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Impairments of brain and behavior: the neurological effects of alcohol
Marlene Oscar-Berman
,
Barbara Shagrin
,
Denise L. Evert
and
Charles Epstein
Alcohol Health & Research World
.
21.1 (Winter 1997): p65.
Copyright:
COPYRIGHT 1997 U.S. Government Printing Office
Abstract:
Heavy alcohol consumption can impair the brain and other components of the nervous system.
Neurological effects can include impaired perception, learning and memory, as well as changes
in personality and emotions.
Full Text:
Alcohol consumption can damage the nervous system, including the brain. Consequently,
alcoholics
(1) and chronic heavy drinkers can suffer abnormalities in their mental functioning and
changes in behaviors associated with brain impairment. The neurological effects of alcohol can
occur directly, because alcohol is a toxic substance, or they can occur indirectly, through
damage to other body organs (e.g., the liver) that subsequently interferes with the workings of
nerve cells in the brain [ILLUSTRATION FOR FIGURE 1 OMITTED].
Images of the brain created with modern neuroradiological techniques, such as magnetic
resonance imaging (MRI) and computed tomography (CT), generally show a relationship
between prolonged alcohol consumption and changes in the brain's structure (Charness 1993;
Pfefferbaum et al. 1995). For example, MRI and CT images have shown brain shrinkage and
tissue damage (i.e., brain lesions) in some alcoholics. These changes can cause poor
temperature regulation, muscle weakness, and alterations in sleep patterns.
This article reviews some of the physical brain changes and neuropsychological(2)
consequences of
alcoholism
, beginning with the effects of chronic alcoholism on memory and
other cognitive functions. This discussion is followed by an examination of the differences
among people that commonly contribute to the many neurological effects of alcoholism,
including medical health, age, gender, and family history of alcoholism. The article concludes
with a consideration of treatment and recovery.
COMMON EFFECTS OF ALCOHOL ON THE NERVOUS SYSTEM
Alcohol has effects on both major components of the nervous system - the central nervous
system (i.e., the brain and the spinal cord) and the peripheral nervous system (i.e., the nerves in
the rest of the body).
Alcohol can have a negative effect on certain neurological processes, such as temperature
regulation, sleep, and coordination. For example, moderate amounts of alcohol lower body
temperature. Severe intoxication in a cold environment may produce massive, life-threatening
declines in temperature (i.e., hypothermia). Many people mistakenly believe that alcohol can
help warm them in cold weather. This notion can be especially dangerous for the homeless, for
elderly people living in inadequately heated quarters, and for those exposed to prolonged cold
temperatures outdoors.
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In addition to its effect on body temperature, alcohol interferes with normal sleep patterns.
Relatively small doses of alcohol can cause early sedation or sleepiness, awaking during the
night, and suppression of rapid-eye-movement (REM) sleep. REM sleep is the dreaming stage
of sleep; when REM sleep occurs near wakefulness, it often produces vivid hallucinations. Most
people fall asleep easily after one or more alcoholic drinks(3) but experience diminution of REM
sleep. Drinkers who attempt to use alcohol as a sedative seldom attain a full night's sleep,
however; after several hours, the natural elimination of alcohol from the body produces arousal
and sleep fragmentation. When chronic drinkers withdraw from alcohol, long-suppressed REM
sleep may rebound excessively. Some authorities (Greenberg and Pearlman 1967) believe that
delirium tremens (known as DT's), a condition occurring 2 to 4 days after alcohol withdrawal that
consists of trembling and agitation with hallucinations, overexcitation, fever, sweating, and rapid
heartbeat, represents a state of continuous REM sleep. In addition, measurable insomnia may
occur many weeks into abstinence.
Another prominent effect of chronic alcohol consumption is harm to the pan of the brain called
the cerebellum [ILLUSTRATION FOR FIGURE 2 OMITTED], resulting mainly in the loss of
muscular coordination. This damage appears as imbalance and staggering, although other
problems also may occur (Raymond et al. 1996).
A peripheral nervous system disorder commonly seen in alcoholics is numbness and weakness
in the hands and feet (i.e., peripheral neuropathy). This condition is thought to be largely a
consequence of malnutrition in severe alcoholics. One type of peripheral nerve damage known
as Saturday night palsy can occur when an alcoholic puts pressure on vulnerable nerves in the
arm while lying in an intoxicated stupor, leaving him or her unable to extend the wrist for days to
weeks.
