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2000, 6:161-168.APTRonan O'CarrollCognitive impairment in schizophrenia

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Cognitive impairment in schizophrenia APT (2000), vol. 6, p. 161

Cognitive impairmentin schizophrenia

Ronan OCarroll

Advances in Psychiatric Treatment (2000), vol. 6, pp. 161168

My whole mental power has disappeared, I havesunk intellectually below the level of a beast(a patientwith schizophrenia, quoted by Kraepelin, 1919, p. 25).

Traditionally, significant cognitive impairment wasthought to be evident only in elderly deterioratedpatients with schizophrenia. However, over the past25 years, evidence has accrued to challenge thisview. It is becoming evident that marked cognitiveimpairment is, in fact, the norm and often pre-datesthe illness. The recent literature has attempted tocharacterise the prevalence, degree and nature of neuropsychological abnormality in schizophrenia(see Box 1). In this brief review, I will attempt tosummarise the current state of knowledge withregard to cognitive impairment in schizophrenia.

Nature and degreeof cognitive impairment

This field evolved from the traditional lesion-basedapproach in neuropsychology, that is, inferringregional brain dysfunction based on poor perfor-mance on putatively localising neuropsychologicaltests. On the basis of such an approach, variousauthors have concluded that schizophrenia ischaracterised by cognitive test profiles indicative of dysfunction of the frontal lobe, temporal lobe, left orright hemisphere, basal ganglia, etc. (Blanchard &Neale, 1994). This lack of consensus may reflect theheterogeneity of schizophrenia, and may also be aresult of the relatively poor localising ability of manystandard neuropsychological instruments. A variety

of candidate brain regions and associated cognitivefunctions have thus been implicated in the psycho-pathology that characterises schizophrenia. Ingeneral, the strongest camps to emerge have beenthose that claim a disproportionate impairment of

memory functioning (McKenna, 1991; Saykin et al,1994) and those arguing for a relatively selectiveexecutive dysfunction (Weinberger et al, 1986).Others have reported more widespread neuropsy-chological dysfunction (Buchsbaum, 1990). Anextreme case is put by Meehl who stated:

I conjecture that whatever is wrong with theschizotaxic CNS is ubiquitous, a functional aberrationpresent throughout, operating everywhere from thesacral cord to the frontal lobes (Meehl, 1990, p. 14).

In many ways, it now seems an old-fashionedapproach to try to localise central nervous system(CNS) dysfunction using cognitive tests that were

largely devised to identify specific brain damage,and were developed in an era before high-resolutionneuroimaging was possible. Many current workerswould agree with Shallice et al (1991) who proposedthat from a neuropsychological perspective, anattempt to understand the nature of the information-processing impairment of schizophrenia shouldprecede an attempt to localise it.

Over the years, many authors have questionedwhether or not schizophrenia is characterised bygenuine cognitive impairment. However, recentstudies have clearly demonstrated its presence. Totake an example, Heinrichs & Zakzanis (1998)carried out a large-scale comprehensive quantitativemeta-analysis of cognitive impairment in schizo-phrenia, which involved comparisons of patientswith schizophrenia v. controls. Their results aresummarised in Table 1. As can be seen, the greatest

Ronan OCarroll is Professor of Psychology at the University of St Andrews (St Andrews, Fife, Scotland KY16 9JU; tel: 01334463041; fax: 01334 463042; e-mail: [email protected]). He trained as a clinical psychologist in Edinburgh and for thepast 10 years has collaborated with colleagues at the Medical Research Council Brain Metabolism Unit and the Department of Psychiatry in Edinburgh investigating clinical neuropsychological aspects of psychiatric disorder.


