and Hécaen, 1970). De· alcohol for 24 hours and from food 4 hours before
crease<! verbal nueney is also characteriSlic of subjeets the experimental session.
acutely intoxicated by alcohol (Hanocollis and John·
son, 1956) and these individuals also alter their
Design and Procedure
responses to free·association tests (Weinganner, 1977).
In the present study, a variety of cognitive·behav. Upon arrivai at the laboratory. all subjects met
ioraI tasks-some sensitive to panicular types of the first of four experimental personnel. They w.,e
neuropsychologica1 impairment-were administered ta then required to sign an informed consent form.
the subject population. Those more sensitive tO fron· Each subject was then weighed and randomly ..."igned
tal function were included to provide a direct test of to one of the following six sroups: told higl: dose.
the hypothesis presented in this anicle. Nonfrontal reeeived high dose (THRH); told low dose, reeeived
and miscollaneous tesL, were administered 10 deter· high dose (TLRH); told high dose, reeeived moderate
mine the specificity or generality of alcohol-icduced dose (THRM); told low dose. reeeived moderate dose
impairment. Tests with well-established !lorms or tests (TLRM); told hir.h cto,",. rer.ived low dose (THRL);
that are apparently affected by highly specific forms 'Uld told low dose, ",ccivO'j Ir>w dose (TLRL). High
of damage were included as fltSt choices, but some dose consisted of 1.32 ml of 95'1. pure pharmaceuticaJ
in use for other reasons (sensitivity to expectaney, alcohol per kilogram of body weight; moderate dose
for example) were aise included. of 0.66 ml/kg; and low dose. which was active
Dose and expectaney confound the effeets of a placebo. of 0.132 ml/kg. Drinks for the high doses
drug, and play crucial roles in determining its be· ""ere mixed 1 pan alconel to 5 pans juic: (3 pans
havioral sequelae (Marlau and Rohsenow, 1981). grapefruit and 2 parts orange). The grapefruit juice
Variation in respanse due to dose and expectallcy help,."!\ mask the presence or absence of alcohoL
was ·,herefore directly measurd. Subjects randomiy Subjects in the moderate· and low-dose conditions
reeeived one of thr.. "'id.ly differing doses of al· reeeived as much juice per kilograrn of body weight
cohol, under two conditioll5 of expectalley, within as the subjeets who reeeived a high dose of alcohoL
the confines of a baJanced-placebo d..,ign. A variety Subjeets in each condition reeeived instructions de-
cf teehniques have been designed to ensure that signed to maximize the effeetiveness of the balanced-
subjeets remain naïve to condition and to therefore placebo design (Ross and Pihl, 19S9). Each subject
maintain the validity of the balanced-placebo design. was given thr.. drinks, and was asked to finish them
Knight et al. (1986) have reeently criticized th... within 20 ntinutes. Arter a 15·minute waiting period.
wchniques. The present experiment was designed with each subject was given the (;'3t of three subjective
th... criticisms in mind, and w.. based on a modi- intoxication scales and 'h-,' first of threc breath
fication of the baJanced-placebo design devise<! by analyzer tests. Subjeets completed their subjeetive
40
116 JOURNAL OF STUDIES ON ALCOHOLIMARCH 1990
intoxication sca1es privatcly. to control for the effects Tests associated with the temporal cortex
of experimcnter rlemand. The subjects wcrc then Logical Memory, Immediate (1); Logica[ Memo,-,.
taken to a separat!: testing area, where they were 25-Minute Delay ID). These Wcchsler memary ,ub-
introduced to th,~ remaining three experimenters, who tests assess the immediate and delayed recall of verbal
were blind to the subjects' condition. ideas from an auditory presentation of two para-
The fallawing tests were divided equally amang graphs. Individuals with temporal lobe damage per-
thesc three investigators. who administered them in farm poarly on these tests (Milner, 1975).
randam arder ta the subjects ta control for differ- Rey~Osterreith Figure, Reproduction Iram .\femory
ences in performance due to praetice, fatigue, the (2) & (3). After the subjcct has capied the Rey figure,
effcets of alcahal metabalism and central nervaus he is subjcctcd ta a delay of 3 minutes and is asked
system ~daptation to alcohol intoxication. ta duplicate the figure from memary. Th. subjcct is
Tests assnciated wUh the frontal cortex then given a series of other tasks. and is finally
asked ta produce a final capy from memary 25
Parteus Maze Test, Extension Series. This test minutes later. Patients with right temporal lobe dam-
measures planning and foresight (Parteus, 1959). age (particularly those with hippocampal lesions) have
Subjccts are required to complete a series of Mazes difficulty in completing this task (Milner, 1975).
rankcd according ta difficulty. Individuals with le- Paired Associates, Difficult (D) and Easy lE). The
sions of the frontal lobes demonstrate impairments Paircd Associate subtest of the Wcchsler Memory
in their ability ta correctly complete this test (Crown, Scale assesses verbal retention (Lezak, 1976). The test
1952; Malmo, 1948; Meuler, 1952; Porteus and Kep- consists of la word pairs; six forming easy associa-
ner, 1944; Porteus and Peters, 1947). tions and four forrning word pairs not easily asso-
Rey-Osterreith Complex Figure, Copy (1). Rey ciated. Individuals with left temporal lesions have
(1941) designed this comple. figure ta investigate difficutly in completing this test (Milner, 1975). Ad-
perceptual organization and visual memory in brain- ditionally, there is evidence that organic brain damage
damagcd patients (Lezak, 1976). The subject is first panicularly impairs recail of the difficult pairs (Walsh,
required to copy the figure Crom an original. Patients 1979).
, .,,>- with prefrantal damage copy this figure (and comple.
figures in general) poorly (Lezak, 1976; Luria, 1980).
Tests assaciated with the parieta/-occipital cortex
Thurstone Ward Fluency Test. This test assesses
the ability ta generate words according ta an abstract Albert's Simple Test of Visual Neglect. Subjccts
conceptual cat,egory. The subject must write as many are given a pencil and a sheet of paper with a
words as he can beginning with the letter S in 5 number of short Iines printcd on it, and are asked
minutes. Individuals with left frontal lobe damage ta biscct each line with another short line. Subjects
consistently demonstrate significant impainnents in who suffer from parietal damage perform panicularly
ward flueney (Benton, 1968; Miller, 1989; Milner, poarly on this test (Albert, 1973).
1967; Ramier and Hécaen, 1970; Tow, 1955). Apraxia Questionnaire. The apraxia questionnaire
Self-Ordered Painting Test, 12 Representational provides a general measure of ideomotor, ideational
Drawings. The Self-Ordercd Painting Test measures and buccofacial apraxia. Apraxia has becn opera-
arganizational ability and sequencing of responses tionally defincd by e.clusion as a disarder of skilled
rather than the reproduction of sequences pre~organ movement not caused by weakness, akinesia, deaf~
izcd by the e.perimenter (Petrides and Milner, 1982). ferentiation, abnormal tone or posture. movement
Subjects must remember the location and sequence disordcrs, intellcctual deterioration, poor comprehen-
of cach of 12 familiar pictures of abjects presented sion or lack of cooperation (Heilman and Valenstein,
12 different ways. Individuals with frontal damage 1985).
consistently maniiest deficits in performance on this
task. Individuals with temporal damage manifest def- Miscel/aneous tests
icits that vary with the severity of the lesion (Petrides
and Milner, 1982). These tests were includcd in the battery for a
Wisconsin Card Sorting Test. This test was deviscd vanety of rcasons. The information and vocabulary
ta study Uabstraet behavior" and Ushift of set" subtests of the WAIS provide a good measure of
(Berg, 1948; Grant and Berg, 1948). The subject is general intelligence but are not generally affected by
given a dcck of 64 cards, and is requircd ta categome frontal trauma in adulthood (Lezak, (976). Analysis
th... according ta a plan establishcd by the investi- of the results of th... tests would help determine
gator. Individuals suffering from dorso-Iateral frontal whether alcohol affectcd the factor of "general in-
lesions perform poorly on this test (Milner, 1964). telligence" or if its action was more specific in nature.
41
PETERSON ET AL. 117
The digit symbol subtest was included because il is T.uu: t. Blood alcohol concentrations
sensitive ta variations in motivation (Lezak, 1976),
Alcohol in high doses impairs certain aspects of DOSAGE GROUP
motor performance (Connors and Maisto, 1980; Hull High dose Medium dose Law dose
and Bond, 19S6; Lewis, 1969). A Reaction Time Test M~n SD Mean SD Mean SD
was included aJong with the Pursuit Rotor Test to
aid in clarifyins the nature of this impairment. Scores On. .093~·b .021 .044' .009 .00l .000'
Two .103a.b .027 .031" .008 .002 .0006
3rc assigned in tenths of a second for the reaetion Th,.. .083~·b .Oll .022' .009 .002 .000'
time test and in seconds for the Pursuit Rotor Test.
The Youns·Pihl Memory Test consists of a list of Nort: Ali rcponed differences are sianificant al p < .01.
40 words taken randomly from the Thorndike·Lorge Il Represenu a sianificant difference bctween the hiah- and 10w-
Analysis of the subjective intoxication scale indi· High dose: lO l.71 1.19 l.5l 1.29
cated that the expectancy manipulation was success· 60 l.10 1.19 2.74 1.64
90 2.l5 1.06 1.86 0.67
fui. Means and stand~'sd deviations are listed in Table Medium dose: lO l.28 0.82 2.9l 1.22
2. Within dosage groups, subjects told that they were 60 2.6l 1.06 1.88 1.01
receiving a hiSh dose of alcohol rated themselves as 9(1 1.48 0.48 1.34 0.51
more intoxicated than subjects told they were receiv. Low dose: lO 2.71 0.75 1.77 0.71
60 1.62 0.91
ing a low dose. Initial (F = 4.IS, 1I6S df, p < .OS) 1.10 0.29
90 1.13 0.l2 1.00 0.00
and mid·session ratings (F = 4.38, 1/6S df, p < .OS)
were significant, whiJe final ratings (F = 3.2g, 1/6S Nott: 5ee Method section for I~els of sisnifi~.
42
1 118 JOURNAL OF STUDlES ON ALCOHOL/MARCH 1990
effects were othcrwise minimal. funher analyses wcre subjects made any errars while carryÎng out the tasks
carried out on means coUapsed within dosage groups. associated with these (wo tests.
mental high-dose effect of alcohol intoxication. The when it did play a role, it was in the opposite
".-::.? direction to that predicted. The fact thal functional
Self·Ordered Pointing and Wisconsin Card Sort Tests
tolerance to alcohol intoxication can be learned
did not appear to be sensitive to the effects of
alcohol consumption. The Self-0rdered Pointing scores (Hoffman and Tabuoff, 1995) May account for the
reported are total errcrs in three trials. The Wisconsin direction of the expectaney effect secn in this study.
If experienced drinkers receive accurate information
Card Sort scores are total errors.
about the dose of alcohol they are consuDÙng they
Tests not directly ossociated with the frontal cane>: May be able to adapt and adjust to that dose if
circumstances demand it.
