Superior Intellectual Ability in Schizophrenia:Neuropsychological Characteristics

James H. MacCabeKing’s College London

Gildas BrebionSant Joan de Deu – Serveis de Salut Mental y CIBERSAM,

Barcelona, Spain

Abraham Reichenberg and Taposhri GangulyKing’s College London

Peter J. McKennaGermanes Hospitalaries del Sagrat Cor de Jesus, Barcelona,

Spain

Robin M. Murray and Anthony S. DavidKing’s College London

Objective: It has been suggested that neurocognitive impairment is a core deficit in schizophrenia. However,it appears that some patients with schizophrenia have intelligence quotients (IQs) in the superior range. In thisstudy, we sought out schizophrenia patients with an estimated premorbid Intelligence Quotient (IQ) of at least115 and studied their neuropsychological profile. Method: Thirty-four patients meeting diagnostic criteria forschizophrenia or schizoaffective disorder, as defined by the Diagnostic and Statistical Manual of MentalDisorders (4th ed.; DSM–IV), with mean estimated premorbid IQ of 120, were recruited and divided into twosubgroups, according to whether or not their IQ had declined by at least 10 points from their premorbidestimate. Their performance on an extensive neuropsychological battery was compared with that of 19IQ-matched healthy controls and a group of 16 “typical” schizophrenia patients with estimated premorbid IQ�110, using one way ANOVAs and profile analysis using MANOVAs. Results: Schizophrenia patientswhose estimated premorbid and current IQ both lay in the superior range were statistically indistinguishablefrom IQ-matched healthy controls on all neurocognitive tests. However, their profile of relative performancein subtests was similar to that of typical schizophrenia patients. Patients with superior premorbid IQ andevidence of intellectual deterioration had intermediate scores. Conclusions: Our results confirm the existenceof patients meeting DSM–IV diagnostic criteria for schizophrenia who have markedly superior premorbidintellectual level and appear to be free of gross neuropsychological deficits. We discuss the implications ofthese findings for the primacy of cognitive deficits in schizophrenia.

Keywords: schizophrenia, psychosis, neuropsychology, intelligence, neuropsychologically normal

Schizophrenia is associated with global cognitive impairmentover a wide variety of domains, which is present in bothfirst-episode and chronic patients, and is often as severe as thatseen in some neurological disorders (Heinrichs & Zakzanis,1998). Some deficits are detectable prior to the onset of clinicalsymptoms (David, Malmberg, Brandt, Allebeck, & Lewis,1997; Reichenberg et al., 2002; MacCabe, 2008; MacCabe etal., 2008). This has led many researchers to conclude that

cognitive deficits are a universal feature of schizophrenia(Weinberger & Gallhofer, 1997) and/or that they are a conse-quence of abnormal neurodevelopment (Marenco & Wein-berger, 2000; MacCabe & Murray, 2004).

In apparent contradiction to this view, some patients withschizophrenia have been documented to have an overall IQ in thenormal range, and a few have above-average performance, at leastin some neuropsychological domains (Palmer et al., 1997; David,

This article was published Online First December 26, 2011.James H. MacCabe, Department of Psychosis Studies, Institute of

Psychiatry, King’s College London, London, United Kingdom; GildasBrebion, Unit of Research and Development, Sant Joan de Deu -Serveis de Salut Mental y CIBERSAM, Barcelona, Spain; AbrahamReichenberg and Taposhri Ganguly, Department of Psychosis Studies,Institute of Psychiatry, King’s College London; Peter J. McKenna,Benito Menni CASM y CIBERSAM, Germanes Hospitalaries del Sa-grat Cor de Jesus, Barcelona, Spain; Robin M. Murray and Anthony S.David, Department of Psychosis Studies, Institute of Psychiatry, King’s CollegeLondon.

J. H. M. has received support for this project from the Stanley Founda-tion, the Psychiatry Research Trust, the United Kingdom Medical ResearchCouncil, and the NIHR Biomedical Research Centre for Mental Health atthe South London and Maudsley NHS Foundation Trust and Institute ofPsychiatry, Kings College London. P. J. M. was supported by the Institutode Salud Carlos III, Centro deInvestigacion en Red de Salud Mental,CIBERSAM. G. B. was supported by CIBERSAM and Lundbeck.

Correspondence concerning this article should be addressed to James H.MacCabe, Department of Psychosis Studies, Institute of Psychiatry, King’sCollege London, De Crespigny Park, London, SE5 8AF, United Kingdom.E-mail: james.maccabe@kcl.ac.uk

Neuropsychology © 2011 American Psychological Association2012, Vol. 26, No. 2, 181–190 0894-4105/12/$12.00 DOI: 10.1037/a0026376

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1999; MacCabe, Aldouri, Fahy, Sham, & Murray, 2002; Wilk etal., 2005; Heinrichs et al., 2008).

By studying patients of normal or superior intelligence, we canattempt to address three important theoretical questions that arerelevant to schizophrenia as a whole. First, using fine-grainedneuropsychological tests, we can evaluate whether these patientsare truly neuropsychologically intact or whether they actually havesubtle cognitive deficits. If it were truly possible to have schizo-phrenia with no cognitive impairment, then this would have im-portant implications for current etiological and neuropsychologicalmodels of schizophrenia, since cognitive deficits could not beregarded as a necessary condition for the illness. If, on the otherhand, subtle cognitive deficits are detectable even in patients withhigh or normal intelligence, then it is likely that cognitive impair-ment is genuinely a core feature of the disorder.

This question has long been debated in the literature. Palmer andcolleagues published an article in 1997 entitled “Is it Possible toBe Schizophrenic Yet Neuropsychologically Normal?” (Palmer etal., 1997) and concluded, on the basis of cognitive testing on 36neuropsychologically normal patients, that it was. However,around a quarter of these neuropsychologically “normal” patientsscored in the impaired range for learning compared with only 10%of controls. This study did not estimate premorbid intelligencequotient (IQ), so it was not possible to investigate whether thepatients with normal cognition had declined from a premorbidlevel in the superior range.

Kremen and colleagues (Kremen, Seidman, Faraone, Toomey,& Tsuang, 2000) performed a similar study but included estimatesof premorbid IQ. They found that neuropsychologically normalpatients had higher estimated premorbid ability but worse currentneuropsychological ability than controls, suggesting that their IQhad declined. In another study, Kremen, Seidman, Faraone, andTsuang (2001) studied the profiles of neuropsychological scores inschizophrenia patients with low-average (80–94) compared toaverage (95–119) current IQ, with each group matched to its owncontrol group. The two patient groups had similar profiles at bothIQ levels, which differed significantly from those of controls.Patients scored higher on verbal than performance subtests andshowed particular impairments in abstraction-executive function.

