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Pretreatment brain activation during stroop task is associated with outcomes in cocaine-dependent patients.

ABSTRACT: Cognitive behavioral and related therapies for cocaine dependence may exert their effects, in part, by enhancing cognitive control over drug use behavior. No prior studies have systematically examined the neural correlates of cognitive control as related to treatment outcomes for cocaine dependence.Twenty treatment-seeking cocaine-dependent individuals performed a Stroop color-word interference task while undergoing functional magnetic resonance imaging (fMRI) prior to initiating treatment. The primary outcome measures were percent of urine drug screens negative for cocaine, percent days abstinent, and treatment retention. Correlations between regional brain activation during Stroop task performance and treatment outcome measures were analyzed.During Stroop performance, individuals activated brain regions similar to those reported in nonaddicted individuals, including the anterior cingulate cortex, dorsolateral prefrontal cortex, parietal lobule, insula, and striatum. Activations at treatment onset correlated differentially with specific outcomes: longer duration of self-reported abstinence correlated with activation of ventromedial prefrontal cortex, left posterior cingulate cortex, and right striatum; percent drug-free urine screens correlated with striatal activation; and treatment retention correlated with diminished activation of dorsolateral prefrontal cortex. A modest correlation between Stroop effect and treatment retention was found.The functions of specific brain regions underlying cognitive control relate differentially to discrete outcomes for the treatment of cocaine dependence. These findings implicate neurocircuitry underlying cognitive control in behavioral treatment outcome and provide insight into the mechanisms of behavioral therapies for cocaine dependence. They also suggest neural activation patterns during cognitive control tasks are more sensitive predictors of treatment response than behavioral measures.

SUBMITTER: Brewer JA

PROVIDER: S-EPMC2601637 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature

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Pretreatment brain activation during stroop task is associated with outcomes in cocaine-dependent patients.

Brewer Judson A JA Worhunsky Patrick D PD Carroll Kathleen M KM Rounsaville Bruce J BJ Potenza Marc N MN

Biological psychiatry 20080717 11

<h4>Background</h4>Cognitive behavioral and related therapies for cocaine dependence may exert their effects, in part, by enhancing cognitive control over drug use behavior. No prior studies have systematically examined the neural correlates of cognitive control as related to treatment outcomes for cocaine dependence.<h4>Methods</h4>Twenty treatment-seeking cocaine-dependent individuals performed a Stroop color-word interference task while undergoing functional magnetic resonance imaging (fMRI) ...[more]

PMID: 18635157

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Project description:Cocaine-dependent individuals demonstrate neural and behavioral differences compared to healthy comparison subjects when performing the Stroop color-word interference test. Stroop measures also relate to treatment outcome for cocaine dependence. Intrinsic connectivity analyses assess the extent to which task-related regional brain activations are related to each other in the absence of defining a priori regions of interest.This study examined 1) the extent to which cocaine-dependent and non-addicted individuals differed on measures of intrinsic connectivity during fMRI Stroop performance; and 2) the relationships between fMRI Stroop intrinsic connectivity and treatment outcome in cocaine dependence.Sixteen treatment-seeking cocaine-dependent patients and matched non-addicted comparison subjects completed an fMRI Stroop task. Between-group differences in intrinsic connectivity were assessed and related to self-reported and urine-toxicology-based cocaine-abstinence measures.Cocaine-dependent patients vs. comparison subjects showed less intrinsic connectivity in cortical and subcortical regions. When adjusting for individual degree of intrinsic connectivity, cocaine-dependent vs. comparison subjects showed relatively greater intrinsic connectivity in the ventral striatum, putamen, inferior frontal gyrus, anterior insula, thalamus and substantia nigra. Non-mean-adjusted intrinsic-connectivity measures in the midbrain, thalamus, ventral striatum, substantia nigra, insula and hippocampus negatively correlated with measures of cocaine abstinence.The diminished intrinsic connectivity in cocaine-dependent vs. comparison subjects suggests poorer communication across brain regions during cognitive-control processes. In mean-adjusted analyses, the cocaine-dependent group displayed relatively greater Stroop-related connectivity in regions implicated in motivational processes in addictions. The relationships between treatment outcomes and connectivity in the midbrain and basal ganglia suggest that connectivity represents a potential treatment target.

Project description:ObjectiveContextual drug-associated memory precipitates craving and relapse in substance users, and the risk of relapse is a major challenge in the treatment of substance use disorders. Thus, understanding the neurobiological underpinnings of how this association memory is formed and maintained will inform future advances in the treatment of drug addiction. Brain endocannabinoids (eCBs) signalling has been associated with drug-induced neuroadaptations, but the role of lipases that mediate small lipid ligand biosynthesis and metabolism in regulating drug-associated memory has not been examined. Here, we explored how manipulation of the lipase fatty acid amide hydrolase (FAAH), which is involved in mediating the level of the lipid ligand anandamide (AEA), affects cocaine-associated memory formation.MethodsWe applied behavioural, pharmacological and biochemical methods to detect cocaine-associated memory formation, eCBs in the dorsal dentate gyrus (dDG), and the activity of related enzymes. We further examined the roles of abnormal FAAH activity and AEA-CB1R signalling in the regulation of cocaine-associated memory formation and granule neuron dendritic structure alterations in the dDG through Western blotting, electron microscopy and immunofluorescence.ResultsIn the present study, we found that cocaine induced a decrease in the level of FAAH in the dDG and increased the level of AEA. A high level of AEA activated cannabinoid type 1 receptors (CB1Rs) and further triggered CB1R signalling activation and granule neuron dendritic remodelling, and these effects were reversed by blockade of CB1Rs in the brain. Furthermore, inhibition of FAAH in the dDG markedly increased AEA levels and promoted cocaine-associated memory formation through CB1R signalling activation.ConclusionsTogether, our findings demonstrate that the lipase FAAH influences CB1R signalling activation and granule neuron dendritic structure alteration in the dDG by regulating AEA levels and that AEA and AEA metabolism play a key role in cocaine-associated memory formation. Manipulation of AEA production may serve as a potential therapeutic strategy for drug addiction and relapse prevention.

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Pretreatment brain activation during stroop task is associated with outcomes in cocaine-dependent patients.

Publications

Pretreatment brain activation during stroop task is associated with outcomes in cocaine-dependent patients.

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