 |
|
Supervisory Attentional System in Nonamnesic Alcoholic Men
Xavier Noël, PhD;
Martial Van der Linden, PhD;
Nicolas Schmidt;
Rita Sferrazza, MD;
Catherine Hanak, MD;
Olivier Le Bon, MD;
Jacques De Mol, PhD;
Charles Kornreich, MD;
Isidore Pelc, MD, PhD;
Paul Verbanck, MD, PhD
Arch Gen Psychiatry. 2001;58:1152-1158.
ABSTRACT
| |
Background Many studies have shown that recently detoxified alcoholic persons perform
poorly on tasks thought to be sensitive to frontal lobe damage, supporting
the hypothesis that the frontal lobes are highly vulnerable to chronic alcohol
consumption. However, it appeared that most of the executive tasks used in
these studies also involved nonexecutive components, and these tasks had been
shown to be impaired as a result of nonfrontal lobe lesions. In this study,
we examined further the "frontal lobe vulnerability" hypothesis using executive
tasks, proved to be associated with frontal lobe functioning, that allowed
us to distinguish the relative importance of executive and nonexecutive processes.
Method Thirty recently detoxified asymptomatic male alcoholic inpatients and
30 control subjects were tested for planning, inhibition, rule detection,
and coordination of dual task, as well as the speed of processing and nonexecutive
functions (such as short-term memory storage).
Results Alcoholics performed worse than controls in almost all tasks assessing
executive functions. However, they were not slower than the controls and showed
normal results for nonexecutive functions.
Conclusions Chronic alcohol consumption seems to be associated with severe executive
function deficits, which are still present after a protracted period of alcohol
abstinence. These data support the idea that the cognitive deficits in recently
detoxified sober alcoholic subjects are due, at least partly, to frontal lobe
dysfunctioning.
INTRODUCTION
ALCOHOLISM continues to be one of the leading public health problems
in the Western World. The economic costs of alcohol dependence to society
are vast.1 Long-term abuse of alcohol in association
with nutritional deficits (thiamine deficiency) can lead to classic neurological
illnesses such as the Wernicke-Korsakoff syndrome.2
However, during the last 2 decades, research has provided evidence of brain
abnormalities in "nonamnesic" chronic alcoholic subjects, including electrophysiological,3 anatomical,4 cerebral
blood flow,5 glucose metabolism,6
and a wide range of neuropsychological deficits.7
Current literature postulates 3 main hypotheses concerning brain structures
that may be vulnerable to the effects of prolonged alcohol abuse: the "right
hemisphere abnormality," the "generalized brain dysfunction," and the "frontal
brain vulnerability.
The right hemisphere abnormality hypothesis states that the nondominant
hemisphere is more vulnerable to alcohol's effects.8
In this view, recently abstinent alcoholic subjects would show difficulties
in nonverbal neuropsychological functions, supposedly related to the right
hemisphere. However, several studies using dichotic listening tasks to determine
whether there was any relationship between functional asymmetry and alcoholism
revealed no significant effects.9, 10
These data suggested that the poorer performance of alcoholic subjects on
nonverbal or visuospatial tasks is a consequence of the psychometric sensitivity
or unfamiliarity of these tests. The generalized brain dysfunction hypothesis
asserts that long-term alcohol abuse produces neurotoxic effects throughout
the brain, resulting in mild to moderate cognitive dysfunction that is global
and nonspecific.11 Although this hypothesis
is consistent with the heterogeneity of neuropsychological, neuroimaging,
and neuropathological data on chronic alcoholism,12, 13
it appears to be so broad that it is difficult to disprove. Lastly, the frontal
brain vulnerability hypothesis suggests that the frontal lobes are greatly
vulnerable to long-term consumption of alcohol.14
Moderate neuronal loss has been reported in the frontal cortex and in the
cingulate gyrus in alcoholic subjects15 supporting
this hypothesis. Functional neuroimaging studies using positron or single-photon
emission computed tomography in recently detoxified alcoholic subjects have
documented global cerebral metabolic or perfusion deficits that are more pronounced
in the frontal regions.16, 17, 18, 19
In addition, frontal lobe hypoperfusion is independent of brain atrophy.20 Finally, neuropsychological studies highlighted "frontal
function" or "executive function" impairments including planning,21 abstraction,22 attention,23 shifting of attention,24
mental flexibility,25 and concept generation
deficits.26 However, it seems as if most of
the executive tasks used in these studies also involved nonexecutive components,
and these tasks had been shown to be impaired as a result of nonfrontal lobe
lesions.27, 28, 29
The main aim of this study was to reexamine the frontal brain vulnerability
hypothesis by using tasks designed to assess separately nonexecutive and specific
executive operations (which proved to be sensitive to frontal lobe dysfunction).