In 2005, Wilk and colleagues responded to Palmer et al.’s(1997) article with one entitled “No, It Is Not Possible to beSchizophrenic Yet Neuropsychologically Normal” (Wilk et al.,2005). In this study, the authors compared a group of patients withmean IQ of 99 with individually matched controls. The patientsscored above controls on verbal tasks but were impaired on mem-ory and visual processing.

Most recently, Heinrichs and colleagues (Heinrichs et al., 2008)examined cognitively superior, as opposed to merely normal,patients with schizophrenia—that is, those who scored above the90th percentile on the vocabulary subtest of the Wechsler AdultIntelligence Scale (WAIS). These patients did not differ on anyneuropsychological measure from controls with similarly highverbal scores.

Other studies have found that apparently neuropsychologicallynormal patients show deficits in psychomotor speed (Holthausen etal., 2002) and executive function (Allen, Goldstein, & Warnick,2003). Overall, the question of whether neuropsychologically nor-mal schizophrenia exists remains controversial.

The second theoretical problem that can be addressed by usingcognitively intact schizophrenia patients is that of confounding byglobal impairment. In most studies of neurocognitive function inschizophrenia, it is difficult to determine to what extent particularcognitive deficits are specific to schizophrenia, because effects onindividual tests are swamped by the general intellectual impair-ment that is also a feature of the disorder—this would tend todepress performance on all specific neuropsychological tests in-discriminately. The most common approach to dealing with thisproblem is to select groups matched on current IQ. However, asnoted by Chapman and Chapman (1973), matching on current IQis not valid if the patient group has undergone an IQ decline—theirIQ will have changed in contrast to that of the control subjects.Another approach is to adjust for IQ in the analysis, but this islikely to lead to an underestimation of any specific neuropsycho-logical deficits, since all neurocognitive tests are correlated withIQ. By studying patients with no global deficits relative to con-trols, we should be able to determine which aspects of neurocog-nitive functioning are specifically impaired in schizophrenia with-out the need to adjust for IQ.

The third issue that we address in this study is that of decline.Several researchers have postulated that schizophrenia patientswith normal intellectual performance may actually have declinedfrom superior premorbid levels (Kremen et al., 2000; Wilk et al.,2005). We therefore sought to identify and study patients who didnot appear to show such decline.

Therefore, this study examined, in detail, the cognitive profilesof schizophrenia patients with a high premorbid IQ, and comparedthem with patients of more typical IQs and with healthy controlsubjects. Unlike previous studies, which selected patients whoscored within the normal range on neuropsychological tests or hada mean IQ close to the population average, we actively sought outand recruited patients with intelligence in the superior range, withestimated premorbid IQ of at least 115.

Method

Subject Recruitment and Classification

Schizophrenia patients with superior intellectual ability are rare.By definition, only a small proportion of the population has supe-rior ability, and in schizophrenia, that proportion is even smaller(MacCabe et al., 2008). It is therefore necessary to screen substan-tial numbers of patients to yield an adequate sample of cases withhigh IQ (Heinrichs et al., 2008).

We were fortunate to have access to a large pool of patients withschizophrenia involved in research and clinical programs at theInstitute of Psychiatry, King’s College London, and the Universityof Cambridge, and their associated clinical services (the SouthLondon and Maudsley National Health Service [NHS] FoundationTrust and the Cambridgeshire and Peterborough NHS FoundationTrust). With the help of our academic and clinical colleagues, wesought outpatients who we considered likely—on the basis ofprevious cognitive testing, academic qualifications, or occupa-tional achievement (e.g., academic scholarships, first class honors,doctorates, or professional qualifications), to have a premorbid IQof 115 or above. Overall, we contacted 59 patients who webelieved to be potential high-IQ cases. Of these, 19 declined toparticipate or did not meet the inclusion criteria, 6 consented but

182 MACCABE ET AL.

were not able to complete testing, and the remaining 34 wereincluded in this study.

We recruited patients who met the following inclusion criteria:(i) a diagnosis of schizophrenia or schizoaffective disorder underthe American Psychiatric Association’s (2000) Diagnostic andStatistical Manual of Mental Disorders (4th ed.; DSM–IV), (ii) noneurological or sensory abnormalities that might interfere withcognitive testing, (iii) age 18–65 years, (iv) no concurrent sub-stance misuse as defined by DSM–IV, (v) English as first language,and (vi) capacity to give informed consent.

We also recruited a patient comparison group of “typical IQ”patients with schizophrenia. These patients were recruited from thesame research and clinical services as the high-IQ cases, using thesame methods and criteria, but here we employed a National AdultReading Test (NART) IQ cutoff of �110. Lastly, we recruitedhealthy controls with above average IQ to allow direct comparisonwith the high-IQ cases. These were recruited from hospital anduniversity staff.

We estimated premorbid IQ using the restandardized version ofNART (Nelson & Willison, 1991), which assesses the ability topronounce irregular words (e.g., “cellist,” “aisle”) whose correctpronunciation cannot be inferred phonetically. Being able to pro-nounce a word correctly implies that an individual knows (or onceknew) the meaning of the word, and this ability tends to bepreserved even when knowledge of the word has been lost due todisease. The NART shows a good correlation with current IQ inhealthy subjects (Bright, Jaldow, & Kopelman, 2002) and is fre-quently used to estimate premorbid IQ in schizophrenia and otherdisorders (Crawford et al., 1992; O’Carroll et al., 1992). In oursample, Pearson’s r was 0.704 in patients and 0.714 in controls,both ps � .001.

Our cutoff for high estimated premorbid IQ was a NART-estimated IQ of at least 1 standard deviation above the populationmean, equivalent to the 84th percentile. Since IQ has a standarddeviation of 15 and a mean of 100 by definition, this equates to aNART-estimated IQ of �115.

Previous research has indicated that even neuropsychologicallynormal schizophrenia patients show a discrepancy between pre-morbid estimates of IQ and current IQ (Kremen et al., 2000).Using the difference between NART and WAIS-III IQ as anestimate of decline, we found that about half of our high-IQpatients did show such a decline, but the other half did not. Wetherefore split patients with high premorbid IQ into two subgroupsaccording to whether or not they showed a decline between theirestimated premorbid IQ (NART) and their current IQ (WAIS-III)of 10 points or more.

