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The Effects of Alcoholism Comorbidity onNeurocognitive Function Following Traumatic BrainInjuryDaniel N. Allen a , Gerald Goldstein b , Janelle M. Caponigro b c & Bradley Donohue aa Department of Psychology , University of Nevada Las Vegas , Las Vegas, Nevadab Mental Illness Research, Educational, and Clinical Center, VA Pittsburgh HealthcareSystem , Pittsburgh, Pennsylvaniac Department of Psychology , University of California-Berkeley ,Published online: 21 Aug 2009.

To cite this article: Daniel N. Allen , Gerald Goldstein , Janelle M. Caponigro & Bradley Donohue (2009) The Effects ofAlcoholism Comorbidity on Neurocognitive Function Following Traumatic Brain Injury, Applied Neuropsychology, 16:3, 186-192,DOI: 10.1080/09084280903098687

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The Effects of Alcoholism Comorbidity on NeurocognitiveFunction Following Traumatic Brain Injury

Daniel N. Allen

Department of Psychology, University of Nevada Las Vegas, Las Vegas, Nevada

Gerald Goldstein and Janelle M. Caponigro

Mental Illness Research, Educational, and Clinical Center, VA Pittsburgh HealthcareSystem, Pittsburgh, Pennsylvania

Bradley Donohue

Department of Psychology, University of Nevada Las Vegas, Las Vegas, Nevada

Alcoholism and traumatic brain injury (TBI) often produce neuropsychological deficits.However, the extent and manner by which these factors interact is unclear. In this study,it was hypothesized that alcoholism would have compounding cognitive effects in indi-viduals with TBI and alcoholism. Participants were divided into three groups, includinga patient comparison (PC) group and groups with TBI with or without alcoholism his-tories. Participants were administered the Wechsler Adult Intelligence Scale-Revisedand major components of the Halstead-Reitan Neuropsychological Test Battery. Com-paring the groups on test performance, the TBI groups performed significantly worsethan the PC group but did not significantly differ from each other. Thus, the effectsof TBI on cognitive function overshadow preexisting deficits from the alcoholism.

Key words: alcoholism, Halstead-Reitan Neuropsychological Battery, traumatic brain injury

Alcohol intoxication and chronic alcohol use are bothrisk factors for traumatic brain injury (TBI), particu-larly in association with automobile accidents. It isestimated that 35% to 50% of TBI’s are alcohol related(Rivara, et al., 1992; Snowden, Miller, Waehrer, &Spicer, 2007) and that from 33% to 72% of those treatedin emergency rooms have positive blood alcohol levels(Corrigan, 1995; Rimel & Jane, 1983). It has beenfurther observed that those who are intoxicated at the

time they sustain TBI experience a greater degree ofbrain damage as evidenced by a number of negativeoutcomes including more severe neuropathology andpoorer performance on neuropsychological tests. Themechanisms underlying this increased impairment areunclear. Some have suggested that it simply representspre-injury impairment associated with alcoholism (e.g.,neurotoxic effects of alcohol, poor nutritional status,liver disease, comorbid psychiatric conditions, etc.), asup to one-third of individuals who are intoxicated atthe time of TBI also have a diagnosis of alcoholdependence (Brismar, Engstrom, & Rydberg, 1983;O’Shanick, Scott, & Peterson, 1984). Alternatively,physiological mechanisms associated with alcohol intox-ication, such as decreased respiration and decreasedblood clotting, may accentuate severity of brain damageresulting from TBI. In attempts to understand the basis

This research was supported by the Mental Illness Research,

Education, and Clinical Center, VA Pittsburgh Healthcare System

and the Medical Research Service, Department of Veterans Affairs.

Janelle M. Caponigro is now at the Department of Psychology,

University of California-Berkeley.Address correspondence to Daniel N. Allen, Department of

