Neuropsychological relationships in paranoid schizophrenia with and without delusional misidentification syndromes. A comparative study

Progress in Neuro-Psychopharmacology & Biological Psychiatry 32 (2008) 1445–1448

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Neuropsychological relationships in paranoid schizophrenia with and without delusional misidentification syndromes. A comparative study L. Lykouras a,⁎, M. Typaldou b, P. Mourtzouchou b, P. Oulis b, C. Koutsaftis b, F. Dokianaki b, P.G. Michalopoulou a,c, M. Havaki-Kontaxaki b, C. Christodoulou a a b c

2nd Department of Psychiatry, Athens University Medical School, “Attikon” Hospital, 1 Rimini Street, 124 62, Athens, Greece 1st Department of Psychiatry, Athens University Medical School, “Eginition” Hospital, 74 Vas Sophias Ave., 115 28, Athens, Greece CSI Laboratory, Department of Psychiatry, Institute of Psychiatry, De Crespigny Park SE5 8AF, London, United Kingdom

A R T I C L E

I N F O

Article history: Received 10 January 2008 Received in revised form 9 April 2008 Accepted 22 April 2008 Available online 29 April 2008 Keywords: Delusional misidentification syndromes Neuropsychological study Paranoid schizophrenia

A B S T R A C T Delusional misidentification syndromes (DMSs) and schizophrenia are strongly associated, since the former occur predominantly in the context of paranoid schizophrenia. However, the possible underlying neuropsychological relationships between DMSs and paranoid schizophrenia have not been thoroughly investigated. The aim of the present study was to investigate whether DMSs in paranoid schizophrenia are associated with a distinct neuropsychological substrate indicative of differential bilateral frontal and right hemisphere dysfunction. We compared two matched groups of paranoid schizophrenic patients with (N = 22) and without (N = 22) DMS(s) on a battery of neuropsychological tests assessing mainly frontal and right hemisphere functions. No statistically significant differences were detected between the two groups. Our findings are indicative of a bilateral frontal and right hemisphere dysfunction of equal severity in both DMS and non-DMS patients with paranoid schizophrenia. © 2008 Elsevier Inc. All rights reserved.

1. Introduction Delusional Misidentification Syndromes (DMSs) have been defined both strictly and broadly. In the strict sense, DMSs consist in delusional beliefs about the identity or rather uniqueness of familiar people or oneself and subsume Capgras syndrome, Fregoli syndrome, the syndrome of intermetamorphosis and the syndrome of subjective doubles (Christodoulou, 1991). The term “delusional misidentification” was first coined by Christodoulou and Malliara-Loulakaki (1981) to cover the above mentioned four main variants. The essential feature of the Capgras syndrome is the negation of identity of familiar person(s) and the delusional belief that this person has been substituted by a double. Fregoli syndrome is characterized by false identification of a familiar person in strangers. The intermetamorphosis syndrome includes false physical resemblance in addition to false recognition. The fourth variety is characterized by delusions of doubles exclusively of the patient's own self. In the broad sense (Cutting, 1991), misidentification syndromes are not limited to persons but also include places, events or objects and are not deemed to be necessarily delusional. However, the issues about the precise boundaries of the concept of DMSs, their subtyping and diagnostic criteria are still widely controversial (Mojtabai, 1998).

Abbreviations: DMSs, Delusional misidentification syndromes. ⁎ Corresponding author. Tel.: +30 210 5832426; fax: +30 210 5326453. E-mail address: [email protected] (L. Lykouras). 0278-5846/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.pnpbp.2008.04.012

Although DMSs occur in a variety of psychiatric and medical conditions (Edelstyn and Oyebode, 1999), they seem to be strongly associated with schizophrenia, since they occur predominantly in the context of paranoid schizophrenia (Joseph, 1994). This strong association raises the issue of the underlying neuropsychological relationship between DMS and paranoid schizophrenia. This relationship has not been thus far thoroughly investigated, since the available studies are mainly case reports (Wilcox and Waziri, 1983; Morrison and Tarter, 1984; Paillére-Martinot et al., 1994; Lykouras et al., 2002), lacking the appropriate controls or small case series with diagnostically heterogenous groups (Kokkevi and Christodoulou, 1985). It has been hypothesized that a neuropsychological impairment of the belief evaluation system, presumably a function of the right frontal lobe (Joseph et al., 1990; Young et al., 1992; Staff et al., 1999; Papageorgiou et al., 2003), is common to both DMS and schizophrenia (Coltheart et al., 2007). Moreover, it has also been hypothesized that the emergence of DMSs in the context of paranoid schizophrenia require the additional dysfunction of the right hemisphere-mediated visual face recognition system (Coltheart, 2007). Thus far, several studies comparing schizophrenic and/or DMS groups to healthy controls have implicated neuropsychological functions associated with bilateral frontal and right hemispheres (Cutting, 1994; Papageorgiou et al., 2005; Coltheart, 2007), though not specifically associated with paranoid schizophrenia (Seltzer et al., 1997; Zalewski et al., 1998). Thus, the aim of the present study was two-fold: first to investigate whether co-occurring DMS in paranoid schizophrenia is associated with a distinct neuropsychological substrate in a diagnostically