The theoretical framework on which this study was based is the control-to-action
model developed by Norman and Shallice.30 This
model distinguishes 2 control-to-action mechanisms. The first, contention
scheduling, is involved in routine situations in which actions are triggered
automatically. The second, the Supervisory Attentional System (SAS) is needed
in situations in which the routine selection of action is unsatisfactory,
and they conceived it as carrying out a variety of processes allowing the
genesis of plans and willed actions.31
An analogy has been established between the SAS and the central executive
(CE) component of the working memory model proposed by Baddeley.32
Working memory is a limited capacity system responsible for the temporary
storage and processing of information while cognitive tasks are performed.
Baddeley's model comprises 2 slave systems ensuring temporary maintenance
of information, the phonologic loop, and the visuospatial sketchpad, as well
as an attentional control system, the CE, the function of which is similar
to that of the SAS. According to Baddeley, an important function of the CE
is to allow the performance of 2 tasks simultaneously.
In the present study, we investigated the performance of recently detoxified
nonamnesic male alcoholic inpatients in 3 SAS functions: planning, inhibition,
and abstraction of logical rules. Additionally, the ability to manipulate
stored information in working memory (a CE function that has been proven to
be frequently affected in alcoholic subjects33)
has been assessed. We also addressed the question of how much a reduction
of processing speed accounts for alcohol-related SAS/CE deficits. To increase
the clinical relevance of this study, we evaluated patients with 3 to 4 weeks
of abstinence at least 7 days after stopping all detoxification medication.
This period corresponds to the moment when patients are usually discharged
from our hospital.
SUBJECTS AND METHODS
SUBJECTS
Thirty male alcoholic subjects were recruited for this study from the
Alcohol Detoxification Program of the Psychiatric Institute, Brugmann Hospital,
Brussels, Belgium. They all received complete medical, neurological, and psychiatric
examinations at the time of selection (Table 1). The subjects had to meet DSM-IV34 criteria for alcohol dependence (made by a board-certified
psychiatrist [P.V.]). Reasons for exclusion were other current DSM-IV Axis I diagnoses, a history of significant medical illness,
head injury resulting in a loss of consciousness for longer than 30 minutes
that would have affected the central nervous system, use of other psychotropic
drugs or substances that influence cognition, and overt cognitive dysfunction.
To increase the reliability of information, alcoholic subjects and their families
were interviewed separately. Blood levels of folate, vitamin B12,
and ß-carotene were measured. The detoxification regimen consisted of
B vitamins and decreasing doses of sedative medication (diazepam). Current
clinical status was rated using the Montgomery-Asberg Depression Rating Scale35 and the Spielberger State-Trait Anxiety Inventory.36
|
|
|
|
Table 1. Demographic and Clinical Variables of Alcoholic Subjects and
Control Subjects*
|
|
|
Thirty controls similar for sex, age, and educational and vocabulary
levels (Mill Hill, French-language adaptation of the multiple choice synonym
subtest37) were recruited by word of mouth
from healthy community members; they were not paid for their participation.
We excluded any who had met an Axis I psychiatric diagnosis assessed by the
Structural Clinical Interview for DSM-III-R38 and DSM-III-R criteria;
who had experienced a drug use disorder during the year before enrollment
in the study; or who had consumed more than 54 g/d of alcohol for longer than
1 month. On the basis of the results of their medical history and physical
examination, they were judged to be medically healthy. Controls were asked
to avoid the use of drugs, including narcotic pain medication, for the 5 days
prior totesting, and to avoid alcohol consumption for the preceeding 24 hours.
All subjects provided written consent.