Five of 14 measures of rtonfrontal' function also The study is interesting because it demonstrates
proved sensitive to the effects of high-dose alcohol that alcohol intoxication per se impairs cenain a3pects
intoxication. Analysis of the Logica1 Memory subtest of neuropsychological functioning. Cognitive skil!>
demonstrated that alcohol intoxication significantly dependent upon the prefrontal cortex suffer deterio· .
impaited delayed recall of verbal information ration. 5uch skil1s are crucial to successful cC"lmpletion
(F = 6.99, 2/64 df, p < .(02). Intoxicated subjects of the Porteus Mazes (Porteus, 1959), the Rey copy
were also impaired in thelr ability to repraduce the (Lhermitte et al.. 1972) and to the copying of complex
Rey·Osterreith figure after a delay (3.minute delay: figu,es in general (Luria and Tsvetkova, 1964). Al-
F = 12.77, 2164 df, p < .001: 25-minute delay: though individuals with parietal lobe damage aise
F = 15.21, 2164 df, p < .(01). Alcohol consumption have difficulty copying complex figures (Walsh, 1978),
significantly impaired recall of the difficult pairs of the pattern of impairments induced by alcohol intox·
the Paired Associates (F = 3.32, 2164 df, p < .05), ication is not suggestive of construetional apraxia.
while the level of impairment approached significance AdditionaJIy, Albert (1973) found that constructional
for recall of the easy pairs (F = 2.52, 2164 df, apraxia was highly correlated with visua! negleet, and
p < .09). The Pursuit·Rotor Test also proved sensi· alcohol intoxication did nol praduce visual neglect in
tive to the detrimental effects of alcohol intoxication the present study. Impairments in word fiueney are
(F = 6.41, 2162 df, p < .(03). Mean.o, standard de· aIso associated with damage to the frontal lobe (Ieft,
viations and leve!> of sill'Ùficance for ail nonfrontal anterior to Broca's area) (Benton, 1968; Milner, 1967;
tests except for the test of visua! neglect and the Ramier and Hécaen, 1970; Tow, 1955). Since the
Apraxia Questionnaire are presented in Table 3. No prefrontal cortex is responsible for the planning and
43
PETERSON ET AL. 119
~
TAn! J. Test of coptitivc funaioninl
li( DOSAGE GROUP
Hia:h dose Medium dose Law dose
Mean SD M.an sb Mean SD
organization of behavior (Damasio, 1985), knowledge interesting given that the funetion of the hippocampus
that alcohol impairs ilS funetioning pharmacologically is not limited tO memor}', and that it and the septum
sheds an interesting light on consideration of intox· play a role in elieiting a variety of eue-specifie states
ication. of anxiety (Gray, 1982). These cues include novelty,
Skills associated classically with the temporal cortex threat of punishment and threat of frustrative nonre-
also deteriorate. Intoxicated subjects manifested def· ward (Gray, (982). An alcohol·impaired septal.hip·
icilS in ail forms of delayed noncued memor}' (verbal pocampal system might weU show reduced sensitivity
and spatial) during tbis study, as weU as perfonning to cues that would nonnally elicit anxiety and aid
poorly on the Wechsler Paired Associates Test. This an individual in maintaining safety. Alcohol intoxi·
pattern of impainnent, overall, suggcslS that alcohol cation may al10w people to engage in activities that
intoxication panicuJarly affects the funetion of the would nonnally produce anxiety, and may produce
hippocampus, which plays a key role in the transfer cognitive impairmenlS that limit their ability to aet
of information from shon·term attention to long· adaplively even if they do become anxious. These
tenn storage and/or in ilS retrieval (Gray, 1982; two factors May aeeount in pan for the pronouneed
Luria, 1980; O'Keefe and Nadel, 1978). Extensive tendeney of intoxicated individuals to become both
support for tbis idea is available within the relevant vietims and vietimizers.
animal literature (Gray, 1982), which suggests that Certain other aspects of this study deserve consid·
the benzodiazepines, barbiturates and alcohol aet eration as weU. The detrimental effcet of alcohol
primarily on the septal·hippocampal system. Recent upon wbat bas bcen dcseribed as Hmotor" perform·
work by Begleiter and Porjesz (19g8) also lends ance has been consistently demonstrated (Connors
credence to tbis supposition. This is particuJarly and Maisto, 1980; Hull and Bond, 1986; Lewis, 1969;
44
120 JOURNAL Of STUDIES ON ALCOHOLIMARCH 1990
Vuchinich and Sobell, 1978). Researchers who study a general descnptor for the dysfunction associated
the effcets of alcohol intoxication have described with damage ta the prefrontal areas of the frontal
bath the Pursuit Rotor and Reaction Time Tests as lobes. The concept is too simplistic. Locale of dam-
indicators of "motar performance" (Williams et al., age, even within an area as specific and apparently
1981). However, in the present study, alcohol intox- nonspecialized as the frontal lobes, still variably
ication did not decrease reaetion time (in threc dif· affects behavior (Damasio, 1985). Althou8h dysfunc-
ferent paradigms) nor performance on the Digit tion associated with circumscribed lesions may be
Symbol WAIS-R subtest, which is sensitive ta deficits usefully described in terms of lobe location, it may
in motor persistence and response speed (Lezak, be mare aceurate ta attribute drug effects ta altera.
1976). However, it did impair complex motor pero tions in neuropsychological systems, which are not
formance, as measured with the Pursuit Rotor. Dif- Iikely ta be lobe-specific. The prefrontal divisions are
ferent pans of the central nervous system control supplicd with rich conncetions ta various Iimbic
diffcreDt aspects of movcment. Recent research al structures, including the hippocampus (Luria, 1980).
the Montreal Neurologica1 Institute suggests that the The hippocampus plays a key raie in memory con-
frontal lobes are particularly imponant in goveming solidation, and the memory deficilS demonstrated by
complex aets of motor performance, but do not intoxicatcd subjects in the present study suggest that
determine motor specd (Leonard et al., 1988). Luria its functions may be impaircd by alcohol consump-
(1980), in his discussion of the motor analyzer, tion. The orbital·frontal conex and various structures
locatcd in the frontal conex, has made similar sugges· in the Iimbic system act as an integratcd unit (Luria,
tians. The", iaeas might help clarify the confusion 1980) and subsume many of the functions that scemcd
about alcohol's effcet on motor performance. Perhaps ta be impalrcd by alcohol during lhis study. This
intoxication has a more profound effeet upon the thenry, admittcd1y post hoc, seems ta fit the facts
sequencing, organizing and control of motor action, more accurately than the hypothesis offercd at the
rather than upon ilS spced of execution. beginning of the study. Nonetheless, the results of
Alcohol intoxication did not produce deficits in the present study are interesting for a variety of
"verbal" or "general" intelligence per se, at least reasons. Research into the effcets of alcohol upon
insofar as these qualities are measured by the Weehs- behavior has lackcd a testable unifying hypothesis
1er Adult Intemgence Scale Vocabulary and Infor- since its inception-and the use of tests validatcd
mation subtests. These tests are robust in the face clinically and experimentally offers the possibility for
of even extensive brain damage. and are often used dceper comprehension of intoxicatcd behavior. In
as indicators of premorbi" ability (Lezak, 1976). addition, the fact that alcohol affects cognition at a
Alcohol intoxication also had no effcet on perform- purely pharmacologieallevel is striking, although Hull
ance during the Self-Ordercd Painting Test. This test and Bond (1986) suggestcd that the expeetaney effcets
was validated on individuals with extensive and var· associatcd with alcohol use primarily affcet social
iable lesions of the frontal conex (Petrides and behavior and not information processing per se. In
Milnor, 1982), and it may be that alcohol affcets a the present study, the effects of expectancy upon
system that docs not participate in the functions cognitive functioning were minimal. Situations that
neeessary ta complete this test successfully. There is involve alcohol consumption May serve as an excuse
no evidence that alcohol intoxication detrimentally for indulging in cenain types of antisocial behavior;
affcets those functions associatcd with the occipital- nonetheless, il is evident that alcohol intoxication
parietal lobes, insofar as the present study is con· pharmacologically induces neurop.ychologica1 impair.
cemcd. Tests for the functioning of this region are ment. It docs not scem unreasonable ta suppose that
somewhat subjective in nature. but in all cases the 5uch impairment has serious behavioral consequences.
performance of the intoxicatcd and sober subjeets
was equally perfeet. No subjcets manifestcd any signs AckDowledcm.Dts
whalSOCver of negicet, of apraxia associated with
The authors would like to thank Debbie Rou and Or. Frank
Iimb and buccofacial gestures and manipulations, or Ervin for the eontribution of their time and knowlcd.e.
serial aets. In summary, it seems as though the
similarities between those behaviors associated with
alcohol intoxication and those associated with pre. Ref.reDces
frontal damage are striking, but that the two con. ALlEU. M.L. A simple test of vÎsuaJ nealect. NEURA. 13:
ditions are certainly not identical. 658-665, 1973.
8EOLEITEJ., H. AND POIJESZ. 8. NeurophysioloaicaJ dysfunetion in
The fundamental hypothesis underlying this study
aJeoholism. la: ROSE, R.M. AlfD 8AUlTT, J.E. (EdJ.) Alea-
suffercd from a number of faults. The concept of hotism: Orilins and Outcomes, New York: Raven Preu, Pubs.,
"frontal·lobe syndrome" itself bas bcen criticizcd as 1988, pp. IS7 -174.
45
PETERSON ET AL. 121
BINTON. A.L. Differentia! behaviouraJ dfecu in frontal lobe PharmacolQlia 23: 99-114, 1972.
dîsease. NcuroPIYchololia 6i: 53-65. 1968. KHIORT. L.J.• BALUEE. R.E. AHD BoLAN1J. F.J. Alcohol and the
BnoWAN. H .• 80&0, 5., Hnro.u.asH, T. t [OUTJ.Ow. C.-M• .uro balaneed.placebo desiln: The role of e;tperimentcr demand.s in
MCTz:!Ll. S. Computed·lom0lfl.phy of the brain and neuro- e;tpeetancy. J. abnorm Psycho!. 95: ]3' - 340, 1986.
psycholoaical useslment of alcoholic patients. In: BI01ElTU. K..ou. P.• SElon. R.. O'NEn.L. B. .um Eow.uos. R.P. Cerebral
H. (Ed.) Biolo,ica1 EC(t'Cts of AJcohol. New York: Plenum cortical atroph, in a1coholic men. J. clin. PsYehial. 41: 417 -421,
Press, 1978. pp. 771-786. 1980.
8W4lAllV, t.M .• JOHNSO"', M.K., HUTUY. J.T• .urt) TAno.., LANO, A.R.• GoECItNEJ.. D.J .• Aoaso. V.J . .uro MAllAn. G.A.
T.H. AJcohol and clabot.live schemas for sct1tences. J. exp. Effeeu of alcohol on auression in male social drinkers. J.
Psychol.: Larn. Mem. CaIO. 6: 293 - 300. 1980. abnorm. riyehol. 14: '08-'18. 197'.
SoLTIa, J.F. ,un:) HAlO/ON, R. Cerebral damqc assoeiated with LEONAJ.D. G•• Mn.Nl:l.. B. AND JoNES. L. PerCormance on uni-
alcoholism: A reexaminadon. Psycho!. Re<:. JO: 165 -119, 1980. manual and bimanual tappinl taJks by patients with Icsions oC
Sat1t1N, K. Sianificance of role and norms in the .maU group (or the Crontal or trntporallobe. Neuropsyehol. 16: 79-91. 1988.
individual behaviorai chanl~ while drinkiDI. Q. J. Stud. LUAIt. M.O. Neuropsychololiw Assessment, New York: Oltford
Alcohol 10: 53 -64. 1959. Uaiv. Press. Ine., 1976.
CONNO.." O.J. AND MA1sTO, S.A. eCreas of alcohol. instruetion LHEJ.WIT1'1!. F.• DUOUESlœ. J. AND SIONOUT, J ,L, Analyse neuro-
and consumption rate on motOt performance. J. Stud. Alcohol psychololique du syndrome frontal. Rev. Neurol. (Paris) 117:
"1: '09-'17. 1980. 41l-44O. 1972.
Ca..ux., FJ.M. Similarities between the effects of alina and LUJ.IA. A.R. Hi,her Cortical Funetions in Man. 2d Edition. New
a1coholic intoxieati..,n on memory performance. COtutrueted York: Basic Boob. Ine.. 1980.
wittlÎn a "levels of procminl" framework. In: Btl.NUt1W. LUJ.IA. A.R•• HoWSItAYA. E.D•• Bt.INJ:Ôv, S.M. AND CmcHLn'.
I.M. AND PAUEl-. E.S. (Eds) A1cohol and Human Memory. M. Impaired seJectivity oC mental processes in a»oeiation with
Hillsdale. N.J.: Lawrence Erlblum Assol:s•• lnc.• 1977. pp. a lesion of the frontal lobe. Neuropsycholopi 5: 10'-117.
9-21. 1967.
ClOWN, S. An e;tperirnental 5tudy of psycholoaical chanles fol· LU1.1A. A.R. AND TsVETltovA. L.D. The proaramminl of construc-
lowinl prefronta! lobotomy. J. len. Psycho!. 41: 3-"1. 19'2. tive aa.lviry in local brain injuries. Neuropsyehololia 2: 9' - 108.
DAMASIO, A.R. The frontal lobes. ln: HIlI1JW'I, K.M. AND VAJ.. 1%4.
