Drug abusers show impaired performance in a laboratory test of decision making

Grant, Steven; Contoreggi, Carlo; London, Edythe D.

doi:10.1016/s0028-3932(99)00158-x

Cited by 571 publications

(445 citation statements)

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“…Drug addicts who predominantly abuse amphetamine, cocaine, heroin, alcohol or phencyclidine exhibit performance deficits on tasks that require response inhibition, decision making and/or cognitive flexibility (Cosgrove and Newell 1991;McKetin and Mattick 1998;O'Malley et al 1992;Rogers et al 1999;Ornstein et al 2000;Grant et al 2000). The deficits exhibited by drug abusers include impairments of set shifting, planning (Ornstein et al 2000) and decision-making (Rogers et al 1999;Grant et al 2000).…”

Section: Relation To Neuropsychological Studies In Drug Addictionmentioning

confidence: 99%

“…Volkow and Fowler 2000;London et al 2000). Second, chronic drug administration affects the neurochemistry and anatomy of these brain regions in animal models (Nestler and Aghajanian 1997;Robinson and Kolb 1997;Wolf 1998;Berke and Hyman 2000; Vandershuren and Kalivas 2000;Robinson et al 2001 (Post et al 1976), altered incentive motivation (Shippenberg and Heidbreder 1995;Taylor and Horger 1999;Robbins and Everitt 1999) and impaired cognitive and executive function (Jentsch et al 1997(Jentsch et al , 2000Rogers et al 1999;Robbins and Everitt 1999;Grant et al 2000;Ornstein et al 2000) after chronic stimulant drug administration.Because of its important role in decision-making (Bechara et al 2000) and inhibitory control over pre-potent behavior (Roberts and Wallis 2000), an involvement of ventromedial regions of the frontal cortex in drug abuse has been proposed. In essence, impairments of frontal lobe function are thought to effectively 'un-gate' subcortically-mediated, conditioned tendencies (such as established instrumental responses to obtain and consume drugs), resulting in the compulsive drug seeking and taking that characterize addiction (Jentsch and Taylor 1999).…”

mentioning

confidence: 99%

“…Second, chronic drug administration affects the neurochemistry and anatomy of these brain regions in animal models (Nestler and Aghajanian 1997;Robinson and Kolb 1997;Wolf 1998;Berke and Hyman 2000;Vandershuren and Kalivas 2000;Robinson et al 2001). Third, neurobehavioral studies in humans and animals have provided evidence for abnor-mal locomotor and stereotypic behavior (Post et al 1976), altered incentive motivation (Shippenberg and Heidbreder 1995;Taylor and Horger 1999;Robbins and Everitt 1999) and impaired cognitive and executive function (Jentsch et al 1997(Jentsch et al , 2000Rogers et al 1999;Robbins and Everitt 1999;Grant et al 2000;Ornstein et al 2000) after chronic stimulant drug administration.…”

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confidence: 99%

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Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

Jentsch

Olausson

Garza

et al. 2002

Neuropsychopharmacology

255

217

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The current experiments examined the effects of acute or repeated, intermittent administrations of cocaine on the acquisition and reversal of object discriminations by Vervet monkeys in order to test the hypothesis that cocaine treatment affects performance of tasks that depend upon the functions of the orbitofrontal cortex and amygdala. An acute dose of cocaine (1 mg/kg; 20 min prior to testing) impaired reversal of a previously learned object discrimination but had no effect on acquisition of a novel one. Specific impairments of reversal learning were also observed in monkeys 9 and 30 days after repeated administrations of cocaine (2 or The compulsive drug seeking and taking behavior that is characteristic of drug addiction has recently been attributed to complex, inter-related dysfunctions in neural systems mediating incentive motivation and behavioral regulation (e.g., the striatum, amygdala and ventral frontal cortex; Jentsch and Taylor 1999;Robbins and Everitt 1999; Volkow and Folwer 2000;Berke and Hyman 2000). Several lines of evidence support this hypothesis. First, drug addicts exhibit altered cerebral blood flow and metabolism within the striatum, amygdala and frontal cortex both at baseline and after drug-induced craving (c.f. Volkow and Fowler 2000;London et al. 2000). Second, chronic drug administration affects the neurochemistry and anatomy of these brain regions in animal models (Nestler and Aghajanian 1997;Robinson and Kolb 1997;Wolf 1998;Berke and Hyman 2000; Vandershuren and Kalivas 2000;Robinson et al. 2001 (Post et al. 1976), altered incentive motivation (Shippenberg and Heidbreder 1995;Taylor and Horger 1999;Robbins and Everitt 1999) and impaired cognitive and executive function (Jentsch et al. 1997(Jentsch et al. , 2000Rogers et al. 1999;Robbins and Everitt 1999;Grant et al. 2000;Ornstein et al. 2000) after chronic stimulant drug administration.Because of its important role in decision-making (Bechara et al. 2000) and inhibitory control over pre-potent behavior (Roberts and Wallis 2000), an involvement of ventromedial regions of the frontal cortex in drug abuse has been proposed. In essence, impairments of frontal lobe function are thought to effectively 'un-gate' subcortically-mediated, conditioned tendencies (such as established instrumental responses to obtain and consume drugs), resulting in the compulsive drug seeking and taking that characterize addiction (Jentsch and Taylor 1999). Nevertheless, few studies have directly investigated the long-term consequences of prolonged exposure to addictive drugs on frontal cortex cognitive function, particularly in non-human primates.The aim of the current studies was to directly evaluate the function of the prefrontocortico-amygdalo-striatal system after repeated, intermittent cocaine administrations to monkeys. Using an animal model in which drug treatment (schedule and dosing) and withdrawal can be experimentally controlled, we employed a wellcharacterized behavioral task, the acquisition and reversal of a 3-choice object discrimination. T...

