Division of Neuroscience and Mental Health, Imperial College and Institute of Neurology, London
Department of Psychology, University of Sussex
Division of Neuroscience and Mental Health, Imperial College London,UK
Correspondence: Dr Eileen Joyce, Institute of Neurology, University College London, Box 19, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. E-mail: e.joyce{at}ion.ucl.ac.uk
Declaration of interest None. Funding detailed in Acknowledgements.
![]() |
ABSTRACT |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Aims To determine whether such heterogeneityis present at illness onset and any relationship to clinical variables.
Method Ninety-three community patients with first-episode schizophrenia and 50 healthy volunteers were assessed for premorbid (Revised National Adult ReadingTest) and current IQ, memory and executive function.
Results Half of those with schizophrenia had preserved IQ in the normal range but there was evidence of a specific impairment in spatial working memory even in those with high/average IQ; 37 out of 93 (40%) had generalised cognitive decline. Those with low premorbid IQ were significantly younger atillness onset. For the entire group, age at onset correlated positively with premorbid but not current IQ.
Conclusions At illness onset, cognitive heterogeneityis present in people with schizophrenia, with a high proportion having undergone general cognitive decline. However, working memory impairment may be a common feature. Lower premorbid IQ is a risk factor for an earlier onset.
![]() |
INTRODUCTION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
METHOD |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Clinical assessments
Patients were assessed with the Scales for the Assessment of Positive and
Negative Symptoms (SAPS; Andreasen,
1983; SANS; Andreasen,
1981). Scores for the three symptom-derived syndromes of
schizophrenia (positive, negative and disorganisation;
Liddle & Barnes, 1990) were calculated for each patient (Table
1). The date at onset of positive psychotic symptoms was
established using a modified questionnaire
(Lieberman et al,
1993; Barnes et al,
2000).
|
Neuropsychological assessments
These were performed when the patients were clinically stable at a time
when they were able to tolerate the testing procedures. This was within 4
weeks of the initial clinical assessment for 68 (72%), within 8 weeks for 85
(91%) and within 20 weeks for 92 (99%) (one patient was tested at 41 weeks).
Premorbid IQ was estimated using the Revised National Adult Reading Test
(NART), which measures reading ability by scoring the pronunciation of 50
irregular words (Nelson & Willison,
1991). Numerous studies have substantiated the use of the NART in
healthy volunteers and in people with a variety of neuropsychiatric disorders
where cognitive decline is suspected
(Nelson & OConnell,
1978; OCarroll,
1987,
1995; Crawford et al,
1989,
2001). Studies have found the
NART is also a valid measure of premorbid IQ in schizophrenia
(Crawford et al,
1992; OCarroll et
al, 1992) and that it is stable over time in this population
(Smith et al, 1998;
Morrison et al,
2000). Current IQ was calculated from four sub-tests of the
Wechsler Adult Intelligence Scale Revised (WAISR) or
WAISIII, which have been shown to provide a reliable measure of
full-scale IQ in schizophrenia (Missar
et al, 1994; Blyler
et al, 2000). During the course of the study, the short
forms of the tests were changed in order to save testing time without
compromising accuracy (Kaufman,
1990) and to accommodate the introduction of the WAISIII.
Subsidiary analyses showed that subgroup allocation of patients and controls
based on current IQ was not a reflection of the short-form tests used.
Memory and executive function tests were taken from the Cambridge Automated Neuropsychological Test Battery (CANTAB; Sahakian & Owen, 1992). These were: (a) spatial short-term memory (spatial span; Owen et al, 1990); (b) episodic memory (pattern recognition memory; Sahakian et al, 1988); (c) spatial working memory (Owen et al, 1990), which measures the ability to remember the location of previously retrieved tokens while searching up to eight boxes for a new token (an error occurs when a participant returns to open a box in which a token has already been found); (d) spatial working memory strategy, measured as the number of times search trials begin with the same box; (e) planning (Owen et al, 1990), a task based on the Tower of London (Shallice, 1982), which measures the ability to plan and execute a sequence of moves for problems requiring a minimum of 2, 3, 4 or 5 moves; and (f) attentional set-shifting (Owen et al, 1991), which has some similarity to the Wisconsin Card Sorting Test, and in which participants are required to learn a series of visual discriminations in which one of two stimulus dimensions (shape or line) is correct; they are also required to deduce and reverse rules governing correct responding.
