Executive functioning in schizophrenia: A thorough examination of

Transcription

Executive functioning in schizophrenia: A thorough examination of
Schizophrenia Research 114 (2009) 84–90
Contents lists available at ScienceDirect
Schizophrenia Research
j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / s c h r e s
Executive functioning in schizophrenia: A thorough examination of
performance on the Hayling Sentence Completion Test compared to
psychiatric and non-psychiatric controls
Nicole Joshua a,b,⁎, Andrea Gogos a,b, Susan Rossell a,b,c
a
Mental Health Research Institute of Victoria, Level 2, 161 Barry Street, Carlton South Victoria 3053, Australia
The University of Melbourne, Parkville Victoria 3010, Australia
c
Monash–Alfred Psychiatry Research Centre, Monash University School of Psychology, Psychiatry and Psychological Medicine, The Alfred Hospital,
Victoria, 3004, Australia
b
a r t i c l e
i n f o
Article history:
Received 20 January 2009
Received in revised form 28 May 2009
Accepted 29 May 2009
Available online 21 June 2009
Keywords:
Schizophrenia
Executive functioning
Inhibition
Suppression
Bipolar disorder
Hayling Sentence Completion Test
a b s t r a c t
Background: The current study examined executive functioning in schizophrenia by assessing
response initiation and suppression in a group of schizophrenia patients, and drawing
comparisons with psychiatric and non-psychiatric control groups.
Method: The Hayling Sentence Completion Test was used as a measure of executive functioning
and was completed by 39 schizophrenia patients, 40 bipolar disorder patients and 44 healthy
control participants. Outcome measures included response initiation and response suppression
latency and error rate.
Results: The schizophrenia group was significantly impaired on all measures of the Hayling
Sentence Completion Test when compared to healthy control participants, and only on some of the
measures when compared to the bipolar disorder group. The bipolar disorder group did not differ
in performance compared to the healthy control group. Overall schizophrenia patients showed
longer response initiation and response suppression latencies, and an increased error rate.
Performance of the schizophrenia patients was associated with higher ratings of cognitive
disorganisation. Performance was not related to age, gender, predicted IQ or any other clinical
characteristics.
Conclusions: Schizophrenia patients show a slowing in baseline response initiation and slowed
suppression of an inappropriate response. Considering the bipolar disorder patients demonstrated
intact performance, altered executive functioning in schizophrenia appears relatively specific to
the disorder rather than reflecting other characteristics common to mental illness. Investigations
examining which neurocognitive domains are impaired in schizophrenia provide direct
implications for treatment options tailored to an individual's cognitive strengths and weaknesses.
© 2009 Elsevier B.V. All rights reserved.
1. Introduction
Neurocognitive impairment is considered a core feature of
schizophrenia (Elvevag and Goldberg, 2000), with impair⁎ Corresponding author. Mental Health Research Institute of Victoria, Level 2,
161 Barry Street, Carlton South Victoria 3053, Australia. Tel.: +61 3 8344 1853;
fax: +61 3 9348 1778.
E-mail addresses: [email protected] (N. Joshua),
[email protected] (A. Gogos), [email protected]
(S. Rossell).
0920-9964/$ – see front matter © 2009 Elsevier B.V. All rights reserved.
doi:10.1016/j.schres.2009.05.029
ment relatively resistant to antipsychotic medication (Goldberg et al., 1993). Impairment is apparent early in the illness,
as it is observed in first episode patients (Saykin et al., 1994).
Longitudinal studies have revealed no difference in the degree
of impairment between first episode and previously treated
patients, both initially and at 19-month follow-up (Censits
et al., 1997), thus indicating that deficits are stable over the
course of the illness. Individuals at high-risk for developing
schizophrenia, i.e. first-degree relatives, also exhibit deficits,
suggesting a familial link (Byrne et al., 1999; Faraone et al.,
N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
1995). Furthermore, schizophrenia patients who demonstrate
the lowest ratings on assessments of global functioning
exhibit greater neurocognitive impairment compared to
higher functioning patients (Loughland et al., 2007).