Psychology, University of Nevada Las Vegas, 4505 Maryland

Parkway, Las Vegas, NV 89154-5030. E-mail: daniel.allen@unlv.edu

APPLIED NEUROPSYCHOLOGY, 16: 186–192, 2009

Copyright # Taylor & Francis Group, LLC

ISSN: 0908-4282 print=1532-4826 online

DOI: 10.1080/09084280903098687

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for this association, some investigators have focused onthe study of pre-injury drug and alcohol use (e.g., Lange,Iverson, & Franzen, 2007; Ponsford, Draper, &Schonberger, 2007), whereas others have studied theeffects of day-of-injury intoxication (e.g., Bombardier &Thurber, 1998; Gordon et al., 2003; Lange et al., 2007;Tate, Freed, Bombardier, Harter, & Brinkman, 1999;Wilde et al., 2004). Studies examining neuropsychologicalfunctioning in those who were intoxicated at the timethey sustained TBI generally support the notion of anegative interaction between intoxication and TBI result-ing in poorer performance on neuropsychologicalmeasures, with the abilities that appear most affectedincluding executive functioning, processing speed,memory, and verbal and spatial abilities (Bombardier &Thurber; Tate et al.; Wilde et al.). However, there are anumber of factors that may influence this relationshipincluding severity of TBI. Lange et al. (2007) recentlysuggested that in cases of mild TBI, alcohol intoxicationon the day of injury may not have any deleterious effectson brain function above and beyond what might beexpected to result from the TBI itself, because in mostof these cases there is an absence of significant braindamage. Similarly, as the severity of brain injuryincreases, the impact of alcohol intoxication on neuraldamage may also be anticipated to increase. Age mayalso be a factor as it has been implicated as one factorthat increases the vulnerability to neuroanatomical andneurocognitive abnormalities in those who abuse alcohol(for review see Oscar-Berman & Marinkovic, 2007).Thus, if present, negative compounding effects ofalcoholism in TBI would be expected to occur in olderindividuals who sustain moderate-to-severe injuries. Con-sistent with these observations, most studies reportingan alcohol TBI interaction have reported on cases withmoderate-to-severe TBI (also see Barker et al., 1999;Lange et al., 2007 for negative findings).

In addition to severity of injury, there is also someevidence that the time since injury may be an importantfactor. For example, in two studies (Draper, Ponsford,& Schoneberger, 2007; Ponsford et al., 2008), functionaloutcome was described 10 years after TBI, examininginjury severity, demographic factors, psychiatric conse-quences, and neuropsychological abilities. Based on areview of outcome studies, Parry-Jones, Vaughan, andMiles Cox (2006) concluded that poorer neuropsycholo-gical outcomes in patients with TBI were associated withpre-TBI alcohol use in general. However, other investi-gations have demonstrated weak relationships betweensubstance misuse and TBI recovery. Along these lines,Vickery et al. (2008) reported that the relationshipbetween the extent of problem drinking and TBI recov-ery was ‘‘modest,’’ with injury severity having a moresignificant association. Lange et al. (2007) came to simi-lar conclusions in their study of the influence of alcohol

use on neuropsychological functioning in patients withmild TBI. However, it is important to emphasize thatalcohol abuse before TBI had a greater influence onshort-term neuropsychological outcome than did intox-ication at the time of injury. It would appear then thatthe existing literature provides an equivocal conclusionabout differential cognitive outcomes among TBIpatients with or without alcoholism. Along these lines,studies have yet to examine the long-term neuropsycho-logical outcomes of individuals who persist in pre-injuryalcohol abuse after an injury is sustained.

Thus, while there is vast neuropsychological litera-ture on the consequences of alcohol and TBI document-ing numerous patterns of individual cognitive deficits,the compounding influence of the two of them occurringtogether is not well understood. Therefore, in this study,we used data from the Wechsler Adult IntelligenceScale-Revised (WAIS-R; Wechsler, 1981) and theHalstead-Reitan Neuropsychological Battery (HRNB)to make comparisons among TBI patients with andwithout chronic alcoholism and a patient control group.Such a comparison could provide insights in determin-ing the extent to which alcohol misuse exacerbates TBIrecovery and assist in providing a foundation on whichto conduct prospective longitudinal studies. While inclu-sion of a group with alcoholism alone and no history ofTBI would be ideal methodologically, such a group wasnot included in the present study, largely for practicalreasons. In examining the test data from such indivi-duals in our database, it became apparent that theyrepresented a subpopulation of veterans with a numberof characteristics that were different from the TBIgroups. For instance, they were characteristically olderand more demented. Thus, they may have created themisleading impression that alcoholism alone producesa greater degree of deficit than does alcoholismcombined with TBI. Preliminary analyses both con-firmed that possibility and produced results essentiallyidentical to what was reported previously in publishedfindings reporting HRNB results in chronic alcoholism(Goldstein, 1976). In any event, the comparison madehere was aimed at determining the extent to which alco-holism exacerbates the neurocognitive effects of TBI,including examination of potential interactive influenceson neuropsychological function. This cross-sectionalthree-group design answers the key question of whetherone disorder overshadows the cognitive consequences ofanother. Thus, does head injury, particularly when it issevere, mask the cognitive consequences of chronicalcoholism?

