Acta Psychiatr Scand 2006: 113: 350–359 Copyright
2005 Blackwell Munksgaard

All rights reserved ACTA PSYCHIATRICA

DOI: 10.1111/j.1600-0447.2005.00626.x
SCANDINAVICA

Neuropsychological test profiles in

schizophrenia and non-psychotic depression
Rund BR, Sundet K, Asbjørnsen A, Egeland J, Landrø NI, Lund A, B. R. Rund1, K. Sundet1,
Roness A, Stordal KI, Hugdahl K. Neuropsychological test profiles in A. Asbjørnsen2, J. Egeland1,
schizophrenia and non-psychotic depression. N. I. Landrø1, A. Lund3, A. Roness3,
K. I. Stordal3, K. Hugdahl4
Objective: The study examined to what degree schizophrenia is 1
Department of Psychology, University of Oslo, Oslo and
characterized by a neuropsychological (NP) test profile specific in Departments of 2Psychosocial Sciences, 3Psychiatry and
shape and level compared with depression and normal functioning. 4
Biological and Medical Psychology, University of
Method: Fifty-three patients with schizophrenia, 45 with non- Bergen, Bergen, Norway
psychotic depression, and 50 normals were assessed with a
comprehensive NP test battery and clinical instruments. NP test scores
were factor analyzed into seven composite scores.
Results: Schizophrenia patients performed significantly below normals
across all seven composite scores, whereas depression patients were
impaired in two. Verbal memory was most impaired. Sixty-two percent
of schizophrenia patients were moderately or severely impaired, the
corresponding figure for depression was 28%. Impairment was Key words: schizophrenia; depression; cognition;
moderately associated with IQ level and clinical symptom load in neuropsychology; intelligence; symptoms
schizophrenia, but not in depression. Bjørn Rishovd Rund, Department of Psychology, PO Box
Conclusion: Schizophrenia is characterized by deficits across a wide 1094 Blindern, University of Oslo, N-0317 Oslo, Norway.
range of NP functions. Thirty-eight percent of the patients are within E-mail: b.r.rund@psykologi.uio.no
normal limits. A mild and limited NP disturbance is apparent in
depression. Accepted for publication July 19, 2005

Significant outcomes
• Patients with schizophrenia showed selective impairments in all four higher order neurocognitive
domains, while the depressed patients evidenced impairment only on measures of processing speed.
• Neurocognitive function constitutes a core trait in schizophrenia as impairments are not fully
explained by symptom load or level of intelligence.
• Subgroups within each diagnostic entity is suggested as nearly two of five patients with schizophrenia
and three of four patients with depression did not show significant neuropsychological (NP)
impairments.

Limitations
• We did not have an adequate control over medication effects.
• Possible different discriminating power of the various NP tasks represents a psychometric limitation.
• Exploratory data analysis may have inflated the chance of type I error.

deficits on a wide range of neuropsychological (NP)

Introduction
tasks compared with normal controls (1, 2). It is also
Studies of neurocognitive function in patients with a common finding that a substantial proportion of
schizophrenia have consistently reported pervasive patients perform within the normal range (3).

350

In order to draw firm conclusions regarding the
magnitude and specificity of cognitive dysfunction
in schizophrenia, this group should be compared
with other psychiatric control groups (4, 5). One
highly relevant comparison group is patients with
recurrent unipolar major depression. Several stud-
ies have reported that this group also shows
cognitive impairment (6–8), and there is empirical
evidence that some of the same brain areas, i.e.
temporal lobe areas and the hippocampus, are
affected in schizophrenia and the recurrent type of
depressive disorder (9–11).
To identify deficits that discriminate between the
two groups of patients, a wide range of cognitive
functions have to be assessed. By analyzing differ-
ences in test profiles rather than measures of
separate functions, it is possible to identify func-
tions that are jointly impaired from those that are
uniquely affected for each diagnostic group. We
have previously presented results on single tests
(12–15). The present study expands the analysis
across all cognitive domains and takes into con-
sideration demographic confounders. Thus, the
first question addressed in the present study was to
what degree patients with schizophrenia present a
specific NP profile, i.e. whether the impairment
varies not only in level but also in type from that of
patients with recurrent depression.
In all but two studies (16, 17) patients with
schizophrenia have been compared with psychotic
or mixed groups of psychotic and non-psychotic
depression. Findings from these two studies, as
well as from comparisons of psychotic and non-
psychotic depression patients (18, 19), provide
support for the conclusion that psychotic depres-
sion is a distinct diagnostic category different
from non-psychotic depression. By comparing
schizophrenia patients with non-psychotic depres-
sion patients we contribute to the understanding
of which aspects of cognition is uniquely impaired
in depression. This was the second aim of the
study.
Our next objective was to analyze how variation
in IQ is associated with NP test performance. A
large body of research shows that low premorbid
IQ increases the risk for developing schizophrenia
(20). To what degree IQ level changes in parallel
with manifestation of schizophrenia symptoms is
still debated (21). Further, little is known about
how patterns of NP function differ at various
levels of current IQ in schizophrenia (22). Weick-
ert et al. (23) and Kremen et al. (22) found that
also patients with normal IQ manifested substan-
tial cognitive deficits. We wanted to replicate their
analyses of how current IQ-level affects NP
performance in schizophrenia and thus shed light
Neuropsychological test profiles
on the question of whether or not neurocognitive
dysfunction is a universal feature of schizophre-
nia.
The last aim of the study was to examine the
relationship between NP impairment and symptom
load. Some studies have found a correlation
between cognitive deficits and negative symptoms
(24–27), while others have not found such an
association (28–30), suggesting that the two
domains are relatively independent. We addressed
this question by investigating to what degree
clinical symptoms influence NP deficits within the
schizophrenia and depression groups separately.
Aims of the study
Four questions were addressed. The first was to
what degree patients with schizophrenia present a
specific NP profile. The second was to enhance our
understanding of how depression per se, free from
psychosis, has a negative effect on neurocognitive
performance. The third was whether variation in
IQ is associated with NP test performance in these
groups. The fourth was whether degree of NP
impairment correlates with clinical symptom load.
Material and methods
The study was approved by the Regional Com-
mittee for Medical Research Ethics.
Participants
Patients were recruited for research purposes from
four clinics in Norway covering two catchment
areas. Fifty-three patients who met the DSM-IV
criteria (31) for schizophrenia (38 in-patients), 50
patients with a major depressive disorder, recurrent
type (296.3) (34 in-patients), and 50 healthy control
subjects invited to participate from newspaper and
community advertisements and recruited from the
same area as the patients, were included. The
Structured Clinical Interview for DSM-IV Axis I
Disorders (32) was used for diagnostic assessment.
Five senior psychiatrists conducted the interviews.
Consensus was reached for selected cases by
clinical discussion and no diagnostic disagreement
occurred. The schizophrenic sample had the
following subdiagnoses: 43 paranoid, three
disorganized, one catatonic, two residual, four
undifferentiated.
Individuals with a history of hypomanic epi-
sodes were excluded from the depression group.
Number of depressive episodes ranged from two
to five. Five of the depression patients were
psychotic at the time of assessment and were
351
Rund et al.