One particularly important aspect of neurocognition is
executive functioning. This is a broad term used to describe
cognitive processes involving control, flexibility, inhibition,
regulation, planning, fluency and execution of goal-oriented
behaviour. Such processes commonly involve abilities
mediated by the prefrontal cortex. Extensive research
indicates deficient executive functioning in schizophrenia
patients (Evans et al., 1997; Morice and Delahunty, 1996). The
Hayling Sentence Completion Test (HSCT) was developed to
assess functioning in patients with cerebral lesions (Burgess
and Shallice, 1996), and is an established measure of
executive functioning. It was used in the current study. The
task was designed to assess basic initiation speed and
response suppression (Burgess and Shallice, 1997). HSCT
performance is impaired in schizophrenia, with investigations reporting a relationship between HCST and clinical
presentation (Chan et al., 2004), cortical activation (McIntosh
et al., 2008), schizotypal personality traits (Laws et al., 2008),
early-onset psychosis (Groom et al., 2008) and high-risk
factors (Byrne et al., 1999). Significantly, HSCT has been
shown to be a strong predictor among genetically high-risk
individuals as to who goes on to develop the illness (Whalley
et al., 2008).
The HSCT is a useful measure as it provides an overall
standardised score to determine level of global impairment.
In addition, the HSCT permits division and analysis of specific
executive abilities evaluated within the task, i.e. response
initiation, response suppression, as well as the error pattern.
The specific profile of impairment in schizophrenia on the
HSCT has not yet been thoroughly examined. Some studies
have evaluated either overall performance (McIntosh et al.,
2005), the speed of response (Groom et al., 2008) or error
rates (Waters et al., 2003), with only one study incorporating
all measures of response latencies over conditions and type of
errors (Marczewski et al., 2001). However, their group sample
size was limited (n = 15). Further, few studies have looked at
the standardised classification of performance according to
the task guidelines. This classification guide provides useful
labels for performance evaluation ranging from ‘impaired’ to
‘high average’ performance.
A further issue common to neurocognitive investigation in
schizophrenia involves the diagnostic specificity of the
impairment. That is, are the performance deficits secondary
to the illness and instead a result of psychopathological
characteristics common to all mental illness, or are the
deficits specific to the underlying aetiology of schizophrenia?
This issue has been addressed in the current study by
incorporating a bipolar disorder (BD) sample as a psychiatric
control group. BD patients also show consistent neurocognitive impairment (Bearden et al., 2001), including executive
functioning (Stoddart et al., 2007). Further, neurocognitive
impairment appears to be independent of current affective
state (Dixon et al., 2004). Both BD and schizophrenia patients
experience psychotic symptoms and as a result share several
psychopathological characteristics. While distinctly separate
disorders, both groups of patients can become severely
unwell, experiencing long periods of time in psychiatric
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institutions or hospitalisation. As a consequence they often
show a reduced ability to maintain employment and/or social
networks. Both groups are often prescribed with antipsychotic medication for extended periods of time. Considering
these similarities, a BD group is an advantageous addition as a
psychiatric control group within schizophrenia research,
providing the opportunity to take into account factors such
as medication, hospitalisation and length of illness. Previous
HSCT studies have addressed this issue to a degree. One study
included a group of attention-deficit hyperactivity disorder
(ADHD) adolescents as a neurodevelopmental control group
for HSCT performance comparisons to adolescent schizophrenia spectrum patients (Groom et al., 2008). Another
study included a sample of schizophrenia and BD patients;
however, they only reported one overall measure of HSCT
performance (McIntosh et al., 2008). Therefore, to our
knowledge, there have been no other studies to date to
compare detailed behavioural performance on the HSCT
between schizophrenia and BD patients.
The aim of the current study was to improve upon
previous research in two main ways. Firstly, by examining
HSCT performance in schizophrenia in greater detail than has
been described previously; and secondly, drawing performance comparisons to both psychiatric and non-psychiatric
control groups. Specifically, the HSCT was used to assess
response initiation, response suppression and an error
pattern. It was expected that the schizophrenia and BD
patients would demonstrate performance deficits compared
to the healthy control group in the form of longer response
latencies and increased error rate. It was further hypothesised
that deficits shown by schizophrenia patients would be
greater than those of the BD patients indicating a diagnosisspecific impairment rather than an impairment that is
secondary to the disorder.