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APT (2000), vol. 6, p. 162 OCarroll

impairment is observed in global verbal memoryfunctioning. However, given the multitude of teststhat show significant impairment, clearly anyspecific impairment (e.g. memory or executivefunctioning) exists within a more widespread reduc-tion in general cognitive functioning. In accordancewith this view, Palmer et al (1997) recently posed thequestion, Is it possible to be schizophrenic yetneuropsychologically normal? They gave acomprehensive neuropsychological battery to 171out-patients with schizophrenia and compared themwith 63 healthy controls. Two experienced neuro-psychologists conducted blind ratings of the testresults. Only 27% of the patients with schizophreniawere classified as neuropsychologically normal .This indicates that significant cognitive impairmentin schizophrenia is, in fact, the norm. However, thisstudy also highlights the fact that a proportion of patients with schizophrenia appear to remainneuropsychologically intact. This suggests that thepathophysiology underlying the cognitive deficitsoften associated with schizophrenia may be distinct

from that causing some of the core clinical features.Evidence in support of this latter view can also bederived from the study by Goldberg et al (1993), whoreported symptomatic improvement followingtreatment with clozapine, but with no accompany-ing improvement in neuropsychological functioning.

Does the cognitiveimpairment pre-date

the illness?

The temporal relationship between cognitiveimpairment and illness has been tackled viastudies where neuropsychological data have beencollated retrospectively from individuals wholater developed schizophrenia. The aim has beento determine whether any pre-existing abnormalitiesin cognitive functioning are apparent before the onset

Table 1 Summary results of meta-analysisof 204 studies of cognitive impairment in

schizophrenia (7420 patients with schizophreniaand 5865 controls; adapted from Heinrichs

& Zakzanis, 1998, with permission)

Test or construct M d s.d. nGlobal Verbal Memory 1.41 0.59 32Bilateral Motor Skill 1.30 0.38 5Performance IQ 1.26 1.00 17Continuous Performance 1.16 0.49 14Word Fluency 1.15 1.00 29Stroop Test 1.11 0.49 6WAIS R IQ 1.10 0.72 35Token 0.98 0.49 7Tactile-Transfer 0.98 1.71 12Selective Verbal Memory 0.90 0.62 7Wisconsin Card Sort 0.88 0.41 43Verbal IQ 0.88 0.66 27Unilateral Motor Skill 0.86 0.39 6

Trail Making Part B 0.80 0.50 15Non-Verbal Memory 0.74 1.98 14Trail Making Part A 0.70 0.36 12Facial Recognition 0.61 0.36 8Digit Span 0.61 0.43 18Line Orientation 0.60 0.63 4Non-WAIS R IQ 0.59 0.51 43Vocabulary 0.53 0.21 38Block Design 0.46 0.39 12

M d , effect size, i.e. average degree of impairment (instandard deviation units), patients v. controls; n, numberof studies; WAIS R, Wechsler Adult Intelligence Scale Revised.

Box 1. Cognitive impairment in schizo-phrenia summary of recent researchfindings

Significant cognitive impairment is commonin schizophrenia, affecting up to 75% of

patientsA wide range of cognitive functions areaffected, particularly memory, attention,motor skills, executive function andintelligence

The cognitive impairment often pre-datesthe illness onset

It is an intrinsic part of the illness and isobserved in young, drug-nave patients

Efforts to explain core features of schizo-phrenia as a consequence of specificneuropsychological abnormalities havebeen disappointing

Cognitive impairment is related to socialand functional outcome

The evidence is mixed regarding theefficacy of newer atypical antipsychoticsin improving cognitive functioning inschizophrenia

Although some laboratory-based studies ofcognitive rehabilitation have providedpromising results, convincing evidenceregarding generalisation to lasting im-provements in day-to-day functioning is,as yet, lacking


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of schizophrenia. Jones et al (1994) used the subjectsfrom the Medical Research Council National Surveyof Health and Development, a random sample of over 5000 births in England, Scotland and Walesduring the first week of March 1946. Out of thissample, 30 cases of schizophrenia arose betweenthe ages of 16 and 43. All the subjects had been testedfor non-verbal, verbal and reading abilities at theages of 8, 11 and 15 years and arithmetic wasmeasured at the ages of 11 and 15 years, withvocabulary being assessed at the ages of 8 and 11years. The main results are shown in Table 2. Ascan be readily observed, children who developedschizophrenia in later life were significantlyimpaired on non-verbal and verbal intelligence testsfrom the age of 8, and on arithmetic/mathematicskills from the age of 11. This result clearly indicatesthe presence of detectable cognitive abnormalitiesin childhood which pre-dated the development of the illness.