Analysis
Data were analysed using the Statistical Package for the Social Sciences
version 10 (SPSS, 1999). For
ordinal data, group comparisons were performed using the t-test or
analysis of variance (ANOVA). Post hoc comparisons were performed
using least squares difference and correlations using Pearsons test.
Nominal data were analysed using the 2-test.
![]() |
RESULTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Premorbid and current IQ
The range of NART IQ was 73122 for controls and 75122 for
patients. For full-scale IQ, these values were 70132 and 72147,
respectively. Paired t-tests between NART and full-scale IQ showed
that these scores differed for patients (t (92)=5.31,
P<0.001) but not for controls (t (49)=0.89,
P=0.38). Examination of the distribution of the scores showed that
there was a downward shift of full-scale IQ compared with NART IQ in the
patients, indicating a decline in IQ from premorbid levels.
IQ subgroups
To determine whether the decline in IQ pertained to all or a subgroup of
patients, we followed the methodology of Weickert et al
(2000) to derive the following
groups: (a) normal and preserved IQ (PIQ), defined as a NART IQ of 90 or more
and a NART-full-scale IQ difference within 10 points; (b)
deteriorated IQ (DIQ), defined as a NART IQ of 90 or more and a
NART-full-scale IQ difference of more than 10 points; (c) premorbid low IQ
(LIQ), defined as a NART IQ and full-scale IQ of less than 90. For
five patients, the NART IQ was lower than the full-scale IQ by more than 10
points and these people were placed in the PIQ category.
Table 1 shows the NART IQ and
full-scale IQ values of the subgroups and relevant statistical comparisons
with the control group. Post hoc comparisons revealed that the NART
IQ values of the PIQ and DIQ groups were similar to those of the control group
whereas the NART IQ of the LIQ group was significantly lower than that of all
other groups (least squares difference: all P<0.001). The
full-scale IQ values of the control and PIQ groups were similar. The
full-scale IQ of the DIQ group had fallen to the same level as the LIQ group
and both were significantly lower than the PIQ group and controls (least
squares difference: both P<0.001). To check the validity of the
NART as a measure of premorbid IQ in those with schizophrenia, the control
group was subjected to the same subgroup analysis. For five controls, NART IQ
was lower than full-scale IQ by greater than 10 points and these were placed
in the PIQ category. The allocation of participants to these categories was
different for patient and control groups (2(2)=8.90,
P=0.012) indicating that more patients than controls fell into the
DIQ category (controls: declined 16%, preserved 74%, low 10% v.
patients: declined 40%, preserved 50%, low 10%).
Comparisons of patients within each group revealed no significant
differences in syndrome scores, gender ratio (see
Table 1), medication status
(2(4)=4.29, NS) or duration of untreated psychosis (F
(2,92)=1.06, NS). The mean ages of the PIQ and DIQ groups were similar to that
of the controls. The LIQ group was significantly younger than the other groups
with respect to age at testing and age at onset of psychosis
(Table 1; least squares
difference: all P<0.05).
Age and IQ
To further investigate the impact of age on the IQ, Pearson correlation
coefficients were calculated between NART full-scale IQ and age at testing in
patients and controls (see Fig.
1). There were no significant correlations with age in controls
(full-scale IQ: r=0.22, P=0.13; NART:
r=0.10, P=0.51). For patients, age correlated significantly
with NART IQ (r=0.37, P<0.001) but not full-scale IQ
(r=0.16, P=0.12). The significant relationship for the
patients between age and NART also held for age at onset of psychosis
(r=0.38, P<0.001), indicating that patients with a lower
IQ had a younger age at onset. This correlation remained significant when the
group with low premorbid IQ was excluded (r=0.29,
P<0.01).
|
|
These results indicate that a substantial subgroup of patients can have neuropsychological function within the normal range at illness onset whereas another has undergone a general intellectual decline. To examine whether specific cognitive impairments are present independently of IQ, we compared cognitive performance in patients and controls with a high/average IQ, defined as a current IQ of 100 or more, closely matched for age, premorbid and current IQ (Table 3). The patients showed a specific impairment in spatial working memory errors.
|
![]() |
DISCUSSION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Intellectual decline in schizophrenia
We confirmed that it is possible for people with a low current IQ to have
had a normal IQ prior to the onset of schizophrenia (e.g.
Nelson et al, 1990;
Goldberg et al, 1993;
Weickert et al, 2000; Kremen et al, 2001).
Our patients who demonstrated a decline in IQ also showed considerable
impairment on tests of memory and executive function. The difference between
this subgroup and those with no evidence of reduced IQ could not be explained
by more severe psychotic symptoms or by the type of antipsychotic medication.