Some evidence consistent with this suggestion isderived from the study of other disorders such as schizo-phrenia where alcoholism also has a high rate of comor-bidity. In such cases, rather than alcoholism causing anotable compounding of neurocognitive deficits already

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present in individuals with schizophrenia, the deficitsassociated with alcoholism are sufficiently subtle so asnot to produce marked differences between individualswith schizophrenia with or without alcoholism. Thesefindings have been interpreted to mean that becausethe neurocognitive deficits of schizophrenia are sosevere, there is little additional observable effectcaused by comorbid alcoholism (Allen, Goldstein, &Aldarando, 1999; Allen et al., 2000; Goldstein, Allen,& Sanders, 2002). If the relationship between alcoholismfollows similar suit, this might suggest outcomes wouldnot be differentially influenced by cognitive function.Indeed, individuals with TBI with and without alcohol-ism would be functioning with essentially the samecognitive capacities. Other behaviors associated withalcoholism could make a difference, but cognitive func-tion would not be a major consideration.

The HRNB and the Wechsler scales are highly appro-priate procedures for this kind of comparison because oftheir extensive use in both alcoholism and head injuryresearch, as well as their widespread clinical application.Possible results would be that there may be a potentiat-ing effect of alcoholism, such that the degree of impair-ment in the comorbid group is substantially greaterthan the other groups, or alternatively that neurocogni-tive function is no more impaired in the comorbid groupthan it is in the group with TBI alone. If this latterhypothesis is confirmed, that would indicate that theeffects of TBI overshadow those of the preexisting alco-holism and leave little or no room for observing thepreexisting effects of alcoholism.

METHOD

Participants

Participants were 103 male veterans who were receivingtreatment at a Veterans Administration hospital. Parti-cipants were referred for neuropsychological testing,suggesting that clinicians were concerned about theircognitive functioning. The study was a three-group com-parison among samples of individuals with (1) historiesof documented TBIs but no evidence of alcoholism (TBIGroup; n¼ 27), (2) histories of TBI in addition toalcoholism (TBIþALC Group; n¼ 27), and (3) a patientcontrol group consisting of patients with no history ofTBI, alcoholism, or several rule-out medical andpsychiatric disorders (PC Group; n¼ 49). Demographicdata for each group is presented in Table 1. With regardto handedness, 84.6% of the TBIþALC group, 84.5% ofthe TBI group, and 87% of the PC group were right-handed. Participants were hospitalized in a neurologicalor neuropsychiatric facility at the time they receivedtheir neuropsychological assessments. The test data for

the present study were not obtained at the hospitaliza-tion for the immediate, acute consequences of thetrauma but for follow-up evaluation and treatmentof residual symptoms of their TBI, such as seizures.The mean length of time since injury was 78.1 months(SD¼ 97.7). Only 17 (20.5%) of the patients had sus-tained their injuries less than one year prior to testing.Individuals with the diagnoses of schizophrenia, aneurological illness other than TBI, or insufficient docu-mentation were not included in the study.

In all cases, the presence of brain damage andalcoholism were unequivocally documented throughcomprehensive neurological evaluation with neuroima-ging and laboratory procedures available at the time.There were often actual descriptions of the injury itselfor neurosurgical data. The head injuries were thereforewell documented and described. Presence of alcoholismwas documented by interview and review of clinicalrecords that had to describe a history of sustainedexcessive use of alcohol and sufficient evidence to indi-cate that the individual met Diagnostic and StatisticalManual of Mental Disorders II or III criteria (AmericanPsychiatric Association, 1952; 1980; 1987) dependingupon time of assessment). The distinction between alco-hol abuse and dependence was not commonly made dur-ing the data collection period. However, the currentsample might best be characterized as having alcoholdependence diagnosis, in that alcoholism was chronicwith a mean length of drinking of 21.75 years(SD¼ 10.77) and ranged from three to 38 years. Seventypercent of these participants had an alcoholic history of10 or more years, the time point that has been suggestedto frequently mark the onset of alcoholism-relateddementia (Beatty, Tivis, Stott, Nixon, & Parsons,2000). Those included in the PC group had no neurolo-gical disorder or history of alcoholism. This group wascomposed of hospital patients, typically being treatedfor other conditions such as orthopedic injury. Theyhad all been referred for neurological and neuropsycho-logical evaluation for suspected brain dysfunction, butall neurodiagnostic and related procedures resulted innegative findings.