In a Swedish study, David et al (1997) were able tocapitalise on a remarkable sample of 50 000 malesconscripted to the Swedish Army between 1969 and1970. Tests of cognitive functioning were recordedat conscription. In later life, 195 subjects wereadmitted to hospital with schizophrenia. Low IQemerged as a clear risk factor for those later diag-

nosed with schizophrenia, and poor performanceon verbal tasks and a mechanical knowledge testconferred a significantly increased risk of schizo-phrenia, even after taking into account generalintellectual ability.

Taken together, the results of these and otherstudies provide strong supportive evidence for theview that neuropsychological abnormalities pre-date the development of schizophrenia. It is temptingto interpret these findings as evidence of a neuro-developmental abnormality in those individualswho develop schizophrenia in late adolescence orearly adulthood. This association could be directlycausal, that is, with cognitive impairment leadingto false beliefs and perceptions, or, alternatively,could act via an indirect mechanism with any factorswhich cause low IQ (such as abnormal braindevelopment) increasing later risk for schizophrenia(David et al, 1997).

Is the cognitive impairmentprogressive?

The assumption of intellectual decline in schizo-

phrenia is evident from the earliest writings on thedisorder for example, the term dementia praecox (Kraepelin, 1919) implies a continuing cognitivedecline. Other writers have proposed that psychoticepisodes may be neurotoxic, with increasing lengthof initial untreated illness associated with a poorprognosis. However, as reviewed above, there isincreasing evidence that cognitive impairment oftenprecedes the illness. One of the outstanding issuesin this area is whether or not the cognitiveimpairment observed in patients with schizophreniadeclines over time. There are opposing views on thissubject. Russell et al (1997) recently proposed thatintellectual decline in schizophrenia was a nothingmore than a myth . They followed up patients whohad received an intelligence test as a child, who thendeveloped schizophrenia, and had their intelligencere-tested some 19 years later. There were nodifferences between the child and adult IQs.However, others have criticised this study on thegrounds that the sample was unrepresentative inthat the individuals had presented to childpsychiatry units and were far more intellectually

Table 2 Premorbid cognitive impairment inpeople assessed as children who subsequently

developed schizophrenia (from Jones et al ,1994, with permission)

MeanTest and Case mean deficit 1

age (years) (s.d.) (% s.d.) F ratio 2 P

Non-verbal8 97.0 (14.1) 5.9 (39%) 3/9 0.0511 98.9 (16.7) 4.4 (29%) 2.1 0.1415 93.6 (15.9) 9.5 (63%) 9.9 0.002

Verbal8 96.6 (15.4) 7.1 (47%) 5.7 0.0211 97.3 (15.8) 5.2 (35%) 3.3 0.0715 96.3 (12.5) 7.5 (50%) 6.5 0.01

Arithmetic/maths11 97.6 (16.4) 6.1 (41%) 5.1 0.02

15 99.2 (13.6) 6.9 (46%) 5.7 0.02Vocabulary8 100.8 (17.7) 31.1 (21%) 1.1 0.311 99.8 (14.6) 4.5 (30%) 2.3 0.2

Reading8 99.6 (16.3) 4.0 (27%) 1.8 0.211 100.1 (14.6) 4.5 (30%) 2.3 0.215 100.2 (12.7) 3.5 (24%) 1.5 0.2

1. Corrected for confounding by gender and social class bymultiple classification analysis.2. ANOVA including gender and social class: main effect of case v. control. No gender case interaction was significant.


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APT (2000), vol. 6, p. 164 O Carroll

impaired than subjects in other studies of childrenwho subsequently developed schizophrenia.

Rund (1998) has reviewed a number of longitud-inal studies and concluded that the cognitive deficitsappear to be relatively stable in schizophrenia,consistent with a static encephalopathy rather thana degenerative process. However, most clinicians

are able to identify individual patients who appearto have severely declined cognitively since the onsetof their illness. It may be that subgroups of patientsshow a particularly poor cognitive outcome. Furtherlongitudinal studies are required in order to settlethis issue.