excluded from the present analyses. Thus, the
total number of patients with recurrent major
depression was 45.
Psychiatric ratings included the Extended Brief
Psychiatric Rating Scale (BPRS) (33), the Global
Assessment of Functioning (GAF) Scale (31),
Hamilton Rating Scale for Depression (HRSD)
(34), and the Positive and Negative Syndrome
Scale (PANSS) (35). Inter-rater reliability was
calculated based on five cases. Average intra-class
correlations were over 0.80 for all rating scales. All
patients with depression had a minimum score of
18 on HRSD at the time of testing, indicating that
they were above the cut-off score for moderate
depression. Four of the schizophrenics did not use
antipsychotic medication. Eleven patients used
typical antipsychotics, 36 atypical antipsychotics,
and two patients both. Three participants with
schizophrenia were using drugs with known anti-
cholinergic effect, and three patients were taking
benzodiazepines.
All but six of the depressed patients were
medicated at the time of NP testing. Thirty-six
patients were using antidepressants (selective sero-
tonin reuptake inhibitor, mianserin, nefazodone,
venlafaxine or moclobemide), and none were on
tricyclic antidepressants. As additional medication,
19 patients were taking benzodiazepines and nine
antipsychotic medication (as a hypnotic). Informa-
tion regarding medication was missing for three
patients.
All participants were Norwegian-speaking adults
between 19 and 51 years old with normal vision
and hearing. Exclusion criteria were: i) history of
head trauma, neurologic disorder or developmen-
tal dysfunction, ii) alcohol or substance abuse, iii)
medical disease likely to affect nervous system
function. Control participants had no previous or
present psychiatric disorders.
Attempts were made to match the three groups
on demographic variables, and there were no
significant differences (P > 0.05) between the
three groups regarding age, education, hand dom-
inance (according to self report), or gender.
Demographic and clinical characteristics are
given in Table 1. A Norwegian short form of the
Wechlser Adult Intelligence Scale–Revised (WAIS-
R) (digit span, similarities, picture completion) (36)
with documented psychometric properties (37) was
administered to estimate current IQ level. Patients
with schizophrenia scored significantly lower than
the other two groups, but none scored below 70 IQ
points. The schizophrenics had higher BPRS and
PANSS scores and lower GAF scores, indicating
greater functional disturbance than the depressed
patients. The depressed group scored significantly
higher than the schizophrenia group on HRSD.
All but two of the schizophrenia patients scored
within the valid range on a measure sensitive to
poor motivation or malingering (Victoria Symp-
tom Validity Test, VSVT) (38) indicating that the
NP test scores may be regarded as reliable
estimates of the groupsÕ neurocognitive perform-
ance level.
Neuropsychological tests
All subjects were tested with a comprehensive NP
test battery. In selecting the NP tests we focused on
cognitive domains that have proved to be sensitive
to dysfunction in these two illnesses. In order of
administration the test battery included: Picture
Completion (WAIS-R) (36), California Verbal
Learning Test (39), Tower of London (40), Paced

Table 1. Characteristics of patients with schizophrenia (n ¼ 53) or recurrent major depression (n ¼ 45) compared with normal control subjects (n ¼ 50)

Group 1: schizophrenia Group 2: depression Group 3: controls Analysis

N N N Chi-square P

Gender (M/F) 33/20 18/27 25/25 v2ð2;N¼148 Þ ¼ 4.9 n.s.

Hand dominance (R/L) 48/4 41/4 42/4 v2ð2;N¼143Þ ¼ 0.1 n.s.
N Mean SD N Mean SD N Mean SD ANOVA Scheff

Age (years) 53 31.5 8.4 45 35.6 8.4 50 32.9 9.0 F2,145 ¼ 2.9 n.s.
Education (years) 53 13.3 3.2 45 13.7 2.8 50 13.9 2.5 F2,145 ¼ 0.6 n.s.
WAIS-R IQ estimate 53 91.0 10.3 45 98.9 10.9 50 103.3 7.6 F2,145 ¼ 21.4*** 1 „ 2, 3
GAF 52 39.3 11.3 45 46.5 8.8 – – – F1,95 ¼ 11.8*** 1 „ 2
BPRS 52 51.9 16.9 45 43.0 6.5 – – – F1,95 ¼ 11.0*** 1 „ 2
PANSS 53 75.6 23.2 45 56.3 11.6 – – – F1,96 ¼ 25.5*** 1 „ 2
HDRS 52 11.1 5.4 44 22.4 4.4 – – – F1,94 ¼ 124.4*** 1 „ 2

Valid test performance: >12 of 16 correct responses on VSVT (5 s delay).

BPRS, Extended Brief Psychiatric Rating Scale; GAF, Global Assessment of Function; HDRS, Hamilton Rating Scale for Depression; PANSS, Positive and Negative Syndrome
Scale; VSVT, Victoria Symptom Validity Scale; WAIS-R, Wechlser Adult Intelligence Scale–Revised.
***P < 0.001.

