lcohol consumption can damage the nervous system, including the brain. Consequently, alco-holics1and chronic heavy drinkers cansuffer abnormalities in their mentalfunctioning and changes in behaviorsassociated with brain impairment. Theneurological effects of alcohol canoccur directly, because alcohol is atoxic substance, or they can occurindirectly, through damage to otherbody organs (e.g., the liver) that subse-quently interferes with the workings ofnerve cells in the brain (see figure 1). Images of the brain created withmodern neuroradiological techniques,such as magnetic resonance imaging(MRI) and computed tomography(CT), generally show a relationshipbetween prolonged alcohol consump-tion and changes in the brains struc-ture (Charness 1993; Pfefferbaum etal. 1995). For example, MRI and CTimages have shown brain shrinkageand tissue damage (i.e., brain lesions)in some alcoholics. These changes cancause poor temperature regulation,VOL. 21, NO. 1, 1997 65Impairments of Brain and BehaviorThe Neurological Effects of AlcoholMARLENE OSCAR-BERMAN, PH.D., BARBARA SHAGRIN, PH.D., DENISE L. EVERT, PH.D., AND CHARLES EPSTEIN, PH.D.Chronicheavydrinkingandalcoholismcanhaveseriousrepercussionsforthefunctioningoftheentirenervoussystem,particularlythebrain.Theseeffectsincludechangesinemotionsandpersonalityaswellasimpairedperception,learning,andmemory. Neuropathological and imaging techniques have provided evidence of physicalbrain abnormalities in alcoholics, such as atrophy of nerve cells and brain shrinkage. Atthecellularlevel,alcoholappearstodirectlyaffectbrainfunctioninavarietyofways,primarilybyinterferingwiththeactionofglutamate,gamma-aminobutyricacid,andother neurotransmitters. Neurological disorders also can result from vitamin deficiencyandliverdisease,twohealthproblemsthatcommonlyoccurwithalcoholism.Otherhypotheses,basedonfactorssuchasaging,gender,andgenetics,havebeendevelopedtoexplainvariousalcohol-relatedneurologicalconsequences.Manypharmacologicaltreatmentstoimproveneuropsychologicalfunctioninginalcoholicshave been tested, but none has proved entirely successful. With prolonged abstinence,however,slowrecoveryofcognitivefunctioningcanoccurinsomecases.KEY WORDS:chronicAODE(alcoholandotherdrugeffects);AODR(alcoholandotherdrugrelated)di sorder;brai nfuncti on;brai ndamage;nervoussystemdi sorder;brai ni magi ng;neuropsychologicalassessment;cognitiveprocess;emotion;memory;learning;personality;neurotransmitters; patient family history; malnutrition; liver disorder; aging; gender differences;drug therapy; hypothesis testing; literature reviewA1The term alcoholism as used in this articlerefers to the criteria for alcohol dependencedefined in the American PsychologicalAssociations Diagnostic and StatisticalManual of Mental Disorders, Fourth Edition(DSMIV).muscle weakness, and alterations insleep patterns. This article reviews some of thephysical brain changes and neuropsy-chological2consequences of alco-holism, beginning with the effects ofchronic alcoholism on memory andother cognitive functions. This discus-sion is followed by an examination ofthe differences among people thatcommonly contribute to the manyneurological effects of alcoholism,including medical health, age, gender,and family history of alcoholism. Thearticle concludes with a considerationof treatment and recovery.COMMON EFFECTS OF ALCOHOLON THE NERVOUS SYSTEMAlcohol has effects on both majorcomponents of the nervous systemthe central nervous system (i.e., thebrain and the spinal cord) and theperipheral nervous system (i.e., thenerves in the rest of the body).Alcohol can have a negative effecton certain neurological processes,such as temperature regulation, sleep,and coordination. For example, mod-erate amounts of alcohol lower bodytemperature. Severe intoxication in acold environment may produce mas-sive, life-threatening declines in tem-perature (i.e., hypothermia). Manypeople mistakenly believe that alcoholcan help warm them in cold weather.This notion can be especially danger-ous for the homeless, for elderly peo-ple living in inadequately heatedquarters, and for those exposed toprolonged cold temperatures outdoors.In addition to its effect on bodytemperature, alcohol interferes withnormal sleep patterns. Relativelysmall doses of alcohol can cause earlysedation or sleepiness, awaking duringthe night, and suppression of rapid-eye-movement (REM) sleep. REMsleep is the dreaming stage of sleep;when REM sleep occurs near wake-fulness, it often produces vivid hallu-cinations. Most people fall asleepeasily after one or more alcoholicdrinks3but experience diminution ofREM sleep. Drinkers who attempt touse alcohol as a sedative seldom attaina full nights sleep, however; afterseveral hours, the natural eliminationof alcohol from the body producesarousal and sleep fragmentation.When chronic drinkers withdraw fromalcohol, long-suppressed REM sleepmay rebound excessively. Some au-thorities (Greenberg and Pearlman1967) believe that delirium tremens(known as DTs), a condition occur-ring 2 to 4 days after alcohol with-drawal that consists of trembling andagitation with hallucinations, overex-citation, fever, sweating, and rapidheartbeat, represents a state of contin-uous REM sleep. In addition, measur-able insomnia may occur many weeksinto abstinence.Another prominent effect of chronicalcohol consumption is harm to thepart of the brain called the cerebellum66 ALCOHOL HEALTH & RESEARCH WORLD3One standard drink is defined as 12 fluidounces (oz) of beer, 5 fluid oz of wine, or 1.5fluid oz of distilled spirits. 2Neuropsychology is the branch of psychologyfocused on the study of the relationship be-tween the brain and behavior.Alcohol and alcoholismPharmacologicalDirect toxic effectsWithdrawalsyndromesLiverdiseaseHead injury UnknownAdverse effects on the nervous systemNutritionaldeficiencyFigure 1 Sources of neurological complications of alcohol and alcoholism.SOURCE: Adapted from Bernat, J.L., and Victor, M. The Neurological Complications of Alcohol andAlcoholism. Unit 7. 