Real-life consequences

It has been claimed that impaired cognitive testperformance in patients with schizophrenia may

be an epiphenomenon, for example, reflecting lackof motivation or distraction by hallucinations. Inorder to convince sceptics that the neuropsycho-logical impairment is important, one would have todemonstrate a clear relationship between cognitivetest performance and real-life functional outcome.An important review of this area was published byGreen (1996), who evaluated studies that usedcognitive measures as predictors and correlates of functional outcome. The most consistent finding toemerge was that verbal memory functioning wasassociated with all types of functional outcome. (Itis notable that verbal memory was the cognitivedomain that showed the greatest impairment in themeta-analysis by Heinrichs & Zakzanis (1998) seeTable 1.) Sustained attention or vigilance was alsofound to be related to social problem-solving andskill acquisition. Interestingly, psychotic symptomswere not significantly associated with outcomemeasures in any of the studies that were reviewed.Green (1996) concluded that deficiencies in verbalmemory and vigilance may prevent patients fromattaining optimal adaptation and hence may act asrate-limiting factors in terms of rehabilitation. It isinteresting that Goldberg et al (1993), who reportedsymptomatic improvement with clozapine treatment,with no associated improvement in neuropsycho-

logical functioning, concluded:This suggests that certain cognitive deficits are

relatively independent of psychotic symptoms inschizophrenia, and are probably central and enduringfeatures of the disorder. Cognitive disability appearedto have been rate-limiting in the sample s rehabil-itation (p. 43).

We have, therefore, moved from a position wherecognitive impairment was not considered to be

particularly important in schizophrenia, to thecurrent view, that it may be a central and rate-limiting feature in terms of rehabilitation.

Velligan et al (1997) has confirmed a poorcorrelation between symptomatology and ability toperform daily living tasks. However, cognitiveimpairment predicted over 40% of the variance in

scores on a functional needs-assessment ratingscale. Addington & Addington (1999) used a novelvideo-taped measure of interpersonal problem-solving skills. In a study of 80 out-patients withschizophrenia, they found that better cognitiveflexibility and verbal memory were positivelyassociated with interpersonal problem-solvingability.

Taken together, the evidence strongly supports theview that cognitive impairment in schizophrenia isdirectly related to social deficits and functionaloutcome for many patients.

Does the neuropsychologicalimpairment relate to clinical

symptoms and signs?

One of the few features of schizophrenia thatmost authors agree on is its heterogeneity. It ispossible that part of the difficulty in detecting aconsistent neuropsychological signature of schizophrenia (Blanchard & Neale, 1994) isthat there is no such thing as schizophrenia .

Syndromes or symptoms may more clearly relate todisordered patterns of information processing.Liddle & Morris (1991) conducted a seminal studyin this area where they assessed a group of patientswith chronic schizophrenia using a battery of neuropsychological tests allegedly sensitive tofrontal lobe dysfunction. Signs and symptoms wereclustered into three syndromes: psychomotorpoverty, disorganisation and reality distortion.Scores for the disorganisation syndrome wereassociated with impairment on tests that requiredthe subject to inhibit a well-established butinappropriate response. Ratings for the psycho-motor poverty syndrome were found to be associatedwith slowness of mental activity. More recently,Baxter & Liddle (1998) confirmed that the psycho-motor poverty syndrome was associated withpsychomotor slowing, and disorganisation wasassociated with impaired performance on the Stroopattentional conflict task, but not with other tests of cognitive inhibition. This led the authors to concludethat the disorganisation syndrome might beassociated with a specific difficulty in suppressing


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irrelevant verbal responses. This approach isappealing, because it tries to integrate neuropsy-chology with the clinical features of schizophrenia.Pursuing this approach to a more specific levelwould result in an attempt to explain specific signsor symptoms in terms of aberrant informationprocessing. As an illustration of this approach,

McKenna (1991) proposed that delusions may ariseas a consequence of a dysfunctional semanticmemory system. Again, this hypothesis has intuitiveappeal, as delusions by definition must representfalse knowledge. However, efforts to try to provideconvincing evidence of a causal relationship betweena specific neuropsychological abnormality and aparticular sign or symptom have, as yet, beendisappointing.

