Psychomotor retardation as a predictor of fluoxetine nonresponse in depressed outpatients.
Item
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Title
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Psychomotor retardation as a predictor of fluoxetine nonresponse in depressed outpatients.
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Identifier
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AAI3115294
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identifier
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3115294
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Creator
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Taylor, Bonnie P.
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Contributor
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Adviser: Jeffrey Halperin
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Date
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2004
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Language
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English
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Publisher
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City University of New York.
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Subject
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Psychology, Cognitive | Psychology, Psychobiology | Biology, Neuroscience
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Abstract
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Although there have been significant advances in the psychopharmacological treatment of depression, roughly 50 percent of patients remain symptomatic after their initial treatment. To date, there is no empirical basis to help guide clinicians as to whether patients will respond more favorably to one medication over another. Current practice is simply a trial and error approach. The potential benefits of discovering predictors of treatment response are considerable as patients could be matched to a treatment that they are most likely to respond to. This study examined whether performance on neuropsychological tests of processing speed, a quantitative measure of psychomotor retardation, predicts response to fluoxetine in depressed outpatients. It was hypothesized that since psychomotor retardation has been linked to reduced dopaminergic functioning, patients with psychomotor slowing would have an unfavorable response to fluoxetine, which enhances serotonergic neurotransmission. Thirty-seven moderately depressed outpatients who were administered a short battery of cognitive tests at baseline completed 12-weeks of treatment with fluoxetine. Patients who were resistant to medication (n = 12) exhibited significantly reduced performance on the FAS test of verbal fluency and the Stroop Color Naming subtest compared to patients who responded (n = 25) (t = -4.10, df = 35, P ≤ 0.001, and t = -2.10, df = 35, P = 0.043, respectively). A trend in the same direction was demonstrated for Stroop Word Reading and the Digit Symbol subtest of the WAIS-III. These findings remained even after controlling for baseline depression severity, suggesting that the psychomotor slowing demonstrated by nonresponders was independent of the severity of depressive symptoms. Moreover, differential treatment response was specific to psychomotor speed, as responders and nonresponders did not perform differently on tasks of executive functioning, attention, visuospatial functioning and verbal intelligence. If confirmed, psychomotor slowing may identify a subgroup of depressed patients who are unresponsive to fluoxetine and should therefore be treated with an alternative agent. Future investigations should utilize anatomical and functional neuroimaging in conjunction with cognitive testing and pharmacological dissection to further elucidate the psychobiological substrates and differential treatment response in this depressive subtype with psychomotor slowness and resistance to fluoxetine.
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