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homogeneous sample of adequately matched patients with confirmed paranoid schizophrenia and second to compare patients' performance in tests of bilateral frontal and right hemisphere neuropsychological functions. We hypothesized that DMS patients with paranoid schizophrenia would exhibit more impaired performance on neuropsychological tests assessing right hemisphere functions compared to their non-DMS counterparts, whereas tests assessing bilateral frontal functions would not show between-group differences. 2. Methods 2.1. Subjects The sample of the study comprised 44 right-handed patients (Annett, 1970), 22 with DMS(s) and 22 without co-occurring or previous history of DMS(s). Patients underwent the Structured Clinical Interview for DSM-IV (First et al., 1995) to establish a DSM-IV diagnosis of paranoid schizophrenia (DSM-IV, 1994) and the strict DMS definition was used for the diagnosis of DMSs in the patients: 7 DMS patients had Capgras Syndrome, 4 Fregoli, 2 Intermetamorphosis and 9 had more than one type. Patients with a current or past neurologic, endocrine disorder or mental retardation were excluded. All patients underwent a computerized tomography brain scan to rule out the possibility of brain lesions. The severity of the illness was assessed by the Positive and Negative Syndrome Scale (PANSS) (Kay et al., 1987). PANSS was administered by two experienced psychiatrists (L.L, P.O), previously involved in the project of its Greek translation with very good interrater reliability, ranging from 0.8–1 (Lykouras et al., 2005). The DMS(s) were active in all patients of the first group at the time of their assessment. Likewise, their counterparts without DMS(s) were also deluded at the time of their assessment and both groups were matched exactly for the severity of delusional beliefs (P1 item of PANSS scale), which in DMS patients included misidentification delusions with secondary persecutory elaborations, whereas in the non-DMS group solely persecutory delusions. DMS patients and their controls were matched for severity of PANSS: positive score (±2 points), negative score (±5 points), general psychopathology score (±6 points), total score (±10 points) (Table 1). DMS patients and their controls were also matched for age (±5 years), gender, educational level (± 2 years) and illness duration (±4 years) (Table 1). The patients of both groups were on medication with comparable doses of atypical antipsychotics. The study protocol was approved by the Ethics Committee of our hospital. All patients gave written informed consent for participation in the study. 2.2. Neuropsychological assessment Based on our hypotheses the neuropsychological test battery included the following tests: A) the subtests Picture Completion, Picture Arrangement, Block Design and Object Assembly from Wechsler Adult Intelligence Scale (WAIS) (Wechsler, 1955), the Rey Complex Figure Test (RCFT) Copy and Immediate-Recall trial (Meyers

Table 1 Sociodemographic and clinical characteristics of the sample DMS group (n = 22) mean (s.d.)

non-DMS group (n = 22) mean (s.d.)

Age Education (years) Duration of illness (years)

34.77 (9.83) 12.77 (2.94) 9.36 (7.32)

38.59 (9.44) 12.36 (2.79) 11.77 (7.17)

PANSS Positive score Negative score General psychopathology score Total score

26.11 (4.67) 23.89 (7.29) 44.21 (11.56) 94.21 (20.44)

24.15 (4.46) 20.60 (3.76) 44.50 (11.24) 88.95 (15.31)

Table 2 Comparisons of neuropsychological test performance between the DMS and the nonDMS Group DMS group (n = 22)

non-DMS group (n = 22)

Wechsler adult intelligence scale subtests

Mean aged scaled scores

Mean aged scaled scores

Information Comprehension Arithmetic Similarities Digit span Vocabulary Digit symbol Picture completion Block design Picture arrangement Object assembly Verbal IQ Performance IQ

10.95 (s.d. 2.79) 8.41 (s.d. 3.65) 7.59 (s.d. 2.59) 10.23 (s.d. 2.54) 7.05 (s.d. 2.73) 9.73 (s.d. 1.80) 7.64 (s.d. 2.48) 7.05 (s.d. 2.28) 7.18 (s.d. 2.52) 6.86 (s.d. 2.49) 5.23 (s.d. 2.54)a 94.36 (s.d. 11.27) 80.64 (s.d. 10.98)