Clinical Assessment

For DSM–IV diagnosis, all patients underwent a detailed clinicalinterview with a consultant psychiatrist (JHM) using the psychosis,affective disorders, and substance misuse sections of the Diagnos-tic Interview for Genetic Studies (Nurnberger et al., 1994). Weabstracted additional material from patients’ case notes and byinterviewing informants wherever possible.

Neuropsychological Assessment

The neuropsychological assessments are summarized in Table 1.All subjects underwent current IQ testing using the Vocabulary,

Similarities, Forward and Backward Digit Span, Letter-NumberSequencing, Arithmetic, Picture Completion, Picture Arrange-ment, and Matrix subtests of the WAIS-III (Wechsler, 1997a).

We also assessed all subjects using selected tests fromthe Cambridge Neuropsychological Test Automated Battery(CANTAB; Robbins et al., 1994). The Stockings of CambridgeTask assesses spatial planning ability and motor control, and isanalogous to the Tower of London Test. The Intradimensional/Extradimensionsal (I/E) Shift Task is a test of rule acquisition andreversal, featuring visual discrimination and attentional set forma-tion, maintenance, and shifting. We recorded two measures: num-ber of stages reached and number of errors.

The Spatial Working Memory Task is a measure of executivefunction, and assesses the subject’s ability to retain spatial infor-mation and to manipulate remembered items in working memory.The test entails searching for tokens hidden inside boxes. In eachtrial, the previously found tokens remain and a new one isadded. Two types of error are possible: returning to a box alreadyshown to be empty within the same trial (within-trial error) orrevisiting a box where a token had been found in a previous trial(between-trial error). The latter is considered the more stringentmeasure (Foong et al., 2000).

We assessed visual spatial working memory using the SpatialSpan Task from the CANTAB. This is a computerized version ofthe Corsi blocks, in which subjects are required to touch blocks inthe same sequence as they were highlighted by the computer. It isdesigned to test executive function.

We used the CANTAB reaction time (RT) test, which measuresspeed of response to a visual target where the stimulus is eitherpredictable (simple) or unpredictable (5-choice).

Table 1Cognitive Tests

Domain Instrument

Estimated Premorbid IQ NARTCurrent IQ (WAIS-III

subtests)Verbal subtestsVocabularySimilaritiesForward and backward digit spanLetter-number sequencingArithmeticPerformance subtestsPicture completionPicture arrangementMatrix reasoning

Executive function ID/ED Shift (CANTAB)Stockings of Cambridge (CANTAB)Spatial working memory (CANTAB)

Verbal memory Rey Auditory Verbal Learning TaskVerbal paired-associates (WMS-III)

Verbal fluency Continuous Oral Word Association TaskLetter (S)Category (Animals)

Working memory Digit Span (Forward and Backward;WAIS-III)

Letter-number sequencing (WAIS-III)Spatial Span (CANTAB)

Reaction time Reaction time (CANTAB)

Note. CANTAB � Cambridge Neuropsychological Test Automated Bat-tery; NART � National Adult Reading Test; WAIS-III � Wechsler AdultIntelligence Scale, 3rd ed.; WMS-III � Wechsler Memory Scale, 3rd ed.

183SUPERIOR INTELLECTUAL ABILITY IN SCHIZOPHRENIA

We assessed verbal episodic memory using the Verbal PairedAssociates task from the Wechsler Memory Scale (WMS-III;Wechsler, 1997b) and the Rey Auditory-Verbal Learning Task(RAVLT) (Rey, 1958). We used the Continuous Oral Word Associ-ation Task (COWAT) to assess verbal fluency by letter (“S”) andcategory (animals, i.e., “name as many animals as you can in oneminute”).

The study was approved by the ethics committee of the Instituteof Psychiatry, and all subjects gave written informed consent.

Statistical Analysis

We analyzed all data using STATA-IC version 10.1 for Macintosh.Using the controls as the reference group, we calculated z scores

for each test, changing the sign where necessary—for example, intimed measures—such that better performance was always indi-cated by numerically higher scores. We then grouped the tests intofour domains, namely, working memory, verbal fluency, verbalmemory, and executive function, as indicated in Table 1. Wecalculated summary z scores for each domain of cognitive func-tion, such as executive functioning, by taking the mean of z scoresin each of the constituent tests.

Conventional analysis. For each test, we conducted one-wayANOVAs. Where the overall ANOVA was significant at the p �.05 level, we conducted all possible pairwise post hoc comparisonsusing the Bonferroni method.

Profile analysis. Profile analysis is a technique that allowsprofiles of scores to be compared between groups. In particular, wewere interested in whether profiles of scores differed in their meanlevels and whether they differed in shape (parallelism). For eachprofile analysis, we performed overall MANOVA tests for differences

in the level of the profiles and for nonparallelism between groups.Where there was evidence that the profiles differed in overall level orwere not parallel, we then performed post hoc comparisons on allpossible pairs of groups. We began by conducting profile analyses onthe summary scores shown in Figure 1, followed by test scores withineach domain of cognitive function (see Figure 2).

Results

Demographic and Clinical Characteristics

Of the 50 patients, 10 met criteria for the high IQ-intact (HI) group,24 for the high IQ-decline (HD) group, and 16 for the typical IQgroup. The demographic and clinical characteristics of the sample arereported in Table 2. The total schizophrenia group was closelymatched with the controls for age and sex distribution, but the HDgroup included more patients over 45 than the other groups. Althoughthis difference was not significant, we were concerned that these olderpatients may have had disproportionately low educational level or IQ.To test this, we excluded the eight patients over 45 years of age. Meanyears of education, NART, verbal, performance, and full-scale IQ andNART-WAIS decline were almost identical in this restricted group, asin the full group.

The groups differed in educational level, as may be expected,given their different IQ profiles. The HI group had the highestproportion of females (40%), while the typical group had thelowest proportion (18.8%). Years of education followed a trend inthe order Controls � HI � HD � typical group. There were nosignificant differences between groups on dose of antipsychotics.In the schizophrenia patients, there was no correlation between

Figure 1. Z scores for summaries of neurocognitive domains.

184 MACCABE ET AL.

antipsychotic dose and current full-scale WAIS IQ (Pearson’s r �.0093, p � .955). The three schizophrenia groups did not signifi-cantly differ from one another in positive symptoms but differedmarkedly in negative symptoms—the HI group having the leastnegative symptoms and the typical patients having the most.

IQ

Premorbid and current IQ is presented in Table 3. The first pointto note is that the control subjects scored well above populationnorms in NART and WAIS IQ. Despite this, the HI schizophreniagroup outperformed them on all IQ subtests except the perfor-

mance subtests of the WAIS. The HD group, by definition, hadhigh scores on the NART and evidence of decline, although theystill performed within the normal range throughout. Typical IQpatients scored significantly below all other groups on almost alltests, and they also showed large NART-WAIS declines. Allpatient groups, including the HI group, scored better on verbal thanperformance subtests of the WAIS.