ENST1!Ilof. E. (Eds.) Cli:Uca.I Neuropsycho!olY, 2d Edition. New MA1wo. R.B. Psyehololieal upcets of frontal JYfCC'lomy :ald
York: Oltford Univ. Press. Inc.• 198'. pp. 339-]7$. frontal lobotomy in mental patienu. Researeh Public:aùoru.
EItKAN. O.• FJ.Al«ENIWluSIlI.. M•• GoLDIDO, L•• HAODAHL. R. Assac. Res. nerv. ment. Dis. 17: '37-564. 1948.
AND MYlST1!N. A.L. Subjec:tive and objective effccu of a1eohol M.u.1ATr. G.A. AND RORSENOW. D.J. Coanitive procesacs in
as funetions of dOSl.le and time. Psychopharm. 6: 399 - 4œ, a1canol use: E;tpectancy and the balanced placebo desian. In:
1%4. MIlllO. N.K. (Ed.) Advances in Substance Abuse: Debavioral
E3UNOSl. P.J. AND DA.WASIo. A.R. Severe ciisturbanee of hilher and Bioloaical Researeh. Greenwich. Conn.: JAl Prm. Ine.•
cOlnition after bilateral frontal lobe ablation: Patient EVR. 1980. pp. Il9-199.
NeurololY 35: 1731-1741, 1985. METr1JiJ,. F.A. Psychosurlical Problems. Philadelphia: Blakiston.
FUNUNUAEUSEJ.. M.• MYUTBN. A.-L. AND J.i.u!. O. Effccu of 19l2.
a moderate dose of alcohol on intellectual funetions. Psycho- MI1.1.EJ.. L. Sex Differences on a Work Auency Tuk. Thesis.
phannacolopa 3: 344-3'1, 1962. MeOill University Medical Library. Montreal. 1988.
0l.AJlAW. K. Theories of intoltieated aurmion. Cano J. Dehav. MELNU. B. Some efrccu of frontal lobectomy in man. In:
sa. 12: 141 -ll8. 1980. WAUEH. LM. AND AuaT. K. (Eds.) The Frontal Oranular
Oa..urr. D.A. AND BIao. E.A. A behlvioural ULI.Iysis of dqrec. Cortex and Behavior. New York: MeOraw-Hill Book Co.•
of reinforcement and e&SC of shiftia; to new resporues in 1 1%4. pp. 313-334.
weial·type card·wninl problcm. J. exp. Psychol. 3;: 0604-411. MD.NEJ.. B. Brain mechanistnJ sUliested by 5tudies of temporal
1948. lobes. In: Ma.1.lxAH. C.H. AND DAJ.1EY. F.L. (EdJ.) Brain
GlAY. J.A. The NeuropsychololY of Anxiety: An Enquiry lnto mechanum.s uaderlyinl speech and IlJ\IUIIe. New York: Orune
the Funetions or the Septo-Hippocampal System. New York: and Stranon, 1967.
Oltford Univ. Press. Ine" 1982. MIUŒJ.. B. Psychololical aspeçu of foc:al epilepsy and ilS neurg..
HUTOCOLLtS. P. AND JOHNSON. D.M. Differeati&l elfccu of aIcobol 5urpcal management. In: Pt1JJ'uu. 0.0•• PEl{J.Y. J.K. AHD
on verbal nuency. Q. J. Stud. Alcohol 17: 183 -189. 19'6. WAJ.TD. R.D. (EdJ.) Advanccs in NeurololY 8. New York:
HEIJ.IWol'. K.M. AND VAUlNSTllIN. E. CUnica1 NeuropsychololY. Raven Press. Pubs.• 197'. pp. 299-321.
New York: O;tford Univ. Press. Ine., 198'. 0·K.Ean. J. AND NADEL, L. The Hippocampw as COlnitive Mal'.
HoPnlAN. P.L. AND T.u.u:oPJ'. B. Ethanol's action on brain New York: O;tford Univ. Press. Ine•• 1978.
biochmùsuy. In: TUTU. R.E. AND VA.."1 Tmm.. D.H. (Eds.)
Aleohol and the brain: Chromc effccu. New York: Plenum
Psnmu. M. AND MILN"Ea. B. Deficits On subject-ordered
alter frontal· and temporal·lobe lesio11S in man. Neuropsy.
w'"
Medical Book Company. 1981. pp. 19-16. ebololia 10: 249 - 262. 1982.
Huu. J.O. A self..wareness madel of the causes and efrec:u of PoaTEUs. S.D. The Maze Test and CUnicai PsyeholOlY. Palo Alto.
alcobol consumptioo. J. ab':lorm. Psyçhol. 90: '86-600, 1981. Caüf.: Pacific Books. Pub.. 19'9.
Huu. J.O. AND BoND. C.F.. JI.. Soc:iaI. and bebavionl eonse. POl.nus. S.D. AND iCIlPND. R.OEM. Mental ehanaes after bUatera.l
quences of aleohol eonsumptioo and expectaDcy: A meta. prefroawlobotomy. Oeaet. Psyçhol. Mono. 19: 97 -1". 1944.
anaIysis. Psycbol. Bull. 9t: 3<17 - 360. 1986. POI.TIU3, S.D. AHD PErDs. H.N. PsycbosurJU')' and test validity.
JI!1lJNU. E.M. AND MAcF.w..um. R.A. ADalysis of psyc:boloaica.l J. aboorm soda! Psycho!. 41: 473-47$. 19017,'
experimenu 00 the efree:u of aleahol. Q. J. Stud. Alcohol 1: R..uaD, A..td. AND fücAmf. H. Role respcctÜ <les atteintes
212-371, 19oW. Crootales et de la laténlisatioD I~NIIe daDI lei déficiu de
JONU. D.M. ANI) VIDA, A. Coanitive performaacc meuured 00 la "fluence vc:rbaIe." Rev. Neural. W: 17-22. 1970.
the ucendiDl and desom<Iinl limb of the blood aleobol <:UlVe. Roos. D.F. """ PœJ.. R.O. Modillcatlom 01 tbe baIaIlecd·pla«bo
46
122 JOURNAL OF 5TUDIE5 ON ALCOHOLIMARCH 1990
dcsilD (or use al hilb blood dcohol levels. Addiet. Beha.... 1": Churchill Livinlslonc. Inc., 1978.
91-97. 1989. WA3H1tmorE. C. Alc:ohol. !leU and the group. Q. J. Stud. Alcohol
T.u.TII.. R.E., JONm, S.M .• SIKnON. C.D. AND VEOA. A. Efrm,s 17: 108 - 123. 1956.
of wk complex.ity and l'factice on performance durinl aeute WEIHOASTNEJl, H. Al'lD MuvKY. D.L. Statc-dcpendcnt stOf:llC
alcohol intoxication. Percept. MOlor Skills 33: 307 - 318. 1971. and reuieval or ellipcrience while into~cat~. In: BIJ.NlAt1W.
TBOlNDWI, E.L. AND La_OE. 1. The tcacher's book of 30,000 I.M. A1'ID P.una, E.S. (EeIs.) Alcohol and Human Memory,
words. New Vork: Columbia University Press. 1944. UiUsdale, N.J.: Lawrence Erlbaum Assoa., Inc.. 1977. pp.
Tow, P.M. Personality Chanl~ FoUowing Frontal Lcucolomy, Il9- 173.
New Yerk: Oxford Uni.... Press, Inc.•. 19~5. YOUNo, J.A. A1'ID Pna.. R.C. Sclr-c:onlto! or the errecu or alcohol
VUCHIN1CH, R.E. AND Souu. M.a. EmpiricaJ separation of into~c.'\tion. J. Stud. AJcohol 41: j67-$71, 1980.
physiololic and Cltpected cffecu of alcohol on c:omplex per· ZEtCHNEa. A. A1'ID Pna., R.C. errecls or alcohol and behavior
ctptual-mOlor pcrronnancc. Psychopharm. 60: 81-85. 1978. continaencies on human auression. J. abnorm. Psychol Il:
WALSH, K.W. Neuropsycholoi)l: A CUnical. Approach, New York: 153 - 160, 1979.
-.s.;..
47
Introduction: Study ~
48
Cognitive Dysfunction and the
Indiana University
Bloomington, Indiana
49
Cognitive Dysfunction
2
Jordan Peterson
Department of Psychology
Montreal, Quebec
CANADA
H3AIBl
,,,,,"';"
li
Key Words
50
Cognitive Dysfunction
3
Abstract
A battery of neuropsychological tests was administered to 22
non-alcoholic sons of male alcoholics (SOMAs) from families
with extensive histories of male alcoholism and to 22 non-
alcoholic controls with no history of familial alcoholism.
Eleven subjects in each group were tested sober; eleven were
tested while alcohol-intoxicated. Analyses of the results of
this battery suggested (1) that SOMAs may be characterized by
comparative decrements in those cognitive functions
associated with the organization of novel information,
dependent in theory upon the prefrontal cortex; and (2) that
alcohol detrimentally affects delayed memory, associated with
the temporal cortex, equally across groups. Twenty of these
SOMAs had previously participated in either of two studies
that demonstrated their cardiovascular hyper-reactivity to
threat/stress and their increased sensitivity to the
reactivity-dampening effects of alcohol intoxication.
Correlational analyses of the results of the present and
prevlous studies demonstrated the existence of a highly
significant relationship between cognitive impairment,
cardiovascular hyper-reactivity, and susceptibllity to the
reactivity-dampening effects of alcohol.
51
Cognitive Dysfunction
4
52
Cognitive Oysfunction
5
53
Cognitive Dysiunction
6
consumption.
Method
Subjects
54
Cognitive Dysfunction
7
55
Cognitive Dysfunction
8
56
Cognitive Dysfunction
9
pharmaceutical alcohol mixed 5:1 in orange juice, or to
receive an equivalent amount of juice by body weight and
0.132 ml/kg pharmaceutical alcohol, to provide "active
placebo" (Ross & Pihl, 1989) control for subject and
experimenter expectancy. All subjects were then submitted to
a battery of neuropsychological tests. An independent-groups
design with random group assignment was chosen specifically
to control for the effect of practice on the
neuropsychological test battery.
It should be noted additionally, that although
57
cognitive Dysfunction
la
58
Cognitive Dysfunction
11
59
Cognitive Dysfunction
12
. a priori) 25 minutes 1ater, after comp1etion of a number of
"i
~-
~ -,
Subjects are required to redraw the figure copied earlier 25
parietal-occipital cortex
printed on it, and are asked to bisect each line with another
GO
Cognitive Dysfunction
13
Miscellaneous tests.
Part Three
61
Cognitive Dysfunction
14
(cardiovascular reactivity-dampening).
..
( ,
62
Cognitive Dysfunction
15
Results
consequences of intoxication.
63
Cognitive Dysfunction
16
Part Three
64
Cognitive Dysfunction
17
0.009), and falls for those ~ho took the test drunk (r =
0.49, P < 0.18). This is an important consideration from the
methodological vie~point, because alcohol detrimentally
65
cognitive Dysfunction
18
decrement.
obviously also involves recall per se. The easy ~ord pairs
cries), and one ~ord serves as a cue for the other during
67
Cognitive Dysfunction
20
68
Cognitive Oysfunction
21
This means that those who made the most errors during the
who made the most errors during the SOP were most susceptible
multigenerational SOMAs.
69
Cognitive Dysfunction
22
shocks were also most susceptible ta alcohol's ability to
eliminate that reactivity.
Conclusion
This study provides tentative support for the hypothesis
that sober SOMAs from families with extensive
multigenerational male alcoholism are characterized by
comparative decrements in the ability to classify or to
attribute meaning to novel information. This ability has been
classically associated with prefrontal cortical function. It
also demonstrates the existence of a significant relationship
between certain aspects of this cognitive deficit and the
cardiovascular hyper-reactivity and alcohol-reactivity-
dampening characteristic of such SOMAs, and that such
reactivity and dampening are integrally related. In addition,
demunstration that alcohol intoxication severely impairs the
transfer of information from short-term storage into
permanent memory in SOMAs and contrals lends additional
credence to Gray's (1982, 1987) idea that alcohol
intoxication particularly impairs hippocampal function.
70
Cognitive Dysfunction
23
References
1 Albert, M.L. A simple test of visual neglect. NEURA 23: 658-
665, 1973.
1952.