ABNORMALITIES IN NEUROPSYCHOLOGICAL FUNCTIONS
In addition to changes in temperature regulation, sleep, and coordination, alcoholism-related
brain changes can cause abnormalities in mental functioning that are detectable using
specialized neuropsychological tests. Behavioral neurologists and neuropsychologists use
these sensitive tests to measure both the obvious and the subtle consequences of brain
damage. Results of the tests often show changes in emotions and personality as well as
impaired perception, learning, and memory (i.e., cognitive abilities) after damage to particular
brain systems (see Evert and Oscar-Berman 1995).
Korsakoff's Syndrome
One of the most severe consequences of long-term alcoholism on mental functioning is
Korsakoff's syndrome (KS), a devastating memory disorder in which a person appears to forget
the incidents of his or her daily life as soon as they occur (see Oscar-Berman 1990). Because of
this dramatic loss of short-term memory (also called anterograde amnesia), patients with KS
virtually live in the past. For example, someone who developed KS in the 1960's might believe
that the President of the United States is Dwight Eisenhower or John Kennedy. Some alcoholics
may have a genetic component or predisposition to develop this amnesic condition: These
patients may have an enzyme deficiency that prevents their bodies from using thiamine (a B
vitamin) efficiently.(4) This deficiency, coupled with a diet high in alcohol and low in thiamine
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(along with other nutrients), may lead to brain damage causing the amnesia.
Although KS destroys short-term memory, it typically spares most long-term memories (i.e.,
memories formed or knowledge gained before the onset of prolonged heavy
drinking
). Thus,
overall intelligence, as measured by standardized IQ tests, does not necessarily deteriorate,
because the types of information and abilities tapped by these tests usually involve long-term
memory.
Other Neuropsychological Problems
Within the past 25 years, clinical and experimental observations of patients with and without KS
have revealed many other neuropsychological dysfunctions associated with alcoholism.
Alcoholics demonstrate poor attention to what is going on around them; need extra time to
process visual information; have difficulty with abstraction, problem-solving, and learning new
materials; exhibit emotional abnormalities and disinhibitions; and show reduced visuospatial
abilities (i.e., the capacity to deal with objects in two-dimensional or three-dimensional space)
(Parsons and Nixon 1993). The once-common view that alcoholics without Korsakoff's
syndrome are cognitively intact has been abandoned in light of accumulating evidence that
cognitive impairments (and associated changes in brain structure) can occur in alcoholics who
do not exhibit obvious clinical signs of anterograde amnesia (see Lishman 1990).
ALCOHOLISM-RELATED BRAIN DAMAGE AND ASSOCIATED NEUROPSYCHOLOGICAL
CHANGES
The type and extent of structural damage to brain tissue can be determined by autopsy (i.e.,
post mortem) examination of the brain's components and individual nerve cells (i.e.,
neuropathological evidence). In addition, neuroradiological techniques, such as MRI and CT
scans, allow the brain to be viewed inside the skull of a living person. Other neuroimaging
techniques (i.e., functional neuroimaging) measure active brain functioning. Functional
neuroimaging can reveal changes in the blood flow in and around the brain, brain metabolism,
and brain electrical activity generated by nerve impulses (i.e., neurophysiological measures).(5)
One type of neurophysiological measure, event-related potentials (ERP's), consists of brain
waves recorded from scalp electrodes while a person is presented with specific pieces of
information or stimuli. Scientists use computers to translate the information obtained from ERP's
and other functional neuroimaging measures into meaningful pictures that, in turn, make it
possible to view brain functioning while a person is thinking or performing a task.
When applied to alcohol research, neuropathological and imaging techniques have helped to
provide cumulative evidence of brain abnormalities in alcoholics, such as atrophy(6) of nerve
cells (i.e., neurons) and brain shrinkage (Hunt and Nixon 1993). Brain shrinkage appears as
abnormal widening of the grooves (i.e., sulci) and fissures on the brain's surface or enlargement
of the fluid-filled cavities deep inside the brain (i.e., the ventricles). Regions of the brain that are
especially vulnerable to damage after years of chronic alcoholism include the cerebellum, the
limbic system (including the hippocampus and amygdala), the diencephalon (including the
thalamus and hypothalamus), and the cerebral cortex [ILLUSTRATION FOR FIGURE 2 AND 3
OMITTED].
Countless intricate pathways of neurons link the different areas of the brain, including the
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regions implicated in alcohol-related neurological dysfunction. Because of the size and
complexity of this network, the consequences of damage to one structure or system often can
resemble the consequences of damage to another. The following sections describe alcohol-
related structural and neuropsychological changes that can occur in the brain.