As mentioned above, one way to simplify theheterogeneity of schizophrenia is to factor-analyseclinical ratings in an attempt to produce syndromes.An alternative to this approach is to try to extractneuropsychological factors from a battery of cognitive tests. This is the approach adopted byHeinrichs & Awad (1993). Patients with schizo-phrenia ( n=104) performed the Wisconsin CardSorting Test to assess executive function, theCalifornia Verbal Learning Test to tap memoryfunctioning, the Purdue Peg Board to assessmotor function and the Wechsler Adult IntelligenceScale Revised to measure general intelligence.The resulting cognitive data were subjected tocluster analysis and five cognitive clustersemerged:

(a) selective executive dysfunction;(b) normative function;(c) executive and motor deficits;(d) dementia/multi-focal disturbance; and(e) relatively selective motor deficits.

Heinrichs & Awad (1993) proposed that clusteranalysis of cognitive test data may thus havepromise in reducing and clarifying the heterogeneityof schizophrenia, and concluded that severalpatterns of neurocognitive dysfunction may underlieschizophrenia, thus contributing to the hetero-geneity of the illness and its variable functionaloutcome.

Frith (1992) has also proposed a fascinatingtheoretical model, where he relates specific signsand symptoms to particular information processingabnormalities. For example, he proposes that theinability to generate spontaneous (willed) intentionscan lead to poverty of action, perseveration andinappropriate action. In contrast, the inability tomonitor the beliefs and intentions of others canlead to delusions of reference, paranoid delusions,certain kinds of incoherence and third-personhallucinations.

Is the cognitive impairmentin schizophrenia caused

by medication?

Most neuropsychological studies in schizophreniahave been conducted on medicated patients. It has

become increasingly clear that neuroleptic medic-ation and the anticholinergic drugs that are givento treat extrapyramidal syndromes can have markedcognitive-impairing effects in patients with schizo-phrenia. Do drug-free patients with schizophreniademonstrate significant cognitive impairment? Theanswer is a definitive yes. Several studies haveappeared over the past few years which have clearlyindicated marked and severe cognitive impairmentin patients who have been taken off their medication,or in patients who have never been prescribed any

neuroleptic or anticholinergic medication (e.g.Blanchard & Neale, 1994; McCreadie et al, 1997;Saykin et al, 1994). Although drugs may make acontribution, they do not account for the cognitiveimpairment that is observed in schizophrenia.

The newer atypicalantipsychotics and cognitive

function

Negative features and neuropsychological impair-ments can cause the greatest problems in terms of rehabilitation and are generally considered to beminimally responsive to conventional neuroleptics.The recent development of novel antipsychoticsraised the hope that these may help alleviate bothnegative symptoms and neuropsychological deficits.However, Hawkins et al (1999) state:

Despite some reports of positive findings, thegrounds for thinking that the novel antipsychoticswill exert direct and significant effects on neurocog-nition nevertheless remain inferential, and infirmlyso (p. 6).

To date, only a few well-controlled studies of theeffects of novel antipsychotics (e.g. clozapine, risper-idone and olanzapine) on cognitive functioninghave been undertaken. The newer drugs are thoughtto have a primary mode of action that consists of acombination of serotonergic and dopaminergic

blockade. It has been proposed tha t it is theserotonergic antagonism that may particularly

benefit cognition (Sharma, 1999). Breier (1999) also


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speculates that cognitive enhancement with atypicalantipsychotics may represent a consequence of N -methyl-D-aspartate antagonism. In relation toneuropsychological outcome, the best-studied agentis clozapine and the results have been mixed. Asstated previously, Goldberg et al (1993) reportedclinical improvement despite no improvement in

neuropsychological status, whereas other studieshave reported cognitive enhancement. Informationis also emerging for other atypicals. For example,Green et al (1997) reported that risperidone improvedverbal working memory, and this effect wasmaintained after controlling for changes in symp-toms. As Hawkins et al (1999) warn us, however, westill do not have convincing evidence that newlydeveloped antipsychotic drugs have a lasting