Summary Scores

The profiles for summary scores are shown in Figure 1. Theprofiles differed overall on level, F(3, 64) � 4.47, p � .0065, and

Figure 2. Profile of z scores in the four groups.

Table 2Demographic and Clinical Characteristics

C HI HD T p

N 19 10 24 16Age (mean[SD]) 36.8 (10.9) 36.5 (8.0) 42.5 (11.2) 34.5 (10.3) 0.10Gender

Male (%) 14 (73.7) 6 (60.0) 17 (70.8) 13 (81.2) 0.695Female (%) 5 (26.3) 4 (40.0) 7 (29.2) 3 (18.8)

Education (years) 16.5 (2.8) 15.5 (2.1) 12.8 (2.2) 11.1 (3.4) �0.001HC � HD; HC � T; HI � T

DiagnosisSchizophrenia — 8 (80) 21 (88) 14 (88) 0.812Schizoaffective disorder — 2 (20) 3 (12) 2 (12)

Age at onset (years; mean [SD]) — 23.2 (7.6) 20.4 (4.8) 22.6 (3.9) 0.204Antipsychotic dose (% BNF maximum) — 39.3 (40.7) 60.3 (40.7) 57.5 (30.5) 0.361SAPS — 18.9 (25.3) 20.9 (21.1) 26.6 (14.0) 0.610SANS — 21.0 (16.8) 37.2 (20.4) 58.7 (28.6) 0.001

Note. Reported p values are for chi-square or ANOVA tests. Post hoc ANOVA multiple comparisons using The Bonferroni method, where p � .05, arelisted. Antipsychotic dose is expressed as percentage of maximum allowable dose according to The British National Formulary (60th ed.; Joint FormularyCommittee, 2010). Where the patient was on more than one antipsychotic, the percentage for each drug was summed. C � control; HD � high IQ-decline;HI � high IQ-intact; SAPS � Scale for the Assessment of Positive Symptoms (Andreasen, 1984); SANS � Scale for the Assessment of NegativeSymptoms (Andreasen, 1983); T � typical IQ.

185SUPERIOR INTELLECTUAL ABILITY IN SCHIZOPHRENIA

parallelism, F(9, 151) � 4.14, p � .0001. In post hoc comparisons,all group profiles differed significantly between one another inboth level and parallelism, with two exceptions: There was nodifference between HI and controls or between HD and typicalgroups, for either level or parallelism.

Executive Function

The pattern of results for executive function was remarkablyconsistent across tests (see Figure 2). For every test, the HI patientsperformed similarly to controls, but the HD and typical patientsperformed substantially worse than controls. These differenceswere statistically significant for the Stockings of Cambridge andSpatial Working Memory tasks, and narrowly failed to reachstatistical significance for the I/E Shift Task (Table 4).

The profiles analysis showed an overall difference on level,which was of borderline statistical significance, F(3, 64) � 2.75,

p � .0498, and a more marked effect on parallelism, F(15, 166) �2.92, p � .0004. In post hoc tests, the results followed the samepattern as for the summary scores: There was no difference be-tween HI and controls or between HD and typical groups, on eitherlevel or parallelism, but all other pairs of groups differed from oneanother on both level and parallelism.

Verbal Memory

All measures of verbal memory were significantly impaired inthe HD and typical groups, compared with controls, while the HIgroup was indistinguishable from the control group on any test.(Table 4, Figure 2). The profiles of verbal memory differed be-tween groups on level F(3, 65) � 13.86, p � .0001, and parallel-ism, F(9, 154) � 4.27, p � .0001. In post hoc tests, the samepattern applied as for summary scores and executive function:There was no difference between HI and controls or between HD

Table 3IQ in the Four Groups

C HI HD T F p Post hoc

NART 114.9 (8.1) 119.9 (2.8) 119.9 (3.4) 101.6 (9.1) 28.76 �0.001 C � T; HI � T; HD � TWAIS-III total 113.4 (10.3) 116.7 (5.4) 102.3 (7.5) 90.3 (12.6) 14.49 �0.001 C � T; HI � HD; HI � T; HD � TWAIS-III verbal 112.6 (11.4) 118.9 (7.8) 106.5 (7.6) 93.6 (14.4) 29.74 �0.001 C � HD; C � T; HI � HD; HI � T; HD � TWAIS-III perform 114.5 (10.8) 113.1 (7.4) 95.0 (9.8) 84.9 (12.8) 23.43 �0.001 C � HD; C � T; HI � HD; HI � T; HD � TDecline 1.5 (7.3) 3.2 (3.1) 17.7 (5.6) 11.3 (11.3) 19.29 �0.001 C � HD; C � T; HI � HD

Note. Post hoc ANOVA multiple comparisons using the Bonferroni method, where p � .05, are listed. C � control; HD � high IQ-decline; HI � highIQ-intact; NART � National Adult Reading Test; T � typical IQ; WAIS-III � Wechsler Adult Intelligence Scale (3rd ed.).

Table 4Cognitive Tests by Group

Test C HI HD T F p Bonferroni post hoc comparison

Executive functionI/E stage 8.79 (0.63) 8.60 (0.84) 7.63 (2.20) 7.44 (2.50) 2.35 0.081 —I/E errors 19.1 (15.1) 22.8 (18.6) 48.9 (51.4) 59.3 (62.0) 3.29 0.026 NSDSOC Errors 1.84 (2.00) 1.68 (1.16) 4.43 (3.07) 5.34 (3.02) 7.93 �0.001 C � HD; C � T; HI � HD; HI � TSOC time 473 (179) 624 (310) 485 (210) 331 (148) 4.09 0.010 HI � TSWM between 16.3 (13.2) 21.7 (20.1) 37.3 (22.2) 48.1 (26.5) 7.99 �0.001 C � HD; C � T; HI � TSWM within 1.11 (1.63) 2.80 (3.55) 2.79 (3.46) 2.56 (3.08) 1.36 0.261 —

Verbal memoryRAVLT (learning) 55.6 (8.1) 56.2 (8.4) 42.4 (8.6) 39.0 (13.9) 12.69 �0.001 C � HD; C � T; HI � HD; HI � TRAVLT (immediate recall) 11.9 (2.1) 10.7 (3.1) 7.6 (2.9) 7.2 (4.1) 10.35 �0.001 C � HD; C � T; HI � TRAVLT (delayed recall) 11.1 (3.6) 10.7 (4.0) 7.0 (4.0) 6.1 (4.4) 6.73 �0.001 C � HD; C � T; HI � TVPA 21.9 (7.1) 22.7 (7.6) 14.7 (7.7) 10.8 (6.9) 9.44 �0.001 C � HD; C � T; HI � HD; HI � T