352

Auditory Serial Addition Test (41), Stroop Color
and Word Test (Stroop) (42), Rey Complex Figure
Test (43), Visual Backward Masking (14), Span of
Apprehension (R.F. Asarnow and K.H. Nuechter-
lein, unpublished data), Continuous Performance
Test–Degraded Stimulus (44), California Compu-
terized Assessment Package (45), Similarities
(WAIS-R) (36), Digit Span (WAIS-R) (36),
Controlled Oral Word Association Test (46),
Wisconsin Card Sorting Test (47), Warrington
Recognition Memory Test (48), and the VSVT
(38). In order to carry out the profile analysis on a
smaller set of empirically defined neurocognitive
composite (NCC) scores representative indices
from each test (49, 50), 16 in total, were selected
for principal component analysis (PCA).
Procedure
After a complete description of the study, written
informed consent was obtained. The NP tests were
administered by a licensed clinical neuropsycholo-
gist, a graduate psychology student or by an MD
supervised by a neuropsychologist, all trained in
standardized testing procedure. Examiners attemp-
ted to obtain maximal performance. The subjects
were tested individually. Time taken to complete
the test battery was approximately 4 h. Subjects
were allowed breaks between the tests, as needed.
All subjects had at least one break, with test
administration typically divided into 1.5–2 h ses-
sions.
Statistical analysis
Analyses were conducted using the statistical
package SPSS for Windows (version 11; SPSS
Inc., Chicago, IL, USA). Scores from the normal
control group on the 16 NP measures were
grouped into six principal components (eigenvalues
>1) by a PCA with Varimax rotation, accounting
for 69.3% of the variation in the data set. Five
components constituted established cognitive
dimensions (working memory, early visual infor-
mation processing, verbal memory, reaction time,
attention and vigilance). One component com-
prised measures from two separate cognitive func-
tions (Visual Memory and Executive Function)
and was thus split in two. Measures loading >0.4
on each component were used to compute seven
composite scores as listed in Table 2, using mean
values and standard deviations from the control
group as norms. Missing data were replaced with
group mean values in order to secure a complete
data set for multivariate analyses of NCCs (see
Table 2 for the prevalence of missing data across
Neuropsychological test profiles
tests and groups). High scores indicate better
performance; where this was not the case, the
direction of the scores was reversed. The intercor-
relations between the NCCs were mainly between
0.0 and 0.2, except for EF and ViM, which showed
a correlation of 0.4. A mean NCC score was
computed across the seven cognitive domains for
correlating cognitive function and clinical symp-
tom load.
The seven NCCs were entered as dependent
variables in a multivariate analysis of variance
(MANOVA) with diagnostic group as the between-
group factor. If the main effect was significant,
univariate analyses of variance (ANOVAs) were
performed for each NCC. Significant univariate
effects were followed by post hoc comparisons
(Scheffé) between each pair of groups.
A second set of MANCOVA and follow-up
ANCOVAs with IQ as covariate were conducted in
order to control for a spurious group effect on the
NCCs due to differences in intellectual capacity.
Subjects were then divided into subgroups defined
by IQ level. None of the control subjects scored
below 85, compared with 12 schizophrenia and
four depression patients. These 16 individuals were
excluded when analyzing how the interaction
between IQ group (below or above mean) and
diagnostic group affected NCC scores. Dividing
diagnostic groups according to IQ level (below
mean: 85–100, above mean: 100–125), the follow-
ing group sizes appeared: 29 and 12 schizophrenia
patients, respectively; 20 and 21 depression
patients, respectively; and 20 and 30 healthy
control subjects, respectively. More schizophrenia
patients were classified in the below mean IQ group
compared with the other two groups [v2(2, N ¼
132) ¼ 8.8, P ¼ 0.012], confirming the general
finding that schizophrenia patients have lower IQ
scores.
To assess within-group contrasts each group’s
score for each NCC was compared with the mean
of the group’s remaining six NCCs by pairwise
t-tests. This procedure has the potential of identi-
fying selective deficits (48), as opposed to a
generalized deficit.
To assess the percentage of patients considered
neuropsychologically impaired on each NCC, a
cut-off score of 1.5 SD below mean in the normal
control group was used as a threshold. To be
classified as moderately impaired a subject had to
perform deviantly on two to four NCCs, and to be
classified as severely impaired in five to seven.
Finally, NP impairment was correlated with
symptom ratings, i.e. GAF for both clinical
groups, HRSD for the depression group, and
BPRS and PANSS for the schizophrenia group.
353
Rund et al.

Table 2. Neuropsychological test results and Z-transformed neurocognitive composite scores for patients with schizophrenia (n ¼ 53) or recurrent major depression (n ¼ 45)
compared with normal control subjects (n ¼ 50)

