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Theory of Mind, Causal Attribution

and Paranoia in Asperger Syndrome
ARTICLE in AUTISM JULY 2001
Impact Factor: 3.5 DOI: 10.1177/1362361301005002005 Source: PubMed
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Theory of Mind, Causal Attribution and Paranoia in Asperger Syndrome

Alison J. Blackshaw, Peter Kinderman, Dougal J. Hare and Chris Hatton
Autism 2001 5: 147
DOI: 10.1177/1362361301005002005
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Theory of mind, causal

attribution and paranoia in
Asperger syndrome
A L I S O N J . B L A C K S H AW
PETER KINDERMAN
D O U G A L J. H A R E
C H R I S H AT T O N
autism 2001
SAGE Publications
and The National
Autistic Society
Vol 5(2) 147163; 017454
1362-3613(200106)5:2
University of Manchester, UK
University of Liverpool, UK
University of Manchester, UK
Lancaster University, UK
Theory of mind (ToM) deficits are central to autistic

spectrum disorders, including Asperger syndrome. Research in psychotic disorders has developed a cognitive model of paranoid delusions
involving abnormal causal attributions for negative events. Possible
aetiologies of these include deficits in social reasoning, specifically ToM.
The present study investigated this attributional model of paranoia in
Asperger syndrome. Participants diagnosed with Asperger syndrome
scored significantly higher on a measure of paranoia and lower on a
measure of ToM, compared with the control group. They did not differ
in self-concept and causal attributions, contrary to the attributional
model of paranoia. A regression analysis highlighted private self-consciousness as the only predictor of paranoia. The theoretical and clinical implications of these findings are discussed.
A B S T R AC T
K E Y WO R D S
Asperger
syndrome;
causal
attributions;
paranoia;
theory of
mind
Correspondence should be addressed to: D R P E T E R K I N D E R M A N ,

Reader in Clinical Psychology, Department of Clinical Psychology, University of Liverpool,
Whelan Building, Quadrangle, Brownlow Hill, Liverpool L69 3GB, UK. e-mail:
p.kinderman@liverpool.ac.uk
ADDRESS
Introduction
In 1944 Hans Asperger described a group of children with very similar
social disturbances to autism but with relatively well preserved language
and general intellectual skills, and the term Asperger syndrome was first
used by Wing (1981). DSM-IV (American Psychiatric Association, 1994)
diagnostic criteria for Asperger syndrome include marked impairments in
social interaction, and restricted, repetitive or stereotyped patterns of
behaviour. These are associated with a clinically significant impairment in
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social functioning, but in the absence of any clinically significant general
delay in language or cognitive development. Prevalence rates for Asperger
syndrome have been estimated at 36 per 10,000 (Fombonne, 1997), but
there is still considerable controversy regarding its distinction from highfunctioning autism (Klin et al., 2000).
The main characteristics that distinguish Asperger syndrome from
autism are normal or near normal intelligence and language abilities. Individuals with this condition have lifelong problems in understanding and
maintaining social relationships coupled with normal intellectual abilities.
Thus, they may be more aware of and distressed by their differences (Hare,
1997), and it has been suggested that they may have serious psychological
difficulties in adult life (Tantam, 1989).
Although there has been a growing interest in various forms of psychotherapeutic work with people with learning disabilities over the past
decade, interventions for individuals with Asperger syndrome are limited
and tend to focus on such aspects as social skills training. There is clearly a
need to develop more appropriate clinical interventions for this group
(Hare, 1997) but before this can be achieved insight needs to be gained
into the cognitions of people with a diagnosis of Asperger syndrome. The
present study focuses specifically on problems in social cognition in individuals with Asperger syndrome, frequently referred to as deficits in theory
of mind (ToM). ToM refers to the ability to think about thoughts and to
attribute mental states to others. It has been suggested that ToM is the key
cognitive ability that autistic people lack (Baron-Cohen et al., 1985) and
that it is this underlying deficit that can account for the triad of impairments associated with autism.
