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Childhood neuropsychological deficits associated with adult obsessive–compulsive disorder

  • Jessica R. Grisham (a1), Tracy M. Anderson (a2), Richie Poulton (a3), Terrie E. Moffitt (a4) and Gavin Andrews (a2)...
Abstract
Background

Existing neuropsychological studies of obsessive–compulsive disorder (OCD) are cross-sectional and do not provide evidence of whether deficits are trait-related (antecedent and independent of symptomatology) or state-related (a consequence, dependent on symptomatology).

Aims

To investigate whether there are premorbid neuropsychological deficits associated with adult OCD.

Method

Longitudinal data were collected from participants of the Dunedin Multidisciplinary Health and Developmental study. Neuropsychological data collected at age 13 were linked with age 32 diagnosis of OCD.

Results

The group who had OCD at age 32 differed significantly from the control group with no OCD on their performance at age 13 on neuropsychological tests of visuospatial, visuoconstructive and visuomotor skills, controlling for gender and socioeconomic status, but did not differ on tests of general IQ or verbal ability. Performance of the group with OCD on tests of executive functioning was mixed.

Conclusions

Individuals with OCD have premorbid impairment in visuospatial abilities and some forms of executive functioning, consistent with biological models of OCD.

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Copyright
Corresponding author
Jessica Grisham, School of Psychology, University of New South Wales, Sydney, Australia 2052. Email: jgrisham@psy.unsw.edu.au
Footnotes
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The Dunedin Multidisciplinary Health and Development Research Unit is supported by the New Zealand Health Research Council. This research was supported by grants from the US National Institute of Mental Health (MH 45070, MH49414), the UK Medical Research Council grant G0100527, and a Postdoctoral Fellowship with the School of Psychiatry, University of New South Wales.

Declaration of interest

None.

Footnotes
References
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1 Insel, TR. Toward a neuroanatomy of obsessive-compulsive disorder. Arch Gen Psychiatry 1992; 49: 739–44.
2 Greisberg, S, McKay, D. Neuropsychology of obsessive-compulsive disorder: a review and treatment implications. Clin Psychol Rev 2003; 23: 95117.
3 Simpson, HB, Rosen, W, Huppert, JD, Lin, S, Foa, EB, Liebowitz, MR. Are there reliable neuropsychological deficits in obsessive-compulsive disorder? J Psychiatr Res 2006; 40: 247–57.
4 Kuelz, AK, Hohagen, F, Voderholzer, U. Neuropsychological performance in obsessive-compulsive disorder: a critical review. Biol Psych 2004; 65: 185236.
5 Frost, LA, Moffitt, TE, McGee, R. Neuropsychological correlates of psychopathology in an unselected cohort of young adolescents. J Abnorm Psychol 1989; 98: 307–13.
6 Wechsler, D. Manual for the Wechsler Intelligence Scale for Children – Revised. Psychological Corporation, 1974.
7 Lezak, MD, Howieson, DB, Loring, DW. Neuropsychological Assessment (4th edn). Oxford University Press, 2004.
8 Kaufman, A. Factor analysis of the WISC-R at age levels between 6.5 and 16.5 years. J Consult Clin Psychol 1975; 43: 135–47.
9 Costello, A, Edelbrock, C, Kalas, R, Kessler, M, Klaric, SA. The National Institute of Mental Health Diagnostic Interview for Children (DISC). National Institute of Mental Health, 1982.
10 Robins, LN, Cottler, L, Bucholz, K, Compton, W. Diagnostic Interview Schedule for DSM–IV. Washington University Press, 1995.
11 Newman, DL, Moffitt, TE, Caspi, A, Magdol, L, Silva, PA, Stanton, WR. Psychiatric disorder in a birth cohort of young adults: prevalence, comorbidity, clinical significance, and new case incidence from ages 11 to 21. J Consult Clin Psychol 1996; 64: 552–62.
12 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorder (4th edn) (DSM–IV). APA, 1994.
13 Zohar, AH, Gross-Isseroff, R, Hermesh, H, Weizman, A. Is there sexual dimorphism in obsessive-compulsive disorder? Neurosci Biobehav Rev 1999; 23: 845–9.
14 Douglass, HM, Moffitt, TE, Dar, R, McGee, R, Silva, P. Obsessive-compulsive disorder in a birth cohort of 18-year-olds. Prevalence and predictors. J Am Acad Child Adolesc Psychiatry 1995; 34: 1424–31.
15 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (3rd edn) (DSM–III). APA, 1980.
16 Crino, R, Slade, T, Andrews, G. The changing prevalence and severity of obsessive-compulsive disorder criteria from DSM-III to DSM-IV. Am J Psychiatry 2005; 162: 876–82.
17 Savage, CR, Keuthen, NJ, Jenike, MA, Brown, HD, Rauch, SL, Jenike, MA. Organizational strategies mediate nonverbal memory impairment in obsessive-compulsive disorder J Neuropsychiatry Clin Neurosci 1999; 8: 99103.
18 Brown, TA, Campbell, LA, Lehman, CL, Grisham, JR, Mancill, RB. Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. J Abnorm Psychol 2001; 110: 585–99.
19 Rosenberg, DR, Keshavan, MS. Toward a neurodevelopmental model of obsessive-compulsive disorder. Biol Psych 1998; 43: 623–40.
20 Grisham, JR, Anderson, TM, Sachdev, PS. Genetic and environmental influences on obsessive-compulsive disorder. Eur Arch Psychiatry Clin Neurosci 2008; 258: 107–16.
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Childhood neuropsychological deficits associated with adult obsessive–compulsive disorder