The Limbic System
The limbic system is an intricate network of structures located deep inside the brain; its
functions are diverse and varied. One function of the limbic system receiving attention from
alcohol researchers is memory. Memory loss similar to the amnesia in KS patients has been
associated with damage to the hippocampus and the amygdala, parts of the limbic system that
are located in the temporal lobes of the brain (see Evert and Oscar-Berman 1995). Although
injury to the limbic system can cause amnesia, researchers are not certain of the degree to
which alcohol-related memory impairments may be linked to damage in that part of the brain.
Alcohol researchers are interested in other functions of the limbic system as well. Damage to
certain parts of the limbic system leads to abnormalities in emotional functioning, the sense of
smell (i.e., olfaction), and the ability to use one sense (e.g., vision) to learn something in another
sense (e.g., touch) (i.e., cross-modal functioning). In all these categories of function,
researchers have observed deficits in alcoholics (Evert and Oscar-Berman 1995). Moreover,
alcoholics with KS appear to have greater impairment in some of these functional areas than do
non-KS alcoholics.
The Diencephalon
The diencephalon, a region nestled in the center of the brain, acts like a way station for nerve
signals moving from one area of the brain to another. Although it is not known precisely what
role diencephalic structures play in human memory functioning, lesions in this region have been
clearly documented in amnesic patients (Victor et al. 1989). Researchers are not certain
whether alcohol-related memory impairments are caused by these lesions, however. An
alternative explanation comes from a study that compared MRI measures of diencephalic
damage in alcoholics with and without KS (Blansjaar et al. 1992). The authors suggested that
diencephalic lesions develop regardless of whether patients acquire the amnesia of KS and are
not so much typical of KS as they are of chronic alcoholism and malnutrition.
The Cerebral Cortex
The cerebral cortex is the intricately folded outer layer of the brain composed of nerve cell
bodies (i.e., gray matter). It is considered to be the center of higher consciousness and the seat
of all intelligent behavior. The cortex makes neural connections, both directly and indirectly, with
all parts of the nervous system and, therefore, with all parts of the body.
As noted previously, neuroradiological evidence has revealed a widening of the fissures and
sulci of the cerebral cortex and enlargement of the ventricles in brains of alcoholics. These
changes suggest cortical atrophy associated with alcoholism (Pfefferbaum and Rosenbloom
1993; Pfefferbaum et al. 1995). The evidence for cortical atrophy has come both from imaging
studies of detoxified alcoholics and from post mortem analyses of the brains of alcoholics. For
example, MRI findings show evidence of significant cortical and subcortical tissue and volume
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loss in non-KS alcoholics compared with nonalcoholic control subjects. Moreover, alcoholics
with KS have greater cortical atrophy than non-KS alcoholics. Researchers also have reported
neuropsychological deficits in alcoholics (e.g., through tests of problem-solving, spatial memory,
visual associations, and learning related to or caused by touch [i.e., tactual learning]) that
indicate alcoholism-related cortical atrophy (Evert and Oscar-Berman 1995).
In most studies of alcohol-related neurological disorders, researchers have assessed
neuropsychological deficits in alcoholics without examining changes in alcoholics' brains. To
better understand brain-behavior relationships, however, neuropsychological, structural, and
functional changes must be evaluated to relate changes in behavior to damage in particular
systems of the brain. In studies using both methods, in fact, results have not revealed
consistent relationships between conical damage and performance on neuropsychological tests.
Some measures of brain structure or function have correlated with cognitive test scores,
whereas others have not. For example, one study reported a relationship between certain
neuropsychological test scores and measures of frontal brain metabolism in long-term
alcoholics; the same study, however, found no correlation between neuropsychological
performance and degree of cortical atrophy as seen using MRI (Wang et al. 1993). The results
were interpreted as reflecting either the preservation of cognitive abilities with mild structural
brain changes or the insensitivity of the tests used to detect mild structural changes.
The most consistently and frequently reported findings in alcoholics, based on functional and
structural imaging techniques, have been abnormalities in frontal brain regions (for reviews, see
Oscar-Berman and Hutner 1993; Pfefferbaum and Rosenbloom 1993). Frontal-system functions
include planning, carrying out, and monitoring goal-directed and socially suitable behaviors.
Compared with nonalcoholic control subjects, some alcoholics have shown significant
reductions in cerebral blood flow in certain areas of the frontal regions as well as in other brain
areas. In addition, greater blood flow reduction in frontal cortical areas has been associated with
greater severity of alcoholism and poorer cognitive test performance. In other studies, alcoholics
showed diminished metabolic functions in frontal areas; this reduction was associated with
impaired neuropsychological functions.