71
Cognitive Dysfunction
24
Finn, P.R., and Pih1, R.O. Men at high risk for a1coholism:
447, 1983.
937-947, 1985.
1948.
72
Cognitive Dysfunction
25
1952.
73
Cognitive Oysfunction
26
.or Vol. 8, New York: Raven Press, 1975, pp. 299-321.
;~.
74
-- Cognitive Dysfunction
75
cognitive Dysfunction
28
Churchill-Livingstone, 1978.
76
Cognitive Dysfunction
29
Porteus Maze Age 13.9 ( 3 . 4 ) +12.7 ( 3 .1) 14.9 (1. 3 ) +13.0 (1. 8)
77
Cognitive Dysfunction
30
Self-Ordered 0.53
Painting 0.0169
.
.~--
:1
/·'",.f
"
78
Comments ~ Study 1 and ~
79
Information Processing, Neuropsychological Function, and the
Innerited Predisposition to Alcoholism
_.
1.
80
Predisposition to Alcoholism
l Jordan Peterson
Department of Psychology
McGill University
1205 Dr. Penfield Avenue
Montreal, Quebec
CANADA
H3AlBl
.. 0:.'
Key Words
alcoholism, heredity, neuropsychology, cognition,
psychophysiology, conduct disorder, hyperactivity, alcohol
intoxication
81
Predisposition to Alcoholism
3
ABSTRACT
82
Predisposition to Alcoholism
4
83
Predisposition to Alcoholism
5
84
Predisposition to Alcoholism
6
85
Predisposition to Alcoholism
7
86
Predisposition to Alcoholism
8
...
.~;
for next contact, or leaves the unexpected in its
87
Predisposition to Alcoholism
9
88
Predisposition ta Alcoholism
10
or coding system (Teylor and Discenna, 1985, 1986) for the
1 higher cortical structures. Each pattern of sensory
experience is accompanied by the activation of ~idespread,
89
Predisposition to Alcoholism
Il
activation: preparation for activity, via the
hypothalamus/pituitary adreno-cortical system, partially
under the inhibitory control of the hippccampus and frontal
cortex (Luria, 1980). Such physiological activation, elicited
prior to engagement in situation-relevant behaviour, might be
considered non-specifie, in that it is not necessarily
directed tovards any particular end (Panksepp, 1986). It is
interesting to note, hovever, that in the absence of
appropriate specifie goal eues, hypothalamic stimulation
evokes not only arousal, in its more general sense, but
generalized searching responses, vhich are amplified if there
are novel objects in the sens ory field of the animal
(Panksepp, 1986). It is for this reason that it may be more
generally use fuI to consider the hypothalamus central to the
integration of physiological state and psychobehavioural
function (Panksepp, 1986), rather than merely responsible for
autonomie regulation. The fact that hypothalamic stimulation
results in generalized searching behaviour (in the
appropriate context) makes it appear reasonable to regard the
cooperative activities of the structures presented in Figure
2 as truly systematic, and integrated in activity.
In addition to physiological activation, mismatch
activates vhat Luria (1973) described as the motor unit
(Gray, 1982), which is composed primarily of the prefrontal,
premotor and motor cortices. The pre frontal cortex, the
primary neocortical representative of the limbic system
90
Predisposition to Alcoholism
12
(Nauta, 1971) provides the physiological basis for the
voluntary, abstract organization of motor behaviour (Granit,
1977) and experience (Luria, 1980), and for the voluntary
direction of attention (Damasio, 1986; Es1inger & Damasio,
1985; Luria, 1980). The premotor and motor cortices appear to
hierarchically arrange intentions into mot or programs, and
execute them in behaviour (Luria, 1973). Intention is thereby
transformed sequentially into action, in the motor unit.
The role of the motor unit in the analysis of the
unexpected can take two parts. Comp1ex non-primates depend
primarily on the action of the premotor/motor cortex to
provide them with additional sensory information, about
unexpected circumstances, or to remove them from danger
(Granit, 1977). The application of search programs, drawn
primarily from the reservoir of learned and instinctual
behaviour, involve behavioural alterations (exploration,
play) and subsequent transformations of sensory input. When
an animal actively explores something new, it changes the
sensory aspect of the object under observation. This change
provides the animal with the opportunity to observe the novel
thing under a variety of circumstances. This adds to its
know1edge about the new situation, transforming the novel
into the known (Gray, 1987). If the unexpected occurs, too
dramatica11y (which means it varies in too many dimensions
simultaneous1y, and/or too quickly), then the animal flees,
..-,-...,
91
Predisposition to Alcoholism
13
92
Predisposition to Alcoholism
14
93
Predisposition to Alcoholism
15
sensitive to experimental variation and (3) because there is
94
Predisposition to Alcoholism
16
~..
Duncan-Johnson & Donchin, 1977; Tueting, Sutton & Z11bln,
'~
1971). From the neuropsychological viewpoint, it is
interesting to note that the P300 component has also been
described as an electrophysiologlcal manifestation of the
orienting reflex (Donchin, 1981; Porjesz & Beg1eiter, 1985),
with its probable origin in the hippocampus and amygdala
(Ha1gren et al., 1980; Okada, Kaufmann & Wllliamson, 1983).
Those studies examining the P300 production of SOMAs
have generally analyzed ERPs recorded during the course of a
visual or auditory "oddball" task. During this task,
participants are elther required to count infrequently
presented stimuli (such as high tones), embedded in a context
of more frequently presented, irrelevant but somewhat slmilar
j' stimuli (like low tones) or to make a judgeme~t regarding the
.. ~ ...
if..
'~ ...-
means that P300 evoked at the beginning of a task might
95
Predisposition to Alcoholism
17
differ from that produced at or near the end. Conclusions
dravn from studies examining P300's averaged over a large
number of trials are limited by their failure to examine this
potentially important possibility. The single study in Table
lA-I vhich presents data bearing directly on this issue in
fact suggests that stimulus novelty and family history
interact to affect P300 production (Elmasian, Neville, woods,
Schuckit and Bloom, 1982). Detailed examination of the data
presented in this study reveals that sober, lov-drinking
SOMAs are actually characterized by increased P300 amplitude,
and by decreased or at least equivalent P300 latency (and
overall reaction time) during the first block of stimulus
presentation (vhen the task is still novel), and by more
rapid deterioration of these responses during presentation of
later blocks and/or vhile under the influence of alcohol.
It is interesting to consider the recent york of Hill,
Steinhauer, Park and Zubin (1990) in the light of this more
detailed analysis of Elmasian et al. (1982). These authors
analyzed the ERP reactions of children of family-history
positive alcoholics and controls, obtained during the course
of an auditory oddball task, according to the conditional
probability of target stimuli appearance. Children of
alcoholics vere actually characterized by the production of
significantly larger mean P300 amplitudes and smaller P300
latencies than their controls, vhen exposed to the most
unpredictable target stimuli, and by cc~trast produced
96
Predisposition to Alcoholism
18
97
Predisposition to Alcoholism
19
unpredictability of the task.
As outlined previously, the hippocampus appears to
determine the intrinsic fascination of novel and/or
threatening ~henomena. By contrast, it appears to be the
prefrontal cortex that regulates the voluntary application of
cognitive resources (attention) in situations like those
described previously, where the significance of a stimuli is
merely dependent upon its social or individual labelling as
significant (Luria, 1980). In other words, those with a
highly functioning pre frontal cortex can concentrate on
performing a task for reasons other than its novelty, or
because it poses a threat. Given this argument, it appears
reasonable to provisionally attribute the differences between
.•.::1;.-•.
those with alcoholic fathers and controls in the experiments
described in Table lA-I to the effects of a specifie type of
attentional deficit characteristic of SOMAs, which makes
itself evident in situations that are boring, defined for the
limited purposes of this discussion as neither novel
(unpredictable) nor threatening, and to further posit that it
is a deficit in those abilities dependent upon the prefrontal
cortex that underlie this attentional deficit. Supportive
evidence for this latter claim will be reviewed later in the
manuscript.
Before these general hypotheses can be accepted as
useful, it is important to examine the minority of ERP
studies whose conclusions differ in part or whole from those
98
Predisposition to Alcoholism
20
99
Predisposition to Alcoholism
21
100
Predisposition to Alcoholism
22
101
Predisposition to Alcoholism
23
"
This latter pnssibility is reinforced by the conclusions
of four additional studies, utilizing a different
methodology, demonstrating that SOMAs may be characterized by
increased psychophysiological response to novel and/or
avers ive stimuli. Finn and Pihl (1987, 1988) demonstrated
that young adult nonalcoholic SOMAs vith extensive
multigenerational family histories of paternal alcohnlism
vere characterized by increased heart-rate and decreased
(OBVA) whe~ anticipating and receiving mild electric shock.
Finn, Zeitouni and Pihl (1990) discovered the same pattern of
cardiovascular hyper-reactivity among SOMAs faced vith and
receiving avoidable and unavoidable signalled electric shock,
and furthermore demonstrated that SOMAs vere characterized by
larger electrodermal orienting responses, shorter orienting
response latencies, and slover rates of habituation vhen
presented vith a short course of novel non-avers ive tones.
Harden and Pihl (submitted) extended the range of this
demonstration, determining that pre- and early adolescent
SOMAs vith extensive multigenerational histories of paternal
alcoholism vere characterized by increased heart-rate and
decreased OBVA during the course of a mental arithmetic task.
It is interesting to note, in this rega~d, that the
hypothalamus appears to be responsible for modulating
physiological preparation-for-activity (such as increased
heart-rate and decreased OBVA) and for integrating such
preparation vithin the context of stimulus-relevant
102
Predisposition to Alcoholism
24
behaviour, and that the hypothalamus is partially under the
inhibitory control of the hippocampus and pre~rontal cortex.
It is directly relevant to this notion that a majority of
the studies designed to address the issue have concluned that
FH+ subjects are characterized by comparatively poor
peLformance on tests of linguistic ability, abstraction and
problem solving. Comparative deficits in total IQ,
performance IQ, memory, visuospatial ability, perceptual-
motor capacity, and auditory/visual attention span have been
described less frequently (Pihl, Peterson, and Finn, 1990).
Those studies which describe such differences are presented
in Table 1-B. SOMAs have often been characterized by reduced
academic achievement, as weil, in many of these reports, and
in various longitudinal studies of children and adolescents
who later develop serious problems with alcohol (see for
example Rydelius, 1981; and the review by Zucker and
Lisansky-Gomberg, 1986). This reduced achievement includes
poorer school performance, more truancy, and completion of
fewer years of school.
The minority of studies which have not provided support
for the notion of reduced cognitive capacity among FH+
subjects can be grouped into three categories. In the first
category are those reports that include a preponderance of
females as subjects or as the alcoholic parent and do not
offer analysis of results by sex (Hesselbrock, Stabenau and
Hesselbrock, 1985; Wilson and Nagoshi, 1988; Workman-Daniels
103
Predisposition to Alcoholism
25
.:.;;,.
1984), especially within larger studies (Schaeffer, Parsons
and Errico, 1988) and sometimes does not provide such
differentiation (Alterman, Gerstley, Goldstein and Tarter,
1987; Reed, Grant and Adams, 1987).
Many of the studies listed in Table 1-B utilized tests
drawn from the neuropsychological literature. This approach,
with aIl its flaws, allows for the production of inferences
based on the relationship between brain function and
behaviour, and such inferences, with regard to SOMAs, have
indeed been drawn (Tarter, Alterman and Edwards, 1985, 1988).
Although the cognitive deficits characteristic of SOMAs have
been defined and measured in a relatively heterogeneous
manner, the abilities many of the most commonly reported
104
Predisposition to Alcoholism
26
apparently share one important feature in common: their
dependence on the proper functioning of the prefrontal
cortex, described in detail by Luria (1980). As noted
previously, this cortical subunit is primarily responsible
for the abstract classification of stimuli and the
organization of behavinur. Tarter et al. (1985, 1988), Pihl,
Peterson and Finn (1987) and Gorenstein (1987) have aIl
observed that the pattern of cognitive impairment typical of
males at increased general risk for alcoholism is similar to
that demonstrated by individuals ~ho have suffered somé form
of mild prefrontal cortical trauma. In addition, the non-
cognitive characteristics of SOMAs and such individuals share
certain features in common. These characteristics include
Test (Petrides and Milner, 1982) and the Wisconsin Card Sort
Test (Milner, 1964)) and their susceptibility to bath aspects
of the cardiovascular hyper-reactivity to anticipation and
receipt of signalled electric shock demonstrated by SOMAs in
105
Predisposition to Alcoholism
27
Finn and Pihl's (1987, 1988) studies. It may be relevant as
well that Whipple et al. (1988) showed that the performance
of SOMAs and their fathers on various tests of "visuo-
perceptual" performance correlated with the average amplitude
of their ERP production to target stimuli. Parsons,
Sinha and Williams (1990) have replicated the latter finding
in a population of FH+ male alcoholics.