  • Jessica R. Grisham (a1), Tracy M. Anderson (a2), Richie Poulton (a3), Terrie E. Moffitt (a4) and Gavin Andrews (a2)...
Submit a response

eLetters

Dr. Grisham and colleagues reply

Jessica R. Grisham, Senior Lecturer
08 October 2009

We thank Drs. Mustaq and Helal for their comments on our article. While they noted the need for longitudinal studies in this area, they expressed several concerns, one regarding the small number of individuals with OCD in our study. We agree and noted this limitation in our original paper. We were constrained, however, by the prevalence of OCD in the population; the proportion of cohort members diagnosed with OCD at age 32 in our study (1.9%) was consistent with other epidemiological studies. Our conclusions nonetheless remain tentative until they may be replicated in another longitudinal study.

Drs. Mustaq and Helal also referred to a previously published study by our group, which examined risk factors for an OCD diagnosis at age 18. We have suggested that this discrepancy may be related to changes in the OCD criteria from DSM-III to DSM-IV, which reduced the reported prevalenceof the disorder in the general population 1. Study members diagnosed withOCD at age 32 may have represented a more severe and persistent subgroup relative to the larger proportion (4%) of cohort members diagnosed with OCD at age 18.

Their letter also referred to a cross-sectional study, conducted by Beers and colleagues, that failed to find cognitive deficits in a group of21 children diagnosed with OCD2. While this study made a valuable contribution, the authors themselves noted the need to supplement their findings with results from “carefully designed longitudinal studies.” 3 Wesuspect that the discrepancy between the results of this earlier study andour recent findings may be partially attributable to sampling differences,including referral bias. Participants in the earlier study were paediatricOCD patients at a prestigious psychiatric institute, whereas the Dunedin cohort comprises a non-treatment seeking population cohort from a range ofsocioeconomic backgrounds. Further, in the previous study, children with OCD who had a lifetime history of any other psychiatric diagnosis were excluded2. OCD, like most emotional disorders, is highly comorbid with other psychiatric conditions4. While creating a “pure” OCD group eliminates the influence of comorbid disorders, this advantage must be weighed against the likelihood of creating a non-representative, potentially less severe, subgroup. Our study aimed to test for neuropsychological risk factors for adult OCD, as it presents in the general population, including comorbity, and regardless of referral and treatment seeking. Thus, our study’s aims, design and inferences differeddecidedly from those of Beers and colleagues.

Finally, Drs. Mustaq and Helal made the valid point that poor performance on neuropsychological tests may help to localize dysfunction in particular neuroanatomical substrates, but it does not provide conclusive evidence for the cause of the pathology. While our results are consistent with research that has demonstrated that children with OCD already show abnormalities in frontal and striatal volumes relative to comparison participants5, we do not suggest that we have provided definitive evidence of causality. OCD is likely to be multiply determinedand not all participants with particular neuropsychological deficits will go on to develop this disorder.

1. Crino R, Slade T, Andrews G. The changing prevalence and severity of obsessive-compulsive disorder criteria from DSM-III to DSM-IV. AmericanJournal of Psychiatry 2005;162:876-82.

2. Beers SR, Rosenberg DR, Dick EL, Williams T, O'Hearn KM, Birmaher B, et al. Neuropsychological study of frontal lobe function in psychotropic-naive children with obsessive-compulsive disorder. American Journal of Psychiatry 1999;156:777-79.

3. Beers SR, Rosenberg DR, Ryan CM. Dr. Beers and Colleagues Reply [Letter to the Editor]. American Journal of Psychiatry 2000;157:1183.

4. Brown TA, Campbell LA, Lehman CL, Grisham JR, Mancill RB. Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. Journal of Abnormal Psychology 2001;110:585-99.