Group 1: schizophrenia Group 2: depression Group 3: controls

Post hoc
N Mean SD N Mean SD N Mean SD Analysis: ANOVA comparison

Component 1: working memory

PASAT: R3 + 2 s 51 60.8 28.7 43 79.2 24.3 50 95.4 16.6 F2,141 ¼ 27.0*** 1 „ 2 „ 3
Digit span backwards 53 5.0 2.1 45 5.8 1.7 50 6.9 2.3 F2,145 ¼ 11.1*** 1, 2 „ 3
Stroop: color word (s) 52 61.4 2r3.3 45 54.8 13.0 50 43.7 9.6 F2,144 ¼ 14.7*** 1, 2 „ 3
COWAT: F + A 53 21.5 7.8 45 23.8 7.7 50 31.0 8.9 F2,145 ¼ 18.6*** 1, 2 „ 3
Composite score 53 )1.5 1.1 45 )0.9 0.9 50 0.0 0.8 F2,145 ¼ 31.1*** 1 „ 2 „ 3
Component 2: executive function
WCST: Perseverative responses 50 31.8 25.3 45 15.1 11.0 49 11.8 9.2 F2,141 ¼ 19.6*** 1 „ 2, 3
Tower of London (trials) 53 14.1 2.7 45 15.8 1.9 50 16.5 1.4 F2,145 ¼ 18.1*** 1 „ 2, 3
Composite score 53 )2.0 1.6 45 )0.5 1.1 50 0.0 0.8 F2,145 ¼ 35.2*** 1 „ 2, 3
Component 3: visual memory
ROCF: delayed recall 50 14.2 6.8 45 20.6 6.6 50 24.5 5.8 F2,142 ¼ 32.7*** 1 „ 2 „ 3
RMT: faces 52 37.1 6.2 45 41.0 6.8 50 42.4 4.4 F2,144 ¼ 11.3*** 1 „ 2, 3
Composite score 53 )1.5 1.0 45 )0.5 1.1 50 0.0 0.8 F2,145 ¼ 32.7*** 1 „ 2, 3
Component 4: verbal memory
CVLT: total A1–A5 53 43.2 13.3 45 55.4 11.0 50 57.3 9.6 F2,145 ¼ 23.0*** 1 „ 2, 3
RMT: words 52 45.9 4.8 45 48.0 3.2 50 49.0 1.2 F2,144 ¼ 10.6*** 1 „ 2, 3
Composite score 53 )2.0 2.2 45 )0.5 1.6 50 0.0 0.8 F2,145 ¼ 19.7*** 1 „ 2, 3
Component 5: early visual information processing
VBM: no-mask condition 50 16.6 2.4 42 17.5 1.9 46 17.8 1.8 F2,135 ¼ 4.7* 1 „ 3
VBM: masking conditions 50 15.7 3.6 42 17.0 3.3 46 17.7 3.0 F2,135 ¼ 4.5* 1 „ 3
Composite score 53 )0.6 1.0 45 )0.2 0.9 50 0.0 0.9 F2,145 ¼ 4.7** 1 „ 3
Component 6: reaction time
CalCAP: SRT 51 356.2 93.8 44 365.3 85.7 48 311.5 68.0 F2,140 ¼ 5.6** 1, 2 „ 3
CalCAP: CRT (mean) 51 591.7 90.9 44 554.8 98.8 48 498.2 77.6 F2,140 ¼ 13.7*** 1, 2 „ 3
Composite score 53 )1.0 1.1 45 )0.8 1.1 50 0.0 0.8 F2,145 ¼ 12.4*** 1, 2 „ 3
Component 7: attention/vigilance
SoA total 53 103.5 14.9 45 109.0 8.8 48 111.4 7.0 F2,143 ¼ 6.9*** 1 „ 3
CPT-DS total dÕ 53 2.26 0.82 44 2.33 0.71 47 2.69 0.92 F2,141 ¼ 3.9* 1 „ 3
Composite score 53 )0.8 1.3 45 )0.4 0.8 50 0.0 0.8 F2,145 ¼ 8.7*** 1 „ 3

MANOVA across the 16 neuropsychological test variables (missing data replaced with group mean): F ¼ 4.763 (k ¼ 0.397), d.f. ¼ 32, 260, P < 0.001.
MANOVA across the seven composite scores: F ¼ 9.239 (k ¼ 0.466), d.f. ¼ 14,278, P < 0.001.
CalCAP, California Computerized Assessment Package; COWAT, Controlled Oral Word Association Test (F + A); CPT-DS, Continuous Performance Test-Degraded Stimuli; CVLT,
California Verbal Learning Test; PASAT, Paced Auditory Serial Addition Test; ROCF, Rey-Osterrieth Complex Figure Test; RMT, Warrington Recognition Memory Test; SoA, Span
of Apprehension Test; VBM, Visual Backward Masking Test; WCST, Wisconsin Card Sorting Test.
*P < 0.05, **P < 0.01, ***P < 0.001.

Results 0.5

Neuropsychological test scores and NCC scores for 0.0

each group are presented in Table 2. The NCC –0.5
z-scores

Z-score profiles of the groups are presented in –1.0

Fig. 1. There was a clear difference in performance
–1.5 Con
across groups, with the overall MANOVA being Dep
–2.0
significant for both the set of 16 test measures [F(32, Sch
260) ¼ 4.8, P < 0.001] and the seven composite –2.5
Working Executive Visual Verbal Visual lnfo Reaction Attention /
scores [F(14, 278) ¼ 9.2, P < 0.001]. Follow-up memory function memory memory processing time vigilance
ANOVAs on the composite scores revealed a
Fig. 1. Scores on seven neurocognitive composite scores for
significant difference between groups on all seven patients with schizophrenia (n ¼ 53) or recurrent major
NCCs (Table 2). Post hoc comparisons (Scheffé) depression (n ¼ 45) compared with normal control subjects
showed that patients with schizophrenia performed (n ¼ 50).
significantly below normal controls on all measures,
and below patients with depression on four NCCs The planned profile contrasts indicated that
(working memory, executive function, visual working memory [t(52) ¼ 2.7, P ¼ 0.01], executive
memory, and verbal memory). Patients with depres- function [t(52) ¼ 4.2, P < 0.001], visual memory
sion performed significantly below normal controls [t(52) ¼ 3.0, P ¼ 0.004], and verbal memory
on two domains (working memory, reaction time). [t(52) ¼ 3.3, P ¼ 0.002] were selectively impaired

354
 Neuropsychological test profiles

60 1.0

Sch 0.5
50
% Impaired subjects

Dep
0.0
Con

z-scores
40
–0.5
30 –1.0

20 –1.5 Con
Dep
–2.0
10 Schi
–2.5
0 Working Executive Visual Verbal Viusal info Reaction Attention /
Working Executive Visual Verbal Visual lnfo Reaction Attention / memory function memory memory processing time vigilance
memory function memory memory processing time vigilance
Fig. 3. Scores on seven neurocognitive composite scores for
Fig. 2. Percentages of subjects scoring 1.5 SD below control patients with schizophrenia (n ¼ 29) or recurrent major
group mean (classified as impaired) on the seven neurocogni- depression (n ¼ 20) compared with normal control subjects
tive composite scores. (n ¼ 20) with current IQ between 85 and 100.