Verbal fluencyCOWAT, letter “S” 20.7 (5.4) 22.6 (6.4) 20.3 (6.0) 16.9 (4.0) 2.54 0.064 —COWAT, animals 26.7 (5.1) 25.6 (4.6) 22.4 (6.1) 16.8 (4.4) 11.60 �0.001 C � T; HI � T; HD � T

Reaction timeSingle choice 515 (180) 631 (252) 743 (219) 891 (407) 6.08 0.001 C � HD; C � T5-choice 526 (101) 670 (150) 777 (255) 846 (248) 8.22 �0.001 C � HD; C � T

Working memoryDS Fwd 10.6 (2.7) 10.9 (2.3) 10.0 (2.0) 9.0 (2.9) 1.71 0.174 —DS Bkwd 8.2 (2.7) 9.3 (2.5) 6.8 (2.1) 6.4 (2.4) 4.15 0.009 HI � TLNSeq 12.2 (2.7) 13.1 (2.5) 9.5 (1.8) 8.4 (3.5) 10.27 �0.001 C � HD; C � T; HI � HD; HI � TSpatial span 6.05 (1.54) 6.10 (1.37) 5.08 (1.10) 5.00 (1.59) 3.02 0.036 —

Note. Standard deviations shown in parentheses. Post hoc ANOVA multiple comparisons using the Bonferroni method, where p � .05, are listed.C � control; COWAT � Continuous Oral Word Association Task; DS � Digit Span Task; HD � high IQ-decline; HI � high IQ-intact; I/E �Intradimensional/Extradimensionsal Shift Task; LNS � Letter-Number Sequencing Task; RAVLT � Rey Auditory-Verbal Learning Task; SOC �Stockings of Cambridge; SWM � Spatial Working Memory Task; T � typical IQ; VPA � Verbal Paired Associates task.

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and typical groups, on either level or parallelism. All other com-binations of groups differed from one another in both level andparallelism.

Verbal Fluency

For semantic fluency, the typical IQ patients scored significantlyworse than all other groups, but there were no significant groupdifferences in phonological fluency (Table 4, Figure 2). Profileanalysis was not attempted since there were only two variables.

Reaction Time

In both the single- and 5-choice RT tasks, the HD and typicalpatients were impaired relative to the HI and control groups. TheHI group appeared somewhat impaired in the single-choice task(Cohen’s d � 0.58), and more so on the 5-choice task (Cohen’sd � 1.25), although in Bonferroni post hoc comparisons, they didnot differ significantly from the control group (Table 4, Figure 2).All the patient groups showed relatively more impairment on the5-choice task than on the single-choice task, suggesting that theunpredictability of the response was similarly problematic for allpatients with schizophrenia, regardless of their IQ. Profile analysiswas not attempted since there were only two variables.

Working Memory

The typical and HD groups performed significantly worse thancontrols on the Letter-Number Sequencing Task, with the HIpatients slightly (but nonsignificantly) outperforming the controls.The Backward Digit Span Task showed a similar pattern of results,although the only significant difference that survived Bonferronicorrection was between HI and typical IQ patients (Table 4, Figure2).

Profile analysis indicated that the group profiles differed on bothlevel, F(3, 65) � 6.52, p � .0006, and parallelism, F(9, 154) �3.04, p � .0022. In post hoc tests, the same pattern of resultsemerged as with all previous profile analyses: There was nodifference between HI and controls or between HD and typicalgroups, on either level or parallelism, but all other combinations ofgroups differed from one another on both level and parallelism.

Discussion

Uniqueness of Sample

In this study, we identified a group of 34 patients who fulfilleddiagnostic criteria for DSM–IV schizophrenia or schizoaffectivedisorder yet were of superior premorbid intelligence, with a meanestimated premorbid IQ of 119.9. Within this group, we identifieda cognitively intact group whose IQs had barely changed fromtheir estimated premorbid level. Although other studies have de-scribed intellectually normal (Elliott, McKenna, Robbins, & Sa-hakian, 1995; Palmer et al., 1997; Kremen et al., 2000; Wilk et al.,2005), nondeclining (Weickert et al., 2000), or even intellectuallysuperior (Heinrichs et al., 2008) patients with schizophrenia, weare not aware of any other study that has described a group ofschizophrenia patients with such high premorbid IQ as this group.

Diagnostic Status of the Sample

We previously reported that cognitively intact patients are morelikely to have prominent mood symptoms (MacCabe et al., 2002),and we recently demonstrated an association between exceptionalacademic ability and increased risk for bipolar affective disorder(MacCabe et al., 2010). These findings suggest that some patientswho appear to have high intelligence and schizophrenia mayinstead be suffering from bipolar disorder with psychotic features.To exclude this possibility, we assessed all our subjects using astructured diagnostic interview, administered by an experiencedclinical psychiatrist, to be certain that all our cases in our samplemet DSM–IV diagnostic criteria for schizophrenia or schizoaffec-tive disorder. Although some patients in our sample did meetcriteria for schizoaffective disorder, the proportion was small, evenin the high-IQ groups. Of those who did meet criteria for schizo-affective disorder, all were bipolar subtype except one with de-pressive subtype, in the typical group.

HI patients did not differ significantly from either the HD ortypical groups in their degree of positive symptoms nor in theirdose of antipsychotics. However, they had remarkably low levelsof negative symptoms. This dissociation between positive andnegative symptoms is in line with previous findings that negativesymptoms are associated with cognitive deficits in schizophrenia(Palmer et al., 1997; Brill et al., 2009; Cohen et al., 2007).

Neuropsychological Findings

The neuropsychological findings are remarkably consistent. Wesaw the same ranking of performance by group in almost all theneuropsychological domains that we tested: The HI group gener-ally performed at around the same level as controls, the HD groupperformed at a lower level, and the typical schizophrenia groupperformed at the lowest level.

On the majority of tests, the HI and control groups were indis-tinguishable from one another, whereas the HD and typical groupswere both markedly impaired and similar to one another. Thispattern of results was replicated in all the profile analyses that weundertook.

The main exception to this general pattern is in the workingmemory tests, on which the HI group performed somewhat betterthan controls. Although this effect is not statistically significant, itis noteworthy, as it seems to challenge the view that workingmemory is a core deficit of schizophrenia (Silver, Feldman, Bilker,& Gur, 2003), may be associated with poor outcome (Leeson et al.,2008), and may be genetically associated with genetic risk forschizophrenia (O’Connor et al., 2009; Toulopoulou et al., 2007).