5. Rosenberg DR, Keshavan MS. Toward a neurodevelopmental model of obsessive-compulsive disorder. Biological Psychiatry 1998;43:623-40.

Jessica R. Grisham, Ph.D.Terrie E. Moffitt, Ph.D.Richie Poulton, Ph.D.
... More

Conflict of interest: None Declared

Write a reply

Childhood neuropsychological deficits and adult OCD

Imran Mushtaq, Locum Consultant Child and Adolescent Psychiatrist
30 September 2009

We read Grisham et al’s paper (1) with some concerns. Without doubt, the study due to its nature, as longitudinal data was used, instead of cross-sectional designs in previous studies, adds positively on the area, which has not been well researched and is far from conclusive results. However, we have number of concerns about the reported results.

This study represents only one type of population and also due to small number of obsessive-compulsive disorder (OCD) cases (only 13/700) found in this study, the authors statement of ‘individuals with OCD have premorbid impairment in visuospatial abilities and some forms of executivefunctioning, consistent with biological models of OCD’, will be consideredoverstatement and cannot be generalized for other subsets of populations.

We also know that a previous study of OCD with the same birth cohortat age 18 found that the OCD group did not differ significantly on any of the neuropsychological tests at age 13 (2), and it will be interesting to know if there were any associations at ages 15, 21 and 26, when the same cohort was also assessed. Although they were also assessed at 3, 5, 7, 9 and 11 years of age, there is some evidence to suggest that there is nocognitive impairment in children with OCD, according to their performance on neuropsychological tests and OCD symptoms may not interfere with cognitive abilities early in the illness(3). However, disturbance of cognitive functions may become significant over time, as we know that psychotropic medications are the main pharmacological treatment that may also influence neuropsychological function (4). Neuroimaging studies suggest that the basal ganglia and ventral prefrontal cortex are most frequently implicated in OCD in adults. If brain dysfunction underlies OCD, decrements on neuropsychological tests should be found (3), so with this in mind, it is difficult to understand how people had neuropsychological deficits before and then developed OCD; when evidences suggest that children with OCD do not exhibit significant cognitive deficits early in the illness. However, disturbance of cognitive function may become evident over time (3).

Evidence is in the favour of late onset OCD (age 13-17) group showingexecutive dysfunction and auditory attention problems than the early onset(prior to 12 years) group. Performing poorly on the neuropsychological tests is not very conclusive as they may help in identifying a dysfunctionin a particular anatomical area; however, they provide little evidence on the actual cause leading towards the pathology. Late onset OCD is also associated with poorer visual memory relative to healthy comparison subjects. Roth et al’s findings (5), suggest that early and late onset OCDmay be the result of at least partially differing neurobiological mechanisms.

There is not much evidence at present to show effects of therapeutic interventions on neuropsychological deficits in OCD (6), and if any, are them curative in order to avoid the illness in future? The majority of the people who had OCD had comorbid illnesses, is it that these illnesses werethe cause of neuropsychological deficits and also later on led towards thedevelopment of OCD (chemical abnormalities such as serotonin)? Probably studies on this aspect may be an area of interest for the researchers.

The numbers of clients in the study are so small that no definitive statements should be made at this stage. We also wonder are there childrenand adolescents with neuropsychological deficits but not diagnosable psychiatric disorders and how we compare them with those with conditions like OCD.

References:

1.Grisham JR, Anderson TM, Poulton R, Moffitt TE, Andrews G. Childhood neuropsychological deficits associated with adult obsessive–compulsive disorder. British Journal of Psychiatry (2009) 195: 138-141

2.Douglass HM, Moffitt TE, Dar R, McGee R, Silva P. Obsessive-compulsive disorder in a birth cohort of 18-year-olds. Prevalence and predictors. J Am Acad Child Adolesc Psychiatry 1995; 34: 1424 -31

3.Beers SR, Rosenberg, DR, Dick, EL,Williams T, O'Hearn KM, BirmaherB, Ryan CM. Neuropsychological Study of Frontal Lobe Function in Psychotropic-Naive Children With Obsessive-Compulsive Disorder. Am J Psychiatry 156:777-779, May 1999

4.Hollander E, Schiffman E, Cohen B, Rivera-Stein MA, Rosen W, Gorman JM, Fyer AJ, Papp L, Liebowitz MR: Signs of central nervous system dysfunction in obsessive-compulsive disorder. Arch Gen Psychiatry 1990; 47:27–32

5.Roth RM et al. Neuropsychological Functioning in Early- and Late-Onset Obsessive-Compulsive Disorder. The Journal of Neuropsychiatry and Clinical Neurosciences 2005; 17:208–213