Almost half (46%) of this subgroup had become psychotic during the 12 months
preceding presentation and the duration of untreated psychosis did not differ
between this group and those with normal preserved IQ. This suggests that
deterioration in IQ from normal levels is not attributable to a longer course
of illness. Thus, in a substantial number of our patients, global
deterioration in intellectual function appears to have occurred as an early
manifestation of the illness.
The finding at first presentation of deterioration in IQ from normal premorbid levels suggests that individuals can be on a normal cognitive trajectory during development. Studies of army conscripts, in which direct measures of premorbid IQ were obtained, found that low IQ is a prominent feature in adults prior to the onset of psychosis (David et al, 1997; Davidson et al, 1999) and that intellectual underperformance is greatest in those nearest the onset of psychosis (Rabinowitz et al, 2000; Gunnell et al, 2002). This suggests that cognitive function is declining during the years immediately preceding the onset of psychosis. Fuller et al (2002), in a longitudinal assessment of premorbid cognitive functioning in people who went on to develop schizophrenia, found that scholastic aptitude actually increased between the ages of 9 and 13 years, prior to a precipitous decline over the following 4 years. Kremen et al (1998) found evidence of a decline in IQ even earlier in childhood, between the ages of 4 and 7 years, in those who subsequently developed psychotic symptoms as adults. In accordance with previous studies (Jones et al, 1994), these researchers found that low IQ per se at the age of 7 years predicted subsequent psychosis. However, a prior decline in IQ, whether from normal or low values, was a stronger predictor. Taken together, these data suggest that individuals destined to develop schizophrenia can undergo deterioration in IQ at various stages during childhood, adolescence and early adulthood. The influences bringing about these changes at different ages are yet to be determined but they may be different for each age level, consistent with the hypothesis that there are several types of morbid process operating at different times during development (e.g. Keshavan, 1999). Whether the timing of this decline has implications for different outcomes also remains to be determined.
In our study, the proportion of patients with pre-existing low IQ may be underrepresented. Weickert et al (2000) found that a quarter of their patients had a low premorbid IQ, compared with a tenth in our study. Although we assessed a large group with schizophrenia, they were self-selecting and it is possible that more patients with lower rather than higher IQ declined to take part in our study. Other studies find that low IQ is overrepresented as far back as childhood in those destined to develop schizophrenia (e.g. Erlenmeyer-Kimling et al, 1991; Ambelas, 1992; Jones et al, 1994), suggesting that low premorbid IQ is a risk factor for the development of schizophrenia or even part of the disorder itself (Jones et al, 1994; Russell et al, 1997). Our data support the view that low IQ is a risk factor for an earlier age at onset of schizophrenia. Those with a low premorbid IQ had a younger age at onset compared with the other two groups, suggesting that IQ development was curtailed by the onset of psychosis, as has been demonstrated in those with childhood-onset childhood-onset psychosis (Bedwell et al, 1999). It is also possible that their low IQ contributed to an earlier age at onset, as concluded by previous investigators (e.g. Erlenmeyer-Kimling & Cornblatt, 1987; Grimes & Walker, 1994). The finding of a significant positive association between premorbid IQ and age at onset for all patients, even when those with low IQ were removed from the analysis, favours the latter explanation. A continuous relationship between IQ and risk of schizophrenia has also been shown in studies with direct premorbid measures of intellectual function (Jones et al, 1994; David et al, 1997).
One limitation of this study is the use of an indirect measure of premorbid IQ. The use of the NART in schizophrenia has been criticised on the grounds that the disorder itself may cause an impairment in verbal ability and thus results in an underestimation of IQ. Against this are studies which have found that a measure of current vocabulary approximates direct measures of premorbid IQ (Russell et al, 2002; Eberhard et al, 2003). Another criticism of the NART is that it can overestimate IQ in the low IQ range and in schizophrenia this may give a spurious impression of IQ decline (Russell et al, 2002). However, this cannot explain our findings because we applied the same analysis to a matched control group and significantly fewer of these showed evidence of IQ decline. Nevertheless 16% of healthy volunteers could be classified as having intellectual decline using this methodology, suggesting that care should be taken in categorising individuals in this way without taking other indices of premorbid function into consideration (Crawford et al, 1990; Russell et al, 2002).