In studies of KS patients, researchers have obtained additional findings supporting frontal-
system dysfunction (Oscar-Berman and Hutner 1993). Neuropsychological studies have shown
that KS patients exhibit clinical signs associated with damage to the frontal cortex (e.g.,
emotional apathy, personality changes and loss of inhibitions, and constant repetition of certain
responses despite feedback indicating that such responses are incorrect or inappropriate [i.e.,
abnormal response perseveration]). Although much debate centers on the connection between
measures of alcohol consumption and the degree of structural or functional impairment in
non-KS alcoholics, research so far has failed to demonstrate a clear connection between
measures of alcohol intake, cognitive dysfunction, and frontal damage.
NEUROTRANSMITTERS AND ALCOHOLISM
At the cellular level, alcohol appears to
affect
brain function in a variety of ways. For example,
alcohol can alter the action of the chemicals that allow neurons to communicate (i.e.,
neurotransmitters). Specialized proteins on the surface of neurons, known as receptors,
recognize neurotransmitters and initiate the cell's response. Neurotransmitters and receptors
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cluster where nerve cells come into close contact; these contacts are called synapses. Some
neurotransmitters stimulate (i.e., excite) a response from the neurons that receive them; others
inhibit neuronal response. Over periods of days and weeks, the levels of receptors change in
response to chemical and environmental influences (e.g., drugs and synaptic activity) on the
neurons. Genes in the neuron's DNA are turned on or off, increasing or decreasing the
synthesis of receptors. Over time, drags that excite a given receptor generally lead to a
reduction in (i.e., down-regulate) the numbers or activity of that receptor type. Drags that inhibit
a receptor eventually tend to lead to an increase in (i.e., up-regulate) that type of receptor.
Up-and down-regulation are means by which the nervous system maintains a functional
balance of neurotransmitters and receptors; when imbalances occur, effects can include
seizures, sedation, depression, agitation, and other mood and behavioral disorders.
Glutamate
The major excitatory neurotransmitter in the human brain is glutamate, an amino acid.
Glutamate has a fundamental role in a cellular adaptation called long-term potentiation, which is
a persistent increase in the efficiency of a neuron's response to a neurotransmitter. Long-term
potentiation may be an important mechanism in learning and memory.
Extremely small amounts of alcohol have been shown to interfere with glutamate action. This
interference could affect multiple brain functions, including memory, and it may account for the
short-lived condition referred to as "alcoholic blackout." Because of its inhibitory effect on
glutamate, chronic consumption of alcohol leads to up-regulation of glutamate receptor sites in
the hippocampus, an area that is crucial to memory and often involved in epileptic seizures.
During alcohol withdrawal, glutamate receptors that have adapted to the continual presence of
alcohol may become overactive. Glutamate overactivity has been linked repeatedly to cell death
in situations ranging from strokes to seizures. Deficiencies of thiamine and magnesium, which
are common in alcoholics as a result of malnutrition, may contribute to this potentially
destructive overactivity.
GABA
Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central
nervous system. Evidence suggests that alcohol initially potentiates GABA effects; in other
words, it increases inhibition, and often the brain becomes mildly sedated. But over time,
chronic alcohol consumption reduces the number of GABA receptors through the process of
down-regulation. When alcohol is eventually withdrawn, the loss of its inhibitory effects,
combined with a deficiency of GABA receptors, may contribute to overexcitation throughout the
brain. This effect, in turn, can contribute to withdrawal seizures (i.e., "rum fits") within 1 or 2
days.
Other Neurotransmitters
Alcohol directly stimulates release of the neurotransmitter serotonin as well as natural
substances related to opioids (i.e., endorphins) that may contribute to the "high" of intoxication.
Serotonin helps regulate functions such as
food
and water intake, sexual response, and
aggression. Changes in other neurotransmitters, such as acetylcholine (which underlies key
cardiovascular mechanisms, including dilation of blood vessels) and the catecholamines (the
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decreased transmission of which has been linked to the memory deficits of patients with KS
[NIAAA 1993]), have been less consistently observed.
Alcohol disrupts neuron activity in various other ways, For example, over several weeks, alcohol
reduces the level of nerve growth factors, proteins important for cellular adaptation and survival.
In addition, alcohol may cause long-term adaptive changes in membrane lipids.