106
Predisposition to Alcoholism
28
107
Predisposition to Alcoholism
29
reason, SOMAs may tend to use search or avoidance strategies,
1···.
.
or to resort (when aIl else fails) to aggression. It i5
interesting to note in this regard that Pihl and Harden
(submitted) have demonstrated that a single group of
108
Predisposition to Alcoholism
30
109
Predisposition to Alcoholism
31
...
~.,~"
effect of alcohol upon SOMAs, within the framework provided
no
Predisposition to Alcoholism
32
theory presented in this manuscript suggests that it is
reduction in the hippocampal response to threat and novelty
that decreases subsequent physiological preparation for
activity, like that described by Finn and Pihl (1987, 1988),
Finn et al. (1990) and Levenson et al. (1987) and which also
reduces the necessity for action in the face of threat, as
described by Levenson et al. (1987).
It also seems possible that SOMAs are more susceptible
to what might be the positively reinforcing effects of
intoxication. Pollock, Volavka, Goodwin, Mednick, Gabrielli,
Knop and Schulsinger (1983) and Pollock, Gabrielli, Mednick
and Goodwin (1988) described SOMAs' comparative1y increased
production of EEG waveforms associated with pleasure and
well-being during alcohol intoxication. This is particularly
interesting given that SOMAs aiso produce more high frequency
beta activlty when sober (Gabrielli, Mednick, Volavka,
Pollock, Schulsinger, and Itil, 1982), like alcoholics
(Mendelson and Mello, 1979), and that these beta waveforms
have been associated with psychological states of tension and
anxiety (Kiloh and Osselton, 1961). Finn and Pihl's (1987,
1988) and Finn, Zeitouni and Pihl's (1990) observation that
the baseline heart-rate of SOMAs increases signlficantly,
when compared to controls, within twenty minutes of alcohol
ingestion could conceivably be indicative of a positively-
reinforcing effect, as drug-related increases in heart rate
have, under sorne clrcumstances, been linked wlth reward (Wise
111
Predisposition to Alcoholism
33
and Bozarth, 1987; Fowles, 1983). Recent research conducted
by Peterson, Pihl, Seguin, and Finn (submitted) suggests that
alcohol-induced heart-rate hyper-react~vLty dampening and
alcohol-induced baseline heart rate increase are associated,
significantly, with increased weekly alcohol consumption.
This is sorne indication that a link exists between putative
markers of alcoholic tendencies and actual drinking behavior.
Conclusion
Sons of male alcoholics are at heightened risk for the
development of alcoholism. This risk is associated with
various observable abnormalities in psychophysiological
response, cognition, behaviour and reaction to alcohol. SOMAs
appear to be characterized by increased amplitude and
decreased latency of the P300 ERP component to stimuli that
are new and/or and unpredictable, and by decreased P300
amplitude and increased latency to stimuli that have lost
their novelty and/or threat. They are aiso characterized by
increased cardiovascular response to novelty and threat, by
decreased performance on tests of verbal ability, problem
solving and abstraction, and by increased rates of conduct
disorder and hyperactivity. SOMAs aiso appear hyper-sensitive
to the cardiovascular-response reducing effect of alcohol
intoxication, to aicohol-intoxication induced reductions in
P300 response to novelty, and to alcohol-induced increases in
baseline heart-rate.
The theoretical model described in the present
112
Predisposition to Alcoholism
34
manuscript is predicated on the notion that deficits in the
function of the pre frontal cortex cou Id underlie
manifestation of aIl these abnormalities. The prefrontal
cortex is responsible for the maintenance of voluntary
attention under conditions of social demand, for the
regulation of psychophysiological response to threat and
novelty, and for many aspects of verbal reasoning,
abstraction and problem solving.
It therefore appears possible that SOMAs are hyper-
reactive to threat and novelty because they are characterized
by deficits in pre frontal function. Their difficulties with
prefrontal function may render them (1) less able to use
~.-.
abstraction to inhibit preparation for activity in the face
~L of novelty and threat, ( 2 ) more likely to revert to action
itse If when confronted with novelty and threat, and ( 3 ) less
likely to maintain attention to stimuli that are no longer
113
Predisposition to Alcoholism
35
. "".,.
......
:~
possible that such interference might be negatively
reinforcing, particularly to those characterized by
hyperactivity of this system.
This the ory makes a' number of specifie and testable
predictions. These include the hypotheses that SOMAs with
well-defined extensive histories of paternal alcoholism will
manifest increased sober reactivity (increased heart-rate,
decreased digital blood volume amplitude, increased P300
amplitude, decreased P300 latency, increased somatic
activity) to unpredictable or novel stimuli or to stimuli
that serve as a eue for punishment and that alcohol-
consumption at or above legally intoxicating doses will
significantly reduce or even eliminate this reactivity. The
theory also predicts that aIl these indices of reactivity
will be correlated, and that such reactivity should be
correlated with alcohol-induced reactivity dampening (no
reactivity, no elimination of that reactivity). The ability
of SOMAs to abstract should be correlated with this increased
reactivity, as weIl, if abstraction is defined as performance
114
Predisposition to Alcoholism
36
il5
Predisposition to Alcoholism
37
References
frontal lobe defect. Res Publ Ass Res Nerv Ment Dis. 27:
479-504, 1948.
Centre, 1984.
310, 1986a.
116
Predisposition to Alcoholism
38
117
Predisposition to Alcoholism
39
1967.
1981.
118
Predisposition to Alcoholism
40
Donchin, E., Ritter, W., & McCallum, W.C. Cognitive
l
psychophysiology: The endogenous components of the ERP.
In: Calla",ay, - .,
r' Tueting, P., and Koslo"" S.H. (Eds.).
Event-Related Brain Potentials in Man. Ne", York,
Academie Press, 1978.
Duncan-Johnson, C.C., & Donchin, E. Quantifying surprise: the
variation of event-related potentials "'ith subjective
probability. Psychophysl. 456-467, 1977.
Elmasian, R., Neville, H., Woods, D., Schuckit, M., & Bloom,
F. Event-related brain potentials are different in
individuals at high and 10'" risk for developing
alcoh01ism. Proc Nat Acad Sei. 79: 7900-7903, 1982.
r
.~.,
~.
119
Predisposition to Alcoholism
41
71, 1983.
832-838, 1970.
120
Predisposition to Alcoholism
42
,"i
~
Goodwin, D.W., Schulsinger, F., Hermansen, L., Guze, S.B. &
Winokur, G. Alcohol problems in adoptees raised apart
from alcoholic biological parents. Archs Gen Psychiat.
28: 238-243, 1973.
Goodwin, D.W., Schulsinger, F., Moller, N., Hermansen, L.,
Winokur, G. & Guze, S.B. Drinking problems in adopted
and non-adopted sons of alcoholics. Archs Gen Psychiat.
131: 164-169, 1974.
Gorenstein, E.E. Cognitive-perceptual deficit in an
alcoholism spectrum disorder. J Stud Alc. 48: 310-318,
1987.
Granit, R. The Purposive Brain. Cambridge: Massachussetts
(~.,.
121
Predisposition to Alcoholism
43
....".
,~.
Heath, A.C. and Martin, N.G. TeeDage alcohol use in the
1984.
65-82, 1985.
1987.
122
Predisposition to Alcoholism
44
Hill, S.Y., steinhauer, S.R., Zubin, J., & Baughman, T.
123
Predisposition to Alcoholism
45
242-253, 1987.
.. ~
modulation and alcohol consumption. J stud Ale. 38:
2049-2056, 1977.
Luria, A.R. The Working Brain. New York: penguin Books, 1973.
124
Predisposition to Alcoholism
46
"'''-''
...
,,1 Milner, B. Sorne effects of frontal lobectomy in man. In:
Warren, J.M. and Akert, K. (Eds.). The Frontal Granular
Cortex and Behaviour. New York: McGraw-Hill Book
Company, 1964, pp. 313-314.
Morrison, J.R., & stewart, M.A. A family study of the
125
Predisposition ta Alcoholism
47
Psychological Association, Anaheim, California, 1983.
Nylander, I. Children of alcoho1ic fathers. Acta Pediatr
Scand. Scandinavia, ~, supplement 121, 1960.
Nylander, I. & Rydelius, P.A. A comparison between children
of alcoholic fathers from excellent versus po or social
conditions. Acta Pediatr Scand. 71: 809-813, 1982.
O'Connor, S., Hesselbrock, V. & Tasman, A. Correlates of
increased risk for alcoholism in young men. Prog
Neuropsychopharmacol Biol Psychiat. 10: 211-218, 1986.
Okada, Y.C., Kaufman, L. & Wi11iamson, S.J. The hippocampal
formation as a source of the slow endogenous potentials.
Electroencephalogr Clin Neuropsychol. 55: 417-426, 1983.
Panksepp, J. The anatomy of emotions. In: Plutchik, R. and
Kellerman, H. (Eds.) Emotion: Theory, Research and
Experience (Vol 3: Bio1ogical Foundations of Emotion),
New York: Academic Press, lnc., 1986 pp. 91-124.
Parsons, O.A., Sinha, R., & Williams, H.L. Relationships
between neuropsychological test performance and event-
related potentials in a1coholic and non-alcoholic
samples. A1coh01: Clin Exp Res. 14: 746-755, 1990.
Peterson, J.B., Rothfleisch, J. Zelazo, P.D. & Pihl, R.O.
Acute alcoho1 intoxication and cognitive functioning. J
Stud Alc., 51, 114-122, 1990.
Peterson, J.B., Finn, P., & Pihl, R.O. Cognitive dysfunction
and the inherited predisposition ta alcoholism. J Stud
Alc., in press.
126
Predisposition to Alcoholism
48
12ï
Predisposition to Alcoholism
49
Pihl, R.a. & Spiers, P. Individual characteristics in the
Po1ich, J., Burns, T., & Bloom, F.E. P300 and the risk for
polich, J., & Bloom, F.E. P300 from norma1s and children of
190, 1988.
psychiat., in press.
ua
Predisposition to Alcoholism
50
340-344, 1987.
129
Predisposition to Alcoholism
51
•.,.....
social background factors, criminality and personality
1983a.
381-385, 1983b.
169: 456-458.
130
predisposition to Alcoholism
52
131
Predisposition to Alcoholism
53
"1·"
'- ," Alcoholism. Toronto: Addiction Research Foundation,
235, 1989.
1985.
132
Predisposition to Alcoholism
54
1985.
133
Predisposition to Alcoholism
TABLE 1
A. ELECTROPHYSIOLOGICAL ABNORMALITIES
I. Reduced P300 ERP Amplitude II. Psychophysiological
and/or Increased P300 ERP Latency Hyper-reactivity
E1masian et al. (1982) Finn & Pihl (1987)
Begleiter et al. (1984) Finn & Pihl (1988)
Whipple & Noble (1986) Finn et al. (1990)
O'Connor et al. (1986) Harden & Pihl (submitted)
Begleiter et al. (1987)
Steinhauer et al. (1987)
Whipple et al. (1988)
Hill et al. (1988)
.,~
134
Figure 1: Theoretical Patll of Information Processing
SENSORY INFORMATION
Mu~imodal Sensory
Integration
ABSTRACT
CLASSIFICATION
~,!'~
~,
Unable to Classily
RELEVANT IRRELEVANT
RewardlPunishment Neutral
ACTION INACTION
Approach
(active exploration)
or
Avoidance
135
Predisposition to Alcoholism
56
136
Figure 2: Neuropsychological Path of Information Processing
SENSORY ORGANS
SENSORY UNIT
HIPPOCAMPAL SYSTEM
PRE FRONTAL
CORTEX
PREMOTOR
AND
MOTOR CORTEX
137
Predisposition to Alcoholism
57
......