1.0
areas in the schizophrenia group. The depressed 0.5
patients were selectively impaired in working 0.0

z-scores
memory [t(44) ¼ 6.2, P < 0.001] and reaction –0.5
time [t(44) ¼ 2.4, P ¼ 0.022]. –1.0
The percentages of subjects in each group –1.5 Con
Dep
scoring more than 1.5 SD below the mean of the –2.0
Schi
normal group (cognitively impaired), are shown in –2.5
Working Executive Visual Verbal Viusal info Reaction Attention /
Fig. 2. More than 40% of the schizophrenia memory function memory memory processing time vigilance

patients showed deficits in working memory, exe-

cutive function, visual memory, or verbal memory, Fig. 4. Scores on seven neurocognitive composite scores for
whereas approximately 25% of the patients with patients with schizophrenia (n ¼ 12) or recurrent major
depression showed impairments in working depression (n ¼ 21) compared with normal control subjects
(n ¼ 30) with current IQ between 100 and 125.
memory or reaction time. In total, 62% of the
schizophrenia group showed impairments within
two or more domains, i.e. 45% were classified as executive functioning (P ¼ 0.006), visual memory
moderately impaired and 17% as severely (P ¼ 0.004) and verbal memory (P ¼ 0.003).
impaired, compared with 24% moderately and Mean NCC score in the schizophrenia group
4% severely impaired in the depression group. correlated moderately with total BPRS score
When using IQ as a covariate in the analysis of [r(52) ¼ )0.42, P ¼ 0.002] as well as all the
group differences, the effect of diagnostic group PANSS scores: total score [r(53) ¼ )0.42, P ¼
remained significant for the set of single tests [F(32, 0.002], positive symptom score [r(53) ¼ )0.28,
258) ¼ 3.3, P < 0.001] and the NCCs [F(14, P ¼ 0.042], negative symptom score [r(53) ¼
276) ¼ 5.8, P < 0.001]. Group differences on )0.37, P ¼ 0.006], and general symptom score
early visual information processing and reaction [r(51) ¼ )0.42, P ¼ 0.002]. No significant corres-
time became non-significant when controlling for pondence between cognitive function and HDRS
IQ. score was found in the depression group. Global
When reiterating the analysis with IQ as the functioning (GAF) showed a weak correlation with
grouping factor instead of as the covariate for the cognitive performance in schizophrenia [r(53) ¼
NCCs, significant main effects for both diagnosis 0.29, P ¼ 0.038], and no correlation in depression.
[F(14, 242) ¼ 8.1, P < 0.001] and IQ group [F(7, Group differences between the two clinical groups
120) ¼ 8.9, P < 0.001] were found. The interac- on executive function and visual memory were still
tion between diagnosis and IQ was non-significant significant when controlling for symptom ratings
(P > 0.05), confirming that the profile for each (BPRS, PANSS total score) in addition to IQ.
diagnostic group remained more or less the same in No significant (P > 0.05) difference was found
shape even though the level of performance on any NCC between patients on conventional and
improved with higher IQ. The NCC scores for atypical antipsychotic medication.
subjects with current IQ between 85 and 100 are
displayed in Fig. 3, and for those with IQ scores
Discussion
between 100 and 125 in Fig. 4. The high-function-
ing schizophrenia group scored below controls on The neurocognitive profiles of the two patient
several measures. This was significantly for groups provide evidence for a pervasive deficit in

355
Rund et al.
schizophrenia and for a mild and restricted distur-
bance in non-psychotic depression. This implies
that neurocognitive deficits found in previous
studies of patients with affective disorder may
partly be due to psychosis and not the depression
per se (16). Consistent with several previous reports
(25, 49, 50, 52–54) the schizophrenia group showed
selective impairments in all four higher order
neurocognitive domains (executive function, work-
ing memory, visual memory, verbal memory). The
presence of selective deficits in both the executive/
working memory domain and the verbal/visual
memory domain, may implicate both frontal and
temporal-hippocampal involvement in the patho-
physiology of schizophrenia.
Thirty-eight percent of the patients with schizo-
phrenia did not show an impaired NP profile,
demonstrating that schizophrenia may exist in the
context of preserved cognition. The percentage of
unimpaired patients in the present study is higher
than in most previous studies where the corres-
ponding figure has varied from approximately 10%
(55, 56) to approximately 55% (3, 57), with
25–30% as the most common estimate (5, 23, 58).
It is possible that the high frequency of paranoid
symptoms in the present sample has contributed to
the relatively high percentage of unimpaired
patients. Patients with a paranoid type of schizo-
phrenia are generally less neuropsychologically
impaired than non-paranoid patients (59, 60). It
is also possible that these patients are impaired
relative to their premorbid level of functioning but
that our research design was unable to detect such
subtle deficits.
Employing the concept of a Ôcontinuum of
neurocognitive functioningÕ (3) may be a meaning-
ful way of understanding these results. This model
is substantiated in the present study by the finding
of 17% of the schizophrenia patients being severely
disturbed, 45% moderately disturbed, and 38%
unimpaired. Further, we cannot rule out the
possibility that a small subsample of patients
shows no evidence of any decline at all in cognitive
functioning relative to their premorbid level.
Finally, cognitive dysfunction also varies with the
phase of the illness, being more pronounced in
acute psychotic phases (61).
At a group level patients with schizophrenia
show a decline in intellectual functioning measured
by IQ tests. We replicated and confirmed the
findings of Kremen et al. (22) that neurocognitive
dysfunction is present in this patient group at all
levels of intellectual ability. The present results
show that even patients with an intellectual ability
above average, manifest substantial neurocognitive
deficits. Thus, a neurocognitive dysfunction
356
beyond the intellectual decline is evident in schi-
zophrenia. In accordance with Kremen et al. (22)
we conclude that these findings provide strong
support for the argument that neurocognitive
dysfunction is a core deficit in schizophrenia.
The finding that degree of NP impairment
among schizophrenia patients was significantly
associated with level of clinical symptoms is in
accordance with some previous studies (5, 25, 51).
However, as symptom load (BPRS and PANSS)
correlated 0.42 with mean NCC score and thus
explained <20% of the variance in neurocogni-
tion, the two dimensions seem to be independent of
each other and should be assessed and treated
separately.
While the impairment in schizophrenia indicates
dysfunction in several aspects of higher order
cognitive domains, depression evidence impair-
ment primarily on measures of processing speed.
Our findings show that depressed patients exhibit
problems within two domains, e.g. working
memory and reaction time. This is in concert
with the study of Landrø et al. (6). They examined
unmedicated patients with non-psychotic major
depression and found that these patients exhibited
an overall NP deficit, but performed dispropor-
tionately worse in the two domains of working
memory and selective attention (a choice reaction
time task). Thiery et al. (62) also found that
subjects with non-psychotic depression were
impaired on a choice reaction time task, and
recently Harvey et al. (63) confirmed a specific
working memory deficit in non-psychotic depres-
sion. These patterns of dysfunction suggest
involvement of fronto-temporal cortical areas in
schizophrenia and subcortical areas in depression.
Although studies of pathogenesis suggest overlap-
ping afflicted brain areas in schizophrenia and
depression (9–11), our findings of differences in
type and magnitude of impairment is supported by
findings of different fMRI activation pattern (64).
Moreover, impaired working memory and reaction
time in depression did not correlate with ratings of
affective disturbance. This strongly suggests that
neurocognitive impairment is not caused by the
affective symptoms characterizing the diagnosis.
One limitation of this study is that the schizo-
phrenia group scored significantly lower than the
two other groups on current IQ, and unfortunately
we do not have an estimate of premorbid IQ. After
controlling for present IQ level by covariance
analysis, group differences in neurocognitive
impairment remained significant for almost all
NCCs. However, some researchers have suggested
that covariance analysis is invalid for pre-existing
disparate groups that differ on the variable to be