The wide age range indicates that the sample includedolder veterans from the times of the second World andKorean Wars and younger individuals in the militaryat the time of the Vietnam conflict. The IQ data suggestthat while the mean scores were in the average range, theextreme range of scores at the low end may reflect thepresence of impairment acquired as a result of TBI.Individuals with IQs within much of this low range areineligible for enlistment in military service, suggestingthat scores within this range reflect acquired cognitiveimpairment rather than preexisting low intellectualfunction. Since the study was retrospective and datawere drawn from an established database, it was not

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possible to achieve demographic matching of partici-pants in advance. Therefore, covariance procedureswere used to adjust for differences in age and education.

All patients provided informed consent to allow theirresults and clinical records to be used for researchpurposes in accordance with established hospitalpolicies and consistent with Institutional Review Boardregulations in place at the time of the assessments.

Procedures

Cases were drawn from a database of Department ofVeterans Administration (DVA) patients containingHRNB test data and copies of pertinent clinical records.Patients in the database first initiated treatment at theTopeka VA Hospital in the mid-1960s for neuropsycho-logical testing, sustaining TBI between 1942 and 1982.Extensive efforts were made, particularly for moreimpaired patients, to communicate to them that testingwas voluntary and that they could discontinue if theywished, that their doctors who referred them wouldreceive a report of the results of the testing, and that

their medical records with identifying material removedwould be used for research purposes. While at the VAfacility, patients received thorough general medicaland neurological evaluations in connection with theneuropsychological assessment. All participants wereadministered the HRNB, including the Category Test,Trail Making Test, Finger Tapping Test, TactualPerformance Test (TPT), Speech Sounds PerceptionTest, and Seashore Rhythm Test. The WAIS was alsoadministered. All tests were administered according tostandard procedures by technicians who were exten-sively trained.

Effort was also evaluated using the subtests I andII of the Category Test and the amount of change inerror score between subtests V and VI. Forrest, Allen,and Goldstein (2004) reported that the best indiceswere more than five errors on subtests I and II, bothof which are simple number identification and countingtasks, and lack of improvement on subtest VI relativeto subtest V, both of which require learning of exactlythe same principle. It was noted in their study thatwhile patients with structural brain damage showed