,
FIGURE 2: NEUROPSYCHOLOGICAL PATH OF INFORMATION PROCESSING:
138
Figure 3: Observable Anomalies in Information Processing
Increased
Motorlc Actlvlty
Increased
Distractlbllity
139
.'!1 '
(,1."
Predisposition to Alcoholism
58
140
Figure 4: TheoreticaJ Effect of AlcohoJ on Information Processing
INTERFERENCE WITH
HIPPOCAMPAL FUNCTION
141
if......
' "'"
Predisposition to Alcoholism
59
FIGURE 4: THEORETICAL EFFECT OF ALCOHOL ON INFORMATION
particularly sensitive.
142
Discussion and Introduction to Study l
The theory outlined above does not provide a simple
explanation for the potentially positively-reinforcing
elevations in heart-rate characteristic of SOMAs during the
ascending limb of the blood alcohol curve, after consumption
of a relatively high dose of alcohol (Levenson et al., 1987;
Finn and Pihl, 1987, 1988; Finn et al., 1990).In addition,
there is no direct evidence linking cardiovascular
reactivity-dampening to negative-reinforcment, or to its
putative consequence - increased voluntary alcohol
consumption. The data analysis (Peterson, Pihl, seguin and
Finn, submitted) designated below as study 3 was designed to
rectify these shortcomings. It provides an examination of the
relationship between alcohol-induced basline heart-rate
increase, cardiac hyper-reactivity to threat of and aversive
stimuli, susceptibility to alcohol-induced elimination of
that reactivity, the multiplicative interactions of these
effects, and voluntary self-reported weekly alcohol
consumption by 36 SOMAs with a multigenerational family
history of alcoholism, 14 SOMAs with alcoholic fathers only,
and 33 sons of nonalcoholics wlth no familial alcoholism.
143
Alcohol-Induced Heart Rate Change, Family History, and
Prediction of Weekly Alcohol Consumption by Non-
Alcoholic Males
Jordan B. Peterson
Robert O. Pihl
Jean R. Séguin
Department of Psychology
McGill University
Montréal, Québec, Canada
Peter R. Finn
Department of Psychology
Indiana University
Bloomingdale, Indiana
144
Alcohol-Induced
2
Abstract
A number of investigations have demonstrated that sons
of male alcoholics with multigenerational family
histories of male alcoholism are characterized by
cardiac hyper-reactivity to avers ive stimuli, by
susceptibility to alcohol-induced elimination of that
reactivity, and by increased baseline heart-rate while
intoxicated. Although it has been assumed that these
characteristics, and others like them, might serve as
markers for the inherited predisposition to alcoholism,
the relationship between their presence and actual use
of alcohol remains unknown. The analyses conducted in
the present paper, completed in an attempt to reduce
this lack of knowledge, demonstrate that all three
psychophysiological factors, and their interactions,
are significantly associated with self-reported weekly
alcohol consumption by 83 non-alcoholic males: 36 who
had at minimum, an alcoholic father, grandfatQer and
uncle or brother; 14 whose familial alcoholism was
limited to the fathcr; and 33 whose familles were not
characterized by alcoholism.
145
Alcohol-Induced
3
146
Alcohol-Induced
4
147
Alcohol-Induced
5
148
A1coho1-Induced
6
149
Alcohol-Induced
7
and (3) that ·,tse and Bozarth (1987) have suggested all
drugs of abuse might share psychomotor stimulant
actIons, and assoclated posltively relnforcing
propertles. Accordlngly, it seems plausIble to poslt
that SOMAs are differentlally susceptible to what might
be the dlrectly relnforclng effect of alcohol, deflned
operationally as heart-rate increase, as weIl as to its
negatlvely-relnforclng propertles. The results of thls
equally testable hypothesis are also reported in this
paper, along wlth an analysls based upon the
Interaction of the two putatively relnforclng effects,
and lts relatlonshlp to alcohol consumptlon.
Method
Data analysed and presented ln thls paper were
collected as part of a continuous high-rlsk project
sponsored by the Douglas Hospital-McGlll UnIversIty
Alcohol Research Project. Various aspects of this
project have been descrlbed ln prevlous communIcatIons
(FInn & Plhl, 1987, 1988; Finn, Zeltoun1 & Pihl, 1990),
and the data lncluded ln the analyses reported herein
have been drawn, from these studles, and from others
completed slnce. However: aIl the analyses descrlbed
150
Alcohol-Induced
8
151
Alcohol-Induced
9
152
Alcohol-Induced
10
AlI subjects were paid $5.00 per hour for their
participation.
Procedure
The majority of the subjects who part~cipated, to
date, in the Douglas Hospital-McGill Univer~ity Alcohol
Research project (and aIl of those described in the
present analysis) were subjected to a standard
procedure, described in detail in Finn and Pihl (1987,
1988) and outlined briefly below. upon arrivaI at the
lab, subjects were required to read and sign an
informed consent form, were weighed, and asked to
complete a self-report questionnaire concerning age,
education, and frequency and quantity of alcohol
consumption. This form of self-report has been
demonstrated to be a valid measure of alcohol
consumption (Sobell & Sobell, 1986). With regards to
freguency: all subjects were asked to estirnate how
often they consurned alcohol per week, on average.
Those who consumed upon less than one occasion weekly
were asked to estimate monthly, or yearly frequency.
With regards to quantity: aIl subjects were asked to
153
l
Alcohol-Induced
11
154
Alcohol-Induced
12
procedure began. Each subject whose data was included
in the present analysis was tested while under the
influence of either 0.75, 1.00, or 1.32 ml/kg of
alcohol. Alcohol administered at these doses
consistently produces measurable psychophysiological
alterations in functioning in MGH SOMAs (stewart, Finn
& Pihl, 1988). Order of participation was not
consistently counter-balanced, as Finn and Pihl (1987)
and Finn, Zeitouni and Pihl (1990) showed no order-
effect.
Results
Demographies and blood alcohol level (BAL)
One-vay analysis of variance revealed that
subjects in th~ three risk groups did not differ
significantly in mean age (M = 23.12, SE = 0.50),
years of school1ng (M = 14.09, SE = 0.21), or BAL (~ =
0.091, ~ = 0.002).
Psychophysiological measures
Results from the first three countdown to and
signalled shock trials are included in the present data
analysis, since a minimum of three trials were
conducted upon every subject. Only one
(..... ~.
155
Alcohol-Induced
13
psychophysiological measure (heart-rate) and one
measure of weekly alcohol consumption are included in
the following analyses. Heart-rate was selected for
sole inclusion (a) because it has varied in previous
investigations conducted upon SOMAs in terms of
~ea~tivity to threat, and merely as a function of
alcohol consumption, as outlined in the introduction;
(b) because its psychological concomitants are
comparatively well-understood, with regards to positive
reinforcement (Fowles, 1983) and preparation-for-
activity (Obrist, 1976); and (c) because it is easily
and reliably assessed, and baseline measures are
comparable within and between subjects (in distinction
to DBVA, which is only comparable within subjects
(Jennings, Tahmoush, & Redmond, 1980). Multiplication
of average weekly frequency and average quantity
provided a simple, easily comprehensible composite
measure of total weekly alcohol consumption. As weIl,
comparison of only two straightforward measures
heightens the parsimollY, utllity and statistical power
of the analyses.
156
Alcohol-Induced
14
157
Alcohol-Induced
15
recorded from sober subjects during the signalled shock
procedure (from the tone signalling trial onset to 7
seconds after shock), divièing that figure by the sober
baseline heart-rate, and multiplying the end result by
100. FH- subjects vere characterized by a mean 6.23%
increase (~= 1.92); UGH subjects by a mean 1.29%
increase (~= 2.87); and HGH subjects by a mean 13.07%
increase (SE = 1.79). One-vay ANOVA revealed
significant differences betveen the groups (~(2,78) =
...
-.
7.11, R< .0015. Post-hoc Fisher's LSD indicated that
the HGH and UGH, and HGH and FH- groups differed
significantly, R< .05.
Per cent a1cohol-induced heart-rate reactivity
change (%ALC-HRRC), also graphically presented in
Figure l, vas calculated by subtracting mean
intoxicated baseline heart-rate (recorded during the
ten-minute rest period prior to the shock trials
administer~d to intoxicated subjects) from heart-rate
recorded from intoxicated subjects during the signalled
shock procedure (from the tone signalling trial onset
to 7 seconds after shock), dividing that figure by the
intoxicated baseline heart-rate, multiplying by 100,
158
Alcohol-Induced
16
the HGH and UGH, and HGH and FH- groups differed
,
d.·
Per cent alcohol-1nduced baseline heart rate
.....
;'I
hoc Fisher's LSD indicated that the HGH and UGH, and
159
Alcohol-Induced
17
~rediction of drinking behaviour
Squared inter-correlations betveen mean drinks per
veek, risk, \SOB-HRR, \ALC-HRRC, \ALC-BLHRC and the
interaction products of the latter three variables are
included in Table 1. Weekly alcohol intake is
significantly correlated vith all the factors and vith
their interactions. As vell, each factor correlates
significantly vith each other factor. This means that
drinking is associated vith sober heart rate
reactivity, alcohol-induced change in that reactivity,
and with alcohol-induced baseline heart rate change.
The multiplicative interaction between sober heart-rate
reactivity and alcohol-induced baseline heart rate
change is assoclated vith drinking almost as well as
the multiplicative interaction between alcohol-induced
heart-rate reactivity change and alcohol-induced
baseline heart rate change.
160
,
•1
Alcohol-Induced
18
~.-
in the model. ALCOHOL-EFFECT, entered in multiple
1
~.
161
Alcohol-Induced
19
ANOVA of these tvo examined alcohol consumption purely
as a function of the primary division. The high
ALCOHOL~EFFECT group consumed significantly more drinks
per veek ,M = 9.68, ~ = 0.65) than the lov ALCOHOL-
162
.j
".\..
Alcohol-Induced
20
UGH a Mean 6.58 drinks per week (SE = 1.491; and
members of the HGH a Mean 7.84 drinks per week (SE =
0.931, [.(2,771 = 0.39, 12.< .6767.
163
Alcohol-Induced
21
Discussion
This study demonstrates most importantly that a
significant relationship exists between three measures
of cardiovascu1ar response and week1y a1coho1
consumption, among non-a1coho1ic social drinkers.
Individua1s characterized by sober heart rate
acce1eration to signa11ed electric shock, by alcohol-
dampening of that acceleration, and/or by heart-rate
acceler~tion to a1cohol consumption consume more
alcoho1 on a week1y basis than those who are not
characterized by these responses. Additionally, those
164
Alcohol-Induced
22
165
.--'.-
.. ..;;;
Alcohol-Induced
23
166
1
".;..
Alcohol-Induced
24
,,'r
.....
167
1
Alcohol-Induced
25
References
American Psychiatrie Association (1980). Diagnostic and
statistical manual of mental disorders (3rd ed.).
Washington, De: Author.
Bohman, M., Sigvardsson, s., & Cloninger, c. R. (1981).
Maternal inheritance of alcoho1 abuse. Archives of
General Psychiatry, ~, 965-959.
Cadoret, R. J., cain, C. A., & Grove, W. H. (1980).
Deve10pment of a1coholism in adoptees raised apart
from alcoholic biological relatives. Archives of
General Psychiatry, 11, 561-563.
cloninger, C. R., Bohman, H. & sigvardsson, S. (1981).
Inheritance of alcohol abuse: A cros5-fostering
analysls of adopted men. Archives of General
Psychiatry, ~, 861-68.
Cotton, N. S. (1979). The familial incidence of
alcoholism. Journal of Studies on Alcohol, ~, 89-
116.
168
Alcohol-Induced
26
169
Alcohol-Induced
27
Goodwin, o. W. (1ge5). Alcoholism and Genetics.
Archives of General Psychiatry, 42, 171-174.
Goodwin, o. W., Schulsinger, F., Hermansen, L., Guze,
S. B., & Winokur, G. (1973). Alcohollsm and the
hyperactive child syndrome. Journal of Nervous and
Mental Oisease, 160, 349-353.
Hrubec, Z., & Omenn, G. S. (1981). Evidence of genetic
predisposition to alcoholic cirrhosls and psychosis:
Twln concordances for a1coho1ism and Its bio1ogical
end points by zygosity among male veterans.