2d ed. Developed by the Project Cork Institute at Dartmouth Medical School.Timonium, MD: Milner-Fenwick, 1994.MARLENE OSCAR-BERMAN, PH.D., is aprofessor in the departments of psy-chiatry and neurology, BostonUniversity School of Medicine, and aresearch scientist in the PsychologyResearch Service, Department ofVeterans Affairs Medical Center,Boston, Massachusetts.BARBARA SHAGRIN, PH.D., is a clinicalassistant professor of psychiatry,Boston University School ofMedicine, Boston, Massachusetts. DENISE L. EVERT, PH.D., is a researchassociate in the department of psychi-atry, Harvard Medical School,Boston, Massachusetts. CHARLES EPSTEIN, PH.D., is associateprofessor of neurology and director ofclinical neurophysiology, EmoryUniversity School of Medicine,Atlanta, Georgia.The writing of this article was support-ed by National Institute on AlcoholAbuse and Alcoholism grants R37-AA07112 and K05-AA00219 and bythe Medical Research Service of theU.S. Department of Veterans Affairs.(figure 2), resulting mainly in the lossof muscular coordination. This damageappears as imbalance and staggering,although other problems also mayoccur (Raymond et al. 1996). A peripheral nervous system disor-der commonly seen in alcoholics isnumbness and weakness in the handsand feet (i.e., peripheral neuropathy).This condition is thought to be largelya consequence of malnutrition in se-vere alcoholics. One type of peripheralnerve damage known as Saturday nightpalsy can occur when an alcoholic putspressure on vulnerable nerves in thearm while lying in an intoxicated stu-por, leaving him or her unable to ex-tend the wrist for days to weeks. ABNORMALITIES IN NEUROPSYCH-OLOGICAL FUNCTIONSIn addition to changes in temperatureregulation, sleep, and coordination,alcoholism-related brain changes cancause abnormalities in mental func-tioning that are detectable using spe-cialized neuropsychological tests.Behavioral neurologists and neuropsy-chologists use these sensitive tests tomeasure both the obvious and thesubtle consequences of brain damage.Results of the tests often show changesin emotions and personality as well asimpaired perception, learning, andmemory (i.e., cognitive abilities) afterdamage to particular brain systems(see Evert and Oscar-Berman 1995).Korsakoffs Syndrome One of the most severe consequencesof long-term alcoholism on mentalfunctioning is Korsakoffs syndrome(KS), a devastating memory disorderin which a person appears to forgetthe incidents of his or her daily lifeas soon as they occur (see Oscar-Berman 1990). Because of this dra-matic loss of short-term memory(also called anterograde amnesia),patients with KS virtually live in thepast. For example, someone whodeveloped KS in the 1960s mightbelieve that the President of theUnited States is Dwight Eisenhoweror John Kennedy. Some alcoholicsmay have a genetic component orpredisposition to develop this am-nesic condition: These patients mayhave an enzyme deficiency that pre-vents their bodies from using thi-amine (a B vitamin) efficiently.4This deficiency, coupled with a diethigh in alcohol and low in thiamine(along with other nutrients), maylead to brain damage causing theamnesia.Although KS destroys short-termmemory, it typically spares most long-term memories (i.e., memories formedor knowledge gained before the onsetof prolonged heavy drinking). Thus,overall intelligence, as measured bystandardized IQ tests, does not neces-sarily deteriorate, because the types ofinformation and abilities tapped bythese tests usually involve long-termmemory.Other NeuropsychologicalProblems Within the past 25 years, clinical andexperimental observations of patientswith and without KS have revealedmany other neuropsychological dys-functions associated with alcoholism.Alcoholics demonstrate poor attentionto what is going on around them; needextra time to process visual informa-tion; have difficulty with abstraction,problem-solving, and learning newmaterials; exhibit emotional abnor-malities and disinhibitions; and showreduced visuospatial abilities (i.e., thecapacity to deal with objects in two-VOL. 21, NO. 1, 1997 67Brain and Behavior ImpairmentsCerebral cortexParietal lobeCerebellumBrain stemMammillary bodyTemporal lobeHypothalamusLateralventricleFrontal lobeCorpus callosumCerebrumThalamusPituitary glandFigure 2 Schematic of a lengthwise cross-section through the human brain. Brainstructures that most frequently have been implicated in alcohol-relatedneurological disorders include parts of the diencephalon (i.e., themammillary bodies of the hypothalamus and the dorsomedial nucleuswithin the thalamus), the cerebral cortex, and several central neuro-transmitter (i.e.,nerve cell communication) systems.4Another disorder, Wernickes encephalopathy,frequently occurs with KS, leading to a diagno-sis in the patient of Wernicke-Korsakoffsyndrome. Patients with Wernickesencephalopathy exhibit confusion, uncoordi-nated gait, and abnormal eye movements, andimaging techniques reveal lesions in thediencephalon, the cerebellum, and the brainstem. Like KS, Wernickes encephalopathy isthought to be caused by a thiamine deficiency;the syndromes acute manifestations often canbe reduced by thiamine administration.Hospitalized alcoholics being administeredintravenous glucose also should receive thi-amine to reduce the possibility of developingacute Wernickes encephalopathy.dimensional or three-dimensionalspace) (Parsons and Nixon 1993). Theonce-common view that alcoholicswithout Korsakoffs syndrome arecognitively intact has been abandonedin light of accumulating evidence thatcognitive impairments (and associatedchanges in brain structure) can occurin