NEUROPSYCHOLOGICAL ASSESSMENT
All subjects had a neuropsychological examination. Alcoholic subjects
were examined after they had abstained from alcohol for a minimum of 19 days
and at least 5 days after a standard detoxification period. All tests were
administered in 4 sessions during a 2-day period by a clinical neuropsychologist
(X.N.) specifically trained in and familiar with the tests used. The order
of the tests within a session was fixed but the sessions were random.
The Alpha-Span Task39 investigated the
ability to manipulate information stored in working memory by comparing the
recall of information in serial order (involving mainly a storage component)
and in alphabetical order (involving storage and manipulation of information).
After having assessed the verbal span level, the subject was asked to repeat
word sequences in 2 different conditions: direct recall and alphabetical recall.
In both conditions, the number of words to be recalled corresponded to the
subject's span minus 1 item. In the direct recall condition, the subject performed
an immediate serial recall of 10 sequences of words. In the alphabetical recall
condition, the subject was asked to recall 10 sequences of words in their
alphabetical order. The comparison of performance in alphabetical recall with
that in serial recall assesses the subject's performance.
Our modified version of the Tower of London test40
explored planning ability and is composed of 12 problems. In each problem,
3 beads of different colors had to be moved from a starting configuration
on 3 sticks to a target configuration in a minimum number of moves. Three
problems needed 3 moves (3N), 9 needed 5 (5N). In 3 of these 9 problems, 1
bead could be moved to its final position on the first move and this allowed
the optimal solution (facilitating, 5F). In another 3 problems, no bead could
be moved to its final position in the first move (neutral, 5N). In the final
3 problems, 1 bead could be moved to the final position in the first move
but this would prevent the optimal solution (misleading, 5M). The time needed
to strategize a plan was estimated by the time taken to execute the first
move (initiation time). We also measured the total time taken to complete
the task. The adequacy of the plan was measured by the number of moves actually
taken to solve the problem.
The Hayling task41 (French-adapted version42) assesses the capacity to suppress (inhibit) a habitual
response. The test consisted of 2 sections (A and B) of 15 sentences each,
in which the last word is missing. Sentences were read aloud by the experimenter.
In section A (initiation-automatic), subjects were asked to give the word
that made sense. In section B (inhibition), subjects were asked to give a
word that made no sense at all in the context of the sentence. These responses
were scored 3 if the word made sense of the sentence; 1 if, although not making
sense, it was semantically connected to the sentence; and 0 if it made no
sense at all. In both sections, subjects were asked to reply as quickly as
possible and performance was measured by the time taken to respond (latency).
The Brixton test43 was used to assess
the capacity to discover and shift logical rules. A series of pages with 10
circles, 1 of which is solid, is displayed. Simple rules determine the position
of the solid circle on subsequent pages but the rules change from time to
time. The subject's task was to suggest which circle will be filled on the
next page and why. We counted the number and type of errors made. The first
type (I) was to continue a rule after it had changed. The second type (II)
was to reapply an earlier rule before the new rule is discovered. The third
type (III) was a guess.
On the phonologic, semantic, and alternate verbal fluency task,44 subjects were given 120 seconds to generate aloud
a list of words beginning with the letter /p/ (phonologic
condition) but excluding proper names and variants of the same word. Then,
we proceeded in the same way with a semantic category (name clothes [categorical
condition]) and with 2 categories alternatively (name tools and animals [alternate
condition]). The number of correct words generated was recorded. In the Trail
Making Test,45 the subject is asked to trace
a line joining in alphabetical order a series of letters distributed randomly
across a sheet of paper (Trail A), and then (Trail B), a trace joining alternatively
the letters of the alphabet and the numbers 1 to 20 in alphabetical or ascending
order.
On the Flexibility test,46, 47
the subjects were instructed to consider some common objects and the task
was to generate orally as many other less common uses for each object as possible.
For example, a newspaper is commonly used for reading, but it can be used
to start a fire, wrap garbage, swat a fly, and others. We calculated the total
number of correct infrequent uses of 3 objects.