covaried for (65, 66). Moreover, available data
suggest a decline of 1/2 to 1 SD from premorbid IQ
(21, 67). If 10 IQ points were added to the current
IQ an estimated average premorbid IQ would be
approximately 103 in the present sample. Thus,
this sample is probably fairly representative with
respect to premorbid IQ.
Another limitation is that we did not have
adequate control over medication effects. Moha-
med et al. (68) compared the performance of
medicated and non-medicated schizophrenia
patients. They found no significant differences in
their performance on any of the NP tasks. In the
current study, no differences were found between
patients on conventional and those on atypical
drugs. Considering the positive effects of atypical
antipsychotics reported in several studies (69) it is
unlikely that antipsychotic medication can explain
the poor performance found in the schizophrenia
group. Further, long-term use of benzodiazepines
seems to be associated with impairment in some
cognitive functions, specifically sustained attention
(70). Finally, findings are inconclusive with respect
to the effects of antidepressants (71). However, the
newer type of antidepressant medication is known
to have a less deleterious effect on neurocognitive
functions than older types (72). In this study, all
depressed patients were on newer types of antide-
pressants. It is therefore unlikely that antidepres-
sants have had any significant effect on NP
performance.
The neurocognitive test battery in the present
study also has a psychometric limitation. The
different discriminating power of the various tasks
represents a confounding variable that does not
allow direct interpretation of differential deficits
(73).
Finally, conducting as many as seven different
comparisons for the profile contrasts may have
resulted in an inflated type I error rate, as these
seven variables to a certain extent are intercorre-
lated. The strength of the present study is that it is
the first comparison of large, well-defined groups
of subjects with schizophrenia and recurrent non-
psychotic depression using a comprehensive NP
test battery. The group sizes are large enough to
lend adequate power to the analyses.
In conclusion, the present study confirms previ-
ous findings that cognitive impairment is a core
deficit in schizophrenia as well as provide evidence
suggesting a great deal of individual variability in
cognition within schizophrenia in that a subgroup
of patients performs within a normal range. This
finding suggests that the schizophrenia comprise
subgroups that should be identified for optimal
treatment and counseling.
Neuropsychological test profiles
Acknowledgements
This study was supported by grants from the
Norwegian Research Council (#122974/320) and
from the National Council for Mental Health/
Norwegian Foundation for Health and Rehabilit-
ation (#1997/007) to Dr Rund.
References
1. Heinrichs RW. In search of madness. Schizophrenia and
neuroscience. New York: Oxford University Press, 2001.
2. Rund BR, Borg NE. Cognitive deficits and cognitive train-
ing in schizophrenic patients: a review. Acta Psychiatr
Scand 1998;100:85–95.
3. Palmer BW, Heaton RK, Paulsen JS et al. Is it possible to be
schizophrenic yet neuropsychologically normal? Neuro-
psychology 1997;11:437–446.
4. Riley EM, McGovern D, Mockler D et al. Neuropsycho-
logical functioning in first-episode psychosis – evidence of
specific deficits. Schizophr Res 2000;43:47–55.
5. Saykin AJ, Shtasel DL, Gur RE et al. Neuropsycholo-
gical deficits in neuroleptic navie patients with first-
episode schizophrenia. Arch Gen Psychiatry 1994;51:
125–131.
6. Landrø NI, Stiles TC, Sletvold H. Neuropsychological
function in nonpsychotic unipolar major depression.
Neuropsychiatry Neuropsychol Behav Neurol 2001;
14:233–240.
7. Veiel HOF. A preliminary profile of neuropsychological
deficits associated with major depression. J Clin Exp
Neuropsychol 1997;19:587–603.
8. Zakzanis KK, Leach L, Kaplan E. On the nature and pattern
of neurocognitive functions in major depressive disorder.
Neuropsychiatry Neuropsychol Behav Neurol 1998;11:
111–119.
9. Bremner JD. Does stress damage the brain? Biol Psychiatry
1999;45:797–805.
10. Kirschbaum C, Wolf OT, May M, Wippich W, Hellhammer
DH. Stress- and treatment induced elevations of cortisol
levels associated with impaired declarative memory in
healthy adults. Life Sci 1996;58:1475–1483.
11. Nelson MD, Saykin AJ, Flashman LA, Riordan HJ. Hippo-
campal volume reduction in schizophrenia as assessed by
magnetic resonance imaging: a metanalytic study. Arch
Gen Psychiatry 1998;55:433–440.
12. Egeland J, Sundet K, Rund BR et al. Sensitivity and spe-
cificity of memory dysfunction in schizophrenia: a com-
parison with major depression. J Clin Exp Neuropsychol
2002;25:79–93.
13. Egeland J, Rund BR, Sundet K et al. Attention profile in
schizophrenia compared with depression: differential
effects of processing speed, selective attention and vigil-
ance. Acta Psychiatr Scand 2003;107:1–9.
14. Rund BR, Melle I, Friis S et al. Neurocognitive dysfunction
in first-episode psychosis: correlates with symptoms, pre-
morbid adjustment, and duration of untreated psychosis.
Am J Psychiatry 2004;161:466–472.
15. Stordal KI, Mykletun A, Asbjørnsen A et al. Executive
functioning in major depression and schizophrenia: Is
impairment determined by general psychopathology or
diagnosis? Acta Psychiatr Scand 2005;111:22–28.
16. Albus M, Hubman W, Wahlheim C, Sobizack N, Franz U,
Mohr F. Contrasts in neuropsychological test profile
between patients with first-episode schizophrenia and
357
Rund et al.
first-episode affective disorders. Acta Psychiatr Scand
1996;94:87–93.
17. Jeste DV, Schelley C, Heaton BA et al. Clinical and neu-
ropsychological comparison of psychotic depression with
nonpsychotic depression and schizophrenia. Am J Psychi-
atry 1996;153:490–496.
18. Basso MR, Bornstein RA. Neuropsychological deficits in
psychotic versus nonpsychotic unipolar depression. Neu-
ropsychology 1999;13:69–75.
19. Schatzberg AF, Posener JA, DeBattista C, Kalehzan BM,