alcoholics who do not exhibit obvi-ous clinical signs of anterograde am-nesia (see Lishman 1990).ALCOHOLISM-RELATED BRAINDAMAGE AND ASSOCIATEDNEUROPSYCHOLOGICAL CHANGESThe type and extent of structuraldamage to brain tissue can be deter-mined by autopsy (i.e., post mortem)examination of the brains compo-nents and individual nerve cells (i.e.,neuropathological evidence). In addi-tion, neuroradiological techniques,such as MRI and CT scans, allow thebrain to be viewed inside the skull ofa living person. Other neuroimagingtechniques (i.e., functional neuro-imaging) measure active brain func-tioning. Functional neuroimaging canreveal changes in the blood flow inand around the brain, brain metab-olism, and brain electrical activitygenerated by nerve impulses (i.e.,neurophysiological measures).5Onetype of neurophysiological measure,event-related potentials (ERPs),consists of brain waves recorded fromscalp electrodes while a person ispresented with specific pieces ofinformation or stimuli. Scientists usecomputers to translate the informationobtained from ERPs and other func-tional neuroimaging measures intomeaningful pictures that, in turn,make it possible to view brain func-tioning while a person is thinking orperforming a task.When applied to alcohol research,neuropathological and imaging tech-niques have helped to provide cumula-tive evidence of brain abnormalities inalcoholics, such as atrophy6of nervecells (i.e., neurons) and brain shrink-age (Hunt and Nixon 1993). Brainshrinkage appears as abnormal widen-ing of the grooves (i.e., sulci) andfissures on the brains surface or en-largement of the fluid-filled cavitiesdeep inside the brain (i.e., the ventri-cles). Regions of the brain that areespecially vulnerable to damage afteryears of chronic alcoholism includethe cerebellum, the limbic system(including the hippocampus and amyg-dala), the diencephalon (including thethalamus and hypothalamus), and thecerebral cortex (see figures 2 and 3). Countless intricate pathways ofneurons link the different areas of thebrain, including the regions implicat-ed in alcohol-related neurologicaldysfunction. Because of the size andcomplexity of this network, the con-sequences of damage to one structureor system often can resemble the con-sequences of damage to another. Thefollowing sections describe alcohol-related structural and neuropsycho-logical changes that can occur in thebrain.The Limbic SystemThe limbic system is an intricate net-work of structures located deep insidethe brain; its functions are diverse andvaried. One function of the limbic sys-tem receiving attention from alcoholresearchers is memory. Memory losssimilar to the amnesia in KS patientshas been associated with damage tothe hippocampus and the amygdala,parts of the limbic system that arelocated in the temporal lobes of thebrain (see Evert and Oscar-Berman1995). Although injury to the limbicsystem can cause amnesia, researchersare not certain of the degree to whichalcohol-related memory impairmentsmay be linked to damage in that partof the brain. Alcohol researchers are interestedin other functions of the limbic systemas well. Damage to certain parts of thelimbic system leads to abnormalitiesin emotional functioning, the sense ofsmell (i.e., olfaction), and the abilityto use one sense (e.g., vision) to learnsomething in another sense (e.g.,touch) (i.e., cross-modal functioning).In all these categories of function,researchers have observed deficits inalcoholics (Evert and Oscar-Berman1995). Moreover, alcoholics with KSappear to have greater impairment insome of these functional areas than donon-KS alcoholics.The DiencephalonThe diencephalon, a region nestled inthe center of the brain, acts like a waystation for nerve signals moving fromone area of the brain to another. Al-though it is not known precisely whatrole diencephalic structures play inhuman memory functioning, lesions inthis region have been clearly docu-mented in amnesic patients (Victor etal. 1989). Researchers are not certainwhether alcohol-related memory im-pairments are caused by these lesions,however. An alternative explanationcomes from a study that comparedMRI measures of diencephalic dam-age in alcoholics with and without KS(Blansjaar et al. 1992). The authorssuggested that diencephalic lesionsdevelop regardless of whether patientsacquire the amnesia of KS and are notso much typical of KS as they are ofchronic alcoholism and malnutrition. The Cerebral Cortex The cerebral cortex is the intricatelyfolded outer layer of the brain com-posed of nerve cell bodies (i.e., graymatter). It is considered to be thecenter of higher consciousness and theseat of all intelligent behavior. Thecortex makes neural connections, bothdirectly and indirectly, with all partsof the nervous system and, therefore,with all parts of the body. As noted previously, neuroradio-logical evidence has revealed awidening of the fissures and sulci ofthe cerebral cortex and enlargementof the ventricles in brains of alco-holics. These changes suggest corti-cal atrophy associated withalcoholism (Pfefferbaum and68 ALCOHOL HEALTH & RESEARCH WORLD5For additional information on imaging tech-niques in alcohol research, see Alcohol Health& Research World Vol. 19, No. 4, 1995. 