The Stroop Interference Test48, 49
comprised 4 different cards shown in a fixed sequence. The "reading condition"
is to read color-words printed in black as quickly as possible. The "denomination
condition" is to name color patches. The "interference condition" is to name
the color of the print of a word printed in an incongruent color. The "flexibility
condition" is similar to the last except that the subject is asked to read
the words rather than name its color when it is underlined. The time to complete
each condition and the sum of errors made on interference and flexibility
conditions were recorded. To measure processing speed, the time to complete
the Trail A, the color-naming part of the Stroop Interference Test, the latency
time of the Tower of London test, and the time to realize part A of the Hayling
task were considered.
STATISTICAL ANALYSIS
With respect to the data collected from the various neuropsychological
tests, analyses of variance (ANOVAs) were performed to determine for which
variables alcoholic subjects and controls differed significantly. Post hoc
analyses were performed by using the Newman-Keuls test. A Pearson product
moment correlation analysis was also conducted to examine the relationships
among demographic and clinical variables and cognitive performance in alcoholic
subjects. All statistical analyses were based on 2-tailed tests of significance
and were performed using SPSS 8.0. (SPSS Inc, Chicago, Ill).
RESULTS
With regard to the Alpha-Span Task, alcoholic subjects' (mean ±
SD, 4.8 ± 0.92 words) and controls' word span (4.9 ± 0.61 words)
did not differ significantly (F1,58 = -0.49, P = .62). The scores for the direct and alphabetical recall conditions
(Figure 1) were then analyzed separately
using a 2-way, 2 (group) x 2 (direct and alphabetical recall) ANOVA.
The analysis revealed a main effect of group (F1,58 = 43.6, P<.001) and of condition (F1,58 = 90.97, P<.001). A significant interaction between the group
and the type of recall was also found (F1,58 = 54.6, P<.001), with the alcoholic subjects showing a more important decrease
of performance from direct to alphabetical recall than the controls, despite
a similar performance in direct recall (Newman-Keuls post hoc comparisons).
|
|
|
|
Figure 1. Comparisons between performances
on the direct and the alphabetical recall conditions of the Alpha-Span Task
in nonamnesic alcoholic male inpatients and control subjects. See the "Neuropsychological
Assessment" subsection of the "Subjects and Methods" section for an explanation
of the Alpha-Span Task. Results are given as mean ± SD. Asterisk indicates
post hoc analysis indicated alcoholic subjects performing less well only in
alphabetical recall condition (P<.01, Newman-Keuls
test).
|
|
|
On the latency time of the Hayling task (Table 2), the 2 (group) x 2 (section) ANOVA revealed a significant
group effect (F1,58 = 12.62, P = .001),
a significant effect of section (F1,58 = 116.1, P<.001) and a significant interaction between these 2 factors (F1,58 = 12.25, P = .001). Post hoc comparisons
revealed that the alcoholic subjects were significantly slower than the controls
in giving an answer in section B (P<.001) but
not in section A (P = .35) (Figure 2).
|
|
|
|
Table 2. Scores on Executive Tests for Alcoholic Subjects and Control
Subjects*
|
|
|
|
|
|
|
Figure 2. Comparisons between the average
responses latencies of the Hayling task in nonamnesic alcoholic male inpatients
and control subjects. See the "Neuropsychological Assessment" subsection of
the "Subjects and Methods" section for an explanation of the Hayling task.
Results are given as mean ± SD. Asterisk indicates post hoc analysis
indicated that alcoholic subjects were significantly slower giving an answer
only when the task required the completion of the sentences with an semantically
unrelated word (Section B; P<.001, Newman-Keuls test).
|
|
|
The section B score of the Hayling task showed that the alcoholic subjects
gave more words semantically linked to the expected word (score 1) (F1,58 = 113.39, P<.001) and fewer unrelated
words (score 0) (F1,58 = 113.39, P<.001)
than the controls. Nevertheless, the alcoholic subjects did not give more
expected words (score 3) (F1,58 = 0.6, P
= .5). Alcoholic subjects showed a higher overall score than the controls
(F1,58 = 12.44, P = .001).
On the Brixton test, alcoholic subjects made more errors than the controls
(F1,58 = 4.46, P<.001). The 2 groups
did not differ with regard to the number of type I errors (F1,58
= 1.35, P = .25) but the alcoholic subjects made
fewer type II errors (reapplication of earlier rule) (F1,58 = 23.6, P<.001) and more type III errors (guesses) (F1,58 = 37.6, P<.001) than the controls.
