Neuropsychological performance of OCD patients before and after treatment with fluoxetine: evidence for persistent cognitive deficits

Background. There is an ongoing debate about the nature of executive dysfunction that accompanies obsessive–compulsive disorder (OCD). One reason for this may be that state-related factors, such as use of medication or co-morbid symptoms, confound with task performance. This study tried to isolate t...

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Bibliographic Details
Published in:Psychological medicine 2003-07, Vol.33 (5), p.917-925
Main Authors: NIELEN, M. M. A., DEN BOER, J. A.
Format: Article
Language:English
Subjects:
Adolescent
Adult
Antidepressive Agents, Second-Generation - therapeutic use
Biological and medical sciences
Cognition - drug effects
Cognitive deficits
Executive function
Female
Fluoxetine
Fluoxetine - therapeutic use
Humans
Male
Medical sciences
Middle Aged
Neuropharmacology
Neuropsychological functioning
Neuropsychological Tests
Obsessive-Compulsive Disorder - drug therapy
Obsessive-Compulsive Disorder - psychology
Obsessive-Compulsive neuroses
Pharmacology. Drug treatments
Psychiatric Status Rating Scales
Psycholeptics: tranquillizer, neuroleptic
Psychology. Psychoanalysis. Psychiatry
Psychopharmacology
Task Performance and Analysis
Treatment
Treatment Outcome
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Summary:Background. There is an ongoing debate about the nature of executive dysfunction that accompanies obsessive–compulsive disorder (OCD). One reason for this may be that state-related factors, such as use of medication or co-morbid symptoms, confound with task performance. This study tried to isolate trait- from state-dependent cognitive impairments by examining variability of cognition following treatment. Method. Nineteen OCD patients were tested on the Cambridge Neuropsychological Test Automated Battery (CANTAB) before and after treatment with fluoxetine. Their pattern of performance was compared to the one observed in healthy volunteers (N=24). Results. OCD patients displayed impairments in planning ability, spatial memory and motor speed that persisted after clinical improvement. With treatment, OCD performance diverged from that of controls on measures of focused attention and strategic ability. However, these effects were rather mild as they did not entail a significant deterioration of performance within the OCD sample. Conclusions. Our data suggest that cognitive impairments in OCD are not secondary to symptoms and therefore form a trait feature of the disorder. The nature of the deficits refers to a chronic dysfunction of the dorsolateral–striatal circuit. The minor effects of treatment on task performance is in line with recent evidence that serotonin mediates cognitive functions of orbitofrontal cortex to a greater extent than those associated with dorsolateral prefrontal regions.
ISSN:0033-2917
1469-8978
DOI:10.1017/S0033291703007682