2. Method
2.1. Participants
The current study included 39 patients diagnosed with
schizophrenia and 40 patients diagnosed with BD. Patients
were recruited via community support groups and community care units and were all out-patients. Diagnosis was
confirmed using the Structured Clinical Interview for DSM-IV
(SCID: First et al., 1996). Current symptomology was acquired
using the Positive and Negative Syndrome Scale (PANSS: Kay
et al., 1987). Only patients with no other co-morbid Axis 1
diagnoses were included in the study. All patients were in a
chronic phase of illness and were not experiencing an acute
psychotic or mood episode at the time of testing. BD patients
were screened for current mood episodes during recruitment
and then a euthymic state was confirmed during the SCID.
Clinical characteristics are presented in Table 1.
Forty-four healthy control participants were recruited via
local advertisements. Control participants were excluded if they
had any history of psychiatric disorder or a first-degree relative
with either schizophrenia or BD. All participants met the
following criteria: a) no history of neurological disorder or head
trauma, b) no current substance abuse, c) English as first
language, d) between the ages of 18–65 years and e) predicted
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N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
Table 1
Demographic and clinical characteristics of the three participant groups
mean (standard deviation).
Group
Controls
n = 44
Age
41.0 (12.0)
Gender
22M 22F
NART
111.8 (6.1)
(predicted IQ)
Age at illness onset
(years)
Illness duration
(years)
PANSS positive
PANSS negative⁎
PANSS general
PANSS total score
Medication CPZe⁎⁎
BD n = 40
Schizophrenia
n = 39
Comparisons
42.1 (11.5)
16M 24F
107.6 (10.3)
42.3 (10.7)
26M 13F
109.2 (9.4)
F = 0.16 a
χ2 = 5.74 b
F = 2.54 a
22.3 (9.3)
23.7 (6.3)
t = 0.78 c
19.8 (11.6)
18.7 (9.9)
t = −0.44 c
10.4 (3.4)
9.2 (2.4)
22.4 (4.6)
42.0 (8.0)
291.2 (198.9)
11.5 (3.2)
11.6 (5.5)
23.5 (6.2)
46.4 (12.4)
494.3 (278.5)
t = 1.46 c
t = 2.59 c
t = .90 c
t = 1.87 c
t = 2.81 c
Note: NART: National Adult Reading Test; CPZe: Chlorpromazine equivalent;
PANSS: Positive and Negative Symptom Scale.
⁎p b 0.05.
⁎⁎p b 0.01.
a
One-way ANOVA between three participant groups.
b
Pearson's Chi-Square test between three participant groups.
c
Independent samples t-test between two patient groups.
IQ N80 as scored by the National Adult Reading Test (NART:
Nelson and Willison, 1991).
2.2. Medication
Schizophrenia patients were taking a higher dose of
antipsychotic medication than the BD patients, as represented
in equivalent mg of Chlorpromazine (CPZe) (Table 1). Of the
schizophrenia patients, 26 were taking antipsychotic medication alone, eight were taking a combination of antipsychotic
and antidepressant medications, one was taking an antidepressant alone, two were taking a combination of antipsychotic, antidepressant and mood stabiliser medications
and two were medication free. Of the BD patients, one was
taking antipsychotic medication alone, one was taking
antidepressant medication alone, nine were taking mood
stabiliser medication alone, one was taking a combination of
antipsychotic and antidepressant medications, eight were
taking a combination of antipsychotic and mood stabiliser
medications, eight were taking a combination of antidepressant and mood stabiliser medications, six were taking a
combination of antipsychotic, antidepressant and mood
stabiliser medications and six were medication free.
2.3. Procedure
The following procedure was approved by the Health
Sciences Human Ethics Sub-Committee of The University of
Melbourne and was carried out in accordance with the latest
version of the Declaration of Helsinki.
The HSCT took each participant approximately 5 min to
complete (Burgess and Shallice, 1997). The task involved two
sections; in each section the investigator read aloud 15
sentences with the last word omitted i.e. ‘The old house will
be torn…’. In section one (response initiation), participants
were required to complete the sentence sensibly as quickly as
possible, i.e. ‘The old house will be torn… down’. In section 2
(response suppression), participants were required to nonsensically complete the sentence as quickly as possible by
giving a word that does not fit in the context of the sentence,
i.e. ‘The old house will be torn… banana’. This requires
suppression or inhibition of the immediate response and then
initiation of an alternative response. For each section the
response latencies for the 15 sentences were recorded and
summed to produce a total time. Participants were also scored
on the number of errors for section two. Category A errors
were scored when participants provided a sensible completion of the sentence, when the response should have been
unconnected to the sentence, i.e. ‘Most cats see very well at…
night’. The possible range for A errors was 0–15. Category B
errors were scored when participants provided a word which
was somewhat semantically related to the sentence but not a
typical direct completion, i.e. ‘Most cats see very well at…
midday’ or ‘Most cats see very well at… dogs’. The possible
range for B errors was 0–10+. The total time scores and the
number of errors were transformed into scaled scores (SS),
according to the manual guidelines, and then summed to
provide an overall SS ranging from 1 (impaired) to 10 (very
superior).
