Mindfulness, Mechanisms and Meaning: Perspectives From the Cognitive Neuroscience of Addiction

McConnell, Patrick A.; Froeliger, Brett

doi:10.1080/1047840x.2015.1076701

Cited by 30 publications

(19 citation statements)

References 85 publications

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“…These limitations notwithstanding findings from the current study support the hypothesis that prolonged prescription opioid use in the context of chronic pain is marked by deficits in frontostriatal morphology and resting‐state functional connectivity, similar to chronic use of other drugs with significant abuse liability. These findings will help guide further research into frontostriatal‐targeted pharmacotherapies producing glutamate homeostasis (eg, N ‐acetylcysteine) and/or behavioral interventions for substance use disorders) that may modulate frontostriatal circuitry function . For example, in a double‐blind, placebo (PBO)–controlled N ‐acetylcysteine (NAC) study in smoking‐abstinent, nicotine‐dependent smokers, NAC was associated with stronger frontostriatal rsFC, less craving, and affective disturbances and remaining smoking abstinent over the medication period .…”

Section: Discussionmentioning

confidence: 96%

Impaired frontostriatal functional connectivity among chronic opioid using pain patients is associated with dysregulated affect

et al. 2019

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Preclinical studies have shown effects of chronic exposure to addictive drugs on glutamatergic-mediated neuroplasticity in frontostriatal circuitry. These initial findings have been paralleled by human functional magnetic resonance imaging (fMRI) research demonstrating weaker frontostriatal resting-state functional connectivity (rsFC) among individuals with psychostimulant use disorders. However, there is a dearth of human imaging literature describing associations between long-term prescription opioid use, frontostriatal rsFC, and brain morphology among chronic pain patients. We hypothesized that prescription opioid users with chronic pain, as compared with healthy control subjects, would evidence weaker frontostriatal rsFC coupled with less frontostriatal gray matter volume (GMV). Further, those opioid use-related deficits in frontostriatal circuitry would be associated with negative affect and drug misuse. Prescription opioid users with chronic pain (n = 31) and drug-free healthy controls (n = 30) underwent a high-resolution anatomical and an eyesclosed resting-state functional scan. The opioid group, relative to controls, exhibited weaker frontostriatal rsFC, and less frontostriatal GMV in both L.NAc and L.vmPFC.Frontostriatal rsFC partially mediated group differences in negative affect. Within opioid users, L.NAc GMV predicted opioid misuse severity. The current study revealed that prescription opioid use in the context of chronic pain is associated with functional and structural abnormalities in frontostriatal circuitry. These results suggest that opioid use-related abnormalities in frontostriatal circuitry may undergird disturbances in affect that may contribute to the ongoing maintenance of opioid use and misuse. These findings warrant further examination of interventions to treat opioid pathophysiology in frontostriatal circuitry over the course of treatment.

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Section: Discussionmentioning

confidence: 96%

Impaired frontostriatal functional connectivity among chronic opioid using pain patients is associated with dysregulated affect

et al. 2019

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“…Moreover, findings herein suggest that individual differences in corticothalamic circuitry function have important implications for smoking cessation and relapse vulnerability. Further research is needed to evaluate the therapeutic benefit of delivering precessation interventions (eg, brain stimulation, 47 cognitive training, 48,49 and combined medications 50 ) to treat the neuropathophysiology of corticothalamic circuitry involved in smoking behavior.…”

