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Impaired visuospatial associative memory and attention in obsessive compulsive disorder but no evidence for differential dopaminergic modulation

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Abstract

Rationale

Patients with obsessive compulsive disorder (OCD) demonstrate impaired cognition in some selected domains. Although serotoninergic dysfunction has been implicated in OCD, recent evidence suggests that dopamine may play a role as well.

Objective

The aim of the study was to evaluate learning and working memory in OCD and to determine the effects of dopaminergic manipulations on these capacities.

Methods

Visuospatial associative memory and spatial and verbal working memory were examined in 18 nondepressed patients with OCD and 18 matched healthy controls. The study further investigated whether acute administration of dopamine D2/D3 receptor agonist and antagonist would differentially modulate cognition in OCD. Each participant underwent the cognitive battery three times in a randomized double-blind, placebo-controlled crossover design.

Results

Significant impairments in patients compared with controls were noted on the Cambridge Neuropsychological Test Automated Battery (CANTAB) paired associates learning (PAL) and a measure of sustained attention (rapid visual information processing, RVIP) that persisted across all sessions, with deficient strategy in the CANTAB spatial working memory task in the first session alone. Although the dopamine D2/D3 agonist, pramipexole, led to poorer performance on the PAL and RVIP tasks, no differential effects were noted between the two groups. No significant effects were noted for the D2/D3 antagonist, amisulpride.

Conclusions

The results are consistent with a specific associative memory deficit in OCD that remained robust despite possible practice effects and compensatory strategies and point to abnormal medial temporal lobe involvement in OCD in addition to the previously implicated frontostriatal loops, with no clear evidence of D2 receptor mediation.

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Acknowledgments

The authors wish to thank the participants who took part in the study. The study was funded by a research grant to TWR from GlaxoSmithKline. The Behavioral and Clinical Neuroscience Institute is cofunded by a grant from the MRC and the Wellcome Trust. SM-Z is funded by a Wellcome Trust Program Grant to TWR. KJC is employed by and is a shareholder in P1vital Ltd., whose clients include several pharmaceutical companies. KDE is supported by a Betty Behrens Clare Hall Research Fellowship. UM has consulted for Janssen-Cilag; has received research support from Alexander von Humboldt Foundation, Janssen-Cilag, Medical Research Council (MRC), and Isaac Newton Trust; and has received honoraria and support to attend and/or lecture at scientific meetings from Bristol-Meyers Squibb, Eli-Lilly, Janssen-Cilag, Lundbeck, Shire, and UCB Pharma. NAF has consulted for Lundbeck, GlaxoSmithKline, Servier, and Bristol Myers Squibb; has received research support from Lundbeck, GlaxoSmithKline, Astra Zeneca, Wellcome, ECNP, and Cephalon; has received honoraria and support to attend and/or lecture at scientific meetings from Janssen, Jazz, Lundbeck, Servier, Astra Zeneca, Cephalon, and Wyeth. EB is employed half-time by the University of Cambridge and half-time by the GlaxoSmithKline and owns shares in GSK. BJS consults for Cambridge Cognition Ltd. and a number of pharmaceutical companies and owns shares in CeNeS. TWR consults for Cambridge Cognition, Pfizer, Lilly, Lundbeck, Allon Therapeutics, and GlaxoSmithKline and currently holds grant funding from GlaxoSmithKline.

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Authors and Affiliations

  1. Department of Psychiatry, University of Cambridge School of Clinical Medicine, Addenbrooke’s Hospital, Hills Road, Box 189, CB2 2QQ, Cambridge, UK

    Sharon Morein-Zamir, Kevin J. Craig, Karen D. Ersche, Ulrich Muller, Edward T. Bullmore & Barbara J. Sahakian

  2. Behavioral and Clinical Neurosciences Institute (BCNI), University of Cambridge, Cambridge, UK

    Sharon Morein-Zamir, Kevin J. Craig, Karen D. Ersche, Sanja Abbott, Ulrich Muller, Edward T. Bullmore, Barbara J. Sahakian & Trevor W. Robbins

  3. Department of Experimental Psychology, University of Cambridge, Cambridge, UK

    Sanja Abbott & Trevor W. Robbins

  4. Department of Psychiatry, Queen Elizabeth II Hospital, Welwyn Garden City, Hertfordshire, UK

    Naomi A. Fineberg

  5. Postgraduate Medical School, University of Hertfordshire, Hatfield, UK

    Naomi A. Fineberg

  6. GlaxoSmithKline, Clinical Unit Cambridge, Cambridge, UK

    Edward T. Bullmore

  7. P1vital Ltd., Oxford, UK

    Kevin J. Craig

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  1. Sharon Morein-Zamir
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Correspondence to Sharon Morein-Zamir.

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Sharon Morein-Zamir and Kevin J. Craig have joint authorship.

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Morein-Zamir, S., Craig, K.J., Ersche, K.D. et al. Impaired visuospatial associative memory and attention in obsessive compulsive disorder but no evidence for differential dopaminergic modulation. Psychopharmacology 212, 357–367 (2010). https://doi.org/10.1007/s00213-010-1963-z

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