6For definitions of this and other technicalterms, see glossary, pp. 9396. Rosenbloom 1993; Pfefferbaum et al.1995). The evidence for corticalatrophy has come both from imagingstudies of detoxified alcoholics andfrom post mortem analyses of thebrains of alcoholics. For example,MRI findings show evidence of sig-nificant cortical and subcortical tis-sue and volume loss in non-KSalcoholics compared with nonalco-holic control subjects. Moreover,alcoholics with KS have greater cor-tical atrophy than non-KS alcoholics.Researchers also have reported neu-ropsychological deficits in alcoholics(e.g., through tests of problem-solv-ing, spatial memory, visual associa-tions, and learning related to orcaused by touch [i.e., tactual learn-ing]) that indicate alcoholism-relatedcortical atrophy (Evert and Oscar-Berman 1995). In most studies of alcohol-relatedneurological disorders, researchershave assessed neuropsychologicaldeficits in alcoholics without examin-ing changes in alcoholics brains. Tobetter understand brain-behavior rela-tionships, however, neuropsychologi-cal, structural, and functional changesmust be evaluated to relate changes inbehavior to damage in particular sys-tems of the brain. In studies using bothmethods, in fact, results have not re-vealed consistent relationships betweencortical damage and performance onneuropsychological tests. Some mea-sures of brain structure or functionhave correlated with cognitive testscores, whereas others have not. Forexample, one study reported a relation-ship between certain neuropsychologi-cal test scores and measures of frontalbrain metabolism in long-term alco-holics; the same study, however, foundno correlation between neuropsycho-logical performance and degree ofcortical atrophy as seen using MRI(Wang et al. 1993). The results wereinterpreted as reflecting either the preser-vation of cognitive abilities with mildstructural brain changes or the insensi-tivity of the tests used to detect mildstructural changes.The most consistently and fre-quently reported findings in alcoho-lics, based on functional and struc-tural imaging techniques, have beenabnormalities in frontal brain regions(for reviews, see Oscar-Berman andHutner 1993; Pfefferbaum andRosenbloom 1993). Frontal-systemfunctions include planning, carryingout, and monitoring goal-directedand socially suitable behaviors.Compared with nonalcoholic controlsubjects, some alcoholics have shownsignificant reductions in cerebralblood flow in certain areas of thefrontal regions as well as in otherbrain areas. In addition, greater bloodflow reduction in frontal corticalareas has been associated withgreater severity of alcoholism andpoorer cognitive test performance. Inother studies, alcoholics showeddiminished metabolic functions infrontal areas; this reduction was asso-ciated with impaired neuropsycho-logical functions. In studies of KS patients, re-searchers have obtained additionalfindings supporting frontal-systemdysfunction (Oscar-Berman andHutner 1993). Neuropsychologicalstudies have shown that KS patientsexhibit clinical signs associated withdamage to the frontal cortex (e.g.,emotional apathy, personalitychanges and loss of inhibitions, andconstant repetition of certain respons-es despite feedback indicating thatsuch responses are incorrect or inap-propriate [i.e., abnormal responseperseveration]). Although much de-bate centers on the connection betweenmeasures of alcohol consumption andthe degree of structural or functionalimpairment in non-KS alcoholics,research so far has failed to demon-strate a clear connection betweenmeasures of alcohol intake, cognitivedysfunction, and frontal damage. VOL. 21, NO. 1, 1997 69Brain and Behavior ImpairmentsFigure 3 Schematic of a cross-section through the human brain. Brain structuresthat have been implicated in alcohol-related neurological disordersinclude parts of the limbic system (i.e., the hippocampus and theamygdala), the mammillary bodies of the hypothalamus, and thedorsomedial nucleus within the thalamus.SOURCE: Adapted from Nieuwenhuys, R.; Voogd, J.; and van Huijzen, C. The Human CentralNervous System: A Synopsis and Atlas. New York: Springer Verlag, 1988.Third ventricleTemporallobeHippocampusMammillarybodyAmygdalaDorsomedialnucleus of thethalamusAnterior nucleusof the thalamusCorpus callosumThalamusNEUROTRANSMITTERS ANDALCOHOLISMAt the cellular level, alcohol appears toaffect brain function in a variety ofways. For example, alcohol can alterthe action of the chemicals that allowneurons to communicate (i.e., neuro-transmitters). Specialized proteins onthe surface of neurons, known as recep-tors, recognize neurotransmitters andinitiate the cells response. Neuro-transmitters and receptors cluster wherenerve cells come into close contact;these contacts are called synapses.Some neurotransmitters stimulate (i.e.,excite) a response from the neurons thatreceive them; others inhibit neuronalresponse. Over periods of days andweeks, the levels of receptors change inresponse to chemical and environmen-tal influences (e.g., drugs and synapticactivity) on the neurons. Genes in theneurons DNA are turned on or off,increasing or decreasing the synthesisof receptors. Over time, drugs thatexcite a given receptor generally lead toa reduction in (i.e., down-regulate) thenumbers or activity of that receptortype. Drugs that inhibit a receptor even-tually tend to lead to an increase in (i.e.,up-regulate) that type of receptor. Up-and down-regulation are means bywhich the nervous system maintains afunctional balance of neurotransmittersand receptors; when imbalances occur,effects can include seizures, sedation,depression, agitation, and other moodand behavioral disorders.GlutamateThe major excitatory neurotransmitterin the human brain is glutamate, anamino acid. Glutamate has a funda-mental role in a cellular adaptationcalled long-term potentiation, which isa persistent increase in the efficiencyof a neurons response to a neuro-transmitter. Long-term potentiationmay be an important mechanism inlearning and memory. Extremely small amounts of alco-hol have been shown to interfere withglutamate action. This interferencecould affect multiple brain functions,including memory, and it may accountfor the short-lived condition referredto as alcoholic blackout. Because ofits inhibitory effect on glutamate,chronic consumption of alcohol leadsto up-regulation of glutamate receptorsites in the