Difficulties in interpreting subtle social clues caused by a deficit in ToM
are highly likely to influence the way in which people diagnosed with
Asperger syndrome explain social situations. Causal attributions such as
these have been widely employed in psychological models of several psychiatric problems. In particular, it has been suggested that attributions feed
into paranoia and persecutory delusions. It is therefore interesting to note
that several clinicians have reported paranoia as a clinical problem in
Asperger syndrome (Hare, 1997;Tantam, 1989;Wing, 1996), although the
frequency with which it is observed is unclear.
Although the cognitive biases in people with Asperger syndrome
remain under-researched, the cognitive basis of paranoia in delusional
states such as schizophrenia has been better documented. Bentall et al.
(1994) and Bentall and Kinderman (1998) have recently proposed a
detailed attributional model of paranoid ideation. In this model, threats to
the self-concept are assumed to make individuals more consciously aware
of latent discrepancies between self-actual and self-ideal representations. In
AU T I S M
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B L A C K S H AW E T A L . : T H E O RY O F M I N D I N A S P E R G E R S Y N D R O M E
the development of persecutory delusions, external, other-blaming attributions are used to explain the occurrence of potential threats (These bad
things are not my fault, someone else is responsible). It is assumed that
this personalizing bias protects the fragile self-concept, but leads to persecutory ideas. Bentall and Kinderman (1998) have developed this model
by explicitly invoking cognitive dysfunction and theory of mind.
The contribution of ToM deficits to the tendency to produce external
personal attributions (other person blaming) in association with paranoid
ideation is easy to imagine. A negative social interaction (e.g. a friend
ignores you) can be explained in two ways. One is in terms of circumstances (e.g. they did not see you, they were in a rush, they were upset and
did not want you to see them upset), which involves making external situational attributions (blaming the situation). The other is in terms of the
friends personality (e.g. they are rude), which involves making external
personal attributions (blaming someone else). The former requires the
ability to appreciate the world from anothers perspective and this requires
an adequate ToM. If the account proposed by Bentall and Kinderman (1998)
is correct then the present study should show that ToM deficits are associated with external personal attributions for negative events.
The model also proposes a possible role for cognitive disorganization,
with reference to ToM. It is hypothesized that ToM performance is dependent on general cognitive resources, in particular executive functioning
(Corcoran et al., 1995; Davis and Pratt, 1995). The making of situational
external attributions is inherently complex, depending on the use of
second-order explanations for events. A deficiency in such complex information processing will affect ToM. This is consistent with findings from
research with individuals with paranoid schizophrenia who have been
shown to experience information processing impairments and ToM deficits
when acutely ill (Bentall and Kinderman, 1998).
Four main hypotheses were investigated in the present study. It was predicted that people with a diagnosis of Asperger syndrome would show difficulties with ToM and central executive functioning when contrasted with
people without a diagnosis of Asperger syndrome. It was also predicted that
people with a diagnosis of Asperger syndrome would show higher levels of
paranoid ideation and self-consciousness than people without a diagnosis
of Asperger syndrome. We predicted that people with a diagnosis of
Asperger syndrome would show specific differences from people without
a diagnosis of Asperger syndrome in scores on a measure of casual attribution. Specifically, we predicted no differences in measures of internalizing bias (self-blame) but a bias towards personal (other blaming) as
opposed to situational attributions, with regards to negative events. Finally,
we predicted that, for the combined population, there would be significant
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negative correlations between scores on ToM measures and measures of
central executive functioning, as well as significant positive correlations
between scores on ToM measures, measures of causal attribution and
measures of paranoid ideation.
AU T I S M
Method
Design
An independent groups design was employed, comparing a normative
group with a group of people with a diagnosis of Asperger syndrome.
Measures were used to investigate ToM, paranoia, attributional style, selfconsciousness, self-representations, anxiety and depression, intellectual
functioning and executive functioning.
Participants
A total of 25 participants with a diagnosis of Asperger syndrome as
recruited, 5 female and 20 male. Ages ranged from 15 to 40 years, mean
age 23 years. Participants were recruited via two routes: 13 were recruited
through the north west regional office of the UK National Autistic Society
and 7 by contacting network managers of small staffed residential houses
for people with learning disabilities. In addition, data from 5 participants
were collected via a postal system.