VULNERABILITIES TO THE NEUROLOGICAL EFFECTS OF ALCOHOLISM
Alcoholism is a multidimensional disorder, and no simple answers exist to questions such as:
"What are the neurological consequences of alcoholism?"; "What makes alcoholism affect
different people in different ways?"; or even "what causes someone to become an alcoholic in
the first place?" Widespread individual differences occur in the manifestation of alcoholism. For
example, according to one estimate, 50 to 85 percent of nonKS alcoholics exhibit signs of
cognitive decline (see Parsons 1993). Thus, anywhere from 15 to 50 percent of such alcoholics
may not exhibit any obvious signs of cognitive impairment. In general, the greater the
consumption of alcohol, the worse the performance on cognitive tasks. However, among those
alcoholics who exhibit neurological problems, researchers have found that measures of
previous alcohol consumption (e.g., duration, frequency, and quantity consumed) do not
correlate consistently with the degree of neuropsychological dysfunction (Parsons 1993). This
finding suggests that variables other than the presumed direct neurotoxic effects of alcohol may
play a role in determining alcohol-related cognitive decline. In response to the variability in the
consequences of alcoholism, researchers have looked for common elements that might help
explain why certain alcoholics develop specific neurological symptoms or mental changes.
Factors that may influence the neurological consequences of alcoholism include coexisting
health problems, such as malnutrition and liver disease; the age at which problem drinking
begins; the gender of the alcoholic; and a family history of alcoholism. These factors are
considered in the sections that follow.
COMMON ALCOHOL-RELATED MEDICAL PROBLEMS
Two common health problems occurring with alcoholism are vitamin deficiency and liver
disease, both of which can result in neurological disorders. As mentioned previously, prolonged
drinking with improper diet and associated malnutrition can lead to thiamine deficiency, a
possible factor in KS-related brain damage. Several investigators have stressed the idea that
damage in the diencephalon of KS patients is caused by thiamine deficiency, whereas cortical
abnormalities, most notably in the frontal lobes, are caused by alcohol neurotoxicity or other
conditions frequently associated with alcoholism (e.g., liver disease or head trauma).
Thiamine Deficiency
Researchers differ in their explanations of how and why particular neuropsychological deficits
are displayed in alcoholics. One theory proposes that alcoholics may fall into subgroups
distinguished by whether their brains are vulnerable to the direct neurotoxic effects of alcohol, to
thiamine deficiency, or to both factors (Lishman 1990). According to this viewpoint, alcoholics
who are susceptible to alcohol toxicity alone may develop permanent or transient cognitive
deficits associated with cortical shrinkage. Those alcoholics who are susceptible to thiamine
deficiency alone will develop a mild or short-lived KS state with anterograde amnesia as a
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salient feature. Alcoholics who suffer from a combination of alcohol neurotoxicity and thiamine
deficiency (i.e., have dual vulnerability) will experience widespread damage to large regions of
the cerebral cortex as well as to structures deep within the brain. These people will exhibit
severe anterograde amnesia as well as other cognitive impairments.
Liver Disease
Alcohol-related liver disease also contributes to neurological disturbances associated with
heavy drinking (Tarter et al. 1993). The risk of alcoholic liver damage depends on factors such
as the drinker's nutrition, gender, and quantity and pattern of alcohol consumption. Recent
research (Tarter et al. 1993) has focused on biological factors involved in protecting liver cells
during metabolism; in some alcoholics, these protective mechanisms appear to be impaired.
One condition associated with advanced liver disease, including alcoholic liver disease, is
hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]). PSE is a
progressive metabolic liver disorder that affects intellectual functioning. Alcoholics with PSE
have livers so damaged by cirrhosis that the flow of venous blood into the liver is obstructed,
allowing toxic substances and metabolic by-products to enter the bloodstream. These toxins,
which can include ammonia and manganese, circulate to the brain, where they interfere with the
actions of neurotransmitters. The effects of PSE can be reversed to some extent with liver
transplantation.
OTHER INFLUENCES ON ALCOHOL-RELATED BRAIN INJURY
Age
When researchers first began to study the effects of alcohol on the brain, they observed
structural brain changes in alcoholics similar to those seen in nonalcoholic subjects as a result
of normal chronological aging. These observations gave rise to the "premature aging
hypothesis." Two versions of the hypothesis exist, each with different propositions concerning
the period in an alcoholic's life during which premature aging begins (for reviews, see Ellis and
Oscar-Berman 1989; Evert and Oscar-Berman 1995). According to the accelerated aging
version of the hypothesis, aging starts to accelerate at whatever age problem drinking begins.
This version predicts that young alcoholics will become old before their time and that
neuropsychological and brain changes in alcoholics will mimic those found in chronologically
older nonalcoholics. According to the increased vulnerability version of the premature aging
hypothesis, vulnerability to alcohol-related brain damage is hastened only in people over age
50, in whom the normal manifestations of aging already have begun. This version suggests that
because of the increased vulnerability of their brains to alcohol-related damage, older alcoholics
will suffer more age-related symptoms and impairment than their nonalcoholic peers and
younger alcoholics.