Rotschild AJ, Shear PK. Neuropsychological deficits in
psychotic versus nonpsychotic major depression and no
mental illness. Am J Psychiatry 2000;157:1095–1100.
20. Zammit S, Allebeck P, David AS et al. A longitudinal
study of premorbid IQ score and risk of developing
schizophrenia, bipolar disorder, severe depression, and
other nonaffective psychosis. Am J Psychiatry 2004;61:
354–360.
21. Sheitman BB, Murray MG, Snyder JA et al. IQ scores of
treatment-resistant schizophrenia patients before and
after the onset of the illness. Schizophr Res 2000;46:
203–207.
22. Kremen WS, Seidman LJ, Farone SV, Tsuang MT. Intelli-
gence quotient and neuropsychological profiles in patients
with schizophrenia and in normal volunteers. Biol Psy-
chiatry 2001;50:453–462.
23. Weickert TW, Goldberg TE, Gold JM, Bigelow LB, Egan
MF, Weinberger DR. Cognitive impairment in patients with
schizophrenia displaying preserved and comprised intel-
lect. Arch Gen Psychiatry 2000;57:907–913.
24. Andreasen NC, Olsen SA, Dennert JW, Smith MR. Ven-
tricular enlargement in schizophrenia: relationship to
positive and negative symptoms. Am J Psychiatry
1982;139:297–302.
25. Bilder RM, Goldman RS, Robinson D et al. Neuropsycho-
logy of first-episode schizophrenia: initial characterization
and clinical correlates. Am J Psychiatry 2000;157:549–559.
26. Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L.
Cerebral ventricular size and cognitive impairment in
chronic schizophrenia. Lancet 1976;11:924–926.
27. Perlick D, Mattis S, Stastny P, Silverstein B. Negative
symptoms are related to both frontal and nonfrontal
neuropsychological measures in chronic schizophrenia.
Arch Gen Psychiatry 1992;49:245–246.
28. Binder J, Albus M, Hubmann W et al. Neuropsychological
impairment and psychopathology in first-episode schizo-
phrenic patients related to the early course of illness. Eur
Arch Psychiatry Clin Neurosci 1998;248:70–77.
29. Hoff AL, Harris D, Faustman WO et al. A neuropsycho-
logical study of early onset schizophrenia. Schizophr Res
1996;20:21–28.
30. Rund BR, Egeland J, Sundet K et al. Early information
processing in patients with schizophrenia or major
depressive disorder. Schizophr Res 2004;68:111–118.
31. American Psychiatric Association. Diagnostic and statis-
tical manual of mental disorders (DSM-IV), 4th edn.
Washington, DC: American Psychiatric Association, 1994.
32. First MB, Spitzer RL, Gibbon M, Williams JBW. The
structured clinical interview for DSM-IV axis I disorders –
patient edition (SCID I/P, version 2.0). New York: Bio-
metrics Research Department, New York State Psychiatric
Institute, 1995.
33. Lukoff D, Ventura D. Manual for the expanded BPRS.
Symptom monitoring in the rehabilitation of schizophrenic
patients. Schizophr Bull 1986;12:594–602.
34. Hamilton M. A rating scale for depression. J Neurol Neu-
rosurg Psychiatry 1960;23:56–62.
358
35. Kay SR, Fiszbein A, Opler LA. The Positive and Negative
Syndrome Scale for schizophrenia. Schizophr Bull
1987;13:261–276.
36. Wechsler D. Wechsler adult intelligence scale – revised.
New York: The Psychological Corporation, 1981.
37. Ward LC, Ryan JJ. Validity and time savings in the selec-
tion of short forms of the Wechsler Adult Intelligence Scale
– Revised. Psychol Assess 1996;8:69–72.
38. Slick D, Hopp G, Strauss E, Thompson GB. Victoria symp-
tom validity test – version 1.0 professional manual. Odessa,
TX: Psychological Assessment Resources, 1997.
39. Delis DC, Kramer JH, Kaplan E, Ober BA. California verbal
learning test (CVLT) manual. New York: The Psycholo-
gical Corporation, 1987.
40. Shallice T. From neuropsychology to mental structure.
New York: Cambridge University Press, 1988.
41. Gronwall D, Wrightson P. Cumulative effects of concus-
sion. Lancet 1975;22:995–997.
42. Comalli PE, Wapner S, Werner H. Interference effects of
Stroop Color-Word Test in childhood, adulthood, and
aging. J Gen Psychol 1962;100:47–53.
43. Meyers JE, Meyers KR. Rey complex figure test and
recognition trial – professional manual. Odessa, TX: Psy-
chological Assessment Resources, 1985.
44. Nuechterlein KH. Signal detection in vigilance tasks and
behavioral attributes among offspring of schizophrenic
mothers and among hyperactive children. J Abnorm Psy-
chol 1983;92:4–28.
45. Miller EN. CalCAP: California computerized assessment
package manual, rev. 4.0. Los Angeles, CA: Eric N Miller,
PhD, and Norland Software, 1993.
46. Spreen O, Strauss E. A compendium of neuropsychological
tests: administration, norms, and commentary, 2nd edn.
New York: Oxford University Press, 1998.
47. Heaton RK, Chelune GJ, Talley JL, Kay GG, Curtiss G.
Wisconsin Card Sorting Test. Manual. Revised and
expanded. Odessa, TX: Psychological Assessment
Resources, 1993.
48. Warrington EK. Recognition memory test. Windsor:
NFER-Nelson, 1994.
49. Saykin AJ, Gur RC, Gur RE et al. Neuropsychological
function in schizophrenia. Arch Gen Psychiatry
1991;48:618–624.
50. Øie M, Rund BR. Neuropsychological deficits in adolescent-
onset schizophrenia compared with attention deficit
hyperactivity disorder. Am J Psychiatry 1999;156:1216–
1222.
51. Addington J, Addington D. Positive and negative symptoms
of schizophrenia: their course and relationship over time.
Schizophr Res 1991;5:51–59.
52. Addington J, Brooks BL, Addington D. Cognitive func-
tioning in first episode psychosis: initial presentation.
Schizophr Res 2003;62:59–64.
53. Goldberg TE, Gold JM, Greenberg R et al. Contrasts
between patients with affective disorders and patients with
schizophrenia on a neuropsychological test battery. Am J
Psychiatry 1993;150:1355–1362.
54. Sullivan EV, Shear PK, Zipursky RB, Sagar HJ, Pfefferbaum
A. A deficit profile of executive, memory, and motor
functions in schizophrenia. Biol Psychiatry 1994;36:641–
653.
55. Seltzer J, Conrad C, Cassens G. Neuropsychological pro-
files in schizophrenia: paranoid versus undifferentiated
distinctions. Schizophr Res 1997;23:131–138.
56. Torrey EF, Bowler AE, Taylor EH, Gottesman II. Schizo-
phrenia and manic-depresive disorder. New York: Basic
Books, 1994.