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Section: Relation To Neuropsychological Studies In Drug Addictionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

Jentsch

Olausson

Garza

et al. 2002

Neuropsychopharmacology

255

217

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“…Patients with lesions in the VMPFC consistently performed more poorly on this task than controls (Bechara et al, 2000a(Bechara et al, , 1999(Bechara et al, , 1997(Bechara et al, , 1994. Substance abusers also show performance deficits on this task (Bartzokis et al, 2000;Grant et al, 2000). Performance on the Iowa Gambling Task appears to be mediated by a neural network composed of the OFC, the amygdala, somatosensory/insular cortices, and the peripheral nervous system (Bechara et al, 1999(Bechara et al, , 1997Ernst et al, 2002).…”

Section: Introductionmentioning

confidence: 98%

Orbitofrontal cortex dysfunction in abstinent cocaine abusers performing a decision-making task

et al. 2003

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Cocaine abusers demonstrate faulty decision-making as manifested by their inability to discontinue self-destructive drug-seeking behaviors. The orbitofrontal cortex (OFC) plays an important role in decision-making. In this preliminary study we tested whether 25-day-abstinent cocaine abusers show alterations in normalized cerebral blood flow (rCBF) in the OFC using PET with 15 O during the Iowa Gambling Task (a decision-making task). This task measures the ability to weigh short-term rewards against long-term losses. A control task matched the sensorimotor aspects of the task but did not require decision-making. Cocaine abusers (N = 13) showed greater activation during performance of the Iowa Gambling Task in the right OFC and less activation in the right dorsolateral prefrontal cortex (DLPFC) and left medial prefrontal cortex (MPFC) compared to a control group (N = 13). Better Iowa Gambling Task performance was associated with greater activation in the right OFC in both groups. Also, the amount of cocaine used (grams/week) prior to the 25 days of enforced abstinence was negatively correlated with activation in the left OFC. Greater activation in the OFC in cocaine abusers compared to a control group may reflect differences in the anticipation of reward while less activation in the DLPFC and MPFC may reflect differences in planning and working memory. These findings suggest that cocaine abusers show persistent functional abnormalities in prefrontal neural networks involved in decision-making and these effects are related to cocaine abuse. Compromised decision-making could contribute to the development of addiction and undermine attempts at abstinence.

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“…Although great advances have been made in the cellular mechanisms of tolerance and dependence to opioids (Bailey and Connor, 2005), little is known about the course of learning and memory deficits after cessation of chronic opiate use in behavioral animal models (Pu et al, 2002;Sala et al, 1994;Spain and Newsom, 1991). In humans, opiate addiction is usually associated with cognitive impairments such as poor impulse control, planning, memory, and decision-making (Chastain et al, 1986;Franken et al, 2000;Grant et al, 2000;Guerra et al, 1987;Lee and Pau, 2002;Strang and Gurling, 1989;Stout and Farrell, 2002). This impairment has been suggested to contribute to the relapse of opiate addiction (Gossop et al, 2002).Thus, understanding the cognitive changes that occur in chronic opiate use may help in developing treatments for opiate addiction.…”

Section: Introductionmentioning

confidence: 99%

Chronic Morphine Selectively Impairs Cued Fear Extinction in Rats: Implications for Anxiety Disorders Associated with Opiate Use

et al. 2007

Neuropsychopharmacol

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Previous studies have shown that opioid transmission plays an important role in learning and memory. However, little is known about the course of opiate-associated learning and memory deficits after cessation of chronic opiate use in a behavioral animal model. In the present study, we examined the effects of chronic morphine on fear extinction, an important preclinical model for behavior therapy of human anxiety disorders. Rats were administrated subcutaneously morphine hydrochloride or saline twice per day for continuous 10 days. Rats received a cued or contextual fear conditioning session 7 days after the last morphine injection. During subsequent days, rats received four cued or contextual extinction sessions (one session per day). Percent freezing was assessed during all phases of training. Chronic morphine did not affect the acquisition of cued fear response or the initial encoding of extinction memory within each session, but produced an impairment in the between-session extinction. However, the same morphine treatment schedule did not affect the acquisition or extinction of contextual fear response. These results suggest that the effects of chronic morphine on memory for fear extinction are complex. Chronic morphine selectively impairs extinction of cued fear response. This deficit in fear extinction may be one of those critical components that contribute to the high prevalence of anxiety disorders in opiate addicts.

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Drug abusers show impaired performance in a laboratory test of decision making

Cited by 571 publications

References 47 publications

Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

Orbitofrontal cortex dysfunction in abstinent cocaine abusers performing a decision-making task

Chronic Morphine Selectively Impairs Cued Fear Extinction in Rats: Implications for Anxiety Disorders Associated with Opiate Use

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