Alcoholism: Clinical and Experimental Research, a,
207-215.
Jennings, J. R., Tahmoush, A. J., & Redmond O. P.
(1980). Non~invasive measurement of peripheral
vascular activity. In 1. Martin & P. H. Venables
(Eds.), Techniques in Psychophysiology (pp. 69-137).
·New York: Wiley.
Lester, o. (1988). Genetie theory: An assessment of the
heritability of alcoholism. In C. o. Chaudron and O.
A. Wilkinson (Eds.), Theories on Aleoholism (pp
73-102). Toronto: Addiction Researeh Foundation.
170
Alcohol-Induced
28
Levenson, R. W., Oyama, O. N., & Meek, P. S. (1987).
Greater reinforce ment from alcohol for those at
rlsk: Parental rlsk, personality rlsk, and sex.
Journal of Abnor.al PsychQiogv, ~, 242-253.
Murray, R. M., Clifford, C. A., and Gurling, H. (1983).
Twln and adoptlon studles: How good ls the evldence
for a genetic role? In M. Ga1anter (Ed.). Recent
Developments ln Alcoholls~ (Vol l, pp. 25-48). New
York: Plenum Press.
Orbrlst, P. A. (1976). The cardiovascular-behavioral
.,,
~
,r•
.-
171
Aleohol-Indueed
29
Pihl, R. O., Finn, P., and Peterson, J. B. (1989).
Autonomie hyperreaetivity and risk for aleoholism.
Progress in Neuro-Psyehopharmaeology and Biologieal
psyehiatry, 11, 489-496.
Pihl, R. O., Peterson, J. B., (in press). Risk
eharaeteristies of men vith a multigenerational
family history of aleoholism. In D. Van Thiel & R.
Tarter (Eds.), Aleohol abuse and aleoholism; Recent
advanees. Nev York: Plenum.
.-.....
.•
Pihl, R. O., Peterson, J. B., & Finn, P. (1990) .
Inherited predisposition to aleoholism:
Charaeteristies of sons of male aleoho1ies. Journal
of Abnor.al Psyehology, ~, 291-301.
Sher, K. (1987). stress response dampening. In H. T.
Blane & K. E. Leonard (Eds.), Psychologieal theories
of drinking and aleoholism (pp. 227-271). Nev York:
Gullford.
Searles, J. S. (1988). The role of geneties in the
pathogenesis of aleoholism. Journal of Abnor.al
Psyehology, i2, 153-167 •
. ..
~
172
Alcohol-Induced
30
Selzer, M. (1971). The Michigan Alcoholism Screening
Test: A quest for a new diagnostic instrument.
American Journal of Psychiat~, 127, 1653-1658.
Sobell, L. c., & Sobell, M. B. (1986). can we do
without a1cohol abuser's self-reports? The Behayior
Therapist, 1, 141-146.
stewart, S. H., Finn, P. R., & Pihl, R. o. (1990). The
effects of alcohol on the cardiovascular stress
response in .en at high risk for alcoholism: A dose
q'--
response study. Manuscript sub.itted for
l publication.
Tarter, R. E., Alter.an, A. 1., & Edwards, K. L.
(1988). Neurobehavioural theory of alcoholism
etiology, in C. D. Chaudron and D. A. Wilkinson
(Eds.) Theories on Alcohollsa, (pp. 73-102).
Toronto: Addiction Research Foundation.
Wise, R. A., & Bozarth, H. A. (1987). A psychomotor
stimulant theory of addiction. Psychologlcal Reyiew,
iL 469-492.
173
Alcohol-Induced
31
B C 0 E F G H 1
F (R2) .199
(12.< ) .0001
G (R2) .200
(12.<> .0001
H (R2) .183
(12.<> .0001
A=Risk F= B*D
B=Sober Heart Rate Reactivity G= C*D
C=Alcohol Induced Heart Rate Reactivity Change H= B*C*D
D=Alcohol Induced Baseline Heart Rate Change I=Drinks/Week
E= B*C
174
Alcohol-Induced
32
Table 2
(Predicted NUmber) 18 13
UGH (AN) 13 1
< (PN) 8 6
1
.....
HGH (AN) 10 26
(PN) 21 15
175
,'......
Per Cent Change
.:.
en
.:.
N o <Xl
0
;,g
0
l'al
;,g
0
•
-,g
0
»
r
»
r
Cf)
." () ()
0
, , ,
CD
I1 CD :c :c
r ::Il ::Il
:c ::Il ::Il
::Il ()
()
..
c
~
Ci)
I
s::
Ci)
I
176
Alcohol-Induced
33
Figure Caption
Figure 1. Per cent change in heart rate. SOB-HRR =
sober heart rate reactivity. ALC-HRRC = alcohol-induced
heart-rate reactivity change. ALC-BLHRC = alcohol-
induced baseline heart-rate change .
.~
'1
'~
177
Mean Drinks/Week
o Cl
m
ï
0
•
:r:
cci"
::E :::r
z
o
» »
C")
0 ë'ï
a :::r 0
:::r
o Q. 0
m
01
~.
:::::
CD
m
:::::
CD
p> .....
C")
.....
C")
éD
-<'.....
JJ
tf)
;;s:;;-
a
o
<
m
::"1.
cr>
Q.
178
Alcohol-Induced
34
Figure Caption
Figure 2. Mean drinks per veek (self-report) by high
and lov susceptibillty to ALCOHOL-EFFECT (AE).
r
...
179
21 1 1
18 • %SOB-HRR
15
lm %ALC-HRRC
12
9
o %ALC-BLHRC
ID
0> 6
c
~ o
..c 3 co
o ri
....... 0+1---'
C
al
o..... -3
al
a.. -6
-9
-12
-15 ;
.,." : 1
LOWAE HIGH AE
, (
Alcohol-Induced
35
Figure Caption
Figure 3. Per cent change in heart rate, by high and
lov sUBceptibility to ALCOHOL-EFFECT (AE). SOB-HRR =
sober heart rate reactivity. ALC-HRRC = alcohol-induced
heart-rate reactivity change. ALC-BLHRC = alcohol-
induced baseline heart-rate change.
181
Final Comments
According to the extant literature, sons of male
alcoholics (SOMAs) are characterized by conduct
.~.
182
The literature examined in the introduction to this
thesis suffers from a number of general faults. Too many
studies use subjects vhose familial alcoholism is
limited at best to the father, and many do not conduct
their analyses by sex. The presence of male alcoholism
in at least tvo concurrent generations of a given
proband's pedigree vould increase the likelihood that
the proband is in tact characterized by the familial
alcoholic predisposition. The nature of alcoholism in
the family, and the long- and short-term patterns of
alcohol use among experimental subjects must be more
carefully specified. Description of alcohol use should
involve investigation of consumption and consequences.
Frequency, duration, intensity and onset of alcohol use
are critical variables. The nature of complications
arising from alcohol use must be clarified in as much
detail. Duration and severity of detrimental effects
upon physical, social, and occupational functioning
should be described. Demographie variables must be given
careful consideration. With regard to age, for example,
the likelihood that a given subject is actually
characterized by an alcoholic predisposition decreases
as he or she ages, vithout actually abusing alcohol.
Younger subjects are therefore more suitable. Finally,
comparison of SOMAs to sons of fathers vith other
psychiatrie disorders vould aid in determining the
specificity, and therefore the utility, of any
·r
183
distinguishing markers. Implementation of these
184
increase that may be indicative of susceptlbllity to
positive reinforcement. Assessment for presence of these
markers or risk factors promises to be relatively
straightforward, and non-invasive. In addition, these
markers are plausible intermediary factors, either from
the viewpoint of heredity or environment.
The story presented in this thesis is predicated
upon a number of assumptions, which may or may not be
grounded ln facto Research conducted upon assumptlon
cannot be made rlsk-free. Over-interpretation of data
may lead to the pursuit of knowledge, where knowledge
does not in fact exist. However, in scientific
endeavour, as elsewhere, the willingness to risk Is
everything.
r
1
.~.
185
References
Adrian, M. (1984). Statistics ~ Alcohol and Drug Use ~
186
Aronson, H. & Gilbert, A. (1963). Preadolescent sons of
480.
187
(1983). P3 and stimulus incentive value. Psycho-
physiology, ~, 95-101.
Bancroft.
188
potentials in normal subjects and alcoholics. In H.
258.
861-68.
189
Cloninger, C.R., Sigvardsson, S., &. Bohman, M. (198S).
Childhood personality predicts alcohol abuse in young
adults. Alcoholism: Clinical Experimental Research, 12,
494-505.
Coger, R.W., DymOnG, A.M., Serafetinides, E.A., Lo~instam,
190
subjective and objective variables over a four-hour
191
Nervous and Mental Disease, 171, 444-447.
349-353.
Goodwin, D., Schulsinger, F., Moller, N., Hermansen, L.,
Winokur, G. & Guze, B. (1974). Drinking problems in
adopted and nonadopted sons of alcoholic$. Archives 2.f
General psychiatry, 21, 164-169.
Gorenstein, E.E. (1987). Cognitive-perceptual deficit in an
alcoholism spectrum disorder. Journal 2.f Studies on
":cohol, i!!., 310-318.
Gorenstein, E.E., & Newman, J.P. (1980). Disinhibitory
psychopathology: A new perspective and a model for
research. psychology Review, [l, 301-315.
Gottfries, C. (1980). Activity of monoamine oxidase and
brain levels of monoamines in alcoholics. In D. Richter
(Ed.) Alcoholism and Brain Damage (pp. 228-239;. New
192
York: tfniversity Park Press.
193
potentials generated in the human hippocampal formation
and amygdala by infrequent events. science, 210, 803-
805.
Harden, P., & Pihl, R.O. Cognitive and Behavioural
characteristics of Adolescent Sons of Alcoholics.
Manus~ript submitted for publication.
Harwood, H.J., Napolitano, D.M. & Kristiansen, H.
(1984). Economie Cost to Societ~ of Alcohol and Drug
Abuse and Mental Illness: 1980. Triangle Park, NC:
Research Triangle Inst.ltute.
Hasin, D.S., Grant, B.F., & Endicott, J. (1988).
severity of alcohol dependence and social/occupational
problems: Relationship to clinical and familial
history. Alcoholism: Clinical and Experimental
Research, 11, 660-664.
Heath, n.G. (1986). The neural substrate for emotion. In
Plutchik, R. and Kellerman, H. (Eds.). Emotion: Theory,
Rese.Hch and Exper ience (Volume 3: Biological
Foundations l i Emotion)(pp 3-36). New York: Academie
Press.
Hechtman, L., weiss, G., & Perlman, T. (1984).
Hyperactives as young adults: Past and current
substance abuse and antisocial behaviour. American
Journal l i Orthopsychiatry, ~, 415-425.
Hegedus, A.M., Alterman, A.L, & Tarter, R.E. (1984)
Learning achievement in sons of alcoholics. Alcoholism:
Clinical and Experimental Research, ~, 330-333.
194
Hegedus, A., Tarter, R. Hill, S.Y., Jacob, T., and
Research, ~, 580-582.
82.
16.
195
490-498.
12.
196
K., Sauna, S., & Rose, R.J. (1987). Genetic influences
Psychology, ~, 262-265.
386-391-
147, 54-57.
197
Lipscomb, T.R., carpenter, J.A., 1; Nathan, P.E. (1979) Static
ataxia: a predictor for alcohollsm? British Journal 2i
(
Addiction, li, 289-294.
Littrell, J. (1988). The Swedish studies of the adopted
children of alcohollcs. Journal of Studies on Alcohol,
i1., 491-499.
Loper, R., Kammeier, M., 1; Hoffman, H. (1973). MMPI
characteristics of college freshman males who later
became a lcoholics. Journal 2.i Abnormal Psychology, !U.,
159-162.
Ludwig, A.M., cain, R.B. 1; Wikler, A. (1977). Stimulus
intensity modulation and alcohol consumption. Journal
2.i Studies QQ Alcohol, ~, 2049-2056.
Lund, C.ll. 1; Landesman-Dwyer, S. (1979). Pre-
stratton.
Luria, A.R. (1980). Higher Cortical Fnnctions ln. t:!ill1.
Moscow: Moscow University Press.