beneficial impact on cognitive status that, in turn,leads to an improvement in everyday functioning.This is not to say that the newer atypicals do nothave such an effect, rather that the evidence has notyet been obtained. Sharma (1999) also cautions thatit is possible that some of the positive effects reportedon cognitive functioning may be a result of wash-out of previous drugs that were impairing cognition,rather than of a true beneficial effect of the atypicalneuroleptic. He also recommends that in order toevaluate the effects of drugs on cognitive function-ing, the duration of treatment should preferably lastone year. A further problem with interpreting thisliterature is that positive effects on a specific neuro-psychological test may be presented but, in fact, mayactually represent the one positive finding out of amultitude of neuropsychological comparisons thatwere conducted. Finally, there is the well-recognised

tendency for researchers not to submit for public-ation studies that produced negative findings,coupled with the reluctance of journals to publishsuch studies.

Cognitive rehabilitation

Given the increasing recognition of cognitiveimpairment in schizophrenia, together with thegeneral failure of conventional drug treatment totreat this impairment, several recent studies haveevaluated the potential for cognitive rehabilitationin schizophrenia. Early studies in this area focusedprimarily on training patients in specific neuropsy-chological tasks, for example, providing coachingor monetary performance incentives for performingthe Wisconsin Card Sorting Test. However, improv-ing cognitive tests with practice or money is unlikelyto have a significant impact on more general day-to-day activities. In order for cognitive rehabilitation

in schizophrenia to prove itself, large-scale properlycontrolled trials are necessary, focusing on: (a)adequacy of the control condition that matches forthe therapist s time, contact and enthusiasm; and(b) demonstration of cognitive gains that extend

beyond the training sessions and material s.Adopting this degree of methodological rigour can

lead to sobering results. For example, Field &Galletly (1997) recently reported a controlled trialusing computer-aided cognitive rehabilitation inattempting to remedy the attentional deficit inschizophrenia. The treatment resulted in significantimprovement on a letter cancellation task. However,the control condition (playing computer games) ledto a similar improvement, suggesting that theimprovement was the result of a non-specificpractice effect.

One approach to cognitive rehabilitation inschizophrenia is to try to: (a) focus on subgroups of patients who have specific cognitive abnormalities;and (b) be guided by the rehabilitation literature from

brain-damaged patients. O Carroll et al (1999)recently reported a study where they selected a groupof patients with schizophrenia who had significantmemory impairment. Drawing on the literature frompatients who suffer from the classic amnesicsyndrome, they evaluated the potential benefitsof an errorless learning approach (see Box 2). Putsimply, patients with the classic amnesic syndromeare thought to have a preserved implicit memorysystem in the presence of a devastatingly impairedexplicit memory system (explicit memory refersto memories of a specific episode, e.g. where onewas yesterday, whereas implicit memory refers to

memory without conscious awareness). Duringlearning, it is proposed that amnesic patientsimplicitly remember the mistakes they madeduring learning. Lacking a functional explicitmemory system, when tested after a delay, theycannot distinguish between errors made duringlearning and correct responses. It has been shownthat such amnesic patients benefit from anerrorless approach to learning, that is, they learn

better when they are prevented from makingmistakes during learning (Baddeley & Wilson, 1994).Adopting this approach, O Carroll et al (1999)showed that memory-impaired patients withschizophrenia benefited significantly from alearning approach where they were not allowed tomake any mistakes during learning. However, thisstudy was restricted to a single session, and furtherwork is required in order to test whether errorlesslearning approaches in schizophrenia will have anylasting benefit beyond the laboratory.