Before participation in the study the participants, or the carers of the
participants, were asked to provide information regarding their diagnosis.
Only participants who had received a diagnosis of Asperger syndrome from
a medical practitioner (psychiatrist or paediatrician) were considered for
entry to the study. Following initial identification, the first author interviewed potential participants to ascertain status according to DSM-IV diagnostic criteria (American Psychiatric Association, 1994). People who were
unable to fill in the test questionnaires independently were excluded from
the study.
Eighteen participants were recruited to the control group, 11 female
and 7 male. Ages ranged from 20 to 46 years, mean age 31 years. All participants were recruited via informal contacts and were not matched to the
clinical sample with regard to gender, age or IQ.
Measures
Paranoia Scale
The Paranoia Scale (Fenigstein and Vanable, 1992) is a 20-item self-report
measure of paranoid ideation derived from MMPI (Minnesota Multiphasic
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Personality Inventory) items. It is designed to be administered to participants who are not psychiatric patients and has been shown to have good
internal consistency, testretest reliability and validity as indicated by its
relationship with a number of theoretically interesting measures (Fenigstein
and Vanable, 1992).
Internal, Personal and Situational Attributions Questionnaire

(IPSAQ)
The IPSAQ (Kinderman and Bentall, 1996a) is a measure of causal attributions, independently measuring three loci of attributions for both positive
and negative events. It consists of 32 items that describe in the second
person 16 positive social situations, for example a friend helped you with
the gardening, and 16 negative social situations, for example a friend
talked about you behind your back. Participants read the statements, try to
imagine themselves in the situation, and then attempt to produce a single,
most likely, causal explanation for each statement. Following this they are
asked to categorize the given cause to one of three domains: internal
(something to do with the participant themselves), personal (something
about another person or persons) and situational attributions (something
about the situation, circumstances or chance).
Two cognitive bias scores are produced from the six subscale scores:
externalizing bias (EB: the number of internal attributions for positive
events minus the number of internal attributions for negative events)
reflecting self-serving bias, and personalizing bias (PB: the proportion of
personal as opposed to situational external attributions for negative events).
Projective Imagination Test (PIT)
The PIT is an unpublished measure of theory of mind (ToM) ability.1 It is
designed to cue open-ended verbal responses about participants conceptions of four scenarios and the thoughts and feelings of the subjects portrayed. It consists of four simple black and white line drawings of social
situations, for example a boy standing leaning against a lamppost. Participants are instructed to produce stories about each picture. It is administered
twice: first uncued, where they are given an open-ended question to
describe what they think is happening in the picture; and second cued,
where they are prompted by the question What do you think the
person/people in the picture is/are thinking or feeling to give mental
states regarding the people in the pictures.
Overall cued and uncued scores are obtained for the four pictures by
adding together the number of mental states produced. The PIT is a new
measure that has been piloted with both psychiatric patients and nonpatient populations and is currently being employed in a number of
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ongoing investigations. The range of mental states generated was also
calculated, defined as the number of non-replicated mental states produced.
AU T I S M
Stroop task
The Stroop task (Stroop, 1935) is a simple and widely used test of executive
functioning, specifically selective attention. Three sets of words are printed
in four different colours, red, yellow, green and blue. The words are either
blocks of noughts; or the colour words printed in the correct ink colour
(blue printed in blue ink); or the colour words printed in the incorrect
ink colour (blue printed in red ink, for example). Participants are timed
reading aloud the colour of the ink in which these words are printed. This
task assesses the degree to which the name of the word interferes with the
ability swiftly to name the ink colours. An interference index is calculated
by subtracting the time taken to name the ink in the consistent condition
from the equivalent time for the interfering condition.
The Stroop task was employed in the present study in order to assess
the hypothesized effect of central executive dysfunction on ToM and, consequently, on attributional style and paranoid ideation.
Hospital Anxiety and Depression Scale (HAD)
The HAD (Zigmond and Snaith, 1983) is a quick and simple measure of
anxious and depressed mood. It consists of 14 statements concerning feelings of depression and anxiety in the past week rated on a four-point scale.