On the verbal fluency tasks, a 2 (groups) x 3 (condition: phonologic,
semantic, and alternate) ANOVA revealed a main effect of group (F1,58 = 5.01, P<.001) and of condition (F2,116 = 5.01, P<.001). The interaction between
these 2 factors was also significant (F2,116 = 7.3, P<.01). Post hoc analysis revealed that alcoholic subjects produced
fewer words than controls only in the alternate fluency condition (P<.001). On the Flexibility test, alcoholic subjects found fewer
uncommon uses of objects than controls (F1,58 = 4.16, P = .04).
On the Stroop Interference Test, the 2 (group) x 3 (condition:
reading plus denomination time, interference time, and flexibility time) ANOVA
revealed a main effect of group (F1,58 = 4.6, P = .05) and of condition (F2,116 = 32, P<.001). There was a significant group by condition interaction
(F2,116 = 13.3, P<.001). Post hoc analysis
revealed that alcoholic subjects were slower than controls only on the flexibility
condition (P<.001). Alcoholic subjects also made
more errors (sum of errors made on interference and flexibility conditions;
mean ± SD, 11.4 ± 6.7) than controls (3.4 ± 1.3) (F1,58 = 7.68, P<.001).
On the Trail Making Test, the 2 (group) x 2 (condition: Trail
A and Trail B) ANOVA revealed a main effect of group (F1,58 = 7.82, P = .007) and of condition (F1,58 = 57.9, P<.001). There was a significant group by condition
interaction (F1,58 = 7.72, P = .007).
Post hoc analysis revealed that the alcoholic subjects were slower than controls
only in Trail B (P<.01).
The Tower of London test (Table 3) results showed that, on the easiest problems (3 moves), alcoholic
subjects and controls did not differ for the number of moves (F1,58
= 0.72, P = .40), for the time needed to initiate
the first move (F1,58 = 0.44, P = .51),
or for the time to solve the problem (F1,58 = 0.34, P = .73). In problems requiring 5 moves, the 2 (group) x 3 (type
of problem: neutral, facilitating, and misleading) ANOVA on the number of
moves revealed a main effect of group (F1,58 = 6.02, P = .02) and showed that the alcoholic subjects took significantly
more moves to solve the problems. There was also a main effect of type of
problem (F2,116 = 6.5, P = .002). Post
hoc analyses revealed that the number of moves was equivalent between the
neutral and misleading problems but was greater for both than for facilitating
problems. There was no significant group by type of problem interaction (F2,116 = 0.99, P = .37). Two-way,
2 (group) x 3 (type of problem) ANOVAs were carried out on the initiation
and subsequent times. For the initiation time, the analysis showed no main
effect of group (F1,58 = 1.3, P = .27)
or type of problem (F2,116 = 1.9, P =
.14). There was no significant group by type of problem interaction (F2,116 = 1.45, P = .23). For the subsequent
time, significant effect of type problem (F2,116 = 29.9, P<.001) was observed. Either significant effect of group
(F1,58 = 0.29, P = .59) or significant
interaction between these 2 factors emerged (F2,116 = 0.42, P = .66).
|
|
|
|
Table 3. Scores on Tower of London (TOL) Test for Alcoholic Subjects
and Control Subjects*
|
|
|
To examine how well the alcoholic subjects and controls were able to
redress their mistakes, we calculated the number of moves to solve the problem
once they put the bead on the first move into a position that was not coherent
with the optimal solution of the neutral and misleading problems. Alcoholic
subjects moved the first bead inadequately 19 times and controls 7 times.
After that, the alcoholic subjects and controls needed 10.43 ± 2.3
and 7 ± 1.2 (mean ± SD) moves, respectively, to solve the problems.
The alcoholic subjects made more moves to achieve the solution than the controls
(F1,28 = 4.5, P<.001).
Finally, none of the correlations among age, number of years of education,
number of prior cures, total lifetime intake of alcohol, number of years of
heavy drinking, depression, anxiety, or those neuropsychological performances
for which a significant group effect had been observed were statistically
significant (all were inferior to P = .22).