In the early observations from which the premature aging hypothesis evolved, researchers
characterized the post mortem appearance of alcoholics' brains as being small and shriveled
compared with the brains of age-matched nonalcoholics (Courville 1966). The appearance was
likened to the shrinkage that is associated with normal chronological aging. Other researchers,
using neuroimaging techniques, have reported comparable findings in support of the
accelerated aging hypothesis; backing the increased vulnerability hypothesis, older alcoholics
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displayed more brain tissue loss in brain scans than did younger alcoholics (see Pfefferbaum
and Rosenbloom 1993). On the whole, most of the structural evidence supports a possible link
between alcoholism and premature aging.
Unlike studies assessing brain atrophy, however, neuropsychological investigations have not
accumulated much support for either version of the premature aging hypothesis. Results of a
few studies favor the increased vulnerability hypothesis, but the evidence is inconsistent (for
reviews, see Ellis and Oscar-Berman 1989; Evert and Oscar-Berman 1995). In support of the
hypothesis, one study demonstrated that on the parts of IQ tests that normally pose difficulties
for elderly nonalcoholic people, alcoholics between the ages of 48 and 74 performed
significantly worse than same-age nonalcoholic control subjects and younger alcoholics (Ellis
1990). The increased vulnerability hypothesis leads to a second prediction, however, which was
not supported by the study.
The second prediction hinges on the considerable evidence from a separate line of research
into possible right-hemisphere brain dysfunction in alcoholics (see Oscar-Berman 1992). Like
patients with damage to the right hemisphere, alcoholics typically perform poorly on visuospatial
tasks. The similarity in performance between alcoholics and patients with right-hemisphere
damage led researchers to hypothesize that right-brain functions are more vulnerable than
left-brain functions to the effects of alcohol. Thus, the increased vulnerability hypothesis predicts
that older alcoholics, the group in whom the effects of aging and alcoholism are combined,
would show deficits out of proportion to their age on specialized tests of right-hemisphere
functioning.(7) This was not the case in the study just described (Ellis 1990). The results of
numerous other studies examining right-hemisphere functional decline in relation to alcoholism
and aging have not been sufficiently consistent to resolve the premature aging issue (for a
review, see Ellis and Oscar-Berman 1989).
Regardless of alcohol's role in aging, older alcoholics, by virtue of their chronological age, may
be particularly susceptible to the effects of alcohol. For example, elderly alcoholics have an
increased risk of accidents, deleterious side effects, and overt toxicity resulting from alcohol
intake. Treatment for medical conditions common among the elderly (e.g., chronic pain and
heart disease) also may increase alcohol-related problems in this group. For example, alcohol-
medication interactions can have neuropsychological consequences ranging from drowsiness to
disorientation; physical effects can include hemorrhage, malnutrition, and liver damage, which
also can lead to neuropsychological problems.
Gender
Controversy exists over whether and to what extent chronic alcoholism affects women's brains
differently from men's brains (Glenn 1993). Results of studies using the same techniques to
measure brain structure and function in men and women have been inconsistent. However,
researchers have found evidence of similar degrees of brain shrinkage and impairment on tests
of mental functioning in men and women, even though the women participating in the study had
shorter drinking histories than the men (Lishman et al. 1987). Such evidence has led
investigators to hypothesize that women's brains may differ from men's brains in their
susceptibility to alcohol-related damage.
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Since research suggests that alcohol may affect brain structure differently in men and women,
one might also expect to see gender differences in the neuropsychological consequences of
alcoholism. One way of studying possible neuropsychological disparities between male and
female alcoholics is to examine gender differences in the functioning of the brain's two
hemispheres (i.e., differences in their functional cerebral laterality patterns). This question may
be important because structural differences in men's and women's brains may be one factor
underlying gender differences in perceptual asymmetries and other neuropsychological
responses to alcohol. Normally, in both men and women, the left and right sides of the brain
have disproportionate (i.e., asymmetrical) abilities to process linguistic (e.g., letters, words, and
phrases) and nonverbal (e.g., visuospatial and musical) information. The left hemisphere
usually is more efficient than the right with linguistic signals, and the right hemisphere is more
efficient than the left for nonverbal signals. Scientists can study differences in hemispheric
asymmetries using procedures called laterality tasks, which are sensitive to left and right
hemisphere functioning. Figure 4 illustrates the neuroanatomy of human laterality (for a detailed
description of laterality tasks, see Oscar-Berman 1992).