Individual statement scores are summed to produce two numerical scores,
for depression and anxiety. The HAD demonstrates good internal consistency and has been widely used in research (Rehm, 1988). The HAD was
used in the present study because depressed mood is known to influence
both causal attributions (Brewin, 1985) and cognitive functioning (Lezak,
1995).
National Adult Reading Test (NART)
The NART (Nelson, 1982) is a brief measure of intelligence based on the
pronunciation of irregularly spelt English words. It comprises a list of 50
words printed on a card in order of increasing difficulty. The words are all
irregular with respect to the common rules of pronunciation. From the
number of errors in pronunciation, it is possible to obtain an estimate of
the individuals IQ. The NART was included in the test battery in order to
control for possible effects of intellectual ability as opposed to more
specific deficits in cognitive function, and to confirm that the intellectual
ability of the participants was consistent with a diagnosis of Asperger
syndrome.
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Self-Discrepancies Questionnaire
The Self-Discrepancies Questionnaire is a straightforward measure of selfrepresentation. It closely follows the original Selves Questionnaire
(Higgins, 1987; Higgins et al., 1986). Participants are required to generate up to 10 words that describe them as they actually are, as they would
ideally like to be and as they believe others see them. Participants are also
required to provide a numerical rating from 1 to 10 depending on to what
degree they felt they actually possessed, or would like to possess, or other
people would say they possessed, each characteristic. Minor amendments
to the nature of these numerical ratings are the only difference between the
original Selves Questionnaire and the version used in the present study.
The Self-Discrepancies Questionnaire resulted in two numerical scores;
self-actual/self-ideal (SASI) consistency and self-actual/other-actual
(SAOA) consistency.The scoring system paralleled that of the original Selves
Questionnaire (for detailed description of the scoring system see Scott and
OHara, 1993). Positive scores therefore reflect consistency, whereas negative scores reflect discrepancy between the domains. Reliability of the Selves
Questionnaire (in its original and modified forms) is very high, with reliability coefficients above 0.9 (Kinderman and Bentall, 1996b; Scott and
OHara, 1993).
The Self-Discrepancies Questionnaire was included in the assessment
battery because, as mentioned above, abnormalities in self-representation
are central to the attributional model of paranoid ideation under investigation (Kinderman and Bentall, 1996a).
Self-Consciousness Scale
The Self-Consciousness Scale (Fenigstein et al., 1975) is a 23-item scale
assessing: private self-consciousness (attention to the private aspects of the
self, such as feelings or motives), public self-consciousness (attention to the
self as a social object, i.e. as an entity that is the object of awareness of
others) and social anxiety. Items are rated on a five-point scale. The questionnaire has good reported reliability (testretest reliability alpha = 0.80;
Fenigstein et al., 1975).
The Self-Consciousness Scale was included in the present study for two
reasons. First, sensitivity to self-referent material is a key element of the
model of paranoid ideation under test (Bentall et al., 1994). In addition, a
slightly different model of paranoid ideation has been proposed by Fenigstein and colleagues (Fenigstein and Vanable, 1992). The use of the SelfConsciousness Scale in the present study allowed for the simultaneous
testing of both models.
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Procedure
Participants and their families were provided, verbally, with standardized
information prior to the interview informing them of the basic aims of the
study, what their involvement would entail, confidentiality and the right to
withdraw from the project at any time. Their agreement was taken to be
informed consent. Administration of the test material took place in a quiet
room in the participants home, in a day centre or in a residential home.
The whole procedure took between 1 and 2 hours.
For five of the participants in the Asperger group, administration of the
measures took place by posting questionnaires out to the participants. For
these individuals a complete data set was unable to be collected as the
Stroop and NART could not be undertaken.
It was necessary to allow the testing session to be flexible and to be
adapted to participants requirements, especially within the Asperger group.
Where motivation, concentration and/or anxiety proved to be a problem
the testing session was divided into separate sessions. Any questionnaires
that were inappropriate were not undertaken, for example, the NART was
not used with one individual who chose not to communicate verbally.