COMMENT
This study investigated the presence of SAS/CE impairments in recently
nonamnesic male alcoholic subjects. It used executive tasks inspired by Norman
and Shallice's control-to-action model30 and
Baddeley's working memory model.32 In addition,
we addressed the question of: by how much does the slowing of processing speed
account for SAS/CE deficits?
The analysis of the Tower of London test results shows that the alcoholic
subjects were able to plan and execute efficiently the easiest problems, but,
once they had begun to solve a problem incorrectly, they had more difficulty
than the controls in redressing their mistake: this suggests a failure of
inhibition or flexibility exploring planning ability (for a similar interpretation
see Joyce and Robbins50).
On the inhibition test (the Hayling task41),
the alcoholic subjects were slower on the inhibition section, but not on the
section requiring production of an automatic response. They also made more
inhibition errors than the controls. The observed dissociation between the
initiation and inhibition sections tackles directly the contention scheduling/SAS
(or automatic-controlled) distinction proposed by the control-to-action model
of Norman and Shallice30: deficits in alcoholic
subjects are observed in the controlled process allowing the inhibition of
a dominant response but not the production of an automatic response. Findings
of a 1999 positron emission tomographic study51
showed that bilateral median frontal activation occurs during section B of
the Hayling task. These data suggest that an alcoholic person's inhibition
deficits might be caused by frontal lobe abnormalities.
Other results are consistent with the existence of an inhibition deficit.
In the Trail Making Test,44 alcoholic subjects
were slower than controls on section B but not on section A. Similarly, they
showed poor performance in the alternate verbal fluency task.44
Finally, patients spent more time to complete the flexibility condition of
the Stroop Interference Test.48 Trail B requires
inhibiting current realization strategy (1, 2, 3 . . . ) to switch between
numbers and letters (1A, 2B, 3C . . . ). Performance in the alternate verbal
fluency task requires, notably, that subjects inhibit one search strategy
to switch to another. In the Stroop test, the flexibility condition requires
the subject to switch between 2 rules alternatively, that is to inhibit the
current rule. However, a puzzling result is that alcoholic subjects were slower
than controls in flexibility but not in the interference condition of the
Stroop test which also clearly requires inhibition. Similarly, they produced
fewer words in the alternate but not the phonologic and semantic fluency tasks
while inhibition process is needed for both (eg, with regard to the phonologic
fluency task, inhibiting the usual search strategy on the basis of the word
meaning49). These dissociations suggest the
view that there exists multiple inhibitory mechanisms52
and/or that the different tasks require various levels of inhibitory resources.
The study's results in the rule detection test (Brixton test43)
show that alcoholic subjects and patients with frontal disorders43
responded similarly: they made more errors than controls, particularly more
illogical responses (guesses).
The results of the Alpha-Span Task39
show that, in alcoholic subjects, the normal storage component (measured by
the span size and the score of direct recall condition) remains healthy but
the ability to manipulate the information stored (measured by the alphabetical
recall condition) is impaired. A recent positron emission tomographic study53 indicated that the executive (manipulation) processes
involved in a modified version of the Alpha-Span Task is distributed between
frontal and parietal attentional systems. These data suggest that, in alcoholic
subjects, this parietofrontal network might be disrupted.
Another interesting result concerns the contribution of a slowing down
of the processing speed to SAS/CE deficits. Similar to the findings of previous
studies,53, 54, 55, 56, 57
alcoholic subjects were not slower than controls in the color-naming part
of the Stroop test, in theTrail A section, in the initiation section of the
Hayling task, and in the Tower of London test. This suggests that processing
speed does not constitute an important contributing factor to their executive
deficits. Since many studies in the Cognitive Aging domain suggest that the
speed of processing is an important mediator between age and cognitive performance,58, 59, 60 our results seem
to be inconsistent with the hypothesis that alcoholic subjects show cognitive
modifications similar to those observed in older nonalcoholic subjects.
Like other studies,61, 62
ours failed to find any correlation between measures of drinking practice
and neuropsychological performance. However, the accuracy of retrospective
recall in patients known to have cognitive impairments is probably low.