2.4. Statistical analysis
Demographic group differences were assessed via Pearson's Chi-Square tests or one-way between groups analysis of
variance (ANOVA) with Bonferroni post-hoc tests. Clinical
group differences were assessed via independent samples ttests.
Task-related group differences were assessed via one-way
between groups ANOVA with Bonferroni post-hoc tests.
Analysis was performed on the Overall SS and on a number
of measures based on response time and error pattern,
including: sensible completion time (Section 1 SS; the time
taken to initiate a response), unconnected completion time
(Section 2 SS; the time taken to inhibit the natural response
and initiate an alternative response), suppression time (total
time Section 2–total time Section 1; the actual time taken for
response inhibition), total errors (Section 2 error SS; the total
number of errors produced), connected errors (A score:
sensible completion of the sentence), somewhat connected
errors (B score; semantically related completion of the
sentence).
Relationships between the HSCT measures and demographic and clinical characteristics were investigated using
exploratory Pearson's product moment correlations with
Bonferroni adjustment made for multiple comparisons. The
relationship between gender and task performance was
investigated via multivariate tests.
3. Results
3.1. Demographics
As shown in Table 1, there was no significant difference in
age, gender or predicted IQ between the three groups. There
was no significant difference in age of illness onset or length
of illness between the two patient groups. Schizophrenia
patients scored significantly higher on the negative factor of
N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
the PANSS, however there were no significant patient group
differences for the positive factor, general factor or total
PANSS scores. Overall, both patient groups were well matched
and showed similar levels of psychopathology.
87
of their response than healthy control participants and BD
patients; however this group difference did not reach
significance (Table 2).
3.4. Response errors
3.2. SCT
As indicated in Table 2, the analysis revealed significant
differences in performance between schizophrenia patients,
BD patients and control participants on measures of the HSCT.
Firstly, the Overall SS is a total measure that combines
response initiation and response suppression as well as error
rate and provides a general indicator of task performance.
Schizophrenia patients demonstrated significantly lower
Overall SS (5.1 out of 10) than both the healthy control
group (6.4) and the BD group (6.0); there were no significant
differences between the BD group and the healthy control
group. According to the classification guidelines (Burgess and
Shallice, 1997), controls and BD patients consistently revealed
‘average’ performance (within the 50th percentile), whereas
the schizophrenia patients performed at ‘moderate average’
levels (within the 25th percentile). Although schizophrenia
patients had poorer performance, they were not considered
to demonstrate any of the lower classifications, such as low
average, poor, abnormal or impaired performance, as indicated in the task guidelines.
3.3. Response latency
The time taken to simply initiate a sensible response to a
sentence or to suppress a response and initiate an alternative
response, was slower for schizophrenia patients compared to
healthy controls as reflected by a significantly lower Section 1
SS and Section 2 SS, respectively. The BD group did not differ
in performance compared to either healthy controls or
schizophrenia patients (Table 2). Again, the standardised
classification indicated that the healthy control group and the
BD group demonstrate average performance and the schizophrenia group demonstrates moderate average performance.
To investigate the actual time to inhibit a response while
taking into account the time to initiate a response, a separate
measure of suppression was created (suppression score: total
time Section 2 in seconds–total time Section 1 in seconds).
Group comparisons on this suppression measure revealed
schizophrenia patients took longer for the actual suppression
Analysis of the overall standardised measure of error
(Section 2 error SS) indicated that the schizophrenia group
made more response errors than the healthy control group.
The BD group did not significantly differ in the rate of
response error compared to the healthy control group or the
schizophrenia group (Table 2). The standardised classification
once again indicated average performance for the healthy
control group and BD group and moderate average performance for the schizophrenia group. Upon investigation of the
pattern of response errors shown by participants, analysis
revealed schizophrenia patients demonstrated more connected errors (A errors) than the healthy control group.