Laterality tasks allow researchers to conduct experiments in which conflicting visual, auditory, or
tactual stimuli are sent simultaneously to the two halves of the brain. These tasks allow
researchers to measure whether the left or the right side of the brain copes better with the
competing information. With visual laterality tasks, the signals are presented on a computer
screen; with auditory laterality tasks, the signals are presented through stereo earphones; and
with touch tasks, the stimuli are given to the right and left hands. When research participants
receive the stimuli, the side of the brain that is dominant for that material will favor the
information coming into the side that is contralateral, or opposite, to that hemisphere. In
experiments using auditory laterality tasks, for example, researchers may present two words
(e.g., "bin" and "pin") or two excerpts of music simultaneously to a subject, who then may be
asked to identify the words or melodies he or she just heard. The left side of the brain, which is
dominant for language, will favor words coming into the right ear, and the right half of the brain,
which is dominant for music, will favor melodies coming into the left ear.
Studies comparing the separate functions of the left and right cerebral hemispheres have relied
mainly on male research participants; no consistent pattern of abnormalities in alcoholics has
emerged (for a review, see Oscar-Berman 1992). In a study that included both male and female
alcoholics and nonalcoholic control participants, however, Drake and colleagues (1990)
measured gender differences in hemispheric asymmetries using words and music presented
simultaneously in each ear (i.e., dichotic listening). The investigators found that compared with
control subjects, male alcoholics were better able to identify words coming into the right ear (a
left-hemisphere function) and not as able to identify melodies coming into the left ear (a right-
hemisphere function). In contrast, female alcoholics' laterality patterns did not differ from those
of control subjects on either of the dichotic listening tasks. The authors interpreted their results
to mean that male alcoholics showed evidence of right hemisphere dysfunction. Results of
numerous other perceptual laterality studies using visual, tactual, and auditory signals have
been inconsistent in showing abnormal asymmetries in alcoholics; these studies, however, have
not addressed gender differences (Oscar-Berman 1992). Continuing research on how
alcoholism may affect the two halves of the brain differently in men and women may suggest
gender-specific strategies for treatment.
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Family History
Researchers have found that adolescent and adult children of alcoholics who do not drink
alcohol nevertheless show deficits in neuropsychological functioning (for reviews, see Babor et
al. 1994; Porjesz and Begleiter 1993). Evidence suggests that children of alcoholics have
difficulty regulating their own behavior, organizing and remembering information, and learning
tasks that involve two- and three dimensional space. In other studies, abnormal brain electrical
activity, measured as a reduced peak in amplitude in one of the electrical components of the
ERP (i.e., the P300 wave), has been observed in nondrinking sons of alcoholics who were
performing cognitive tasks. Because the electrophysiological abnormalities in the children of
alcoholics are similar to those displayed by abstinent alcoholics, researchers have inferred that
brain waves may provide an observable marker for potential alcoholism in children of alcoholics
even before the initiation of drinking behavior.
Family history of alcoholism has been associated with other notable results. In one study,
intoxicated alcoholics, both with and without a family history of alcoholism, had problems on
cognitive tests sensitive to temporal lobe functions (e.g., memory). On tests sensitive to frontal
lobe functions (e.g., planning and judgment) however, only alcoholics with a positive family
history of alcoholism performed poorly (Peterson et al. 1992).
RECOVERY AND TREATMENT
Studies suggest that slow recovery of cognitive functioning occurs in alcoholics who remain
abstinent for at least 4 weeks, and certain indicators of impairment (i.e., CT and MRI images
and brain glucose metabolism) have been shown to improve with prolonged abstinence
(Pfefferbaum et al. 1995; Volkow et al. 1994). Although numerous pharmacological treatments
have been given to alcoholics to improve neuropsychological functioning, none has proved
entirely successful (Martin and Nimmerrichter 1993). Researchers have not established whether
recovery is complete in most alcoholics (or what constitutes complete recovery), and they have
not yet determined the typical length of the recovery period. With abstinence, some alcoholics
show a slow reversal of neuropsychological impairment. Other alcoholics, however, display
apparently irreversible deficits on specific tasks of cognitive function.
For example, in a study of cognitive recovery over a 14-month period, alcoholics who remained
abstinent performed better than relapsers (Glenn et al. 1994), but abstainers did not perform as
well as nonalcoholic control subjects. In another study, drinkers with a positive family history of
alcoholism who had been abstinent for up to 4 months showed poorer performance on tests of
cognition than either drinkers with a negative family history of alcoholism or abstainers with a
positive family history (Drake et al. 1995). However, alcoholics both with and without a positive
family history of alcoholism showed significant improvement with abstinence. Hence, a positive
family history of alcoholism did not impede recovery of cognitive function among abstinent
alcoholics. In most studies of neuropsychological deficits, length of abstinence typically has
approximated 4 weeks. It is possible that past research may have overestimated permanent
neuropsychological deficits related to chronic alcoholism by examining alcoholics whose mental
functioning continued to improve following the studies' conclusion.
