Literature DB >> 18722390

A somatic marker theory of addiction.

Antonio Verdejo-García1, Antoine Bechara.   

Abstract

Similar to patients with ventromedial prefrontal cortex (VMPC) lesions, substance abusers show altered decision-making, characterized by a tendency to choose the immediate reward, at the expense of negative future consequences. The somatic marker model proposes that decision-making depends on neural substrates that regulate homeostasis, emotion and feeling. According to this model, there should be a link between alterations in processing emotions in substance abusers, and their impairments in decision-making. Growing evidence from neuroscientific studies indicate that core aspects of addiction may be explained in terms of abnormal emotional/homeostatic guidance of decision-making. Behavioral studies have revealed emotional processing and decision-making deficits in substance abusers. Neuroimaging studies have shown that altered decision-making in addiction is associated with abnormal functioning of a distributed neural network critical for the processing of emotional information, and the experience of "craving", including the VMPC, the amygdala, the striatum, the anterior cingulate cortex, and the insular/somato-sensory cortices, as well as non-specific neurotransmitter systems that modulate activities of neural processes involved in decision-making. The aim of this paper is to review this growing evidence, and to examine the extent to which these studies support a somatic marker theory of addiction. We conclude that there are at least two underlying types of dysfunction where emotional signals (somatic markers) turn in favor of immediate outcomes in addiction: (1) a hyperactivity in the amygdala or impulsive system, which exaggerates the rewarding impact of available incentives, and (2) hypoactivity in the prefrontal cortex or reflective system, which forecasts the long-term consequences of a given action.

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Year:  2008        PMID: 18722390      PMCID: PMC2635337          DOI: 10.1016/j.neuropharm.2008.07.035

Source DB:  PubMed          Journal:  Neuropharmacology        ISSN: 0028-3908            Impact factor:   5.250


  166 in total

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