Further, schizophrenia patients also demonstrated significantly more semantically related errors (B errors) than both
the healthy control group and the BD group who did not
significantly differ from one another. As indicated in Table 2,
the standard deviation of the schizophrenia group was
particularly large for the number of B errors made. To
investigate this spread of response, a plot of the raw data
can be observed in Fig. 1. This figure indicates while there was
a greater spread in the number of errors for schizophrenia
patients, there are no definable subgroups. The spread is
therefore most likely indicative of the heterogeneity in
cognitive capacity common to schizophrenia samples.
3.5. HSCT performance correlations with demographic and
clinical characteristics
Analysis revealed only one correlation between predicted
IQ and HSCT, this was in the BD patients between IQ and
Section 1 SS (r = 0.56, p b 0.007). Similarly, there were no
significant relationships between age and HSCT performance
for the three participant groups, with one exception; age of
healthy control participants was significantly correlated with
the Section 2 SS (r = −0.42, p b 0.007). Analysis also revealed
there was no overall relationship between gender and HSCT
performance. Moreover, there was no interaction between
gender and group for any of the HSCT measures, indicating
Table 2
Comparison of schizophrenia patients and control participants on the HSCT mean (standard deviation).
Overall scaled score (range 1–10)
Section 1 scaled score (range 1–7)
Section 2 scaled score (range 1–8)
Suppression score (seconds)
Section 2 error scaled score (range 1–8)
A errors–Connected errors (range 0–15)
B errors–unconnected errors (range 0–10+)
Controls n = 44
BD n = 40
Schizophrenia n = 39
Comparisons a
Post-hoc comparison
6.4 (1.2)
6.0 (0.8)
6.1 (0.8)
15.8 (16.8)
6.6 (1.5)
0.5 (0.8)
1.8 (1.8)
6.0 (1.3)
5.7 (0.9)
5.9 (0.9)
18.7 (25.4)
6.2 (2.1)
0.9 (1.4)
2.2 (2.2)
5.1 (1.5)
5.3 (1.3)
5.5 (1.0)
26.2 (25.8)
5.3 (2.3)
1.2 (1.4)
3.4 (2.6)
F = 9.44⁎⁎⁎
F = 4.80⁎
F = 5.38⁎⁎
SZ b CTRL, BD
SZ b CTRL
SZ b CTRL
F = 2.27, p = 0.11
F = 4.91⁎⁎
F = 3.29⁎
F = 6.44⁎⁎
SZ b CTRL
SZ N CTRL
SZ N CTRL, BD
SZ: Schizophrenia, CTRL: Healthy control, BD: Bipolar disorder.
⁎p b 0.05.
⁎⁎p b 0.01.
⁎⁎⁎p b 0.001.
a
Comparisons refer to one-way ANOVA between three participant groups with Bonferroni Post-hoc tests.
88
N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
Fig. 1. Plot of the raw data corresponding to the number of B errors (range = 0–10+) made by schizophrenia patients, bipolar disorder patients and control
participants.
males and females from the three different groups performed
similarly to one another.
For the schizophrenia and BD patients, there were no
significant correlations between medication, illness duration,
or PANSS ratings with the HSCT measures. One of the most
significant findings of this data is that of elevated semantic
errors in the schizophrenia group. There is a prominent
literature that has established that schizophrenia patients
with delusions (Rossell et al., 1999) and/or thought disorder
(Rossell and Stefanovic, 2007) are the most likely to show
semantic errors. These relationships were investigated in the
current study. For the schizophrenia patients there were no
significant correlations between the PANSS rating P1 (delusions) and the HSCT measures, there were however correlations for the PANSS rating P2 (conceptual disorganisation)
(r = .34–.41, p b .05). There were no apparent P1 or P2
correlations for the BD patients.
4. Discussion
To our knowledge this is the first study to report
comprehensive HSCT data in schizophrenia patients with
the inclusion of both psychiatric and non-psychiatric control
groups for comparison. Consistent with expectations, schizophrenia patients' revealed impaired performance compared
to healthy control participants. Discordant with expectations
the BD patients were more similar in their performance to the
healthy controls than the schizophrenia group.