Magnusson, D., 1; Bergman, L.R. (1988). Individual and
variable-based approaches to longitudinal research on
early risk factors. In M. Rutter (Ed.) Studies 2i
Psychosocial Risk: The Power 2.i Longitudinal Data (pp.
45-61). New York: Cambridge University Press.
Major, L.F., Hawley, R.J., saini, N., Garrick, N.A., 1;
198
Murphy, D.L. (1985). Brain and liver monoamine oxidase
Psychiatry, l, 189-195.
l§., 888-891.
199
alcoholism. Archives Qi General Psychiatry, il, 1137-
1141.
Moss, H.B., Yao, J.K., and Maddock, J.M. (1989).
Responses by sons of alcoholic fathers to alcoholic and
placebo drinks: Perceived mood, intoxication, and
plasma prolactin. Alcoholism: Clinical and Experimental
Research, 12, 252- 257.
Murphy, W.J., McBride, W.J., Gatto, L., Lumeng, L., &
Li. T.K., (1988). Effects of acute ethanol
administration on monoamine and metabolite content in
forebrain reglons of ethanol-tolerant and
nontolerant alcohol-preferring (P) rats. Pharmacology
Blochemistry !. Behavior, li, 169-174.
Murray, R.M., Clifford, C.A., and Gurling, H. (1983).
Ne ... lln, O.B., "Thomson, J,B. (1990). Alcohol challenge ... ith
California, USA.
276.
201
P3ychiatry, !Q, 211-218.
O'Halley, s.s., &. Haisto, S.A. (1985). Bffects of
family history and expectancies on responses to alcohol
in men. Journal Qi Studies ~ Alcohol, ~, 289-297.
Oreland, L., von Knorring, L., von Knorring, A.L., &
202
Petrie, A. (1978). Individuality in Pain and Sufferinq
Charles C. Thomas.
291-301.
Polich, J., Burns, T., & BloOffi, F.E. (1988). P300 and
203
Polich, J., & Bloom, F.E. (1988). Event-related brain
potentials in individuals at high and low risk for
developing alcoholism: Failure to replicate. Alcoholism:
Clinical and Experimental Research, lI, 368-373.
Polich, J., & Bluom, F.E. (1986). P300 and alcohol
consumption in normals and individuals at risk for
alcoholism. A preliminary report. Prugress in
Neuropsychopharmacology. and Biological Psychiatry, lQ.,
201-210.
Polich, J. & Bloom, F.E. (1987). P300 from normals
and children of alcoholics. Alcohul, i, 301-305.
Polich, J., Haier, R.J., Buchsbaum, M., & Bloom, F.E.
(1988). Assessment of young men at risk for alcoholism
with P300 from a visual discrimination task. Journal
of Studies on Alco~ol, il, 186-190.
:'f
...
".1
i~
Pollock, V.E., Gabrielli, W.F., Mednick, S.A., &
Goodwin, D.W. (in press). EEG identification of
subgroups of men at risk for alcoholism? Psychiatry
Research.
Pollock, V.E., Teasdale, T.W., Gabrielli, W.F. & Knop,
J. (1986). Subjective and objective measures of
response to alcohol among young men at risk for
alcoholism. Journal Qi studies on Alcohol, .il, 297-304.
Pollock, V.E., Volavka, J., Goodwin, D.W., Gabrielli,
W.F., Mednick, S.A., Knop, J., & Schu1singer, F.
(in press). Pattern reversaI visual evoked potentials
after alcohol administration among men at risk for
alcoholism. Biological Psychiatry.
JI
"':,i ...
204
Pollock, V.E., Volavka, J., Goodwin, D.W., Mednick,
.-,.-,. S.A., Gabrielli, W.F., Knop. J. & Schulsinger, F .
(1983). The EEG after alcohol administration ln men at
risk for alcoholism. ~rchive$ ~ General Psychiatry,
iQ., 857-861.
Porjesz, B., & Begleiter, H. (1985). Human brain
electrophysiology and alcoholism. In R.E. Tarter & D.H.
Thiel (Eds.). Alcohol and the Brain, (pp. 139-182).
Plenum Publishing Corporation.
Porjesz, B., Begleiter, H. & Samuelly, I. (1980).
Cognitive deficits in chronic alcoholics and elderly
subjects ,~ssessed by evoked brain potentials. Acta
Psychiatrica_ Scandinavi.:l, g, (Suppl. 286), 15-29.
Porjesz, B., & Begleiter, H. (1981). Human evoked
brain potentials and alcohol. Alcoholism: Clinical and
Experimental Research, ~, 304-317.
Propping, P., Kruger, J. & Mark, N. (1981). Genetic
predisposition to alcoholism: An EEG study in alcoholics
and their relatives. Human Genetics, 59, 51-59.
Reed, R., Grant, 1., & Adams, K.M. (1987). Family
history of alcoholism does not predict
neuropsychological performance in alcoholics.
Alcoholism: Clinic,~l and Exper imental Research, li,
o
340-344.
Ricks, D. 1< Berry, J. (1970). Family & symptom
patterns that precede schizophrenia. In M. Roff and
F. Ricks (Eds.). Life History Research in
205
Psychopathology (pp. 31-50). Minneapolis:
University of Minnesota Press.
Robins, L.N. (1966). Deviant Children Grown ~ ~
i2., 497-520.
Roy, A., Virkunnen, M., Guthrie, S., & Linnoila, M.
(1986). Indices of serotonin and glucose metabolism in
violent offenders, arsonists and alcoholics. Annals ~
206
psychiatrica Scandinavia, ~, 368-380.
Research, i, 117.
Schuckit, M.A. (1980). Biological markers: metaLolism
and acute reactions to alcoh01 in sons of alcoholics.
Pharmacology Biochemistry ~ Behavior, 11, (Suppl. 1), 9-
207
16.
Schuckit, M.A. (1984). Differences in plasma cortisol
after ingestion of ethano1 in relatives of alcoholics
and controls: Preliminary results. Journal of Clinical
PsychiatrY, 12, 374- 376.
Schucki t, M.A. (1988). Reactions to alcohol in sons of
alcoholics and controls. Alcoholism: Clinical and
Experimental Research, 11., 465-470.
Schucklt, M.A. (1980b). Self-rating of alcohol
intoxication by young men with and without family
histor ies of alcoholism. Journal 2.i Studies Q.!l
208
Schuckit, M.A., Gold, E.O., Croot, F., Finn, P., &
55.
209
young men at high risk for alcoholism: Social and
psychological. characteristics. Archives Qi General
psychiatry, il, 755- 760.
Searles, J.S. (1988). The role of genetics in the
pathogenesis of alcoholism. Journal of Abnormal
Psychology, 12, 153-167.
Sher, K.J., li Alterman, A.1. (1988). The HK/MBD
questionnaire: Replication and validation of distinct
factors in a nonclinical sample. Alcoholism: Clinical
and Experimental Research, 11" 233- 238.
Simons, R.F. (1982). Physical anhedonia and future
psychopathology: An electrocortical continuity?
Psychophysiology, li, 433- 441.
Sokolov, E.J. (1969). The modeling properties of the
nerv0us system. In 1. Maltzman li Cales, K. (Eds.).
Handbook of Contemporary Soviet Psychology (pp. 671-
704). New York: Basic Books.
stahl, S.M. and Kravitz, K.D. (1986). A critical review
of the use of laboratory tests in psychiatrie
disorders. In P. Berger and K.H. Brodie (Eds.1 American
Handbook Qi Psychiatry, Vol. ~ ~ 1048- 10841. New
York: Basic Books.
Steinhauer, S.R., Hill, s.Y., li Zubin, J. (1987).
Event- related potentials in alcoholics and their first-
degree relatives. Alcohol, i, 307-314.
Stewart, M.A., de Blois, C.S., li Singer, S.S. (1978).
Alcoholism and hyperactivity revisited. A preliminary
210
report. Currents in Alcohol Research lllL 1-3, 349-357.
Sullivan, J.L., Cavenar, J.O. Jr., & Maltby, A.A.
(1979). Familial biochemical and clinical correlates
of a1coholics with low platelet monoamine oxidase
activity. Biological Psychiatry, li, 385-39.
Sullivan, J.L., Stanfield, C.N., Schanberg, S., &
Cavenar, J. (1978). Platelet monoamine oxidase and
serum dopamine beta- hydroxylasc ùctivity in chronic
alcoholics. Archives Qi General Psychiatry, 12, 1209-
1212.
swartz., C.M., Drew5, V., and Cadoret, R. (1987).
Decreased epinephrine in familial alcoholism. Archives
Qi General Psychiatry, !i, 938-941.
Tarter, R.E., Alterman, A.r., & Edwards, K.L. (1985).
Vulnerability to alcoholism in men: A behavior-genetic
perspective. Journal Qi Studies on Alcohol, ii, 329-
356.
Tarter, R.E., Alterman, A.r., & Edwards, K.L. (1988).
Neurobehavioural theory of alcoholism etiology, in C. D.
Chaudron and D. A. Wilkinson (Eds.) Theories Qll
Alcoholism 1I2J2. 73-102). Toronto: Addiction Research
Foundation.
Tarter, R.E., Hegedu5, A.M., Goldstein, G., shelly, C.
& Alterman, A.I. (1984). Adolescent sons of
a1coholics: Neuropsycho1ogical and personality
characteristics. Alcoholism: Clinical and Experimental
Research, ~, 216-222.
211
Tarter, R.E., Jacob, T., and Bremer, D.A. (1989).
Cognitive status of sons of a1coh01ic men. A1coh01ism:
Clinical and Experimental Research, 11, 232-235.
Tarter, R.E., McBride, H., 8uonpane, N., & Schneider,
D. (1977). Differentiation of alcoholics: Childhood
history of minimal brain dysfunction, family history,
and drinking pattern. Archives of General psychiatry,
il, 761-768.
Tueting, P., sutton, s. & Zubin, J. (1971).
Quantitative evoked potential correlates of the
probability of events. Psychophysiology, l, 385-394.
Vaillant, G.E. (1983). The Natural History of
Alcoholism. Cambridge, MA: Harvard University Press.
von Knorring, L. (1976). Vieual averaged evoked
responses in patients suffering from alcoholism.
Neuropsychobiology,~, 233-238.
von Knorring, A.L., Bohman, M., von Knorring, L. &
Oreland, L. (1985a). Plate let MAO activity as a
biological marker in subgroups of alcoholism. Acta
Psychiatrica Scandinavia, li, 51- 58.
von Knorring, L., Palm, U., & Andersson, H.E. (1985b).
Relationship between treatment outcome and subtype of
alcoholism in men. Journal Qi Studies Qll Alcohol, ii,
388- 391.
von Knorring, L., von Knorring, A.L., Smigan, L.,
Lindberg, U., & Edholm, M. (1987). personality traits
in subtypes of alcoholics. Journal of Studies on
Alcohol, i!, 523-527.
212
Whipple, S., & Noble, E.P. (1986). The effects of
familial alcoholism on visual event-related potentials.
Psychophysiology, 23, 470-
Whipple, S.C., Parker, E.S., & Noble, E.P. (1988). An
atypical neurocognitive profile in alcoholic fathers and
their sons'. Journal .Qi. Studies 2.!l Alcohol, i2., 240-244.
Wilson, J.R., & Nagoshi, C.T. (1988). Adult children
of alcoholics: cognitive and psychomotor
characteristics. British Journal .Qi. Addiction, ~, 809-
820.
Winokur, G., Rimmer, J., & Reich, T. (1971).
Alcoholism. IV. Is there more than one type of
alcoholism? British Journal .Qi. psychiatry, 118, 525-
531.
.-. Wood, D., Wender, P.H., & Reimherr, F.W. (1983). The
prevalence of attention deficit disorder, residual type,
or minimal brain dysfunction, in a population of male
alcoholic patients. American Journal .Qi. psychiatry, 140,
95-98.
Workman-Daniels, K.L. and Hesselbrock, V.M. (1987).
Childhood problem behaviour and neuropsycho1ogica1
functioning in persons at risk for alcoho1ism. Journal
Qi Studies 2.!l A1coho1, 11, 187-193.
Zucker, R.A. & Lisansky-Gomberg, E.S. (1986). Etio1ogy
of alcoho1ism reconsidered: The case for a
biopsychosocia1 process. American Psycho1ogist, il,
783-793.
213
Zuckerman, M., Murtagh, T., & Siegel, J. (1974).
214