SUMMARY AND CONCLUSIONS
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Several hypotheses have been proposed to explain the diversity of neuropsychological
abnormalities shown by chronic alcoholics: (1) In patients with KS, alcoholism can selectively
interfere with short-term memory, emotion, and other functions associated with damage to
limbic system and diencephalic structures; and (2) alcoholics can also suffer diffuse cortical
damage that affects the functioning of both brain hemispheres (e.g., abstracting and problem-
solving abilities, poor attention, disinhibition, and perseverative responding). No definite
relationships have been established, however, between damage to specific cortical regions and
concurrent cognitive impairments, although findings from neuroimaging and neuropathology
studies point to increased susceptibility of frontal brain systems.
Factors that contribute to differences among people in the neurological consequences of
alcoholism are numerous and include nutritional deficiencies, liver disease, the age and gender
of the drinker, and family history of alcoholism. The notion that neurological disorders result
from the prolonged consumption of alcohol by certain vulnerable alcoholics is a plausible
hypothesis, but identifying what makes certain alcoholics "vulnerable" remains a problem for
further investigation.
Research on alcohol-related neurological disorders has centered on damage to the limbic
system, diencephalon, and cerebral cortex. In addition, damage to central neurotransmitter
systems has been considered as possibly contributing to alcohol-related abnormalities with
harmful neurological consequences. Future research should help clarify the relative importance
of the many biochemical effects of alcohol at all levels, from its effects on the preservation and
replication of the genetic code embodied in DNA and the synthesis of new proteins, to the
activities of neurotransmitters, receptors, neurons, and the entire brain. This information will link
cellular changes directly to specific neurological consequences observed clinically. In the
absence of a cure for alcohol addiction, a detailed understanding of the biochemical actions of
alcohol on nerve cells may help in designing therapies to ameliorate its devastating neurological
effects.
ACKNOWLEDGMENTS
The authors thank Dr. Mark Lewis and Mr. Michael Ward for their helpful comments.
1 The term "alcoholism" as used in this article refers to the criteria for alcohol dependence
defined in the American Psychological Association's Diagnostic and Statistical Manual of Mental
Disorders, Fourth Edition (DSM-IV).
2 Neuropsychology is the branch of psychology focused on the study of the relationship
between the brain and behavior.
3 One standard drink is defined as 12 fluid ounces (oz) of
beer
, 5 fluid oz of
wine
, or 1.5 fluid oz
of distilled spirits.
4 Another disorder, Wernicke's encephalopathy, frequently occurs with KS, leading to a
diagnosis in the patient of Wemicke-Korsakoff syndrome. Patients with Wernicke's
encephalopathy exhibit confusion, uncoordinated gait, and abnormal eye movements, and
imaging techniques reveal lesions in the diencephalon, the cerebellum, and the brain stem. Like
KS, Wernicke's encephalopathy is thought to be caused by a thiamine deficiency; the
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syndrome's acute manifestations often can be reduced by thiamine administration. Hospitalized
alcoholics being administered intravenous glucose also should receive thiamine to reduce the
possibility of developing acute Wernicke's encephalopathy.
5 For additional information on imaging techniques in alcohol research, see Alcohol Health &
Research World Vol. 19, No. 4, 1995.
6 For definitions of this and other technical terms, see glossary, pp. 93-96.
7 Specialized tests that compare right-hemisphere functioning with left-hemisphere functioning
are called laterality tests. Laterality tests are discussed in a later section; see also Oscar-
Berman (1992).
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MARLENE OSCAR-BERMAN, PH.D., is a professor in the departments of psychiatry and
neurology, Boston University School of Medicine, and a research scientist in the Psychology
Research Service, Department of Veterans Affairs Medical Center, Boston, Massachusetts.
BARBARA SHAGRIN, PH.D., is a clinical assistant professor of psychiatry, Boston University
School of Medicine, Boston, Massachusetts.
DENISE L. EVERT, PH.D., is a research associate in the department of psychiatry, Harvard
Medical School, Boston, Massachusetts.
CHARLES EPSTEIN, PH.D., is associate professor of neurology and director of clinical
neurophysiology, Emory University School of Medicine, Atlanta, Georgia.
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The writing of this article was supported by National Institute on Alcohol Abuse and Alcoholism
grants R37AA07112 and K05-AA00219 and by the Medical Research Service of the U.S.
Department of Veterans Affairs.
Source Citation
(MLA 8
th
Edition)
Oscar-Berman, Marlene, et al. "Impairments of brain and behavior: the neurological effects of
alcohol."
Alcohol Health & Research World
, Winter 1997, p. 65+.
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