hippocampus, an area thatis crucial to memory and often in-volved in epileptic seizures. Duringalcohol withdrawal, glutamate recep-tors that have adapted to the continualpresence of alcohol may becomeoveractive. Glutamate overactivity hasbeen linked repeatedly to cell death insituations ranging from strokes toseizures. Deficiencies of thiamine andmagnesium, which are common inalcoholics as a result of malnutrition,may contribute to this potentiallydestructive overactivity.GABAGamma-aminobutyric acid (GABA) isthe major inhibitory neurotransmitterin the central nervous system.Evidence suggests that alcohol initial-ly potentiates GABA effects; in otherwords, it increases inhibition, andoften the brain becomes mildly sedat-ed. But over time, chronic alcoholconsumption reduces the number ofGABA receptors through the processof down-regulation. When alcohol iseventually withdrawn, the loss of itsinhibitory effects, combined with adeficiency of GABA receptors, maycontribute to overexcitation through-out the brain. This effect, in turn, cancontribute to withdrawal seizures (i.e.,rum fits) within 1 or 2 days.Other NeurotransmittersAlcohol directly stimulates release ofthe neurotransmitter serotonin as wellas natural substances related to opi-oids (i.e., endorphins) that may con-tribute to the high of intoxication.Serotonin helps regulate functionssuch as food and water intake, sexualresponse, and aggression. Changes inother neurotransmitters, such asacetylcholine (which underlies keycardiovascular mechanisms, includingdilation of blood vessels) and thecatecholamines (the decreased trans-mission of which has been linked tothe memory deficits of patients withKS [NIAAA 1993]), have been lessconsistently observed.Alcohol disrupts neuron activity invarious other ways. For example, overseveral weeks, alcohol reduces thelevel of nerve growth factors, proteinsimportant for cellular adaptation andsurvival. In addition, alcohol maycause long-term adaptive changes inmembrane lipids.VULNERABILITIES TO THENEUROLOGICAL EFFECTSOF ALCOHOLISMAlcoholism is a multidimensionaldisorder, and no simple answers existto questions such as: What are theneurological consequences of alco-holism?; What makes alcoholismaffect different people in differentways?; or even What causes some-one to become an alcoholic in the firstplace? Widespread individual differ-ences occur in the manifestation ofalcoholism. For example, according toone estimate, 50 to 85 percent of non-KS alcoholics exhibit signs of cogni-tive decline (see Parsons 1993). Thus,anywhere from 15 to 50 percent ofsuch alcoholics may not exhibit anyobvious signs of cognitive impairment.In general, the greater the consumptionof alcohol, the worse the performanceon cognitive tasks. However, amongthose alcoholics who exhibit neurologi-cal problems, researchers have foundthat measures of previous alcoholconsumption (e.g., duration, frequency,and quantity consumed) do not corre-late consistently with the degree ofneuropsychological dysfunction(Parsons 1993). This finding suggeststhat variables other than the presumeddirect neurotoxic effects of alcoholmay play a role in determining alcohol-related cognitive decline. In responseto the variability in the consequencesof alcoholism, researchers have lookedfor common elements that might helpexplain why certain alcoholics developspecific neurological symptoms ormental changes. Factors that may influ-ence the neurological consequences ofalcoholism include coexisting health70 ALCOHOL HEALTH & RESEARCH WORLDproblems, such as malnutrition andliver disease; the age at which problemdrinking begins; the gender of thealcoholic; and a family history of alco-holism. These factors are considered inthe sections that follow.COMMON ALCOHOL-RELATEDMEDICAL PROBLEMSTwo common health problems occur-ring with alcoholism are vitamin defi-ciency and liver disease, both ofwhich can result in neurological disor-ders. As mentioned previously, pro-longed drinking with improper dietand associated malnutrition can leadto thiamine deficiency, a possiblefactor in KS-related brain damage.Several investigators have stressed theidea that damage in the diencephalonof KS patients is caused by thiaminedeficiency, whereas cortical abnor-malities, most notably in the frontallobes, are caused by alcohol neurotox-icity or other conditions frequentlyassociated with alcoholism (e.g., liverdisease or head trauma). Thiamine DeficiencyResearchers differ in their explana-tions of how and why particular neu-ropsychological deficits are displayedin alcoholics. One theory proposes thatalcoholics may fall into subgroupsdistinguished by whether their brainsare vulnerable to the direct neurotoxiceffects of alcohol, to thiamine defi-ciency, or to both factors (Lishman1990). According to this viewpoint,alcoholics who are susceptible to alco-hol toxicity alone may develop perma-nent or transient cognitive deficitsassociated with cortical shrinkage.Those alcoholics who are susceptibleto thiamine deficiency alone will de-velop a mild or short-lived KS statewith anterograde amnesia as a salientfeature. Alcoholics who suffer from acombination of alcohol neurotoxicityand thiamine deficiency (i.e., havedual vulnerability) will experiencewidespread damage to large regions ofthe cerebral cortex as well as to struc-tures deep within the brain. Thesepeople will exhibit severe anterogradeamnesia as well as other cognitiveimpairments.Liver DiseaseAlcohol-related liver disease alsocontributes to neurological distur-bances associated with heavy drinking(Tarter et al. 1993). The risk of alco-holic liver damage depends on factorssuch as the drinkers nutrition, gender,and quantity and pattern of alcoholconsumption. Recent research (Tarteret al. 1993) has focused on biologicalfactors involved in protecting livercells during metabolism; in