Functional Magnetic Resonance Imaging of Human Brain Activation During Cue-Induced Cocaine Craving

Maas, Luis C.; Lukas, Scott E.; Kaufman, Marc J.; Weiss, Roger D.; Daniels, Sarah; Rogers, Veronica W.; Kukes, Thellea J.; Renshaw, Perry F.

doi:10.1176/ajp.155.1.124

Cited by 400 publications

(336 citation statements)

References 8 publications

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“…These include various portions of the cingulate gyrus (Breiter et al, 1997;Childress et al, 1999;Garavan et al, 2000;Grant et al, 1996;Kilts et al, 2001;Mass et al, 1998;Wexler et al, 2001;Brody et al, 2002), the orbital cortex (Grant et al, 1996;Mass et al, 1998;Wang et al, 1999), the nucleus accumbens (Breiter et al, 1997;George et al, 2001;Kilts et al, 2001), and the insula (Breiter et al, 1997;Wang et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Differential Brain Activity in Alcoholics and Social Drinkers to Alcohol Cues: Relationship to Craving

Myrick

Anton

et al. 2003

Neuropsychopharmacol

471

345

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Using fMRI, our group previously found that after a sip of alcohol and exposure to alcohol beverage pictures, alcoholics compared to social drinkers had increased differential brain activity in the prefrontal cortex and anterior thalamus. This study extends this earlier work with several improvements including imaging the entire brain (rather than the anterior half previously) and recording craving, while the subjects viewed images within the scanner. In a Philips 1.5 T MRI scanner, 10 nontreatment-seeking alcoholics and 10 age-matched healthy social drinkers were given a sip of alcohol before viewing a 12 min randomized presentation of pictures of alcoholic beverages, nonalcoholic beverages, and two different visual control tasks. During picture presentation, changes in regional brain activity were measured in 15 transverse T2*-weighted blood oxygen level dependent slices. Subjects rated their urge to drink after each picture sequence. After a sip of alcohol, while viewing alcohol cues compared to viewing other beverage cues, the alcoholics, but not social drinkers, reported higher craving ratings and had increased activity in the prefrontal cortex and anterior limbic regions. Brain activity in the left nucleus accumbens, anterior cingulate, and left orbitofrontal cortex significantly correlated with subjective craving ratings in alcohol subjects but not in control subjects. This study suggests, as did our earlier study, that alcoholics and not social drinkers, when exposed to alcohol cues, have increased brain activity in areas that reportedly subserve craving for other addictive substances.

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Section: Discussionmentioning

confidence: 99%

Differential Brain Activity in Alcoholics and Social Drinkers to Alcohol Cues: Relationship to Craving

Myrick

Anton

et al. 2003

Neuropsychopharmacol

471

345

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“…Consistent with these animal models, brain imaging studies in humans have shown that cue-induced cocaine craving is associated with activation of the amygdala and anterior cingulate cortex (Childress et al 1999;Maas et al 1998). The neurochemical substrates underlying such conditioned reinforcement effects are under intense investigation but have been hypothesized to involve glutamatergic afferents from the basolateral amygdala and ventral subiculum as well as dopaminergic projections to the basolateral amygdala and other cortical areas (Berke and Hyman 2000).…”

Section: Brain Stress Systems and Vulnerability To Relapsementioning

confidence: 98%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,544

1,962

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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drugtaking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to BACKGROUNDDrug addiction is a chronically relapsing disorder that is defined by two major characteristics: a compulsion to take the drug with a narrowing of the behavioral repertoire toward excessive drug intake, and a loss of control in limiting intake (American Psychiatric Association 1994; World Health Organization 1992). An important challenge for neurobiological research is to understand the neuroadaptive differences between controlled drug use and loss of control, and by extension, the molecular, cellular and system processes that lead to addiction (Koob and Le Moal 1997).Animal models are critical for understanding the neuropharmacological mechanisms involved in the development of addiction. While there are no complete animal models of addiction, animal models do exist for many elements of the syndrome. These elements can be derived from symptoms or diagnostic criteria for addiction or conceptual frameworks such as different sources of reinforcement (American Psychiatric Association 1994; World Health Organization 1992). Linking neu- 24 , NO . 2 ropharmacological events to animal models can occur at multiple levels of analysis -molecular, cellular and system -and it will only be the integration of these changes across dimensions of analysis that will allow a full understanding of the neurobiology of drug addiction.Advances in neuroscience research are rapidly unr...

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“…Research suggests that cue-related cocaine craving involves the activation of a network of cortical regions involved in the engagement of attention, and the subsequent ruminations also involve the fronto-parietal network seen in WM rehearsal (Childress et al, 1999;Garavan et al, 2000;Grant et al, 1996;Kilts et al, 2001;Maas et al, 1998). Although speculative, a link between WM demands, cocaine craving and poor error awareness may help explain why cocaine users selfmonitoring, or insight into their own behavior, is particularly poor during craving for the drug (Miller and Gold, 1994).…”

Section: Error Awarenessmentioning

confidence: 99%

Post-Error Behavior in Active Cocaine Users: Poor Awareness of Errors in the Presence of Intact Performance Adjustments

Hester

Simões‐Franklin

Garavan

2007

Neuropsychopharmacol

107

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Active cocaine abusers have a diminished neural response to errors, particularly in the anterior cingulate cortex thought critical to error processing. The inability to detect, or adjust performance following errors has been linked to clinical symptoms including the loss of insight and perseverative behavior. We investigated the cognitive implications of this diminished error-related activity, using response inhibition tasks that required error awareness and performance adaptation. Twenty-one active cocaine users (six female subjects, mean age ¼ 40.3) and 22 non-drug using adults (six female subjects, mean ¼ 39.9) participated. The results indicated that cocaine users consistently demonstrated poorer inhibitory control, a deficit accompanied by reduced awareness of errors. Adaptation of post-error reaction times did not differ between groups, although a different measure of adaptive behavior: exerting inhibitory control on the trial immediately after failing to inhibit, was significantly poorer in the cocaine using sample. In summary, cocaine users demonstrated a diminished capacity for monitoring their behavior, but were able to perform post-error adjustment to processes not already suffering an underlying deficit. These difficulties are consistent with previous reports of cocaine-related hypoactivity in the neural system underlying cognitive control, and highlight the potential for cognitive dysfunction to manifest as behavioral deficits that likely contribute to the maintenance of drug dependence.

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Functional Magnetic Resonance Imaging of Human Brain Activation During Cue-Induced Cocaine Craving

Abstract: These results suggest that functional MRI may be a useful tool to study the neurobiological basis of cue-induced craving.

Cited by 400 publications

References 8 publications

Differential Brain Activity in Alcoholics and Social Drinkers to Alcohol Cues: Relationship to Craving

Differential Brain Activity in Alcoholics and Social Drinkers to Alcohol Cues: Relationship to Craving

Drug Addiction, Dysregulation of Reward, and Allostasis

Post-Error Behavior in Active Cocaine Users: Poor Awareness of Errors in the Presence of Intact Performance Adjustments

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