Wykes et al (1999) recently reported the initialoutcome of an important cognitive remediationstudy. They conducted a randomised controlled trial


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of intensive cognitive remediation (targetingcognitive flexibility, working memory and planning)involving individual daily sessions for up to threemonths v. a control condition of intensive occupationaltherapy. The cognitive remediation also includedprocedural and errorless learning, targeted reinforce-ment and massed practice. Cognitive remediationsignificantly improved performance on selected testsof cognitive flexibility and memory relative to thecontrol condition. Interestingly, those patients whowere receiving atypical antipsychotic medicationappeared to benefit most from cognitive remediation,suggesting that such a combination treatment may

be optimal. It is noteworthy that improvement occur-red on cognitive tasks that were dissimilar to thoseused in the remediation package, that is, generalis-ation was evident. In addition, improvements in cog-nitive flexibility were related to improvements inself-esteem. This is a promising finding, but furtherwork is required to determine: (a) the specific effec-tive ingredients; and (b) the long-term outcome. Thiswas an extremely time-intensive individualised inter-vention, which is likely to prove expensive in clinicalpractice. However, if the results are robust andreplicable, they may well be worth the investment of time and money. As Wykes et al (1999) concluded,costs of such treatment may well be offset by improve-ments in functioning and reduced dependence onmore expensive (e.g. in-patient) services.

References

Addington, J. & Addington, D. (1999) Neurocognitive andsocial functioning in schizophrenia. Schizophrenia Bulletin,25 , 173182.

Baddeley, A. & Wilson, B. A. (1994) When implicit learningfails: amnesia and the problem of error elimination.Neuropsychologia, 32, 5368.

Baxter, R. D. & Liddle, P. F. (1998) Neuropsychologicaldeficits associated with schizophrenic syndromes.Schizophrenia Research, 30, 239249.

Blanchard, J. J. & Neale, J. M. (1994) The neuropsychologicalsignature of schizophrenia: generalized or differential deficit? American Journal of Psychiatry , 151, 4048.

Breier, A. (1999) Cognitive deficit in schizophrenia and itsneurochemical basis. British Journal of Psychiatry , 174(suppl. 37), 16 18.

Buchsbaum, M. S. (1990) Frontal lobes, basal ganglia, temporallobes three sites for schizophrenia? Schizophrenia Bulletin,16 , 377378.

David, A. S., Malmberg, A., Brandt, L., et al (1997) IQ and risk forschizophrenia: a population-based cohort study. Psychological Medicine, 27, 13111323.

Field, C. D. & Galletly, C. (1997) Computer-aided cognitiverehabilitation: possible application to the attentionaldeficit of schizophrenia, a report of negative results.Perceptual and Motor Skills , 85, 9951002.

Frith, C. D. (1992) The Cognitive Neuropsychology of Schizophrenia.Hove: Lawrence Erlbaum.

Goldberg, T. E., Greenberg, R. D., Griffin, S. J., et al (1993)The effect of clozapine on cognition and psychiatricsymptoms in patients with schizophrenia. British Journalof Psychiatry, 162 , 4348.

Green, M. F. (1996) What are the functional consequences of neurocognitive deficits in schizophrenia? American Journal of Psychiatry , 153, 321330.

, Marshall, B. D., Jr., Wirshing, W. C., et al (1997) Doesrisperidone improve verbal working memory in treatment-resistant schizophrenia? American Journal of Psychiatry , 154,799804.

Hawkins, K. A., Mohamed, S. & Woods, S. W. (1999) Will thenovel antipsychotics significantly ameliorate neuropsycho-logical deficits and improve adaptive functioning inschizophrenia. Psychological Medicine, 29, 18.

Heinrichs, R. W. & Awad, A. G. (1993) Neurocognitivesubtypes of chronic schizophrenia. Schizophrenia Research,9, 4958.

& Zakzanis, K. K. (1998) Neurocognitive deficit inschizophrenia: A quantitative review of the evidence.Neuropsychology, 12, 426445.

Jones, P., Rodg er s, B. , Murr ay, R. , et al (1994) Childdevelopment risk factors for adult schizophrenia in theBritish 1946 birth cohort. Lancet, 344 , 13981402.

Kraepelin, E. (1919) Dementia Praecox and Paraphrenia .Reprinted 1971, Huntingdon, NY: Robert E. KriegerPublishing.

Liddle, P. F. & Morris, D. L. (1991) Schizophrenic syndromesand frontal lobe performance. British Journal of Psychiatry,158, 340345.