somealcoholics, these protective mecha-nisms appear to be impaired. Onecondition associated with advancedliver disease, including alcoholic liverdisease, is hepatic encephalopathy(also called portal-systemicencephalopathy [PSE]). PSE is a pro-gressive metabolic liver disorder thataffects intellectual functioning.Alcoholics with PSE have livers sodamaged by cirrhosis that the flow ofvenous blood into the liver is obstruct-ed, allowing toxic substances andmetabolic by-products to enter thebloodstream. These toxins, which caninclude ammonia and manganese,circulate to the brain, where theyinterfere with the actions of neuro-transmitters. The effects of PSE canbe reversed to some extent with livertransplantation.OTHER INFLUENCES ON ALCOHOL-RELATED BRAIN INJURYAgeWhen researchers first began to studythe effects of alcohol on the brain,they observed structural brain changesin alcoholics similar to those seen innonalcoholic subjects as a result ofnormal chronological aging. Theseobservations gave rise to the prema-ture aging hypothesis. Two versionsof the hypothesis exist, each withdifferent propositions concerning theperiod in an alcoholics life duringwhich premature aging begins (forreviews, see Ellis and Oscar-Berman1989; Evert and Oscar-Berman 1995).According to the accelerated agingversion of the hypothesis, aging startsto accelerate at whatever age problemdrinking begins. This version predictsthat young alcoholics will become oldbefore their time and that neuropsy-chological and brain changes in alco-holics will mimic those found inchronologically older nonalcoholics.According to the increased vulnera-bility version of the premature aginghypothesis, vulnerability to alcohol-related brain damage is hastened onlyin people over age 50, in whom thenormal manifestations of aging al-ready have begun. This version sug-gests that because of the increasedvulnerability of their brains to alcohol-related damage, older alcoholics willsuffer more age-related symptoms andimpairment than their nonalcoholicpeers and younger alcoholics. In the early observations fromwhich the premature aging hypothesisevolved, researchers characterized thepost mortem appearance of alcoholicsbrains as being small and shriveledcompared with the brains of age-matched nonalcoholics (Courville1966). The appearance was likened tothe shrinkage that is associated withnormal chronological aging. Otherresearchers, using neuroimaging tech-niques, have reported comparablefindings in support of the acceleratedaging hypothesis; backing the increasedvulnerability hypothesis, older alco-holics displayed more brain tissue lossin brain scans than did younger alco-holics (see Pfefferbaum andRosenbloom 1993). On the whole,most of the structural evidence sup-ports a possible link between alco-holism and premature aging. Unlike studies assessing brainatrophy, however, neuropsychologicalinvestigations have not accumulatedmuch support for either version of thepremature aging hypothesis. Resultsof a few studies favor the increasedvulnerability hypothesis, but the evi-dence is inconsistent (for reviews, seeEllis and Oscar-Berman 1989; EvertVOL. 21, NO. 1, 1997 71Brain and Behavior Impairmentsand Oscar-Berman 1995). In supportof the hypothesis, one study demon-strated that on the parts of IQ teststhat normally pose difficulties forelderly nonalcoholic people, alco-holics between the ages of 48 and 74performed significantly worse thansame-age nonalcoholic control sub-jects and younger alcoholics (Ellis1990). The increased vulnerabilityhypothesis leads to a second predic-tion, however, which was not sup-ported by the study. The second prediction hinges onthe considerable evidence from aseparate line of research into possibleright-hemisphere brain dysfunction inalcoholics (see Oscar-Berman 1992).Like patients with damage to the righthemisphere, alcoholics typically per-form poorly on visuospatial tasks.The similarity in performance betweenalcoholics and patients with right-hemisphere damage led researchers tohypothesize that right-brain functionsare more vulnerable than left-brainfunctions to the effects of alcohol. Thus,the increased vulnerability hypothesispredicts that older alcoholics, thegroup in whom the effects of agingand alcoholism are combined, wouldshow deficits out of proportion totheir age on specialized tests of right-hemisphere functioning.7This was notthe case in the study just described(Ellis 1990). The results of numerousother studies examining right-hemi-sphere functional decline in relationto alcoholism and aging have not beensufficiently consistent to resolve thepremature aging issue (for a review,see Ellis and Oscar-Berman 1989). Regardless of alcohols role inaging, older alcoholics, by virtue oftheir chronological age, may be partic-ularly susceptible to the effects ofalcohol. For example, elderly alco-holics have an increased risk of acci-dents, deleterious side effects, andovert toxicity resulting from alcoholintake. Treatment for medical condi-tions common among the elderly (e.g.,chronic pain and heart disease) alsomay increase alcohol-related problemsin this group. For example, alcohol-medication interactions can haveneuropsychological consequencesranging from drowsiness to disorien-tation; physical effects can includehemorrhage, malnutrition, and liverdamage, which also can lead to neuro-psychological problems.GenderControversy exists over whether andto what extent chronic alcoholismaffects womens brains differentlyfrom mens brains (Glenn 1993).Results of studies using the sametechniques to measure brain structureand function in men and women havebeen inconsistent. However,researchers have found evidence ofsimilar degrees of brain shrinkage andimpairment on tests of mental func-tioning in men and women, eventhough the women participating in thestudy had shorter