11.59 (s.d. 2.06) 8.91 (s.d. 2.76) 9.23 (s.d. 2.25) 9.73 (s.d. 2.71) 7.73 (s.d. 3.18) 9.95 (s.d. 2.30) 7.36 (s.d. 2.34) 7.45 (s.d. 2.24) 8.18 (s.d. 3.00) 6.68 (s.d. 2.55) 6.09 (s.d. 2.54) 97.64 (s.d. 10.94) 82.91 (s.d. 12.58)

Wisconsin card sorting test Number of categories completed Total number of errors Total number of perseverative responses

Mean raw scores 2.50 (s.d. 2.06)b

Mean raw scores 2.91 (s.d. 2.33)b

Stroop colour word test Colour-word score WISC-R mazes

Hedges' ga

0.500 0.740 0.031 0.645 0.441 0.535 0.506 0.512 0.246 0.632 0.184 0.307 0.391

0.26 0.15 0.66 0.19 0.23 0.10 0.11 0.17 0.36 0.07 0.33 0.29 0.19

0.609

0.18

63.40 (s.d. 24.01) 52.05 (s.d. 40.32)b

b

52.82 (s.d. 26.39) 38.86 (s.d. 30.75)b

0.131 0.358

0.41 0.36

29.37 (s.d. 8.74)b 19.05 (s.d. 7.19)b

30.91 (s.d. 12.81)b 19.32 (s.d. 6.46)b

0.917 0.820

0.14 0.04

4.68 (s.d. 2.21)b

0.953

0.02

7.68 (s.d. 4.05)b

0.715

0.22

30.34 (s.d. 7.33)b 10.36 (s.d. 8.51)b

0.139 0.535

0.37 0.28

73.95 (s.d. 29.66)b 176.09 (s.d. 94.20)b 42.68 (s.d. 4.22)

0.098 0.952 0.986

0.37 0.13 0.26

b

Benton visual retention test Number of correct 4.73 (s.d. 2.25)b reproductions Number of errors 6.86 (s.d. 3.09)b Rey complex figure test Copy-score Immediate recall-score

p⁎

27.57 (s.d. 7.50)b 8.48 (s.d. 7.58)b

Trail making test(response time in seconds) Part A 62.59 (s.d. 29.85)b Part B 165.43 (s.d. 68.28)b Test of facial recognition 40.92 (s.d. 9.88)

a Indicative values of Hedges' g values are as follows: 0.2 = low effect, 0.5 = medium effect, 0.8 = large effect. b Values are in neuropsychological impaired range i.e. below normative data *p ≤ 0.05 (Mann–Whitney test).

and Meyers, 1995), the Benton Visual Retention Test (BVRT) (Benton, 1963) and the Benton Test of Facial Recognition (Benton et al., 1994), which assess visual recognition, non-verbal reasoning, perceptual organization, visual perception, visuospatial memory, and are mainly associated with right hemisphere B) the Wisconsin Card Sorting Test (WCST) (Heaton et al., 1993), the Stroop Colour Word Test (SCWT) (Golden, 1978), the subtest Mazes from the Wechsler Intelligence Scale for Children Revised (WISC-R) (Wechsler, 1974), the Trail Making Test (TMT) Part A and Part B (Davies, 1968), which assess executive and complex attention functions, and are mainly associated with frontal lobes areas (Lezak, 2004) and C) The Verbal Scale of the WAIS was administered to detect mental retardation, which was among the exclusion criteria in our study. The same test sequence was employed to all patients to eliminate possible order effects. 2.3. Statistical analyses Mann–Whitney U test was applied in the statistical analysis of the patients' scores in the various scales used. In order to account for multiple comparisons, the level of significance has been subjected to