The findings of the present study show that uncomplicated alcoholic
subjects near the end of a period of detoxification manifest executive function
deficits: these could have important clinical implications, particularly concerning
relapse. Tiffany63 suggests that drug use behavior
in addicts is largely controlled by automatic processes and, therefore, that
executive functions are needed to block this and maintain abstinence. Thus,
the existence of executive function deficits in alcoholic subjects, as shown
in the present study, could affect the capacity to maintain abstinence. However,
further studies are needed to explore this relationship.
There are 2 main limitations to the present study. First, we do not
know whether cognitive deficits in alcoholic subjects recover after a longer
period of abstinence. Second, it does not show whether an alcoholic subject's
executive dysfunction developed as the result of a long-term use of alcohol
(a neurotoxic effect) or constituted a developmental predisposing factor to
substance abuse. Further longitudinal studies should be conducted to explore
both questions.
CONCLUSIONS
The findings of the present study showed that inhibition, planning,
rule detection, and coordination of dual tasks were impaired in recently detoxified
male alcoholic subjects. It seems as if these SAS/EC deficits were probably
not caused by reduced processing speed. More generally, these findings are
consistent with the view that the cognitive deficits in recently detoxified
sober alcoholic subjects are due, at least partly, to frontal lobe dysfunctioning.
AUTHOR INFORMATION
Accepted for publication June 26, 2001.
From the Department of Psychiatry (Drs Noël, Sferrazza, Hanak,
Le Bon, De Mol, Kornreich, Pelc, and Verbanck) and the Cognitive Sciences
Research Unit (Mr Schmidt), Free University of Brussels, and the Psychiatric
Institute, Brugmann University Hospital (Drs Noël, Sferrazza, Hanak,
Le Bon, De Mol, Kornreich, Pelc, and Verbanck), Brussels, Belgium; and the
Department of Cognitive Psychopathology, University of Geneva, Geneva, Switzerland
(Dr Van der Linden).
Corresponding author and reprints: Xavier Noël, PhD, Psychiatric
Institute, Brugmann University Hospital, Van Ghuchten 4, Brussels 1020, Belgium
(e-mail: xnoel{at}ulb.ac.be).
REFERENCES
| |
1. Rice DP. Economic costs of substance abuse, 1995. Proc Assoc Am Physicians. 1999;111:119-125.
FULL TEXT
|
ISI
| PUBMED
2. Kopelman MD. The Korsakoff syndrome. Br J Psychiatry. 1995;166:154-173.
FREE FULL TEXT
3. Porjesz B, Begleiter H. Evoked brain potentials and alcoholism. In: Parsons OA, Butter N, Nathan P, eds. Neuropsychology
of Alcoholism: Implications for Diagnosis and Treatment. New York,
NY: Guilford Press; 1987:45-63.
4. Harper C, Kril J. Brain atrophy in chronic alcoholic patients: a quantative pathological
study. J Neurol Neurosurg Psychiatry. 1985;48:211-217.
FREE FULL TEXT
5. Risberg J, Berglund M. Cerebral blood flow and metabolism in alcoholics. In: Parsons OA, Butter N, Nathan P, eds. Neuropsychology
of Alcoholism: Implications for Diagnosis and Treatment. New York,
NY: Guilford Press; 1987:64-75.
6. Gilman S, Adams K, Koeppe RA, Berent S, Kluin KF, Modell JG, Kroll P, Brunberg JA. Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration
studies with positron emission tomography. Ann Neurol. 1990;28:775-785.
FULL TEXT
|
ISI
| PUBMED
7. Knight RG, Longmore BE. Cognitive impairment in alcoholics. In: Clinical Neuropsychology of Alcoholism.
Hillsdale, NJ: Lawrence A Erlbaum Associates; 1994:225-240.
8. Bertera JH, Parsons OA. Impaired visual search in alcoholics. Alcohol Clin Exp Res. 1978;2:9-14.
PUBMED
9. Ellis RJ, Oscar-Berman M. Alcoholism, aging, and functional cerebral asymmetries [review]. Psychol Bull. 1989;106:128-147.