57. Strauss BS, Silverstein ML. Luria-Nebraska measures in
neuropsychologically nonimpaired schizophrenics: a com-
parison with normal subjects. Int J Clin Neuropsychol
1986;8:35–38.
58. Taylor MA, Abrams R. Cognitive dysfunction in schizo-
phrenia. Am J Psychiatry 1984;141:186–201.
59. Rund BR. The effect of distraction on focal attention in
paranoid and non-paranoid schizophrenic patients com-
pared to normals and non-psychotic psychiatric patients.
J Psychiat Res 1983;17:241–250.
60. Silverstein ML, Zervick MJ. Clinical psychopathologic
symptoms in neuropsychologically impaired and intact
schizophrenics. J Consult Clin Psychol 1985;53:288–296.
61. Rund BR. A review of longitudinal studies of cognitive
functions in schizophrenia patients. Schizophr Bull
1998;24:425–435.
62. Thiery P, Axman D, Giedke H. Slow brain potentials and
psychomotor retardation in depression. Electroencepha-
logr Clin Neurophys 1986;63:570–581.
63. Harvey PO, Le Bastard G, Pochon JB, Allilaire JF, Dubois
B, Fossati P. Executive functions and updating of the
contents of working memory in unipolar depression.
J Psychiat Res 2004;38:567–576.
64. Hugdahl K, Rund BR, Lund A et al. fMRI brain activation
to a mental arithmetic task in schizophrenia and major
depression. Am J Psychiatry 2004;161:286–293.
Neuropsychological test profiles
65. Miller GA, Chapman JP. Misunderstanding analysis of
covariance. J Abnorm Psychol 2001;110:40–48.
66. Cohen J, Cohen P. Applied multiple regression/correlation
analysis for the behavioral sciences. Hillsdale, NJ: Erl-
baum, 1975.
67. Frith C, Leary J, Cahill C, Johnstone E. Performance on
psychological tests: demographic and clinical correlates of
the results of these tests. Br J Psychiatry 1991;13:26–29.
68. Mohamed S, Paulsen JS, O’Leary D, Arndt S, Andreasen
NC. Generalized cognitive deficits in schizophrenia. A
study of first-episode patients. Arch Gen Psychiatry
1999;56:749–754.
69. Purdon SE, Jones BDW, Stip E et al. Neuropsychological
change in early phase schizophrenia during 12 months
treatment with olanzapine, risperidone, or haloperidol.
Arch Gen Psychiatry 2000;57:249–258.
70. Golombok S, Moodley P, Lader M. Cognitive impairment in
long-term benzodiazepine users. Psychol Med
1988;18:365–374.
71. Amadore-Boccara J, Gougoulis N, Littrè MFP, Galinowski
A, Loo H. Effects of antidepressants on cognitive functions:
a review. Neurosci Biobehav Rev 1992;19:479–493.
72. Elliot R. The neuropsychological profile in unipolar
depression. Trends Cogn Sci 1998;2:447–454.
73. Chapman LJ, Chapman JP. The measurement of differential
deficit. J Psychiat Res 1978;14:303–311.
359