Results
Comparative studies
T-test analysis for independent groups was used to allow for comparison
of the age of the two groups. For this and all other t-test analyses, normality of the data was assured via one-sample KolmogoroffSmirnoff tests and
consideration of skewness and kurtosis. All variables met basic criteria for
parametric analysis. Levenes test for equality of variance was carried out to
determine the appropriate statistic, t-value and probability. The data for all
variables of interest are presented in Table 1.
As can be seen in Table 1, there was a significant difference in the mean
age of the two groups. Participants with a diagnosis of Asperger syndrome
were significantly younger than the control group (t(40) = 3.83, p <
0.001). There was also a significant difference in the gender of the two
groups (chi square (1) = 6, p < 0.02) with more women in the control
group.
Participants with a diagnosis of Asperger syndrome obtained lower
NART estimated full-scale IQ scores than the control group (t(34) = 4.35,
p < 0.005). Because of this difference, NART full-scale IQ score was used
as a covariate in ANCOVA comparisons of all other variables. It is worth
noting that, although the participants with a diagnosis of Asperger syndrome on average recorded a lower estimated IQ score than the control
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Table 1
Summary statistics for all variables

Group
Control
People with a
diagnosis of
Asperger syndrome

Mean
(SD)
Mean
(SD)
Age
NART full-scale IQ
Paranoia Scale
31.39
109.50
(7.85)
(10.73)
22.71
93.33
(6.82)
(11.54)
t-value
3.83
4.35
p-value
<0.001
<0.001
38.72
(11.53)
52.18
(17.32)
F-ratio
5.26
<0.01
Internal, Personal and

Situational Attributions
Questionnaire (IPSAQ):
Externalizing bias
Personalizing bias
2.24
0.515
(3.61)
(0.274)
0.85
0.618
(4.40)
(0.263)
0.54
1.77
0.467
0.195
Projective Imagination
Test (PIT):
ToM uncued
ToM cued
ToM range uncued
ToM range cued
8.00
9.08
7.53
8.08
(4.49)
(3.20)
(4.35)
(2.71)
4.32
6.67
3.72
5.21
(3.38)
(4.63)
(2.67)
(4.51)
9.13
7.26
10.00
5.76
<0.005
<0.05
<0.005
<0.024
66.50
(17.88)
92.18
(29.80)
2.00
0.167
Hospital Anxiety and

Depression Scale (HAD):
Anxiety
Depression
6.89
3.61
(3.83)
(2.75)
8.74
4.58
(5.51)
(3.67)
3.41
0.59
0.074
0.448
Self-Discrepancies
Questionnaire:
SASI consistency
SAOA consistency
0.56
4.89
(4.33)
(4.41)
0.39
2.32
(5.40)
(4.68)
0.08
2.22
0.775
0.147
18.67
18.22
13.94
(5.43)
(5.36)
(5.97)
23.48
17.09
13.39
(5.62)
(4.86)
(4.84)
8.01
0.11
0.01
<0.005
0.744
0.939
Stroop discrepancy
Self-Consciousness Scale:
Private
Public
Social anxiety
Note: t-test statistics refer to comparisons of the control and experimental groups. F-ratios refer to
comparisons of the two groups by ANCOVA, with NART full-scale IQ score as covariate. SASI and
SAOA consistencies refer to consistency scores between the self-actual and self-ideal and between the
self-actual and other-actual domains on the Self-Discrepancies Questionnaire. Other variables are
explained in the text.
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group, all participants scored within the normal range of IQ. Although participants with a diagnosis of Asperger syndrome appeared to perform significantly slower on the Stroop task (Stroop interference effect between
speed of colour naming for concordant and discordant words: (t(31) =
2.98, p < 0.01)), this difference disappeared when NART estimated fullscale IQ was entered as a covariate (F(1, 30) = 2.00, p = 0.167).
On the central dependent variable, participants with a diagnosis of
Asperger syndrome scored significantly higher on a measure of paranoia
than did the control group (F(1, 31) = 5.26, p < 0.01).
There were no significant differences observed in levels of anxiety (F(1,
32) = 3.41, p = 0.074) or depression (F(1, 32) = 0.59, p = 0.448) as
measured by the HAD between the two groups. The participants did not
differ in terms of self-actual/self-ideal discrepancy (F(1, 32) = 0.08, p =
0.775) or self-actual/other-actual self-discrepancy scores (F(1, 32) = 2.22,
p = 0.147).
As can be seen in Table 1, participants with a diagnosis of Asperger syndrome produced fewer mental states in both uncued (F(1, 32) = 9.13, p <
0.005) and cued (F(1, 26) = 7.26, p < 0.05) domains than participants in
the control group. The range of mental state terms produced followed a
similar pattern, for both cued (F(1, 32) = 10.00, p < 0.005) and uncued
(F(1, 26) = 5.76, p < 0.05) domains. It is worth noting, also, the results
of simple t-tests comparing the two groups without the addition of NART
full-scale estimated IQ as a covariate. In the uncued domain the difference
in number of mental states generated was highly significant (t(40) = 3.03,
p = 0.004), but in the cued domain the difference was not significant (t(34)
= 1.62, p = 0.115).
As can also be seen from Table 1, there were no significant differences
between the participants with a diagnosis of Asperger syndrome and the
control group in terms of either externalizing bias (F(1, 28) = 0.54, p =
0.467) or personalizing bias (F(1, 28) = 1.77, p = 0.195) on the IPSAQ.
This finding was contrary to our predicted hypotheses.
A multivariate analysis of covariance (MANCOVA) was conducted,
comparing the three subscales of self-consciousness (private, public and
social anxiety) between the two groups with NART estimated full-scale IQ
as a covariate. This revealed that the two groups did not differ significantly
on public self-consciousness (F(1, 32) = 0.108, p = 0.744) or social
anxiety (F(1, 32) = 0.006, p = 0.939).The participants with a diagnosis of
Asperger syndrome did, however, report significantly more private selfconsciousness than the control group (F(1, 32) = 8.01, p < 0.01).
Participants responses on the Paranoia Scale and the Self-Consciousness
Scale were subjected to metric analysis, to examine the possibility that
different patterns of responses were recorded by the two groups. A
AU T I S M
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repeated-measures multivariate analysis of variance was conducted on the

number of responses made by each participant to each of the five possible
answers to each item on these scales, with group membership as a betweensubjects variable.This revealed that there were no relative differences in the
frequency with which each option was endorsed (Paranoia scale, F(4, 35)
= 1.16, p = 0.347; Self-Consciousness Scale, F(4, 35) = 1.07, p = 0.387).
Correlational analysis
For the combined participant group, estimated full-scale IQ did not significantly correlate with the number of uncued (r(35) = 0.09, p = 0.593)
or cued (r(30) = 0.34, p = 0.062) mental states produced. The number of
mental states produced correlated with Stroop discrepancy, both cued
(r(29) = (0.41, p = 0.028) and uncued (r(33) = (0.35, p = 0.043). That
is, the poorer the performance on the Stroop, the fewer mental states produced in both the uncued and cued conditions of the PIT.
For the combined group of participants, full-scale IQ (estimated by the
NART) and performance on the Stroop task were significantly negatively
correlated (r(33) = (0.62, p < 0.001), such that higher estimated IQ was
correlated with a smaller discrepancy on the Stroop task.
A stepwise multiple regression analysis with paranoia scale scores as the
dependent variable was undertaken on the combined data from both participant groups. Independent variables were entered into the analysis if
identified as potentially significant by between-group comparisons. These
were: group (forced in), full-scale estimated IQ, Stroop discrepancy, age,
sex, number of uncued mental states and private self-consciousness. The
combined model was a significant predictor of paranoia (F(2, 28) = 10.14,
p < 0.0005). However, the only significant individual variable was private
self-consciousness (beta = 0.529, t = 3.42, p = 0.0019). None of the other
variables was a significant predictor of paranoid ideation. In a supplementary analysis, the regression procedure was repeated with the same variables as before, but omitting private self-consciousness and with all
variables entered, in order to examine the possibility that private self-consciousness shared explanatory variance with other variables. However, this
analysis revealed no significant predictors of paranoia (overall model: F(6,
24) = 1.75, p = 0.152).
Discussion
As predicted, individuals who were diagnosed with Asperger syndrome
scored lower on a test of theory of mind and higher on a measure of paranoia than did a group of control participants. However, the two groups did
not show specific differences on a measure of causal attribution. People in
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both groups were equally as likely to attribute negative events to themselves
as they were positive events, and to use both personal and situational
external attributions.
The present study questioned whether the paranoia observed clinically
in Asperger syndrome would stem from the same precipitating factors as
that observed in studies of schizophrenia. To reiterate, the model proposed
by Bentall and Kinderman (1998) assumes that a perceived threat to the
self-concept opens up discrepancies between the self-actual and the selfideal. This promotes defensive, paranoid attributions, where people
attribute the cause of the negative event to another person/people (personal external) rather than themselves (internal).This allows closure of the
self-actual/self-ideal discrepancies.
However, no significant associations were found between causal attributions, paranoia and ToM in the present study. The paranoia observed in
Asperger syndrome therefore does not appear to stem from the same factors
as seen in the paranoia observed in people with a diagnosis of schizophrenia.The question therefore is what may be governing paranoia in people
diagnosed as having Asperger syndrome. One possibility is that the paranoia seen in Asperger syndrome is of a different quality to that observed
in schizophrenia. Rather than stemming from a defensive strategy, it may
stem from a confusion of not understanding the subtleties of social interactions and social rules. For example, if a person with a diagnosis of schizophrenia is questioned about the paranoia they feel, they may well tell you
that someone is plotting to hurt them. Negative events are seen as part of
this plot. However, if a person with a diagnosis of Asperger syndrome is
questioned in the same way it is likely that there will be no plot but rather
a recurrent pattern of concerns in an area of threat from other people, stemming from a confusion or perplexity about social rules. If this is the case,
there are no reasons to make abnormal attributions.
Such an interpretation is consistent with Frith and Corcorans (1996)
observation that never having a theory of mind is different from temporarily losing ones ability to infer mental states. ToM abnormalities in
schizophrenia appear to be present only during acute, symptomatic phases
of illness (Corcoran et al., 1995). It is likely that an individual who has
developed a rich social cognitive schema involving the intentions and plans
of other people will use a similar (if distorted) schema when temporarily
unable to understand the actions of other people. On the other hand, an
individual with Asperger syndrome will never be likely to use such a social
cognitive system.
This suggestion relates well to the literature. Bowler (1992) suggests
that people with Asperger syndrome do not actually lack a theory of mind,
but rather acquire one later on in development. This untuned theory of
AU T I S M
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mind has missed a critical period important for normal development and
therefore the person with Asperger syndrome struggles with the subtleties
of social communication. Using their underdeveloped ToM to learn social
rules, these may then become overlearned and rigid. Therefore when
prompted into attributing mental states they are able to do so only by using
these rigid, learned rules. When left to describe a social interaction
impromptu, they have difficulties in so doing. This is also consistent with
the findings that people with autism perform well on tests of recognition
and cued recall, but poorly on tests of free recall (Bennetto et al., 1996;
Bowler et al., 1997).
Following a regression analysis, the only significant predictor of paranoia in the present study was private self-consciousness. It could be hypothesized that if a person with Asperger syndrome has a preponderance of
learned and rigid social rules then they are likely to be very privately selfconscious.
There are many considerations when evaluating the present study. With
regard to ToM, do people with Asperger syndrome actually have a deficit in
ToM, or do they have normal ToM but with a deficit in central executive
functioning that does not allow them to use their ToM? This study has taken
the results to highlight a deficit in ToM, and indeed there is evidence (cf.
Bowler, 1992) that seems to support this conclusion.
Problems in executive functioning, which implicate the frontal lobes
and subcortical structures in the brain, may also fit in with other problems
in Asperger syndrome such as perseveration and motor clumsiness.To refer
back to the paranoia literature, this links in with the finding of Kinderman
and Bentall (1997a) who proposed that people with a diagnosis of schizophrenia, when ill, also show a deficit in cognitive processing and ToM.
However, a further line of thought comes from Frith (1994), who suggests
that deficits are qualitatively different when you are born with them as
opposed to when you acquire them, and therefore the link between the two
studies may not be as strong as first thought.
There are also methodological issues to consider. None of the measures
used within the project were designed specifically for use with people with
Asperger syndrome. Features of Asperger syndrome such as difficulties in
thinking in shades of grey or in abstract as opposed to concrete terms may
have impeded the understanding and scoring of some of the questionnaires, especially the Paranoia Scale and the Self-Consciousness Scale.
However, metric analysis of the responses of participants revealed no tendency for any different pattern of scores to be recorded by the two groups.
People with Asperger syndrome who tended to score at the borderline of
learning disability were excluded from the study because of the nature of
the tasks required. The findings of the present study therefore relate to a
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5(2)
specific sample of people with Asperger syndrome who had the ability to
fill in the questionnaires independently and the motivation to complete
them. The generalizability of the findings is thereby reduced. Furthermore
in the present study a DSM-IV diagnosis of Asperger syndrome was used.
We did not differentiate between high-functioning autism and true
Asperger syndrome. Finally, although the groups used were not matched
for sex or age, it was felt that these discrepancies do not undermine the
findings of the study. The present study was undertaken as a preliminary
study to determine the validity of the relationships proposed and the findings have proved promising.
AU T I S M
Clinical implications
Although it is increasingly recognized that adults with Asperger syndrome
may have serious psychological difficulties in adult life (Tantam, 1989),
these difficulties are frequently overlooked and many people with this condition fail to receive the help they require.
With regard to interventions, there are no known behavioural or pharmacological interventions that will have any effect on the underlying
impairments of Asperger syndrome or autism. The interventions that are
available target the behavioural manifestations of the syndrome and are
often adapted from the field of learning disabilities. They tend to include
habilitative education-based treatment plans that concentrate on turning
eccentricities into strengths, and the didactic teaching of information and
skills, e.g. social skills, that most other people learn intuitively.
However, there is a growing interest in various forms of psychotherapeutic work with people with learning difficulties with a particular need
to develop more appropriate clinical intervention for people with Asperger
syndrome (Hare, 1997). Hare and Paine (1997) outlined three interventions general counselling, personal construct psychology (PCP) and cognitive behaviour therapy (CBT) that have been successfully used with
clients with Asperger syndrome. However, there is no one single therapy
that appears to be generally effective with this group of clients, possibly
due to the heterogeneous nature of the condition and the problems it
encompasses.
With regard to the cognitive aspects of Asperger syndrome researched
in the present study, the findings would suggest that an intervention for
paranoia in Asperger syndrome should be based on a model for social
anxiety and self-consciousness.This contrasts with an approach that focuses
on the defensive nature of the paranoia, such as attributional therapy. In
such an approach the client would be taught to attribute negative events to
benign situational reasons rather than personalize them (Kinderman and
Bentall, 1997b).
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Further work expanding on the findings from the present study could
culminate in a CBT model for paranoia in Asperger syndrome focusing on
the self-consciousness and anxiety aspects, the principles of which could
be based on an existing model, such as that of Wells (1997). CBT aims to
change dysfunctional thoughts and emotions via evidence-based reasoning
in association with a change in dysfunctional behaviour using behavioural
techniques.
A more specific intervention could be schema focused cognitive therapy
(Young, 1990). Because the paranoia observed in Asperger syndrome probably revolves around themes, recurrent patterns of concerns in an area of
threat from other people, it may be a more appropriate intervention to
address the recurrent themes.
It should be noted that any form of CBT used with Asperger syndrome
requires adaptation to the client group. Many problems regarding clinical
work with people with Asperger syndrome have been identified by Hare
(1997), such as how they view the clienttherapist relationship and the
rigid nature of interactions. In addition to developing therapies, the
research could pave the way for paranoia to become recognized as a feature
of Asperger syndrome and therefore open up opportunities to be treated
by professionals in the mental health field rather than in learning disabilities.
Notes
1 Information on the Projective Imagination Test (PIT) is available from: Dr Peter
Kinderman, Department of Clinical Psychology, University of Liverpool, Whelan
Building, Brownlow Hill, Liverpool L69 3GB, UK.
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