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Bonferroni correction. However, owing to the relative small sample size of our study, an index of effect size (Hedges g) in patients' differential performance on neuropsychological tests were also computed (Table 2). 3. Results No significant differences were found between the two groups in all neuropsychological measures with the exception of the WAIS “Arithmetic” subtest (p = 0.031), which did not remain significant after Bonferroni correction (Table 2). Post hoc power analysis performed on the results obtained from the comparison between the two groups disclosed that in order to attain statistical significance the order of magnitude of our sample should be tenfold greater. The performance of both groups was impaired compared to the normative data in several neuropsychological tests (Table 2). Normative data were derived from the mean scores reported in the relevant clinical manuals in relation to the patients' age, or for some tests, both age and education. Impaired range performance was defined as scores below the mean normative scores – adjusted for age or, for some tests both age and education – by 1.5 SD or more. Classifying these tests according to the cognitive functions they are considered to measure (Lezak, 2004), our findings suggest that both groups showed deficits in four neuropsychological domains: a) Visuospatial Ability (WAIS-Subtest Object Assembly and RCFT-Copy) b) Executive Functions (WCST and WISC-R Mazes) c) Complex Attention Functions (SCWT and TMT A and B) and d) Visual Constructional Memory (BVRT and RCFT-Recall). The small size of our DMS-subgroups did not allow us to perform comparisons between them in order to investigate the possible differences in their performance. 4. Discussion Building on previous findings, we investigated whether DMS in paranoid schizophrenia is associated with a distinct neuropsychological substrate, indicative of a differential bilateral frontal and right hemisphere dysfunction. Our analyses revealed no significant differences between the patients with paranoid schizophrenia with and without DMS(s) with respect to their performance on a neuropsychological test battery assessing mainly bilateral frontal and right hemisphere functions. Only a trend towards a higher number of errors in WSCT in the DMS group-indicative of more severe frontal lobe impairment-was noted, vanishing however after the Bonferroni correction. The values of the calculated effect sizes were in the low-medium range (Table 2). Overall, our findings are indicative of a bilateral frontal and right hemisphere dysfunction of equal severity in both DMS and non-DMS patients with paranoid schizophrenia. The findings of our study are in line with the cases describing DMSs in patients with paranoid schizophrenia, which have showed evidence of frontal (Morrison and Tarter, 1984; Lykouras et al., 2002) and right hemisphere dysfunction (Lykouras et al., 2002). Evidence of differential right hemisphere dysfunction in a group of psychotic patients with DMS compared to a group of psychotic patients without DMS was demonstrated in the study of Kokkevi and Christodoulou (1985). The same study also revealed a greater verbal vs. performance score difference in the DMS group. The diagnostic heterogeneity of this study sample (paranoid schizophrenia, mood disorder, organic psychosis) may account for the discrepancy between its neuropsychological findings and those of our study. Neuroimaging evidence from another study revealed more severe frontal lobe atrophy in twelve paranoid schizophrenic patients with Capgras syndrome compared to twelve without, suggesting a greater degree of frontal dysfunction in the former group (Joseph et al., 1990). It is likely that the small sample size of this study and the inclusion of patients with schizophrenia and pure Capgras syndrome, could account for the divergence of its findings from ours.

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As mentioned previously, DMS has been associated with dysfunctions in both frontal and right cerebral regions (Cutting, 1994). Ellis (1994) proposed a model implying a right hemisphere mechanism, according to which there are two pathways to face recognition: ventral and dorsal. The ventral route, from the visual cortex to the temporal lobes, is involved in the cognitive processing of information, whereas the dorsal route, from the inferior parietal lobe to the limbic regions, carries indications about a stimulus' emotional significance. According to this model, the former route is intact in the DMSs whereas the latter is impaired. By contrast, according to another model (Hirstein and Ramachandran, 1997), the pathways to face recognition in DMS are intact, whereas there is a disconnection between the inferior temporal and limbic components of the visual recognition system that accounts for the emergence of the delusional misidentifications. Nevertheless, brain lesion studies have demonstrated that face recognition processing abnormalities do not necessarily result in delusional misidentifications. Thus, an additional abnormality is also required for the impaired face processing to lead to DMS. This additional abnormality is hypothesized to consist in a presumably right frontal lobe dysfunctional belief evaluation system (Joseph et al., 1990; Young et al., 1992; Staff et al., 1999; Papageorgiou et al., 2003), which prevents delusional patients from rejecting their abnormal beliefs despite recalcitrant evidence (Coltheart et al., 2007). According to this hypothesis, paranoid schizophrenia and DMS share the same neuropsychological impairment in belief evaluation, which is considered necessary for the maintenance of delusional beliefs. Accordingly, DMS will occur in the context of paranoid schizophrenia wherever a dysfunction in the dorsal pathway of face recognition system or a disconnection between the inferior temporal and limbic components of the visual recognition occur. Nevertheless, the findings of our study are indicative of frontal and right hemisphere dysfunction of equal severity in both DMS and non-DMS patients with paranoid schizophrenia. Therefore, they do not seem to support the hypothesis of a differential right hemisphere dysfunction in DMS vs. non-DMS patients with paranoid schizophrenia. The performance of the DMS group was found to be significantly lower on WAIS “Arithmetic” subtest. A distributed network involved in arithmetic abilities that includes prefrontal and posterior parietal regions has been demonstrated in control subjects and in patients with cerebral lesions using neuropsychological and functional neuroimaging techniques (Menon et al., 2000; Stanescu-Cosson et al., 2000). Parietal regions have been demonstrated to play a direct role in numerical processing, while frontal regions participate in the working memory aspects of complex computations. The abnormalities found in our study may be indicative of differentially impaired posterior parietal regions in DMS compared to non-DMS patients with paranoid schizophrenia. Although the between-group differences did not remain significant after Bonferroni correction, the calculated effect sizes were in the medium range (Table 2). Among the limitations of our study, we should underscore the following: to begin with, the size of our DMS group was small, since DMSs are quite rare. However, the results of our power analysis support the adequacy of our sample size. Moreover, the design of our study was only cross-sectional and thus unable to address issues of causation, which would require a longitudinal design. Furthermore, the neuropsychological battery used did not include, apart from BVRT-which in addition tends to produce ceiling effects-other tests sensitive enough to detect abnormalities in face processing. In addition, since the aim of the present study was to investigate whether co-occurring DMS in paranoid schizophrenia is possibly associated with a distinct neuropsychological substrate, we did not include a non-paranoid schizophrenia control group. Therefore, we cannot rule out the possibility that the neuropsychological impairments found in our study could be common to all patients with schizophrenia regardless the clinical subtype of the disorder and/or the co-occurrence of DMS(s). Finally, in order to evaluate patients' performance we used individual test norms and not a healthy