As expected, overall HSCT performance of the schizophrenia group was lower than that of the healthy control
group. This impairment in performance was further observable on each specific aspect of the HSCT. Schizophrenia
patients exhibited longer average response latency for simple
response initiation and response suppression, and demonstrated an increased rate of response error (as also reported in
Groom et al., 2008; Nathaniel-James et al., 1996; Waters et al.,
2003). These results indicate that not only did the schizophrenia group show a slowing in baseline response initiation,
but there was also slowing of the suppression of the response.
The suppression of an inappropriate response is thought to
engage the Supervisory Attentional System (SAS) which
controls intentional cognitive processes (Shallice, 1988),
involving prefrontal cortical activation. Indeed, the HSCT
promotes activation in the prefrontal cortex (Collette et al.,
2001), and the deficits in performance on the HSCT shown by
schizophrenia patients have been related to functional
abnormalities in prefrontal cortical regions (Whalley et al.,
2004).
Inspection of the error rate data indicated that compared
to healthy controls, schizophrenia patients exhibited more
errors that were sensible completions of the sentence (A
errors) as well as more errors that were semantically related
to the sentence (B errors). Interestingly, upon inspection of
the actual responses given by the schizophrenia patients, it
appeared they did not utilise the strategies commonly
employed by the control participants, including providing
sentence completions from items around the room, or all
from one particular semantic category. This is consistent with
previous literature that has reported impaired strategy
utilisation in schizophrenia (Kim et al., 2007). It also relates
to research that has shown schizophrenia patients are more
likely to produce semantically or associated errors to simple
questions (Rossell and Batty, 2008). The actual responses
given by the schizophrenia patients were examined for any
consistencies in incorrect responses. There was no obvious
pattern to the incorrect responses. There were, however,
some consistent errors within several items. For example, for
the sentence “Most cats see very well at…”, the majority of
the schizophrenia patients who demonstrated a B category
error, responded with the name of an animal e.g. dog. Another
example can be observed for the sentence “The whole town
came to hear the mayor…”. The majority of the schizophrenia
patients who demonstrated a B error, responded with a sound
e.g. sing. These B category errors were clearly connected to the
sentence, often being fairly concrete, semantically related
responses. However, it must be noted such a consistent
pattern was only found for approximately one third of
sentences, thus response errors were context-dependent
and variable.
A hallmark feature of schizophrenia is formal thought
disorder, whereby patients show disorganised, tangential and
illogical thought often reflected by incoherent speech
(American Psychiatric Association, 2000). There are a number
of studies that have suggested that thought disorder is a
N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
product of impaired planning and response inhibition, and
thus is related to performance on executive function tasks (i.e.
Kerns and Berenbaum, 2002). Our results did indicate a
tendency for schizophrenia patients who scored higher on the
PANSS measure of thought disorder (P2), to demonstrate
greater impairment on the task. However, the current sample,
in general, only showed low ratings on the P2 variable,
making conclusions difficult to draw. This could be a point of
interest for future studies, involving patients with greater
thought disorder. The error data, and the relationship of the
task with thought disorder, do highlight the possibility that
some language disturbances in schizophrenia may be the
product of faulty executive control, implying that some
positive symptoms of psychosis may be better described as
cognitive deficits. Interestingly, the same frontal circuitry has
been implicated in ‘at risk’ psychosis patients for HCST
(Whalley et al., 2008) and executive language measures
(verbal fluency, Broome et al., 2009).
The results of the current study clearly indicated that
schizophrenia patients showed impaired performance compared to the healthy control group. Interestingly, however, the
schizophrenia group also showed impairment when the
overall performance score and the number of B errors was
compared to the psychiatric control group of BD patients.
Both patient groups were matched on age at illness onset,
illness duration and total PANSS rating, further there were no
significant correlations between these measures and task
performance. Consequently, the deficits shown by the
schizophrenia patients appear to be specific to the diagnosis
rather than reflecting these other psychopathological characteristics. To our knowledge, this is the first study to make
detailed comparisons between schizophrenia and BD patients
on the HSCT measures of response initiation, response
suppression and response error. While McIntosh et al.
(2005) compared both patient groups, only overall performance measures were reported with limited depth of
analysis. The current results are in agreement with a recent
neuroimaging paper that revealed schizophrenia and BD
patients demonstrate different frontal activation patterns
during an adapted HSCT paradigm (McIntosh et al., 2008).
The schizophrenia group showed reduced activation in the
left dorsolateral prefrontal cortex, and the BD group showed
increased activation in this area. This suggests that the
cognitive profile and neurobiological substrates are different
in schizophrenia and BD.