Core cognitive impairments in first-episode schizophrenia
Half of our patients with first-episode schizophrenia had no evidence of
deterioration in IQ, and their performance on a range of memory and executive
tests was no different from controls. Studies of people with chronic
schizophrenia have also found evidence for intact cognition in a subgroup
(Heinrichs & Awad, 1993; Palmer et al, 1997),
suggesting that cognitive impairment might not be a core feature of
schizophrenia. However, Kremen et al
(2001) suggest that even in
patients with high IQ, evidence of neuropsychological impairment can be found.
Indeed, when we closely matched subgroups of controls and patients with
high/average premorbid and current IQ, we found that the patients exhibited a
particular impairment of executive function, indicated by an increased number
of spatial working memory errors. Weickert et al
(2000) also found that their
subgroup with preserved IQ displayed subtle impairments in executive function
and this is in turn consistent with studies finding empirically derived
subgroups with preserved general cognitive function and mild executive
impairment (Heinrichs & Awad,
1993; Goldstein &
Shermansky, 1995). Thus, there is accumulating evidence that
executive dysfunction is a pervasive abnormality, intrinsic to schizophrenia,
which is not accounted for by illness chronicity, antipsychotic treatment or
antipsychotic type.
Working memory as a marker of cognitive impairment at first episode
In previous studies of cognitive heterogeneity the most consistent
indicator of executive dysfunction has been impaired performance on the
Wisconsin Card Sorting Test. This is a complex task subsuming several
executive processes, including working memory, planning and response
inhibition. We examined each of these processes separately and found that
patients with high/average preserved IQ at first episode of schizophrenia show
a specific impairment in working memory. Our spatial working memory task
measures the ability to remember the location of a number of tokens previously
retrieved while searching for new tokens. This suggests that a disturbance of
executive function, of the type required to hold information in memory while
performing other cognitive operations, is present in all patients independent
of IQ. In a recent family study there was a doseresponse relationship
between the degree of spatial working memory impairment and increasing genetic
predisposition to schizophrenia, suggesting that impaired spatial working
memory may constitute an effective endophenotype of the disorder
(Glahn et al, 2003).
It has recently been argued that increased antisaccade errors, which are also
considered to be a promising endophenotype for schizophrenia, reflect a more
fundamental deficit in spatial working memory processes
(Hutton et al, 2004).
Thus, in our patients presenting for the first time with schizophrenia, the
spatial working memory deficit, which permeated all cognitive subgroups, may
represent such a genetic marker.
![]() |
Clinical Implications and Limitations |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
LIMITATIONS
![]() |
ACKNOWLEDGMENTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
REFERENCES |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Ambelas, A. (1992) Preschizophrenics: adding to the evidence, sharpening the focus. British Journal of Psychiatry, 160, 401 -404.[Medline]
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSMIV) . Washington, DC: APA.
Andreasen, N. (1981) Scale for the Assessment of Negative Symptoms (SANS). Iowa City, IA: University of Iowa.
Andreasen, N. (1983) Scale for the Assessment of Positive Symptoms (SAPS). Iowa City, IA: University of Iowa.
Barnes, T. R. E., Hutton, S. B., Chapman, M. J., et al
(2000) West London first-episode study of schizophrenia:
Clinical correlates of duration of untreated psychosis. British
Journal of Psychiatry, 177, 207
-211.
Bedwell, J., Keller, B., Smith, A., et al
(1999) Why does post-psychotic IQ decline in childhood-onset
schizophrenia. American Journal of Psychiatry,
156, 1996
-1997.
Blyler, C. R., Gold, J. M., Iannone, V. N., et al (2000) Short form of the WAISIII for use with patients with schizophrenia. Schizophrenia Research, 46, 209 -215.[CrossRef][Medline]
Crawford, J., Parker, D., Stewart, L., et al (1989) Prediction of WAIS IQ with the National Adult Reading Test; cross validation and extension. British Journal of Clinical Psychology, 28, 267 -273.
Crawford, J. R., Allan, K. M., Cochrane, R. H. B., et al (1990) Assessing the validity of using NART-estimated pre-morbid IQs in the individual case. British Journal of Clinical Psychology, 29, 435 -436.[Medline]
Crawford, J. R., Besson, J. A., Bremner, M., et al (1992) Estimation of premorbid intelligence in schizophrenia. British Journal of Psychiatry, 161, 69-74.[Abstract]
Crawford, J. R., Deary, I. J., Starr, J., et al (2001) The NART as an index of prior intellectual functioning: a retrospective validity study covering a 66 year interval. Psychological Medicine, 31, 451 -458.[Medline]
David, A., Malmberg, A., Brandt, L., et al (1997) IQ and risk for schizophrenia. A population based cohort study. Psychological Medicine, 27, 131 -132.[CrossRef][Medline]
Davidson, M., Reichenberg, A., Rabinowitz, J., et al
(1999) Behavioural and intellectual markers for schizophrenia
in apparently healthy male adolescents. American Journal of
Psychiatry, 156, 1328
-1335.