FULL TEXT
|
ISI
| PUBMED
10. Ellis RJ. Dichotic asymmetries in aging and alcoholic subjects. Alcohol Clin Exp Res. 1990;14:863-871.
PUBMED
11. Tivis R, Beatty WW, Nixon SJ, Parson OA. Patterns of cognitive impairment among alcoholics: are there subtypes? Alcohol Clin Exp Res. 1995;19:496-500.
FULL TEXT
|
ISI
| PUBMED
12. Oscar-Berman M. Neuropsychological consequences of alcohol abuse: questions, hypotheses,
and models. In: Parsons OA, Butters N, Nathan PE, eds. Neuropsychology
of Alcoholism: Implications for Diagnosis and Treatment. New York,
NY: Guilford Press; 1987:59-79.
13. Harper C. The neuropathology of alcohol-specific brain damage, or does alcohol
damage the brain? J Neuropathol Exp Neurol. 1998;57:101-110.
ISI
| PUBMED
14. Tarter RE. Psychological deficit in chronic alcoholics: a review. Int J Addict. 1975;10:327-368.
ISI
15. Kril JJ, Halliday GM, Svoboda MD, Cartwright H. The cerebral cortex is damaged in chronic alcoholics. Neuroscience. 1997;79:983-998.
FULL TEXT
|
ISI
| PUBMED
16. Erbas B, Bekdik C, Erbengi G, Enunlu T, Aytac S, Kumbasar H, Dogan Y. Regional cerebral blood flow changes in chronic alcoholism using Tc-99m
HMPAO SPECT: comparison with CT parameters. Clin Nucl Med. 1992;17:123-127.
FULL TEXT
|
ISI
| PUBMED
17. Gilman S, Adams K, Koeppe RA, Berent S, Kluin KF, Modell JG, Kroll P, Brunberg JA. Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration
studies with positron emission tomography. Ann Neurol. 1990;28:775-785.
18. Adams KM, Gilman S, Koeppe RA, Kluin KJ, Brunberg JA, Dede D, Berent S, Kroll PD. Neuropsychological deficits are correlated with frontal hypometabolism
in positron emission tomography studies of older alcoholic patients. Alcohol Clin Exp Res. 1993;17:205-210.
FULL TEXT
|
ISI
| PUBMED
19. Dao-Castellana MH, Samson Y, Legault F, Martinot JL, Aubin HJ, Crouzel C, Feldman L, Barrucand D, Rancurel G, Féline A, Syrota A. Frontal dysfunction in neurologically normal chronic alcoholic subjects:
metabolic and neuropsychological findings. Psychol Med. 1998;28:1039-1048.
FULL TEXT
|
ISI
| PUBMED
20. Nicolas JM, Catafau AM, Estruch R, Lomena FJ, Salamero M, Herranz R, Monforte R, Cardenal C, Urbano-Marquez A. Regional cerebral blood flow-SPECT in chronic alcoholism: relation
to neuropsychological testing. J Nucl Med. 1993;34:1452-1459.
FREE FULL TEXT
21. Pishkin V, Lovallo WR, Bourne LE Jr. Chronic alcoholism in males: cognitive deficit as a function of age
of onset, age and duration. Alcohol Clin Exp Res. 1985;9:400-406.
ISI
| PUBMED
22. Parker ES, Parker DA, Harford TC. Specifying the relationship between alcohol use and cognitive loss:
the effects of consumption and psychological distress. J Stud Alcohol. 1991;52:366-373.
ISI
| PUBMED
23. Smith ME, Oscar-Berman M. Resource-limited information processing in alcoholism. J Stud Alcohol. 1992;53:514-518.
ISI
| PUBMED
24. Sullivan EV, Mathalon DH, Zipursky RB, Kersteen-Tucker Z, Knight RT, Pfefferbaum A. Factors of the Wisconsin Card Sorting Test as measures of frontal-lobe
function in schizophrenia and in chronic alcoholism [review]. Psychiatry Res. 1993;46:175-199.
FULL TEXT
|
ISI
| PUBMED
25. Glenn SW, Errico AL, Parsons OA, King AC, Nixon SJ. The role of antisocial, affective, and childhood behavioral characteristics
in alcoholics' neuropsychological performance. Alcohol Clin Exp Res. 1993;17:162-169.
FULL TEXT</ |