TABLE 1

Demographic and Test Data for the TBIþALC, TBI, and PC Groups

TBIþALC TBI PC

Variable M SD M SD M SD F p

Demographics

Age 45.7 10.7 45.8 10.7 33.0 10.5 18.57 0.000

Education (Yrs.) 10.7 2.6 11.1 2.3 12.8 2.4 8.06 0.001

WAIS-R

Information 8.7 2.6 9.3 2.5 12.0 2.5 18.78 0.000

Comprehension 9.3 2.9 9.2 2.6 12.2 3.1 12.91 0.000

Arithmetic 9.2 2.9 8.5 3.0 10.6 2.5 5.96 0.004

Similarities 9.0 3.4 8.4 3.2 11.9 2.2 16.41 0.000

Digit Span 7.3 2.4 8.2 3.6 11.3 3.0 18.73 0.000

Vocabulary 8.8 2.5 8.9 2.8 11.5 2.5 13.54 0.000

Digit Symbol 5.2 2.7 5.0 2.7 9.5 2.1 40.75 0.000

Picture Completion 8.5 3.0 8.3 2.6 10.6 1.8 11.64 0.000

Block Design 7.3 3.4 7.0 3.1 10.2 2.3 15.09 0.000

Picture Arrangement 7.6 2.7 6.2 2.7 9.6 1.9 18.63 0.000

Object Assembly 7.2 3.0 6.9 3.0 10.0 2.9 13.06 0.000

Verbal IQ 93.9 14.0 93.9 13.4 109.5 11.6 19.16 0.000

Performance IQ 90.2 15.7 87.2 14.5 103.1 10.0 16.25 0.000

Full Scale IQ 91.9 14.5 90.3 12.9 107.1 9.9 22.57 0.000

HRNB Tests

Category-Errors 83.9 29.4 95.1 23.6 45.0 21.5 44.54 0.000

TPT-Time 24.0 5.9 24.7 6.2 13.5 4.2 53.84 0.000

TPT-Memory-Blocks 5.5 2.5 5.7 1.8 7.8 1.3 19.22 0.000

TPT-Location-Blocks 1.4 1.9 1.4 1.6 4.1 2.1 24.73 0.000

Speech Sounds-Errors 17.1 9.9 17.0 8.5 6.9 3.1 27.05 0.000

Rhythm-Errors 7.8 4.0 9.4 4.8 3.7 3.1 21.98 0.000

Trails A-Seconds 60.6 32.8 75.6 65.2 29.8 9.7 14.31 0.000

Trails B-Seconds 165.6 91.3 168.7 84.5 65.4 17.8 31.81 0.000

Tapping-Right-Taps 36.7 11.9 42.0 11.2 50.1 5.7 19.88 0.000

Tapping- Left-Taps 34.2 13.4 36.4 11.4 45.8 5.4 15.20 0.000

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such improvement, coached malingerers showed lessimprovement than patients with structural braindamage. It was also found that coached malingerersproduced an excessive number of errors on subtests Iand II. For this evaluation we used unpublished datafrom a larger sample of patients with TBI (n¼ 87),containing the participants in the sample used in thepresent study.

Data Analysis

Analysis of variance (ANOVA) was used to compare theTBI, TBIþALC, and PC groups on demographic vari-ables and showed that the TBI and TBIþALC groupswere significantly older, had fewer years of education,and lower Wechsler Full Scale IQ scores than the PCgroup (see Table 1).

For the main analyses, two multivariate analysesof covariance were used (MANOVA) to compare thethree groups on the WAIS-R subtest scores and on themajor tests of the HRNB. Because of significant groupdifference on age and education, MANCOVAs werealso accomplished with education used as a covariatefor the WAIS-R analyses (subtest scores were alreadycorrected for age) and both age and education for theHRNB tests. Significant differences identified by themultivariate tests were followed up with one way ANO-VAs (or ANCOVAs) to examine for differences amongthe groups on the individual WAIS-R and HRNB testscores.

RESULTS

WAIS Subtests

The results of the analyses for the WAIS-R subtests arepresented in Table 1. The MANOVA was significant(F¼ 3.82, df¼ 22, 178, p< .001). When education wasincluded as a covariate in a MANCOVA, the test resultremained significant (F¼ 3.17, df¼ 22, 176, p< .001). Inboth of these analyses, examination of the individualsubtests scores using ANOVA indicated that there weresignificant differences among the groups for all of thesubtests. These differences were accounted for by thePC group obtaining better scores than the TBI andTBIþALC group, which did not differ from each other.Figure 1 presents the WAIS-R subtest profiles for thegroups.

HRNB Tests

The results of the analyses for the HRNB tests are alsopresented in Table 1. The overall MANOVA was signif-icant (F¼ 5.93, df¼ 20, 174, p< .001). When age and

education were included as covariates in a MANCOVA,the test result remained significant (F¼ 4.39, df¼ 20,170, p< .001). Whether or nor age and education wereincluded as covariates, examination of the individualtest scores indicated that there were significant differ-ences among the groups for all of the tests. Again, thesedifferences were accounted for by the PC group obtain-ing better scores than that TBI and TBIþALC group,who did not differ from each other. Figure 2 presentsthe HRNB subtest differences among the groups asz-scores which were calculated using the mean and

FIGURE 1 Wechsler intelligence scale profiles for the TBIþALC,

TBI, and PC Groups.

FIGURE 2 HRNB profiles for the TBIþALC and ALC groups.

Note: Because of the way in which the Z-Scores were computed, all

of the mean scores for the PC group are by definition zero.

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standard deviation (SD) from the PC group. Higherscores indicate poorer performance. Similar to theWAIS-R results, both of the TBI groups performed sig-nificantly worse than the PC group. The greatestdifference from controls was noted on the Trail MakingTest Parts A and B, Speech Perception, and the TPT.Few differences were present between the TBI andTBIþALC groups, although there was some separationon the Category Test and Finger Tapping with thedominant hand. When demographically adjustedZ-scores were used, all HRNB mean scores still fell atleast one SD above the baseline of zero produced bythe PC group. Comparing the demographically cor-rected with the uncorrected scores, the overall profilepatterns were essentially identical. In general, larger dif-ferences were present between the PC and TBI groupsfor the HRNB tests than for the WAIS-R tests, appar-ently reflecting the relatively greater sensitivity of theHRNB to brain injury (Reitan & Wolfson, 1993).