Eberhard, J., Riley, F. & Levander, S. (2003) Premorbid IQ and schizophrenia. Increasing cognitive reduction by episodes. European Archives of Psychiatry and Clinical Neuroscience, 253, 84 -88.[Medline]
Erlenmeyer-Kimling, L. & Cornblatt, B. (1987) The New York high-risk project. A follow-up report. Schizophrenia Bulletin, 13, 451 -461.[Medline]
Erlenmeyer-Kimling, L., Rock, D., Squires-Wheeler, E., et al (1991) Early life precursors of psychiatric outcomes in adulthood in subjects at risk for schizophrenia or affective disorders. Psychiatry Research, 39, 239 -256.[CrossRef][Medline]
Fuller, R., Nopoulos, P., Arndt, S., et al (2002) Longitudinal assessment of pre-morbid cognitive functioning in patients with schizophrenia through examination of standardised scholastic test performance. American Journal of Psychiatry, 158, 183 -189.
Glahn, D., Therman, S., Manninen, M., et al (2003) Spatial working memory as an endophenotype for schizophrenia. Biological Psychiatry, 53, 624 -626.[CrossRef][Medline]
Gold, J. M., Goldberg, R. W., McNary, S.W., et al
(2002) Cognitive correlates of job tenure among patients with
severe mental illness. American Journal of Psychiatry,
159, 1395
-1402.
Goldberg, T., Hyde, T., Kleinman, J., et al (1993) Course of schizophrenia: neuropsychological evidence for a static encephalopathy. Schizophrenia Bulletin, 19, 797 -804.[Medline]
Goldstein, G. & Shermansky,W. (1995) Influences on cognitive heterogeneity in schizophrenia. Schizophrenia Research, 18, 59-60.[CrossRef][Medline]
Grimes, K. & Walker, E. (1994) Childhood emotional expression, educational attainment and age of onset of illness in schizophrenia. Journal of Abnormal Psychology, 103, 784 -790.[CrossRef][Medline]
Gunnell, D., Harrison, G., Rasmussen, E., et al
(2002) Associations between premorbid intellectual
performance, early-life exposures and early-onset schizophrenia. Cohort study.
British Journal of Psychiatry,
181, 298
-305.
Heinrichs, R. & Awad, A. (1993) Neurocognitive subtypes of chronic schizophrenia. Schizophrenia Research, 9, 49 -58.[CrossRef][Medline]
Hill, S., Ragland, J., Gur, R. (2002) Neuropsychological profiles delineate distinct profiles of schizophrenia, an interaction between memory, executive function and uneven distribution of clinical subtypes. Journal of Clinical and Experimental Neuropsychology, 24, 765 -780.
Hutton, S. H., Puri, B. K., Duncan, L.-J., et al (1998) Executive function in first episode schizophrenia. Psychological Medicine, 28, 463 -473.[CrossRef][Medline]
Hutton, S. B., Huddy,V., Barnes, T. R. E., et al (2004) The relationship between antisaccades, smooth pursuit and executive dysfunction in first episode schizophrenia. Biological Psychiatry, 56, 553 -559.[CrossRef][Medline]
Jones, P., Murray, R., Rodgers, B., et al (1994) Child developmental risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet, 344, 1398 -1402.[CrossRef][Medline]
Kaufman, A. (1990) Assessing Adolescent and Adult Intelligence. Boston, MA: Allyn and Bacon.
Keshavan, M. (1999) Development, disease and degeneration in schizophrenia: a unitary pathophysiological model. Journal of Psychiatric Research, 33, 513 -521.[CrossRef][Medline]
Kremen,W. S., Buka, S., Seidman, L. J., et al
(1998) IQ decline during childhood and adult psychotic
symptoms in a community sample: a 19-year longitudinal study.
American Journal of Psychiatry,
155, 672
-677.