McCreadie, R. G., Latha, S., Thara, R., et al (1997) Poor memory,negative symptoms and abnormal movements in never-treatedIndian patients with schizophrenia. British Journal of Psychiatry , 171, 360363.

McKenna, P. J. (1991) Memory, knowledge and delusions. British Journal of Psychi atry , 159 (suppl. 14), 36-41.

Meehl, P. E. (1990) Toward an integrated theory of schizotaxia, schizotypy and schiozphrenia. Journal of Personality Disorders , 4, 199.

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Rund, B. R. (1998) A review of longitudinal studies of cognitive functions in schizophrenia patients. SchizophreniaBulletin, 24, 425435.

Box 2. Errorless learning

Patients with memory problems appear tohave a particular difficulty distinguishingbetween errors and correct responsesmade during learning

Training using errorless learning principlesinvolves preventing patients from makingany mistakes during learning

This is achieved by starting with very easytasks, and very gradually increasing thedifficulty level

Preliminary results suggest that memory-impaired patients with schizophreniamay benefit from this type of approachas part of a comprehensive package ofcognitive rehabilitation


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MCQ answers

1 2 3 4 5a T a T a F a F a Tb T b T b F b F b Tc T c F c F c T c Td F d F d T d T d Fe F e F e F e T e T

Saykin, A. J., Shtasel, D. L., Gur, R. E., et al (1994) Neuro-psychological deficits in neuroleptic naive patients withfirst-episode schizophrenia. Archives of General Psychiatry ,51 , 124131.

Shallice, T., Burgess, P. W. & Frith, C. D. (1991) Can theneuropsychological case-study approach be applied toschizophrenia? Psychological Medicine, 21, 661673.

Sharma, T. (1999) Cognitive effects of conventional andatypical antipsychotics in schizophrenia. British Journal of Psychiatry , 174 (suppl. 38), 44 51.

Velligan, D. I., Mahurin, R. K., Diamond, P. L., et al (1997) Thefunctional significance of symptomatology and cognitivefunction in schizophrenia. Schizophrenia Research, 25, 2131 .

Weinberger, D. R., Berman, K. F. & Zec, R. (1986) Physio-logical dysfunction of dorsolateral prefrontal cortex inschizophrenia. I. Regional cerebral blood flow evidence. Archives of General Psychia try, 43, 114124.

Wykes, T., Reeder, C., Corner, J., et al (1999) The effects of neurocognitive remediation on executive processing inpatients with schizophrenia. Schizophrenia Bulletin, 25 ,29 1307.

Multiple choice questions

1. Cognitive impairment in schizophrenia is:a consistent with the neurodevelopmental

theory of schizophrenia b present in drug-na ve patientsc present in the majority of patients with

schizophreniad clearly related to specific symptomse is only found in chronic elderly patients.

2. Studies of people before they developed schizo-phrenia generally show:a significant impairment of intelligence

b cognitive deficits present by the age of eightyears

c no obvious cognitive abnormalitiesd that the cognitive impairment clearly causes

schizophreniae a reliable cognitive marker for subsequent

development of schizophrenia.

3. Measures of cognitive impairment in schizo-phrenia:a show no relationship with functional

outcome b have been shown to be clearly related to

brain dopamine levels

c always improve in tandem withsymptomatic improvement

d are related to interpersonal problem-solvingdeficits

e are consistently and reliably improved withtreatment with atypical neuroleptics.

4. Cognitive rehabilitation in schizophrenia:a is always effective b has been conclusively shown to produce

lasting, generalised improvements thatimpact on day-to-day functioning

c has not been thoroughly evaluated in asufficient number of well-controlled studies

d has been shown to produce some promisingresults

e requires further evaluation using appropriatecontrol conditions and dependent measuresthat differ sufficiently from the trainingmaterials.

5. Patients with schizophrenia:a may show no cognitive decline following

illness onset b often have marked impairment covering a

variety of cognitive domainsc often have particular verbal memory

impairmentd always have a characteristic neuropsycho-

logical signature e often show a pre-existing cognitive

impairment which can be exacerbated withanticholinergic medication.

jurnal inggris8

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