Section: Discussionmentioning

confidence: 99%

Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability

et al. 2017

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IMPORTANCE Tobacco use disorder is associated with dysregulated neurocognitive function in the right inferior frontal gyrus (IFG)—one node in a corticothalamic inhibitory control (IC) network. OBJECTIVE To examine associations between IC neural circuitry structure and function and lapse/relapse vulnerability in 2 independent studies of adult smokers. DESIGN, SETTING, AND PARTICIPANTS In study 1, treatment-seeking smokers (n = 81) completed an IC task during functional magnetic resonance imaging (fMRI) before making a quit attempt and then were followed up for 10 weeks after their quit date. In study 2, a separate group of smokers (n = 26) performed the same IC task during fMRI, followed by completing a laboratory-based smoking relapse analog task. Study 1 was performed at Duke University Medical Center between 2008 and 2012; study 2 was conducted at the Medical University of South Carolina between 2013 and 2016. MAIN OUTCOMES AND MEASURES Associations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse. RESULTS Of the 81 study participants in study 1 (cessation study), 45 were women (56%), with mean (SD) age, 38.4 (10.2) years. In study 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P threshold = 0.03), greater IC task-related blood oxygenation level–dependent (BOLD) response in the right IFG (F1,78 = 14.87) and thalamus (F1,78 = 14.97) (P < .05), and weaker corticothalamic task-based functional connectivity (tbFC) (F1,77 = 5.87; P = .02). Of the 26 participants in study 2 (laboratory study), 15 were women (58%), with mean (SD) age, 34.9 (10.3). Similar to study 1, in study 2, greater IC-BOLD response in the right IFG (t23 = −2.49; β = −0.47; P = .02), and weaker corticothalamic tbFC (t22 = 5.62; β = 0.79; P < .001) were associated with smoking sooner during the smoking relapse-analog task. In both studies, corticothalamic tbFC mediated the association between IC performance and smoking outcomes. CONCLUSIONS AND RELEVANCE In these 2 studies, baseline differences in corticothalamic circuitry function were associated with mediated IC and smoking relapse vulnerability. These findings warrant further examination of interventions for augmenting corticothalamic neurotransmission and enhancing IC during the course of tobacco use disorder treatment.

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“…According to the Mindfulness‐to‐Meaning Theory, mindfulness meditation can be used to disengage from automatic schema into a metacognitive state of awareness in which attention expands to encompass previously unattended data from which new cognitive structures can be constructed through a process of memory reconsolidation. Applying this theory to addiction, mindfulness may be used to interrupt drug‐use action schema, which can then be consciously reconfigured in working memory to subserve adaptive goal pursuit (i.e., abstinence). Insofar as mindfulness allows access to an expanded set of information from which semantic and conditioned associations may be restructured, it can be used to enhance interoceptive awareness of the salience of various courses of action and experiences, thereby optimizing prediction error signaling in the brain to increase goodness‐of‐fit between behavior and goal states .…”

Section: Transforming Addiction Through the Synergy Of Mindfulness Rmentioning

confidence: 99%

Restructuring reward processing with Mindfulness‐Oriented Recovery Enhancement: novel therapeutic mechanisms to remediate hedonic dysregulation in addiction, stress, and pain

Garland

2016

Annals of the New York Academy of Sciences

118

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Though valuation processes are fundamental to survival of the human species, hedonic dysregulation is at the root of an array of clinical disorders, including addiction, stress, and chronic pain, as evidenced by the allostatic shift in the relative salience of natural reward to drug reward observed among persons with severe substance use disorders. To address this crucial clinical issue, novel interventions are needed to restore hedonic regulatory processes gone awry in persons exhibiting addictive behaviors. This article describes a theoretical rationale and empirical evidence for the effects of one such new intervention, mindfulness-oriented recovery enhancement (MORE), on top-down and bottom-up mechanisms implicated in cognitive control and hedonic regulation. MORE is innovative and distinct from extant mindfulness-based interventions in that in unites traditional mindfulness meditation with reappraisal and savoring strategies designed to reverse the downward shift in salience of natural reward relative to drug reward, representing a crucial tipping point to disrupt the progression of addiction, which no other behavioral intervention has been designed to do. Though additional studies are needed, clinical and biobehavioral data from several completed and ongoing trials suggest that MORE may exert salutary effects on addictive behaviors and the neurobiological processes that underpin them.

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Mindfulness, Mechanisms and Meaning: Perspectives From the Cognitive Neuroscience of Addiction

Cited by 30 publications

References 85 publications

Impaired frontostriatal functional connectivity among chronic opioid using pain patients is associated with dysregulated affect

Impaired frontostriatal functional connectivity among chronic opioid using pain patients is associated with dysregulated affect

Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability

Restructuring reward processing with Mindfulness‐Oriented Recovery Enhancement: novel therapeutic mechanisms to remediate hedonic dysregulation in addiction, stress, and pain

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