Working memory is strongly correlated with intelligence, bothin the general population and in schizophrenia (Aukes et al., 2009).Our results suggest that, among patients with high premorbid IQ,working memory may be a useful predictor or index of postonsetdecline, such that individuals with better working memory maysuffer less decline. Further research, particularly in longitudinalsamples, would be useful in elucidating whether working memoryor other neuropsychological measures could serve as predictors ofdecline, and such investigations may inform efforts to preservecognitive function following the onset of psychosis (Leeson et al.,2009).

187SUPERIOR INTELLECTUAL ABILITY IN SCHIZOPHRENIA

Implications of the Existence of the HI Patients

If the HI group is truly free of cognitive deficits, the implicationwould be that cognitive deficits are not a core feature of schizo-phrenia. Rather, they may, like auditory hallucinations or delu-sions, be features of the illness that are present in the majority ofcases, but not in all cases. Similarly, if the cognitive deficits foundin schizophrenia are an artifact of impaired neurodevelopment,then the existence of patients without such deficits would implythat neurodevelopmental impairment is not a prerequisite forschizophrenia.

However, whether the individuals in this HI group are truly freeof any cognitive impairment remains open to doubt. The HIpatients certainly performed at a level that is statistically indistin-guishable from controls in all the tests that we have used in thisstudy, and this was despite the controls themselves having anabove average IQ. Nevertheless, visual inspection of Figure 2suggests that the profile of scores in the HI group does bear someresemblance to the profile of scores in the other schizophreniagroups. In particular, the HI patients scored relatively poorly onRT, where, like the HD and typical groups, they were relativelymore impaired in the 5-choice than in the single-choice condition.They showed relatively worse performance in semantic than letterfluency, supporting the view that semantic fluency deficits are acandidate “core” deficit (studies reviewed in Reichenberg & Har-vey, 2007). HI patients also scored relatively worse on error thantime in the Stockings of Cambridge Task, and they performed aspoorly as the other schizophrenia groups on within-trial errors inthe Spatial Working Memory Task.

One possible explanation for these subtle deficits could be thatthey are a consequence of impairment by antipsychotic drug treat-ment. To explore this possibility, we examined correlations be-tween antipsychotic dose and the RT, Stockings of Cambridge, andSpatial Working Memory tasks in the schizophrenia patients. Wefound that higher antipsychotic doses were associated with betterperformance on almost all tasks. Thus, in the Stockings of Cam-bridge Task, drug dose had no significant correlation with errors(R � 0.099, p � .55), but higher doses were significantly associ-ated with faster times (R � �0.483, p � .002). Similarly, higherdoses were associated with significantly fewer within-search errors(i.e., better performance) in the Spatial Working Memory Task(R � �0.478, p � .002). There were also nonsignificant correla-tions between higher medication dose and faster RTs, in both thesimple and 5-choice tasks.

Considering the low power to detect differences between sub-groups, the resemblance of the profiles in the three schizophreniagroups leads us to suspect that these may be real, albeit subtle,abnormalities in the cognitive profile of the HI patients.

One final possibility is that cognitive deficits in schizophreniaarise through more than one neurobiological mechanism. A recentstudy (Wexler et al., 2009) comparing brain structural abnormal-ities in neuropsychologically near-normal versus neuropsychologi-cally impaired patients with schizophrenia, found that white matterloss was present in the impaired group but not the intact group,suggesting that white matter loss was responsible for the majorityof the cognitive deficit. Gray matter, however, was reduced in bothgroups, suggesting that it was a core pathology. Thus, it may bethat neuropsychologically intact patients have little or no whitematter damage and that the subtle deficits present in the intact

patients reflect gray matter loss, which appears to be common toall schizophrenia.

Limitations

With a cross-sectional study design, we are only able to inferpremorbid IQ using the NART. The apparent declines in IQ aretherefore also inferred rather than measured directly, and theirtiming cannot be determined. Although the timing of decline is notclear, there is increasing evidence of a decline between premorbidand postonset IQ (Woodberry, Giuliano, & Seidman, 2008). Ittherefore seems reasonable to interpret the discrepancies betweenNART and WAIS IQ in our sample as representing a real declinein IQ, possibly occurring around the time of illness onset.

Another limitation of the NART, particularly in this patientgroup, is its ceiling effect: The estimated premorbid IQ score forsomeone scoring the maximum raw score of 50 on the NART isonly 131 (Deary et al., 2007). Therefore, although the HI patientsappear not to show a discrepancy between NART-estimated pre-morbid IQ and current IQ, it is possible that some of theseindividuals may in fact have declined from premorbid IQs thatwere too high to be accurately estimated by the NART. On theother hand, if this were the case, one might expect to see severalpatients in this group, with NART-estimated premorbid IQ scoresat or near the ceiling of 131, but the highest NART IQ wemeasured was 124.

We believe we have gone further than any previous study instudying a subgroup of patient with superior, rather than merelyaverage, intellectual functioning. However, studies on rare indi-viduals will always tread a fine line between selecting as pure asubgroup as possible and restricting power. We acknowledge thatour HI group, while unique, is relatively small. If we had been ableto recruit a larger group, it is possible that the small differencesbetween HI patients and controls would have reached statisticalsignificance.

In common with most neuropsychological literature, the inter-pretation of z scores depends on the assumption that the tests areequally reliable: Less reliable tests will produce higher standarddeviations, giving a lower z score for a given difference in rawscore.

Finally, while the HI group has grossly preserved intellectualfunctioning on our test battery, it remains possible that this grouphas deficits in some other neurocognitive domain that we did notmeasure.

Conclusions

In keeping with previous studies (Torrey, Bowler, Taylor, &Gottesman, 1994; Palmer et al., 1997; Kremen et al., 2000; Hei-nrichs et al., 2008), our results confirm the existence of patientsmeeting DSM–IV diagnostic criteria for schizophrenia who havemarkedly superior premorbid intellectual functioning. Our dataindicate that within these patients, some undergo a decline incognitive functioning and develop cognitive deficits that are sim-ilar to those of typical schizophrenia patients, but of a lesserdegree. However, some patients remain indistinguishable fromhealthy controls on all cognitive tests.