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control group. However, we think that, as we attempted to investigate the possible differences in neuropsychological functions between patients with paranoid schizophrenia with and without co-occurring DMS(s), a healthy control group was not indispensable. Overall, our findings are indicative of a bilateral frontal and right hemisphere dysfunction of equal severity in both DMS and non-DMS patients with paranoid schizophrenia. However, further research with neuropsychological batteries more sensitive in the detection of face processing abnormalities is fully warranted. References American Psychiatric Association. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994. Annett M. A classification of hand preference by association analysis. Br J Psychol 1970;61:303–21. Benton AL. The Revised Visual Retention Test. 3rd ed. The Psychological Corporation; 1963. Benton AL, Sivan AB, Hamsher Kde S, Varney NR, Spreen O. Facial recognition. Contributions to neuropsychological assessment: A Clinical Manual. 2nd edn. Oxford University Press; 1994. p. 35–52. Christodoulou GN, Malliara-Loulakaki S. Delusional misidentification syndromes and cerebral “ dysrhythmia ”. Psychiatria Clin; 1981;14:245–51. Christodoulou GN. The delusional misidentification syndromes. Br J Psychiatry 1991;159(suppl.14):65–9. Coltheart M. The 33rd Sir Frederick Bartlett lecture. Cognitive neuropsychiatry and delusional belief. Q J Exp Psychol 2007;60:1041–62. Coltheart M, Langdon R, McKay. Schizophrenia and monothematic delusions. Schizophr Bull 2007;33:642–7. Cutting J. Delusional misidentification and the role of right hemisphere in the appreciation of identity. Br J Psychiatry 1991;14:70–5 (Suppl). Cutting JC. Evidence for right hemisphere dysfunction in schizophrenia. In: David AS, Cutting JC, editors. The neuropsychology of schizophrenia. Lawrence Erlbaum Associates Ltd; 1994. p. 231–41. Davies AD. The influence of age on trail making test performance. J Clin Psychol 1968;24:96–8. Edelstyn NMJ, Oyebode F. A review of the phenomenology and cognitive neuropsychological origins of the Capgras syndrome. Int J Geriatr Psychiatry 1999;14:48–59. Ellis HD. The role of the right hemisphere in the Capgras delusion. Psychopathology; 1994;27:177–85. First MB, Spitzer RL, Gibbon M, Williams JBW. Structured clinical interview for DSM-IV axis I disorders. The New York State Psychiatric Institute, Biometrics Research, New York; 1995. Golden GC. Stroop color and word test. Α Manual for Clinical and Experimental uses. Stoelting Co; 1978. Heaton RK, Chelune GJ, Talley JL, Kay GK, Curtiss G. Wisconsin Card Sorting Test Manual Revised and Expanded. Psychological Assessment Resources Inc; 1993. Hirstein W, Ramachandran VS. Capgras syndrome: a novel probe for understanding the neural representation of the identity and familiarity of persons. Proc R Soc Lond B 1997;264:437–44. Joseph AB, O' Leary DH, Wheeler HG. Bilateral atrophy of the frontal and temporal lobes in schizophrenic patients with Capgras syndrome: a case-control study using computed tomography. J Clin Psychiatry 1990;51:322–5.

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