drinking historiesthan the men (Lishman et al. 1987).Such evidence has led investigators tohypothesize that womens brains maydiffer from mens brains in their sus-ceptibility to alcohol-related damage.Since research suggests that alcoholmay affect brain structure differentlyin men and women, one might alsoexpect to see gender differences in theneuropsychological consequences ofalcoholism. One way of studyingpossible neuropsychological dispari-ties between male and female alco-holics is to examine gender differencesin the functioning of the brains twohemispheres (i.e., differences in theirfunctional cerebral laterality patterns).This question may be important be-cause structural differences in mensand womens brains may be one factorunderlying gender differences in per-ceptual asymmetries and other neu-ropsychological responses to alcohol.Normally, in both men and women,the left and right sides of the brainhave disproportionate (i.e., asymmetri-cal) abilities to process linguistic (e.g.,letters, words, and phrases) and non-verbal (e.g., visuospatial and musical)information. The left hemisphere usu-ally is more efficient than the rightwith linguistic signals, and the righthemisphere is more efficient than theleft for nonverbal signals. Scientistscan study differences in hemisphericasymmetries using procedures calledlaterality tasks, which are sensitive toleft and right hemisphere functioning.Figure 4 illustrates the neuroanatomyof human laterality (for a detaileddescription of laterality tasks, seeOscar-Berman 1992).Laterality tasks allow researchersto conduct experiments in which con-flicting visual, auditory, or tactualstimuli are sent simultaneously to thetwo halves of the brain. These tasksallow researchers to measure whetherthe left or the right side of the braincopes better with the competing infor-mation. With visual laterality tasks,the signals are presented on a computerscreen; with auditory laterality tasks,the signals are presented through stereoearphones; and with touch tasks, thestimuli are given to the right and lefthands. When research participantsreceive the stimuli, the side of thebrain that is dominant for that materialwill favor the information coming intothe side that is contralateral, or oppo-site, to that hemisphere. In experi-ments using auditory laterality tasks,for example, researchers may presenttwo words (e.g., bin and pin) ortwo excerpts of music simultaneouslyto a subject, who then may be asked toidentify the words or melodies he orshe just heard. The left side of thebrain, which is dominant for language,will favor words coming into the rightear, and the right half of the brain,which is dominant for music, will favormelodies coming into the left ear.Studies comparing the separatefunctions of the left and right cerebralhemispheres have relied mainly onmale research participants; no consis-tent pattern of abnormalities in alco-holics has emerged (for a review, seeOscar-Berman 1992). In a study thatincluded both male and female alco-holics and nonalcoholic control partic-ipants, however, Drake and colleagues(1990) measured gender differences in72 ALCOHOL HEALTH & RESEARCH WORLD7Specialized tests that compare right-hemisphere functioning with left-hemispherefunctioning are called laterality tests. Lateralitytests are discussed in a later section; see alsoOscar-Berman (1992).hemispheric asymmetries using wordsand music presented simultaneouslyin each ear (i.e., dichotic listening).The investigators found that comparedwith control subjects, male alcoholicswere better able to identify words com-ing into the right ear (a left-hemispherefunction) and not as able to identifymelodies coming into the left ear (aright-hemisphere function). In con-trast, female alcoholics lateralitypatterns did not differ from those ofcontrol subjects on either of the di-chotic listening tasks. The authorsinterpreted their results to mean thatmale alcoholics showed evidence ofright hemisphere dysfunction. Resultsof numerous other perceptual laterali-ty studies using visual, tactual, andauditory signals have been inconsis-tent in showing abnormal asymme-tries in alcoholics; these studies,however, have not addressed genderdifferences (Oscar-Berman 1992).Continuing research on how alco-holism may affect the two halves ofthe brain differently in men and wom-en may suggest gender-specific strate-gies for treatment.Family HistoryResearchers have found that adoles-cent and adult children of alcoholicswho do not drink alcohol neverthelessshow deficits in neuropsychologicalfunctioning (for reviews, see Babor etal. 1994; Porjesz and Begleiter 1993).Evidence suggests that children ofalcoholics have difficulty regulatingtheir own behavior, organizing andremembering information, and learn-ing tasks that involve two- and three-dimensional space. In other studies,abnormal brain electrical activity,measured as a reduced peak in ampli-tude in one of the electrical compo-nents of the ERP (i.e., the P300wave), has been observed innondrinking sons of alcoholics whowere performing cognitive tasks.Because the electrophysiologicalabnormalities in the children of alco-holics are similar to those displayedby abstinent alcoholics, researchershave inferred that brain waves mayprovide an observable marker forpotential alcoholism in children ofalcoholics even before the initiation ofdrinking behavior.Family history of alcoholism hasbeen associated with other notableresults. In one study, intoxicated alco-holics, both with and without a familyhistory of alcoholism, had problems oncognitive tests sensitive to temporallobe functions (e.g., memory). On testssensitive to frontal lobe functions (e.g.,planning and judgment) however, onlyalcoholics with a positive family histo-ry of alcoholism performed poorly(Peterson et al. 1992).RECOVERY AND TREATMENTStudies suggest that slow recovery ofcognitive functioning occurs in alco-holics who remain abstinent for atVOL. 