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      Decision-making and Related Processes in Internet Gaming Disorder and Other Types of Internet-Use Disorders

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      Current Addiction Reports
      Springer Nature

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            Is Open Access

            Integrating psychological and neurobiological considerations regarding the development and maintenance of specific Internet-use disorders: An Interaction of Person-Affect-Cognition-Execution (I-PACE) model.

            Within the last two decades, many studies have addressed the clinical phenomenon of Internet-use disorders, with a particular focus on Internet-gaming disorder. Based on previous theoretical considerations and empirical findings, we suggest an Interaction of Person-Affect-Cognition-Execution (I-PACE) model of specific Internet-use disorders. The I-PACE model is a theoretical framework for the processes underlying the development and maintenance of an addictive use of certain Internet applications or sites promoting gaming, gambling, pornography viewing, shopping, or communication. The model is composed as a process model. Specific Internet-use disorders are considered to be the consequence of interactions between predisposing factors, such as neurobiological and psychological constitutions, moderators, such as coping styles and Internet-related cognitive biases, and mediators, such as affective and cognitive responses to situational triggers in combination with reduced executive functioning. Conditioning processes may strengthen these associations within an addiction process. Although the hypotheses regarding the mechanisms underlying the development and maintenance of specific Internet-use disorders, summarized in the I-PACE model, must be further tested empirically, implications for treatment interventions are suggested.
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              Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On.

              A decade ago, we hypothesized that drug addiction can be viewed as a transition from voluntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transition from prefrontal cortical to striatal control over drug seeking and taking as well as a progression from the ventral to the dorsal striatum. Here, in the light of burgeoning, supportive evidence, we reconsider and elaborate this hypothesis, in particular the refinements in our understanding of ventral and dorsal striatal mechanisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments in top-down prefrontal cortical inhibitory control over this behavior. We further review animal and human studies that have begun to define etiological factors and individual differences in the propensity to become addicted to drugs, leading to the description of addiction endophenotypes, especially for cocaine addiction. We consider the prospect of novel treatments for addiction that promote abstinence from and relapse to drug use.
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                Author and article information

                Journal
                Current Addiction Reports
                Curr Addict Rep
                Springer Nature
                2196-2952
                September 2017
                June 20 2017
                : 4
                : 3
                : 262-271
                Article
                10.1007/s40429-017-0156-9
                e2d81245-058e-4346-acaa-0e424d062324
                © 2017

                http://www.springer.com/tdm

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