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References

Allen, D. N., Goldstein, G., & Warnick, E. (2003). A consideration of neuro-psychologically normal schizophrenia. Journal of the International Neuro-psychological Society, 9, 56–63. doi:10.1017/S135561770391006X

American Psychiatric Association. (2000). Diagnostic and statistical man-ual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Andreasen, N. C. (1983). The Scale for the Assessment of Negative Symp-toms (SANS). Iowa City, IA: The University of Iowa.

Andreasen, N. C. (1984). The Scale for the Assessment of Positive Symp-toms (SAPS). Iowa City, IA: The University of Iowa.

Aukes, M. F., Alizadeh, B. Z., Sitskoorn, M. M., Kemner, C., Ophoff,R. A., & Kahn, R. S. (2009). Genetic overlap among intelligence andother candidate endophenotypes for schizophrenia. Biological Psychia-try, 65, 527–534. doi:10.1016/j.biopsych.2008.09.020

Bright, P., Jaldow, E., & Kopelman, M. D. (2002). The National AdultReading Test as a measure of premorbid intelligence: A comparison withestimates derived from demographic variables. Journal of the Interna-tional Neuropsychological Society, 8, 847– 854. doi:10.1017/S1355617702860131

Brill, N., Levine, S. Z., Reichenberg, A., Lubin, G., Weiser, M., & Rabinowitz,J. (2009). Pathways to functional outcomes in schizophrenia: The role ofpremorbid functioning, negative symptoms and intelligence. SchizophreniaResearch, 110, 40–46. doi:10.1016/j.schres.2009.02.016

Chapman, L. J., & Chapman, J. P. (1973). Problems in the measurement ofcognitive deficit. Psychological Bulletin, 79, 380–385. doi:10.1037/h0034541

Cohen, A. S., Saperstein, A. M., Gold, J. M., Kirkpatrick, B., Carpenter,W. T. J., & Buchanan, R. W. (2007). Neuropsychology of the deficitsyndrome: New data and meta-analysis of findings to date. Schizophre-nia Bulletin, 33, 1201–1212. doi:10.1093/schbul/sbl066

Crawford, J. R., Besson, J. A., Bremner, M., Ebmeier, K. P., Cochrane,R. H., & Kirkwood, K. (1992). Estimation of premorbid intelligence inschizophrenia [see comments]. British Journal of Psychiatry, 161, 69–74. doi:10.1192/bjp.161.1.69

David, A. S. (1999). Intelligence and schizophrenia. Acta PsychiatricaScandinavica, 100, 1–2. doi:10.1111/j.1600-0447.1999.tb10907.x

David, A. S., Malmberg, A., Brandt, L., Allebeck, P., & Lewis, G. (1997).IQ and risk for schizophrenia: A population-based cohort study. Psy-chological Medicine: A Journal of Research in Psychiatry and the AlliedSciences, 27, 1311–1323. doi:10.1017/S0033291797005680

Deary, I. J., Ferguson, K. J., Bastin, M. E., Barrow, G. W. S., Reid, L. M.,Seckl, J. R., & MacLullich, A. M. J. (2007). Skull size and intelligence,and King Robert Bruce’s IQ. Intelligence, 35, 519–528. doi:10.1016/j.intell.2007.04.003

Elliott, R., McKenna, P. J., Robbins, T. W., & Sahakian, B. J. (1995).Neuropsychological evidence for frontostriatal dysfunction in schizo-phrenia. Psychological Medicine: A Journal of Research in Psychiatryand the Allied Sciences, 25, 619–630. doi:10.1017/S0033291700033523

Foong, J., Rozewicz, L., Chong, W. K., Thompson, A. J., Miller, D. H., &Ron, M. A. (2000). A comparison of neuropsychological deficits inprimary and secondary progressive multiple sclerosis. Journal of Neu-rology, 247, 97–101. doi:10.1007/PL00007804

Heinrichs, R. W., Miles, A. A., Smith, D., Zargarian, T., Vaz, S. M.,Goldberg, J. O., & Ammari, N. (2008). Cognitive, clinical, and func-tional characteristics of verbally superior schizophrenia patients. Neu-ropsychology, 22, 321–328. doi:10.1037/0894-4105.22.3.321

Heinrichs, R. W., & Zakzanis, K. K. (1998). Neurocognitive deficit inschizophrenia: A quantitative review of the evidence. Neuropsychology,12, 426–445. doi:10.1037/0894-4105.12.3.426

Holthausen, E. A., Wiersma, D., Sitskoorn, M. M., Hijman, R., Dingemans,P. M., Schene, A. H., & van den Bosch, R. J. (2002). Schizophrenicpatients without neuropsychological deficits: Subgroup, disease severityor cognitive compensation? Psychiatry Research, 112, 1–11. doi:10.1016/S0165-1781(02)00184-1

Joint Formulary Committee. (2010). British National Formulary (60th ed.).London, England: British Medical Association and Royal Pharmaceuti-cal Society.

Kremen, W. S., Seidman, L. J., Faraone, S. V., Toomey, R., & Tsuang,M. T. (2000). The paradox of normal neuropsychological function inschizophrenia. Journal of Abnormal Psychology, 109, 743–752. doi:10.1037/0021-843X.109.4.743

Kremen, W. S., Seidman, L. J., Faraone, S. V., & Tsuang, M. T. (2001).Intelligence quotient and neuropsychological profiles in patients withschizophrenia and in normal volunteers. Biological Psychiatry, 50, 453–462. doi:10.1016/S0006-3223(01)01099-X

Leeson, V. C., Barnes, T. R., Harrison, M., Matheson, E., Harrison, I.,Mutsatsa, S. H., . . . Joyce, E. M. (2010). The relationship between IQ,memory, executive function, and processing speed in recent-onset psy-chosis: 1-year stability and clinical outcome. Schizophrenia Bulletin, 36,400–409. doi:10.1093/schbul/sbn100

Leeson, V. C., Sharma, P., Harrison, M., Ron, M. A., Barnes, T. R., &Joyce, E. M. (2011). IQ trajectory, cognitive reserve, and clinical out-come following a first episode of psychosis: A 3-year longitudinal study.Schizophrenia Bulletin, 37, 768–777. doi:10.1093/schbul/sbp143

MacCabe, J. H. (2008). Population-based cohort studies on premorbidcognitive function in schizophrenia. Epidemiologic Reviews, 30, 77–83.doi:10.1093/epirev/mxn007

MacCabe, J. H., Aldouri, E., Fahy, T. A., Sham, P. C., & Murray, R. M.(2002). Do schizophrenic patients who managed to get to university havea non-developmental form of illness? Psychological Medicine, 32, 535–544. doi:10.1017/S0033291702005391