Kremen,W. S., Seidman, L. J., Faraone, S.V., et al (2001) Intelligence quotient and neuropsychological profiles in patients with schizophrenia and in normal volunteers. Biological Psychiatry, 50, 453 -462.[CrossRef][Medline]
Liddle, P. F. & Barnes, T. R. (1990) Syndromes of chronic schizophrenia. British Journal of Psychiatry, 157, 558 -561.[Medline]
Lieberman, J., Jody, D., Geisler, S., et al (1993) Time course and biological correlates of treatment response to first episode schizophrenia. Archives of General Psychiatry, 50, 369 -376.[Abstract]
Missar, C., Gold, J., Goldberg, T. (1994) WAISR short forms in chronic schizophrenia. Schizophrenia Research, 12, 247 -250.[CrossRef][Medline]
Morrison, G., Sharkey,V., Allardyce, J., et al (2000) Nithsdale Schizophrenia Surveys: a longitudinal study of National Adult Reading Test stability. Psychological Medicine, 30, 717 -720.[CrossRef][Medline]
Nelson, H. & OConnell, A. (1978) Dementia: the estimation of pre-morbid intelligence levels using the new adult reading test. Cortex, 14, 234 -244.[Medline]
Nelson, H. & Willison, J. (1991) The Revised National Adult Reading Test (NART) Test Manual (2nd edn) . Windsor: NFERNelson.
Nelson, H., Pantelis, C., Carruthers, K., et al (1990) Cognitive functioning and symptomology in chronic schizophrenia. Psychological Medicine, 20, 357 -365.[Medline]
OCarroll, R. (1987) The inter-rater reliability of the National Adult Reading Test (NART). A pilot study. British Journal of Clinical Psychology, 26, 229 -230.[Medline]
OCarroll, R. (1995) The assessment of pre-morbid ability. A critical review. Neurocase, 1, 83-89.[CrossRef]
OCarroll, R.,Walker, M., Dunan, J., et al (1992) Selecting controls for schizophrenia research studies: the use of the National Adult Reading Test (NART) as a measure of pre-morbid ability. Schizophrenia Research, 8, 137-141.[CrossRef][Medline]
Owen, A., Downes, J., Sahakian, B., et al (1990) Planning and spatial working memory following frontal lobe lesions in man. Neuropsychologia, 28, 1021 -1034.[CrossRef][Medline]
Owen, A. M., Roberts, A. C., Polkey, C. E., et al (1991) Extra-dimensional versus intra-dimensional set shifting performance following frontal lobe excisions, temporal lobe excisions or amygdalo-hippocampectomy in man. Neuropsychologia, 29, 993 -1006.[CrossRef][Medline]
Palmer, B., Heaton, R., Paulsen, J., et al (1997) Is it possible to be schizophrenic yet neuropsychologically normal? Neuropsychology, 11, 437 -446.[CrossRef][Medline]
Rabinowitz, J., Reichenberg, A.,Weiser, M., et al
(2000) Cognitive and behavioural functioning in men with
schizophrenia both before and shortly after first admission to hospital.
Cross-sectional analysis. British Journal of
Psychiatry, 177, 26
-32.
Russell, A., Munro, J., Jones, P., et al (1997) Schizophrenia and the myth of intellectual decline. American Journal of Psychiatry, 154, 635 -639.[Abstract]
Russell, A. J., Munro, J., Jones, P. B., et al (2002) The National Adult Reading Test as a measure of premorbid IQ in schizophrenia. British Journal of Clinical Psychology, 39, 297 -305.[CrossRef]
Sahakian, B. & Owen, A. (1992) Computerised assessment in neuropsychiatry using CANTAB. Journal of the Royal Society of Medicine, 85, 399 -402.[Medline]
Sahakian, B., Morris, R., Evenden, J., et al (1988) A comparative study of visuospatial memory and learning in Alzheimer-type dementia and Parkinsons disease. Brain, 111, 695 -718.[Abstract]
Shallice, T. (1982) Specific impairments of planning. Philosophical Transactions of the Royal Society of London Series B: Biological Sciences, 298, 199 -209.
Smith, D., Roberts, S., Brewer,W., et al (1998) Testretest reliability of the National Adult Reading Test as an estimate of pre-morbid IQ in patients with schizophrenia. Cognitive Neuropsychiatry, 3, 71-80.[CrossRef]
SPSS (1999) SPSS for Windows, Release 10. Chicago, IL: SPSS.
Weickert, T., Goldberg, T., Gold, J., et al
(2000) Cognitive impairment in patients with schizophrenia
displaying preserved and compromised intellect. Archives of General
Psychiatry, 57, 907
-913.
Received for publication November 28, 2003. Revision received March 17, 2005. Accepted for publication March 24, 2005.
Related articles in BJP: