J Psychopathol Behav Assess (2011) 33:246253

DOI 10.1007/s10862-011-9224-y

Systematic Review of the Clinical Presentation

of Schizophrenia in Intellectual Disability
Killian A. Welch & Stephen M. Lawrie & Walter Muir &
Eve C. Johnstone

Published online: 8 March 2011

# Springer Science+Business Media, LLC 2011

Abstract Schizophrenia and intellectual disability (ID) cooccur three times more than would be expected by chance. This
has led to speculation that a particular form of schizophrenia
may give rise to both the symptoms of schizophrenia and the
intellectual impairment. If this was the case, one may expect
the presentation of schizophrenia in an ID population to differ
from that in a population with average/high IQ. A systematic
review and meta-analysis was undertaken of studies comparing
the clinical presentation of schizophrenia in people with mild/
borderline ID to that in people with average/high IQ. Five
studies were eligible for inclusion. Four reported more negative
symptoms in the ID population, while two reported more
positive symptoms. Meta-analysis demonstrated that the ID
population experienced more negative symptoms. The
available evidence supports the proposal that the clinical
presentation of schizophrenia in an ID population differs from
that in a population with normal IQ.
Keywords Schizophrenia . Learning disability . Intellectual
impairment . Dual diagnosis . Symptoms

Introduction
In the first half of the twentieth century there was considerable
interest in the occurrence of psychosis in people with
intellectual impairment. Both the feasibility and potential
reasons for such co-occurrence were topics of much debate,
these discussions frequently being influenced by the prevailing psychodynamic and eugenic theories of the time (Turner
1989). One of the earliest and most influential contributors to
this discussion was Emil Kraepelin. He estimated that some
K. A. Welch (*) : S. M. Lawrie : W. Muir : E. C. Johnstone
Division of Psychiatry, School of Molecular and Clinical
Medicine, University of Edinburgh, Royal Edinburgh Hospital,
Edinburgh, UK EH10 5HF
e-mail: kwelch1@staffmail.ed.ac.uk

7% of all cases of dementia praecox arose in individuals with

premorbid intellectual impairment, and proposed these
individuals had a very early onset illness involving pathological processes that actually led to the intellectual disability
(Kraepelin 1919). He named this putative condition
pfropfschizophrenie, and suggested that this particular
manifestation of dementia praecox was associated with
mannerisms, stereotypies and negativistic features.
Turner undertook a comprehensive historical review of
schizophrenia in intellectual disability (ID) in 1989 (Turner
1989). This established that in this population schizophrenia
had a point prevalence of 3%, three times that of the general
population. When detailed, the IQ of participants in included
studies ranged from around 50 to 85. A recent study of a large
Glaswegian cohort arrived at a similar figure (Cooper et al.
2007), while an Australian report estimated prevalence as
slightly higher, at 3.75.2% (Morgan et al. 2008). Both these
studies included individuals with all severities of ID, with the
latter also including borderline cases (i.e. those with IQ 7074).
In Turners review, studies which address the clinical
features of schizophrenia in the intellectually disabled population are notable by their scarcity. It is reported nevertheless,
that symptoms in this population are often shallow or banal
and that disturbed behaviour is commonplace (Lund 1985;
Turner 1989). Additionally, and of particular interest given
the observations of Kraepelin, an association with catatonic
symptoms is a repeated observation. Turner even suggests
that the observed decline of catatonic symptoms in the
psychiatric population may in fact be a consequence of the
care of people with mental handicap being undertaken by
specialist services rather than general psychiatrists.
It is now accepted that in people with mild ID (IQ 5055 to
70) (American Psychiatric Association 1994) there is an
increased prevalence of schizophrenia. This suggests that the
co-occurrence of the two conditions is not random, a
proposition supported by studies illustrating a particularly
strong familial relationship between ID and schizophrenia

J Psychopathol Behav Assess (2011) 33:246253

(Doody et al. 1998; Greenwood et al. 2004). It has also been

suggested that the schizophrenic phenotype may be subtly
different in the intellectually disabled population. These
observations are in-keeping with the concept of Pfropfschizophrenia, and raise the possibility that schizophrenia as manifest
in the ID population may be clinically distinguishable from that
in people with normal IQ. It may be that schizophrenia as
manifest in the ID population represents a particularly severe
from of the condition, these being reflected in these patients
experiencing a particularly great symptom load.
The aim of this systematic review is to address the above
question by ascertaining if the severity of symptoms
experienced by people with schizophrenia and ID differs
from that in people with normal/high IQ. To maximise the
data that can be utilised we will include studies focusing on
patients with borderline intellectual function (BIF) as well
as mild ID. To maximise chances of identifying such a
distinction total, positive and negative symptom ratings will
be examined separately, and if feasible data will be subject
to meta-analytic comparison. Standard diagnostic tools and
rating scales have been shown to have validity in the mildly
intellectually disabled population (Davidson et al. 1995;
Hatton et al. 2005), but this is not the case for the more
severely intellectually impaired. Consequently, studies
identified investigating symptom load in individuals with
more severe intellectual disability (i.e. IQ less than 50) will
not be included in meta-analytic comparison. Studies which
characterise the schizophrenia phenotype within this population are clearly also of value however; they will therefore
be discussed if they meet the other inclusion criteria.

Methods
The following databases were searched: Medline (1950 to
August 2008), PsychINFO (1950 to August 2008) and
EMBASE (1980 to August 2008). The aim was to identify
all English language studies comparing the clinical features
of schizophrenia in adults (aged 1665) with ID or
borderline intellectual functioning (BIF) to those in individuals with average/high IQ. Participants with BIF,
described in DSM-IV as those in the IQ range 7184
(American Psychiatric Association 1994), were included to
increase the yield of studies. The search terms were
schizophrenia or psychosis, combined using the AND
operator with learning disability, mental retardation,
intellectual disability, intellectual impairment or borderline intellectual functioning, AND symptoms, or
psychopathology. Both free-text and expanded medical
subject headings were used. Subject headings were adapted
to the specific subject headings of the biomedical databases
used. The search strategy was supplemented by inspecting
the reference lists of included articles.

247

A total of 2,021 abstracts were assessed for inclusion by

the author, and articles in full text were retrieved if
appropriate. Primary research studies were considered for
inclusion if they were published as a peer-reviewed article
in English and compared people with schizophrenia and a
mild or borderline intellectual disability to those with
schizophrenia and average/high IQ. We required that
schizophrenia spectrum disorder diagnosis was made using
either ICD or DSM criteria, and that a recognised symptom
rating scale was used to quantify symptoms. Studies were
excluded if the recruitment method itself could have
potentially resulted in individuals with differing severity
of illness being included in either the ID or comparator
groups (e.g. recruiting the ID individuals from among
inpatients and comparator subjects from the community).
Relevant data was extracted from studies identified as
eligible for inclusion. To enable meta-analytic comparison,
mean score on the relevant symptom rating scale (for
positive, negative and total symptoms) together with
standard deviation of this score and sample size was
extracted for the ID and non-ID patient groups in each
study. If standard deviation was not given in the paper but
was calculable from other data (e.g. 95% confidence
interval), then this was done. If it could not be derived
from the paper it was requested from the author. If usable
data was available for any symptom category from three or
more studies, then meta-analytic analysis was undertaken in
STATA 10 (StataCorp, College Station, TX, USA) using
the user-contributed command for meta-analyses metan
(Bradburn et al. 1999). The mean difference in scores
between ID and none-ID groups was standardized by
calculating Cohens d, the difference between the two raw
means divided by the pooled standard deviation (Rosenberg
et al. 2000). The standard error of each studys standardized
effect size was calculated from the estimated effect and the
group sizes of the two groups using the method of Cooper
and Hedges (1994), which is implemented in metan.
Standardised effects were then pooled using a random
effects model. The small number of studies available meant
that assessment for publication bias was not feasible.

2021 publications identified by

literature search

14 full text articles retrieved

5 articles included in review

Exclusions: no non-intellectually
disabled schizophrenic comparison
group (5), no recognised scale for
the assessment of psychotic
symptoms used (4).

Fig. 1 Flow of citations through the publication identification process

248

The process of publication identification is outlined in

Fig. 1. For the vast majority of studies identified in the
literature search it was clear from the abstract that the study
was not a case controlled comparison of the groups of
interest. The issues addressed in these studies was very
varied, ranging from basic science reports to outlines of
service structures delivered to this patient group. Fourteen
studies were potentially eligible for inclusion and were
retrieved in full text form, five were excluded as there was
no non-intellectually disabled comparator group, (Catinari
et al. 2005; Cooper et al. 2007; Hatton et al. 2005; Reid
1972; Wright 1982), and four did not use a recognise
symptom rating scale (Emerson 2003; Glick and Zigler
1995; Linaker and Helle 1994; Schultze-Lutter and
Klosterktter 1995). In total, five studies met the inclusion
criteria. These are shown in Table 1. The exclusion of one
particular study must be discussed further. This was a study
by Shultze-Lutter and Klosterkotter comparing symptoms
in intellectually disabled and non-intellectually disabled
groups with schizophrenia using the Bonn Scale for the
Assessment of Basic Symptoms (Schultze-Lutter and
Klosterktter 1995). These basic symptoms are attentional-perceptive-cognitive disturbances, regarded as subtle
subclinical signs rather than frank symptoms of schizophrenia.
As they are not comparable to the symptoms measured by
rating scales, this study was felt not to meet inclusion criteria.

Results
Those studies eligible for inclusion together compared a
total of 280 individuals with schizophrenia and mild ID/BIF
to 909 individuals with schizophrenia and average/high IQ.
In the case of all studies those with intellectual impairment
had an IQ greater than or equal to 50 and less than or equal
to 81. In two studies there was a significant age difference
between the two groups, the older group being the learning
disabled group in one of these studies and the comparison
group the elder in the other. Similarly, in one study illness
duration was greater in the group with intellectual impairment, and in one study it was greater in the comparator
group (though statistical significance of the latter finding
could not be ascertained). When it could be ascertained
from the data provided, in all but one study gender
distribution of the two groups was balanced.
The mild ID/BIF group scored higher on scales measuring
negative symptoms in four of the five studies reviewed, higher
on scales measuring positive symptoms in two, and higher on
scales measuring general symptoms in two. Meta-analytic
comparison of positive, negative and general symptomatology
in the two groups would have been desirable. Unfortunately
however meta-analytic comparison could only be undertaken
for negative symptoms. This included only three studies,

J Psychopathol Behav Assess (2011) 33:246253

which together compared 151 people with schizophrenia and

mild ID/BIF to 400 people with schizophrenia and average/
high IQ. Inclusion of data from the two other studies was not
possible because there was inadequate data in the published
paper. Sufficient data for meta-analysis of load of both positive
and general symptoms was available in only two studies. Data
from only two studies was inadequate for meta-analysis.
The meta-analysis of ratings on scales measuring negative
symptoms produced an effect size of 1.72 (see Fig. 2). This is
an extremely large effect size, indicating that ID individuals
with schizophrenia experience substantially greater negative
symptoms than patients with average/high IQ.
The identification of studies comparing the clinical
presentation of schizophrenia in people with moderate or
severe intellectual disability to that in people with normal
IQ was not the objective of this systematic review. One
such study was encountered during the undertaking of the
exhaustive search process however; it suggested an excess
of incoherence and flat affect in the ID group, though fewer
delusions (Linaker and Helle 1994).

Discussion
Only three case controlled studies could be identified
comparing the clinical presentation of schizophrenia in ID
to that in people with average/high IQ. This increased to
five when individuals with borderline intellectual functioning were included. Given the historical interest in this
population this paucity of studies is surprising. It may
however be partially explained by the fact that one of the
earliest modern studies addressing the clinical presentation
of schizophrenia in people with ID indicated a clinical
picture much like that of people without ID (Meadows et al.
1991). This essentially negative finding may have reduced
interest in further studies. The reasons for this negative
finding do need explanation, which may be provided by the
studys sole reliance on the Schizophrenia and Affective
Disorders Schedule-Lifetime Version (SADS-L) for detection of psychopathlogy (Endicott and Spitzer 1978). It is
widely recognised that rating scales vary in their ability to
detect negative symptoms, with the SANS regarded as a
particularly sensitive tool (Foussias and Remington 2008).
The Positive and Negative Syndrome Scale (PANSS) (Kay
et al. 1987) was derived from the SANS (Andreasen 1989),
and it seems significant that all four studies employing
either of these scales did find more negative symptoms in
the ID group, whereas that using only the SADS-L did not.
When the study of Meadows et al. is excluded, the two
other studies addressing the clinical presentation of schizophrenia in individuals with mild ID both found increased
negative symptoms (Bouras et al. 2004; Doody et al. 1998).
This was also the case in the two studies investigating

Study group (as described in original study)

34

482

53

313

Doody et al. (1998)

Hassiotis et al. (1999)

Bouras et al. (2004)

Chaplin et al. (2006)

No data

No data

No data

22.8

26.8 (8.7)*

Mean age illness

onset (s.d.)

43.2*

41.1

35 (median, not mean)

48.6

43.2*

Mean age

39

SADS-L
PANSS
CPRS
SANS

59

PANSS

No data

matched

9.0* (median,not mean)

5.0

17.0*

<81

50-70

No data

41:12**

n.s.d.

n.s.d

!8:8 (69%)

Ratio M:F

53

CPRS
SANS

Mean illness durtn.

(years)

5070

5070

104 58-81

25

SADS-L
4.9

12.9*

45.4*

39.5

No data

matched

Borderline intellectual impairment group had higher scores

on positive (p=0.004) and negative (p<0.001) symptoms
scales of PANSS.

LD group showed greater levels of psychopathology on

observed (p<0.001), though not reported CPRS..
LD higher score on SANS (p<0.001)

Lower IQ group had more negative symptoms (p=0.045).

No significant difference between groups in
psychopathology as measured by CPRS.

No data

27:26**

n.s.d.

n.s.d

16:9 (64%)

Negative symptoms: 0.77

Positive symptoms: 0.38

General symptoms: 0.61

Negative symptoms: 1.08

Negative symptoms: 3.38

Positive symptoms: -1.45

General symptoms: 1.72

Standardised effect size

(when derivable)

36.5 (median, not mean) 10.1* (median, not mean)

48.6

35.4*

Mean illness durtn. (years) Ratio M:F

Generally similar clinical presentation in both groups.

Normal IQ group significantly greater prevalence of
persecutory delusions and thought disorder.
Comorbid group significantly more negative symptoms
(p<0.01), no difference in positive, general or total
symptom profiles.

Main findings

No data

No data

No data

24.4

22.5 (6.5)*

Symptom rating Schizophrenia with intellectual impairment

scales used
N
IQ range Mean age illness Mean age
onset (s.d.)

*P<0.05; **P<0.01; ***P<0.001; insufficient data to calculate statistical significance

n.s.d. Reported as no significant difference in source paper, further information not available

Those with schizophrenia spectrum psychoses included rather than just schizophrenia

Borderline intellectual impairment refers to IQ in range 7181. The methodology of both studies identifying these individuals will have resulted in the inclusion of people with mild ID. By use
of the Weschler Adult Intelligence Scale-Revised, the Hassiotis et al. study estimated these to be 43% of the total. This estimation was not undertaken in the Chaplin et al. study

Abbreviations: NART National Adult Reading Test (Nelson 1982), CPRS Comprehensive Psychopathological Rating Scale (Asberg et al. 1978), SANS Scale for the Assessment of Negative Symptoms
(Andreasen 1989), PANSS Positive and Negative Syndrome Scale (Kay et al. 1987), SADS-L Schizophrenia and Affective Disorders Schedule-Lifetime Version (Endicott and Spitzer 1978)

26

Schizophrenia with normal IQ

Meadows et al. (1991)

Study (year)

Meadows et al. (1991) People comorbid for mild mental retardation and schizophrenia,
identified from mental handicap services caseloads
Doody et al. (1998)
People comorbid for mild learning disability and schizophrenia,
identified from records of psychiatric admissions
Hassiotis et al. (1999) People with borderline intellectual impairment (or mild ID)
determined on basis of NART score. Recruited from
general adult psychiatric services
Bouras et al. (2004)
People comorbid for mild intellectual disability and
schizophrenia spectrum psychosis. Recruited from a
specialist service for people with ID
Chaplin et al. (2006)
People with borderline intellectual impairment (or mild ID)
determined on basis of NART score. Recruited from
general adult psychiatric services

Study (year)

Table 1 Studies investigating the clinical features of schizophrenia in ID populations

J Psychopathol Behav Assess (2011) 33:246253

249

250

J Psychopathol Behav Assess (2011) 33:246253

Study

Standardised mean difference

ES (95% CI)
% Weight

Chaplin et al. (2006)

0.77 (0.73, 0.81)

33.82

Doody et al. (1998)

3.38 (3.12, 3.65)

32.47

Bouras et al. (2004)

1.09 (1.00, 1.17)

33.71

Overall

1.72 (0.99, 2.46)

100.00

0
3.65
Standardised mean difference

Fig. 2 Forrest plot for data comparing negative symptoms experienced by people with schizophrenia with and without ID. The studies
of Chaplin et al. and Doody et al. used the SANS, while Bouras et al.
used the PANNS. Items on the SANS are: Affective flattening or
blunting (unchanging facial expression, decreased spontaneous movements, paucity of expressive gestures, poor eye contact, affective
nonresponsivity, lack of vocal inflections, global rating of affective
flattening, inappropriate affect); Alogia (poverty of speech, poverty of
content of speech, blocking, increased latency of response, global
rating of alogia), Avolition-apathy (grooming and hygiene, impersis-

tence at work or school, physical anergia, global rating of avolitionapathy); Anhedonia-asociality (recreational interests and activities,
sexual interest and activity, ability to feel intimacy and closeness,
relationship with friends and peers, global rating of asociality and
anhedonia); Attention (social inattentiveness, inattentiveness during
mental status testing, global rating of attention). Negative items on the
PANNS are: Blunted affect; Emotional withdrawal; Poor rapport;
Passive/apathetic social withdrawal; Difficulty in abstract thinking;
Lack of spontaneity and flow of conversation; Stereotyped thinking

individuals with BIF (Chaplin et al. 2006; Hassiotis et al.

1999). In contrast, greater positive symptom ratings in the
intellectually impaired population was found in only one of
the former (Bouras et al. 2004) and one of the latter studies
(Chaplin et al. 2006). That schizophrenia in the context of
ID is particularly associated with negative symptoms is of
course further supported by the very large effect size which
emerged from the meta-analysis.
Given the paucity of studies undertaken in this area,
extending the inclusion criteria to individuals with borderline
intellectual functioning was necessary. The characteristics of
the patients who constitute the ID/BIF groups requires further
discussion however. The two studies focusing on BIF patients
identified intellectually impaired individuals on the basis of
performance on the National Adult Reading Test (NART)
(Nelson 1982). As they acknowledge, this methodology will
also identify some individuals in the mild ID IQ range. The
proportion of participants actually in the mild ID rather than
BIF IQ range was only formally estimated in one of these two
studies (Hassiotis et al. 1999). This study estimated, by use of
the Wechsler Adult Intelligence Scale-Revised (WAIS-R)
(Wechsler 1981), that the proportion of participants identified
as having intellectual impairment actually in the mild ID
range was a striking 43%. Given that similar methodology
was used to identify intellectually impaired individuals in the
two studies, a similar proportion may be expected in the

Chaplin et al. report. A degree of caution is however required

in interpreting this unexpectedly high estimate. Though the
NART should yield a measure of IQ resistant to change
(Crawford 1992), IQ as measured by the WAIS-R will be
influenced by any IQ loss consequent to the development of
schizophrenia: the proportion of participants with true mild
ID is likely fewer than 43%.
Albeit with the proviso that it may have been overestimated, the potential implications of the high proportion
of individuals in the Hassiotis et al. study thought to be in
the mild ID rather than BIF IQ range requires further
discussion. Taken together with evidence that the prevalence of schizophrenia may be less elevated in people with
BIF than those with mild ID (and thus the former condition
may have a weaker association with schizophrenia)
(Hassiotis et al. 2008), this has consequences for our ability
to comment on the nature of schizophrenic illness in people
with BIF. It raises the possibility that the higher ratings of
schizophrenic symptomatology seen in intellectually impaired individuals in these two studies is fact driven largely
by those individuals with IQs below 70, and thus actually in
the mild ID IQ category. Given these considerations,
ideally people in these two IQ categories would have
been analysed separately; unfortunately this was not
possible with the data provided. In this context it is
however interesting to note that a recent study of

J Psychopathol Behav Assess (2011) 33:246253

intellectually compromised individuals derived from a

non-learning disabled population (mean IQ 79.9, verbal
IQ 81.7) did report that negative symptoms were
particularly prominent in this subgroup (Potter and
Nestor 2010). It may thus be that though not as
pronounced as in those with schizophrenia and frank ID,
those with BIF do exhibit more negative symptoms than
those with normal or superior IQ.
The limitations of this study must be acknowledged.
Most importantly, the number of eligible studies available
for review was limited. Furthermore it was not possible to
extract from the available data the specific symptoms
driving the higher ratings on symptom rating scales in the
dual diagnosis groups. Nonetheless, it is the case that these
data do support the contention that people with a dual
diagnosis of both schizophrenia and mild ID have greater
ratings of negative symptoms than those with schizophrenia
alone. This may also be the case for those with BIF and
schizophrenia. That either of these groups also have
experience more positive symptoms, though certainly
suggested, remains more contentious.
Why May Those with Dual Diagnosis Have Higher Ratings
on Symptom Rating scales?
A possible explanation for the greater scores on symptom
rating scales in individuals with both ID and schizophrenia
compared to those with schizophrenia alone could be that
this is a manifestation intellectual disability rather than
arising from the schizophrenic illness. It may be, for
example, that having an intellectual disability itself results
in high ratings on scales of negative symptoms. Though the
fact that structured interviews and rating scales have been
shown to have validity in this population does reduce this
concern to some degree, this issue is best addressed by
including non-schizophrenic intellectually disabled controls.
Such data was included in the Doody et al. study, which
showed the non-schizophrenic, non-syndromal intellectually
disabled group to score very low on both the positive and
negative symptom subsets (Doody et al. 1998). It thus seems
unlikely that the excess of symptoms in the dual diagnosis
group is simply a consequence of their intellectual disability.
If the greater symptom ratings observed in dual
diagnosis individuals is something intrinsic to their
schizophrenic illness, why should this occur? A possible
explanation is that this reflects the existence of a severe
schizophrenia phenotype within the intellectually disabled population (Doody et al. 1998). This proposal was
initially postulated to explain the threefold increased
prevalence of schizophrenia seen in this population. The
thrust of this argument is that in some comorbid
individuals the cognitive impairment manifesting as
intellectual disability is in fact arising from the schizo-

251

phrenic illness itself, this resulting in an elevated rate of

co-occurrence of the two conditions. Evidence supporting
this proposition include structural brain changes in the
dual diagnosis sample strongly resembling those of the
schizophrenia sample yet being very different from the
group with intellectual disability alone (Bonnici et al.
2007; Sanderson et al. 1999). It does thus seem that there
is indeed commonality between the conditions affecting
the dual diagnosis and schizophrenia groups. Given the
differences that exist between the dual diagnosis and nonsyndromal intellectually disabled groups, this in turn
suggests that it is from the schizophrenia itself that the
intellectual impairment of the former group arises. Though
cognitive impairment is of course associated with schizophrenia in general (Johnstone et al. 2007), in the case of
the dual diagnosis group this impairment is of sufficient
magnitude to place them in the intellectually disabled IQ
range because of the greater severity of illness they
manifest; they have a particularly severe schizophrenia.
This review therefore adds further weight to the proposal
that individuals with both ID and schizophrenia exhibit a
particularly severe manifestation of the condition.
This being the case it suggests that further study of this
population, (involving genetic and imaging studies as well
as phenomenological characterisation), has the potential to
provide important insights in to the genesis of schizophrenia. It may be, for example, that the aetiology of this
severe schizophrenia is more independent of environmental exposures, and individuals affected by it exhibit greater
differences from normal controls than is the case in those
without ID. While the mechanism/s underpinning this
posited severe schizophrenia are at this time unclear, high
rates of both positive family histories of schizophrenia and
chromosomal variants and abnormalities in dual diagnosis
individuals (Muir et al. 1998), suggests that genetic factors
may play a significant role. Interestingly, and of considerable interest in relation to the finding of greater negative
symptoms in dual diagnosis individuals, earlier studies
undertaken by our group have suggested that amygdala
volume reductions are particularly associated with higher
negative symptom ratings in individuals with special
educational needs who are at elevated risk of schizophrenia
(Moorhead et al. 2009; Welch et al. 2010).
In addition to providing further evidence for the existence
of a severe schizophrenia phenotype, this review also has
clinical relevance. If, as well as simply having the dual burden
of both intellectual disability and schizophrenia these dual
diagnosis individuals also tend to have more schizophrenic
symptomatology, then this has clear implications for service
provision. Care providers need not only to be vigilant to the
presence of this increased (particularly negative) symptomatology, but also have sufficient resources to provide adequate
levels of care for this already disadvantaged group.

252
Acknowledgements

J Psychopathol Behav Assess (2011) 33:246253

Nil

Conflicts of interests Nil

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