The present data also revealed that the BD patients did not
differ in HSCT performance compared to the healthy control
participants. This finding was contrary to our hypothesis as
well as previous studies utilising the HSCT in BD (Dixon et al.,
2004; Stoddart et al., 2007). There has however, been one
other study to show intact HCST in BD (Rocca et al., 2008).
Inspection of the demographic and clinical characteristics did
not reveal any clearly differentiating variables to explain why
some studies reveal impaired performance by BD patients and
others reveal intact performance. The BD patients in the
current sample were tested during a euthymic state. Euthymic
patients have demonstrated both impaired performance
(Dixon et al., 2004) and intact performance (Rocca et al.,
2008) in the literature. One potential conclusion is that the
discrepant findings may be due to procedural, instructional
and/or scoring differences between studies. Interestingly,
89
category fluency has also reported to be intact in BD (Rossell,
2006); with BD patients producing no out of category errors.
Category fluency is certainly a comparable task, both requiring a verbal response, speech planning and response
suppression of inappropriate responses: again, highlighting
the parallels with some executive function and language
tasks.
One potential limitation of this study was that the
schizophrenia and BD patient groups were not matched on
dose of antipsychotic medication and were taking a different
range of medications. Although there is considerable overlap
between the two disorders, a difference in medication was
expected; the illness presentation for schizophrenia and BD is
distinctly different and accordingly require different courses
of treatment. As the medication characteristics were not
matched for the two groups, it may be possible that
pharmaceutical treatment impacted on task performance.
Indeed, previous work has shown that antipsychotic medication can adversely affect cognitive skill when given to healthy
control participants (Peretti et al., 1997). The current results,
however, indicated no significant correlations between
medication and task performance, therefore it is unlikely
the impairment demonstrated by schizophrenia patients was
a result of medication effects. Previous findings in schizophrenia (McIntosh et al., 2005) and BD patients (Stoddart
et al., 2007) have suggested performance appears relatively
independent of medication.
The current study revealed schizophrenia patients show a
clear slowing in response initiation as well as problems with
suppression of response. These deficits do not appear
secondary to the illness as they remain evident when
compared to individuals sharing similar characteristics
resultant of psychiatric illness. Response suppression is a
key feature of executive functioning, and is an aspect of
neurocognitive functioning that is crucial to carrying out dayto-day tasks. A review of the schizophrenia literature shows
that neurocognitive ability is clearly linked to functional
outcome (Green, 1996; Green et al., 2000). Interestingly, the
relationship between neurocognitive impairment and functional outcome appears much stronger than that between
psychotic symptomatology and functional outcome. This
provides direct implication for targeted neurocognitive
remediation strategies for schizophrenia (Medalia and Lim,
2004). Further, considering the wide heterogeneity in
neurocognitive performance in schizophrenia, it may be
appropriate to tailor remediation tools to an individual's
cognitive strengths and weaknesses (Green et al., 2000).
Role of funding source
Nicole Joshua was funded by the Sir Robert Menzies Memorial Research
Scholarship for Allied Health Sciences from The Menzies Foundation. Further,
Andrea Gogos was supported by a National Health and Medical Research
Council (NHMRC) fellowship (ID 435690). This research was also supported
by Operational Infrastructure Support (OIS) from the Victorian State
Government. The funding bodies had no further role in study design; in
the collection, analysis and interpretation of data; in the writing of the
report; or in the decision to submit the paper for publication.
Contributors
Authors Nicole Joshua and Andrea Gogos designed the study and
collected the data. Nicole Joshua managed literature searches, undertook
the statistical analysis and wrote the first draft of the manuscript. Andrea
Gogos provided thorough edits to the first draft of the manuscript. Author
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N. Joshua et al. / Schizophrenia Research 114 (2009) 84–90
Susan Rossell managed the study design, data collection and data analysis
and edited the first draft of the manuscript. All authors contributed to and
have approved the final manuscript.
Conflict of interest
The authors declare they have no conflicts of interest.
Acknowledgements
The authors would like to acknowledge the Menzies Foundation and the
National Health and Medical Research Council (NHMRC) for the financial
support of Nicole Joshua and Andrea Gogos. Many thanks also go to Alison
O'Regan for assistance with some of the clinical interviewing and Prof David
Castle for assistance with patient recruitment.
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