21, NO. 1, 1997 73Brain and Behavior ImpairmentsL RRRRLLR LLLRLMainlanguagecenter CalculationROlfactionnostrilSpeechWritingOlfactionnostrilStereognosisearR. earearL. earVisualhalffieldVisualhalffieldSpatialconstructionSimple languagecomprehensionNonverbalideationStereognosis(i.e., tactual learning) (i.e., tactual learning)Figure 4 Schematic representation of perceptual and language functions in theright and left cerebral hemispheres of the human brain.least 4 weeks, and certain indicatorsof impairment (i.e., CT and MRIimages and brain glucose metabolism)have been shown to improve withprolonged abstinence (Pfefferbaum etal. 1995; Volkow et al. 1994). Al-though numerous pharmacologicaltreatments have been given to alco-holics to improve neuropsychologicalfunctioning, none has proved entirelysuccessful (Martin and Nimmerrichter1993). Researchers have not estab-lished whether recovery is complete inmost alcoholics (or what constitutescomplete recovery), and they have notyet determined the typical length ofthe recovery period. With abstinence,some alcoholics show a slow reversalof neuropsychological impairment.Other alcoholics, however, displayapparently irreversible deficits onspecific tasks of cognitive function. For example, in a study of cogni-tive recovery over a 14-month period,alcoholics who remained abstinentperformed better than relapsers (Glennet al. 1994), but abstainers did notperform as well as nonalcoholic con-trol subjects. In another study, drinkerswith a positive family history of alco-holism who had been abstinent for upto 4 months showed poorer perfor-mance on tests of cognition than ei-ther drinkers with a negative familyhistory of alcoholism or abstainerswith a positive family history (Drakeet al. 1995). However, alcoholics bothwith and without a positive familyhistory of alcoholism showed signifi-cant improvement with abstinence.Hence, a positive family history ofalcoholism did not impede recovery ofcognitive function among abstinentalcoholics. In most studies of neu-ropsychological deficits, length ofabstinence typically has approximated4 weeks. It is possible that past re-search may have overestimated per-manent neuropsychological deficitsrelated to chronic alcoholism by ex-amining alcoholics whose mentalfunctioning continued to improvefollowing the studies conclusion.SUMMARY AND CONCLUSIONSSeveral hypotheses have been pro-posed to explain the diversity of neu-ropsychological abnormalities shownby chronic alcoholics: (1) In patientswith KS, alcoholism can selectivelyinterfere with short-term memory,emotion, and other functions associat-ed with damage to limbic system anddiencephalic structures; and (2) alco-holics can also suffer diffuse corticaldamage that affects the functioning ofboth brain hemispheres (e.g., abstract-ing and problem-solving abilities,poor attention, disinhibition, and per-severative responding). No definiterelationships have been established,however, between damage to specificcortical regions and concurrent cogni-tive impairments, although findingsfrom neuroimaging and neuropath-ology studies point to increased sus-ceptibility of frontal brain systems. Factors that contribute to differ-ences among people in the neurologicalconsequences of alcoholism are numer-ous and include nutritional deficien-cies, liver disease, the age and genderof the drinker, and family history ofalcoholism. The notion that neurologi-cal disorders result from the prolongedconsumption of alcohol by certain vul-nerable alcoholics is a plausible hypo-thesis, but identifying what makescertain alcoholics vulnerable remainsa problem for further investigation.Research on alcohol-related neuro-logical disorders has centered on dam-age to the limbic system, diencephalon,and cerebral cortex. In addition, dam-age to central neurotransmitter systemshas been considered as possibly con-tributing to alcohol-related abnormalitieswith harmful neurological conse-quences. Future research should helpclarify the relative importance of themany biochemical effects of alcohol atall levels, from its effects on thepreservation and replication of thegenetic code embodied in DNA andthe synthesis of new proteins, to theactivities of neurotransmitters, recep-tors, neurons, and the entire brain. Thisinformation will link cellular changesdirectly to specific neurological conse-quences observed clinically. In theabsence of a cure for alcohol addic-tion, a detailed understanding of thebiochemical actions of alcohol onnerve cells may help in designingtherapies to ameliorate its devastatingneurological effects.IACKNOWLEDGMENTSThe authors thank Dr. Mark Lewisand Mr. Michael Ward for their help-ful comments.REFERENCESBABOR, T.F.; HESSELBROCK, V.; MEYER, R.;AND SCHOEMAKER, W., eds. 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Functionalimportance of ventricular enlargement andcortical atrophy in healthy subjects and alco-holics as assessed with PET, MR imaging, andneuropsychologic testing. Radiology 186(1):5965, 1993.JOIN US IN CHICAGO, NEW ORLEANS,BALTIMORE, AND INDIANAPOLISThe National Institute on Alcohol Abuse and Alcoholism (NIAAA) invites you to visit itsscientific exhibit at these upcoming conferences:VOL. 21, NO. 1, 1997 75Brain and Behavior ImpairmentsIAmerican Psychological AssociationAugust 1519, 1997Hyatt Regency HotelChicago, ILISociety for NeuroscienceOctober 2530, 1997Morial Convention CenterNew Orleans, LAIAmerican Society of Human GeneticsOctober 28November 1Baltimore Convention CenterBaltimore, MDIAmerican Public Health AssociationNovember 913, 1997Indiana Convention CenterIndianapolis, INThe Alcohol and Alcohol Problems Science Database (ETOH), recent NIAAA publications, and research grant information will be on display.