6.Bolton D et al. Neurological and neuropsychological signs in obsessive compulsive disorder: interaction with behavioural treatment. Behaviour Research and Therapy. 38;7, 2000, 695-708

Authors:

Imran Mushtaq, Locum Consultant Child and Adolescent Psychiatrist, Northampton CAHMS, 8-Notre Dame Mews, Northampton NN1 2BG

Muhammad Nabeel Helal, Staff Grade Psychiatrist, Cabot CMHT, 12 GroveRd, Redland, Bristol, BS6 6UJ

Declaration of Interests: None declared
... More

Conflict of interest: None Declared

Write a reply

Childhood neuropsychological deficits and adult OCD

Imran Mushtaq, Locum Consultant Child and Adolescent Psychiatrist
02 September 2009

We read Grisham et al’s paper (1) with some concerns. Without doubt, study due to its nature as longitudinal data was used, instead of cross-sectional designs in previous studies, adds positively on the area, which has been not well researched and is far from conclusive results. However, we have number of concerns about reported results.

This study represents only one type of population and also due to small number of obsessive-compulsive disorder (OCD) cases (only 13/700) found in this study, authors statement of ‘individuals with OCD have premorbid impairment in visuospatial abilities and some forms of executivefunctioning, consistent with biological models of OCD’, will be consideredoverstatement and cannot be generalized for other subsets of populations.

We also know that a previous study of OCD with this same birth cohortat age 18 found that the OCD group did not differ significantly on any of the neuropsychological tests at age 13 (2), and it will be interesting to know if there were any associations at ages 15, 21 and 26, when the same cohort was also assessed. Although they were also assessed at 3, 5, 7, 9 and 11 years of age but there is some evidence to suggest that there is nocognitive impairment in children with OCD, according to their performance on neuropsychological tests and OCD symptoms may not interfere with cognitive abilities early in the illness. However, disturbance of cognitive functions may become significant over time, so with this in mind, it is difficult to understand how people had neuropsychological deficits before and then developed OCD (3).

Whilst, the late onset OCD (age 13-17) group shows executive dysfunction and auditory attention problems than the early onset (prior to12 years) group. Performing poorly on the neuropsychological tests is not very conclusive as they may help in identifying a dysfunction in a particular anatomical area; however, they provide little evidence on the actual cause leading towards the pathology. Late onset OCD is also associated with poorer visual memory relative to healthy comparison subjects (4).

There is not much evidence at present to show effects of therapeutic interventions on neuropsychological deficits in OCD (5), and if any, are them curative in order to avoid the illness in future? Majority of the people who had OCD had comorbid illnesses, is it that these illnesses werethe cause of neuropsychological deficits and also later on led towards thedevelopment of OCD (chemical abnormalities such as serotonin)? Probably studies on this aspect may be an area of interest for the researchers.

Numbers of clients in the study are so small that no definitive statements should be made at this stage. We also wonder are there childrenand adolescents with neuropsychological deficits but not diagnosable psychiatric disorders and how we compare them with those with conditions like OCD.

References:

1.Grisham JR, Anderson TM, Poulton R, Moffitt TE, Andrews G. Childhood neuropsychological deficits associated with adult obsessive–compulsive disorder. British Journal of Psychiatry (2009) 195: 138-141

2.Douglass HM, Moffitt TE, Dar R, McGee R, Silva P. Obsessive-compulsive disorder in a birth cohort of 18-year-olds. Prevalence and predictors. J Am Acad Child Adolesc Psychiatry 1995; 34: 1424 -31

3.Beers SR, Rosenberg, DR, Dick, EL,Williams T, O'Hearn KM, BirmaherB, Ryan CM. Neuropsychological Study of Frontal Lobe Function in Psychotropic-Naive Children With Obsessive-Compulsive Disorder. Am J Psychiatry 156:777-779, May 1999

4.Roth RM et al. Neuropsychological Functioning in Early- and Late-Onset Obsessive-Compulsive Disorder. The Journal of Neuropsychiatry and Clinical Neurosciences 2005; 17:208–213

5.Bolton D et al. Neurological and neuropsychological signs in obsessive compulsive disorder: interaction with behavioural treatment. Behaviour Research and Therapy. 38;7, 2000, 695-708

Authors:

Imran Mushtaq, Locum Consultant Child and Adolescent Psychiatrist, Northampton CAHMS, 8-Notre Dame Mews, Northampton NN1 2BG

Muhammad Nabeel Helal, Staff Grade Psychiatrist, Cabot CMHT, 12 GroveRd, Redland, Bristol, BS6 6UJDeclaration of Interests: None declared
... More

Conflict of interest: None Declared

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