MacCabe, J. H., Lambe, M. P., Cnattingius, S., Sham, P. C., David,A. S., Reichenberg, A., . . . Hultman, C. M. (2010). Excellent schoolperformance at age 16 and risk of adult bipolar disorder: Nationalcohort study. British Journal of Psychiatry, 196, 109 –115. doi:10.1192/bjp.bp.108.060368

MacCabe, J. H., Lambe, M. P., Cnattingius, S., Torrang, A., Bjork, C.,Sham, P. C., . . . Hultman, C. M. (2008). Scholastic achievement at age16 and risk of schizophrenia and other psychoses: A national cohortstudy. Psychological Medicine: A Journal of Research in Psychiatry andthe Allied Sciences, 38, 1133–1140. doi:10.1017/S0033291707002048

MacCabe, J. H., & Murray, R. M. (2004). Intellectual functioning inschizophrenia: A marker of neurodevelopmental damage? Journal ofIntellectual Disability Research, 48, 519 –523. doi:10.1111/j.1365-2788.2004.00619.x

Marenco, S., & Weinberger, D. R. (2000). The neurodevelopmental hy-pothesis of schizophrenia: Following a trail of evidence from cradle tograve. Development and Psychopathology, 12, 501–527.

Nelson, H. E., & Willison, J. R. (1991). The Revised National AdultReading Test: Test manual. Windsor, England: NFER-Nelson.

Nurnberger, J. I., Jr., Blehar, M. C., Kaufmann, C. A., York-Cooler, C.,Simpson, S. G., Harkavy-Friedman, J., . . . Reich, T. (1994). Diagnosticinterview for genetic studies. Rationale, unique features, and training.NIMH Genetics Initiative. Archives of General Psychiatry, 51, 849–859; discussion 863–864.

O’Carroll, R., Walker, M., Dunan, J., Murray, C., Blackwood, D., Ebmeier,K. P., . . . Goodwin, G. M. (1992). Selecting controls for schizophreniaresearch studies: The use of the National Adult Reading Test (NART) isa measure of premorbid ability. Schizophrenia Research, 8, 137–141.doi:10.1016/0920-9964(92)90030-9

O’Connor, M., Harris, J. M., McIntosh, A. M., Owens, D. G., Lawrie,S. M., & Johnstone, E. C. (2009). Specific cognitive deficits in a groupat genetic high risk of schizophrenia. Psychological Medicine, 39,1649–1655. doi:10.1017/S0033291709005303

Palmer, B. W., Heaton, R. K., Paulsen, J. S., Kuck, J., Braff, D., Harris,M. J., . . . Jeste, D. V. (1997). Is it possible to be schizophrenic yetneuropsychologically normal? Neuropsychology, 11, 437– 446. doi:10.1037/0894-4105.11.3.437

189SUPERIOR INTELLECTUAL ABILITY IN SCHIZOPHRENIA

Reichenberg, A., & Harvey, P. D. (2007). Neuropsychological impairmentsin schizophrenia: Integration of performance-based and brain imagingfindings. Psychological Bulletin, 133, 833– 858. doi:10.1037/0033-2909.133.5.833

Reichenberg, A., Weiser, M., Rabinowitz, J., Caspi, A., Schmeidler, J.,Mark, M., . . . Davidson, M. (2002). A population-based cohort study ofpremorbid intellectual, language, and behavioral functioning in patientswith schizophrenia, schizoaffective disorder, and nonpsychotic bipolardisorder. American Journal of Psychiatry, 159, 2027–2035. doi:10.1176/appi.ajp.159.12.2027

Rey, A. (1958). L’examen clinique en psychologie. (The clinical examin-sation in psychology). Paris, France: Presse Universitaire de France.

Robbins, T. W., James, M., Owen, A. M., Sahakian, B. J., McInnes, L., &Rabbitt, P. (1994). Cambridge Neuropsychological Test Automated Bat-tery (CANTAB): A factor analytic study of a large sample of normalelderly volunteers. Dementia, 5, 266–281.

Silver, H., Feldman, P., Bilker, W., & Gur, R. C. (2003). Working memorydeficit as a core neuropsychological dysfunction in schizophrenia. TheAmerican Journal of Psychiatry, 160, 1809–1816. doi:10.1176/appi.ajp.160.10.1809

Torrey, E. F., Bowler, A. E., Taylor, E. H., & Gottesman, I. I. (1994).Schizophrenia and manic-depressive disorder. New York, NY: BasicBooks.

Toulopoulou, T., Picchioni, M., Rijsdijk, F., Hua-Hall, M., Ettinger, U.,Sham, P., . . . Murray, R. M. (2007). Substantial genetic overlap betweenneurocognition and schizophrenia: Genetic modeling in twin samples.Archives of General Psychiatry, 64, 1348–1355. doi:10.1001/archpsyc.64.12.1348

Wechsler, D. (1997a). WAIS-III: Wechsler Adult Intelligence Scale (3rded.). San Antonio, TX: Psychological Corporation/Harcourt Brace.

Wechsler, D. (1997b). WMS III: The Wechsler Memory Scale (3rd ed.). SanAntonio, TX: Psychological Corporation (Harcourt).

Weickert, T. W., Goldberg, T. E., Gold, J. M., Bigelow, L. B., Egan, M. F.,& Weinberger, D. R. (2000). Cognitive impairments in patients withschizophrenia displaying preserved and compromised intellect. Archivesof General Psychiatry, 57, 907–913. doi:10.1001/archpsyc.57.9.907

Weinberger, D. R., & Gallhofer, B. (1997). Cognitive function in schizo-phrenia. International Clinical Psychopharmacology, 12, S29–S36. doi:10.1097/00004850-199709004-00006

Wexler, B. E., Zhu, H., Bell, M. D., Nicholls, S. S., Fulbright, R. K., Gore,J. C., . . . Peterson, B. S. (2009). Neuropsychological near normality andbrain structure abnormality in schizophrenia. The American Journal ofPsychiatry, 166, 189–195. doi:10.1176/appi.ajp.2008.08020258

Wilk, C. M., Gold, J. M., McMahon, R. P., Humber, K., Iannone, V. N., &Buchanan, R. W. (2005). No, it is not possible to be schizophrenic yetneuropsychologically normal. Neuropsychology, 19, 778 –786. doi:10.1037/0894-4105.19.6.778

Woodberry, K. A., Giuliano, A. J., & Seidman, L. J. (2008). Premorbid IQin schizophrenia: A meta-analytic review. The American Journal ofPsychiatry, 165, 579–587. doi:10.1176/appi.ajp.2008.07081242

Received July 2, 2010Revision received May 9, 2011

Accepted May 25, 2011 �

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