Effort

With regard to effort, the mean score for CategoryTest subtest I was .14 (SD¼ .47) and .54 (SD¼ .83)for subtest II. There was also a mean improvement onsubtest V relative to VI of 5.35 (SD¼ 5.40). Errors onsubtests I and II were substantially lower than thoseobtained by the coached malingering group in Forrestet al. (2004), and improvement from subtest V to VI isalso greater. In examining individual cases, there wasonly one patient who made an excessive number oferrors on subtest II (12). This patient made 149 errorson the total test, had brain surgery for a subdural hema-toma, and multiple well-documented other illnesses. Notall participants improved on subtest VI relative to V, butonly six participants made more than one more error onsubtest VI relative to V while 80% of the participantsshowed some improvement. Thus, overall findings andintercluster differences are not readily attributable toeffort-related considerations.

DISCUSSION

This comparison of individuals with TBI, TBI andalcoholism, and a PC group did not confirm the hypoth-esis that alcoholism would compound the neurocogni-tive effects of TBI. Rather, there was little differencebetween neurocognitive profiles of the TBI and TBIþALC groups, even after adjustment for demographicdifferences, with both groups doing significantly morepoorly than a PC group. The differences obtainedbetween the TBI and TBIþALC groups were small,and the direction of these differences did not reliablyfavor one or the other group.

These results are consistent with those obtained fromcomparing neurocognitive performances of patients withschizophrenia with and without alcoholism comorbidity.The deficits associated with the schizophrenia appearedto be sufficiently severe to overshadow those that mightbe related to the alcoholism. Differences when foundwere again subtle and primarily involved deficits specifi-cally associated with alcoholism, including sensory,visual-spatial deficits and peripheral nerve disordersnot typically associated with schizophrenia (Goldsteinet al., 2002). However, a compounding of cognitiveimpairments generally associated with both schizophre-nia and alcoholism was not apparent. The same maskingprocess appears to occur in regard to TBI.

There is a possibility that the absence of a compound-ing effect was because the participants with alcoholismhad mild forms of the disorder not sufficient to producesubstantial cognitive impairment in itself. That did notappear to be the case for several reasons. Several studiesinvolving the same population of hospitalized veteranswith alcoholism revealed substantial neuropsychologicaldeficits, reviewed some time ago by Goldstein (1976).These patients typically had long histories of chronicalcoholism, and many of the participants in this studywere hospitalized at some time for inpatient alcoholismrehabilitation.

Implications of the current findings provide someexplanation for those studies (Vickery et al., 2008;Lange, et al., 2007) that did not find major outcome dif-ferences in TBI patients between those with and withoutalcoholism histories. That is, the TBI overwhelmed theindependent consequences of the alcoholism history,putting both groups on an equal footing from the stand-point of cognitive function. Once having sustained aTBI, differences in outcome between subgroups thatdo and do not experience a history of alcoholism mayoccur. This might be understood in the context thatpost-injury members of these subgroups may haveroughly equal cognitive status, but the ensuing historicaldifferences may be the major determinant of outcome.

The current work was not designed to allow forestablishment of the temporal relationship between theTBI and alcoholism in the TBIþALC group. Thus, itwas unclear whether for some patients alcoholism wasof recent onset, if it predated their TBI, or if they wereintoxicated at the time of the accident. However, whilethis lack of information provides a limitation of thisstudy, the results appear to have implications for inter-pretation of such research. From a clinical standpoint,it might be useful to understand that patients withTBI do not have remarkably different cognitive statusesdepending upon whether they have a prior history ofalcoholism. While members of both groups may havesignificant cognitive impairment, its severity will prob-ably not differ remarkably. The retrospective nature of

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this study did not permit definitive determinations of theseverity of the alcoholism or the head injuries althoughhead injuries in this population are typically moderate tosevere, and it is clear that future research involving thesecommonly occurring comorbid conditions needs to con-sider these matters in more detail.

Lange, Iverson, and Franzen (in press) pointed outthis matter also has forensic implications. In litigation,the neuropsychologist is often asked to testify whetheran observed cognitive deficit is a consequence of a pre-vious TBI. The data from Lange et al. (in press) andthe present study would strongly suggest that it is notpossible to reliably make this determination in indivi-duals with comorbid alcoholism if that determinationis made on the basis of a post-trauma evaluation with-out information concerning premorbid status.

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