Adolescence is a developmental period characterized by suboptimal decisions and actions that are associated with an increased incidence of unintentional injuries, violence, substance abuse, unintended pregnancy, and sexually transmitted diseases. Traditional neurobiological and cognitive explanations for adolescent behavior have failed to account for the nonlinear changes in behavior observed during adolescence, relative to both childhood and adulthood. This review provides a biologically plausible model of the neural mechanisms underlying these nonlinear changes in behavior. We provide evidence from recent human brain imaging and animal studies that there is a heightened responsiveness to incentives and socioemotional contexts during this time, when impulse control is still relatively immature. These findings suggest differential development of bottom-up limbic systems, implicated in incentive and emotional processing, to top-down control systems during adolescence as compared to childhood and adulthood. This developmental pattern may be exacerbated in those adolescents prone to emotional reactivity, increasing the likelihood of poor outcomes.

The Adolescent Brain

OBJECTIVE: Studies of the neurobiological processes underlying drug addiction primarily have focused on limbic subcortical structures. Here the authors evaluated the role of frontal cortical structures in drug addiction. METHOD: An integrated model of drug addiction that encompasses intoxication, bingeing, withdrawal, and craving is proposed. This model and findings from neuroimaging studies on the behavioral, cognitive, and emotional processes that are at the core of drug addiction were used to analyze the involvement of frontal structures in drug addiction. RESULTS: The orbitofrontal cortex and the anterior cingulate gyrus, which are regions neuroanatomically connected with limbic structures, are the frontal cortical areas most frequently implicated in drug addiction. They are activated in addicted subjects during intoxication, craving, and bingeing, and they are deactivated during withdrawal. These regions are also involved in higher-order cognitive and motivational functions, such as the ability to tr...

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Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex

At the moment, there is no single conceptual theoretical model of gambling that adequately accounts for the multiple biological, psychological and ecological variables contributing to the development of pathological gambling Advances in this area are hampered by imprecise definitions of pathological gambling, failure to distinguish between gambling problems and problem gamblers and a tendency to assume that pathological gamblers form one, homogeneous population with similar psychological principles applying equally to all members of the class The purpose of this paper is to advance a pathways model that integrates the complex array of biological, personality, developmental, cognitive, learning theory and ecological determinants of problem and pathological gambling It is proposed that three distinct subgroups of gamblers manifesting impaired control over their behaviour can be identified These groups include (a) behaviourally conditioned problem gamblers, (b) emotionally vulnerable problem gamblers and (c) antisocial, impulsivist problem gamblers The implications for clinical management are discussed

https://www.uv.es/~choliz/ModeloJuego.pdf

A pathways model of problem and pathological gambling

The role of impulsivity in the development of substance use and eating disorders

Because little is known about the human trait of affiliation, we provide a novel neurobehavioral model of affiliative bonding. Discussion is organized around processes of reward and memory formation that occur during approach and consummatory phases of affiliation. Appetitive and consummatory reward processes are mediated independently by the activity of the ventral tegmental area (VTA) dopamine (DA)-nucleus accumbens shell (NAS) pathway and the central corticolimbic projections of the u-opiate system of the medial basal arcuate nucleus, respectively, although these two projection systems functionally interact across time. We next explicate the manner in which DA and glutamate interact in both the VTA and NAS to form incentive-encoded contextual memory ensembles that are predictive of reward derived from affiliative objects. Affiliative stimuli, in particular, are incorporated within contextual ensembles predictive of affiliative reward via: (a) the binding of affiliative stimuli in the rostral circuit of the medial extended amygdala and subsequent transmission to the NAS shell; (b) affiliative stimulus-induced opiate potentiation of DA processes in the VTA and NAS; and (c) permissive or facilitatory effects of gonadal steroids, oxytocin (in interaction with DA), and vasopressin on (i) sensory, perceptual, and attentional processing of affiliative stimuli and (ii) formation of social memories. Among these various processes, we propose that the capacity to experience affiliative reward via opiate functioning has a disproportionate weight in determining individual differences in affiliation. We delineate sources of these individual differences, and provide the first human data that support an association between opiate functioning and variation in trait affiliation.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/41885C410FD7476B2730780AFF265769/S0140525X05000063a.pdf/div-class-title-a-neurobehavioral-model-of-affiliative-bonding-implications-for-conceptualizing-a-human-trait-of-affiliation-div.pdf

A neurobehavioral model of affiliative bonding: Implications for conceptualizing a human trait of affiliation.

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces “reward” when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. “The reward cascade” involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or “reward site.” It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the “pleasure molecule” and/or the “antistress molecule.” When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in ...

Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors.

Six children were provided with long-term biofeedback and academic treatment for attention deficit disorders. Their symptoms were primarily specific learning disabilities, and, in some cases, there were varying degrees of hyperkinesis. The training consisted of two sessions per week for 10 to 27 months, with a gradual phase-out. Feedback was provided for either increasing 12- to 15-Hz SMR or 16- to 20-Hz beta activity. Inhibit circuits were employed for blocking the SMR or beta when either gross movement, excessive EMG, or theta (4-8 Hz) activity was present. Treatment also consisted of combining the biofeedback with academic training, including reading, arithmetic, and spatial tasks to improve their attention. All children increased SMR or beta and decreased slow EEG and EMG activity. Changes could be seen in their power spectra after training in terms of increased beta and decreased slow activity. All six children demonstrated considerable improvement in their schoolwork in terms of grades or achievement test scores. None of the children are currently on any medications for hyperkinetic behavior. The results indicate that EEG biofeedback training, if applied comprehensively, can be highly effective in helping to remediate children who are experiencing attention deficit disorders.

Electroencephalographic biofeedback of SMR and beta for treatment of attention deficit disorders in a clinical setting.

Abnormal behaviors involving dopaminergic gene polymorphisms often reflect an insufficiency of usual feelings of satisfaction, or Reward Deficiency Syndrome (RDS). RDS results from a dysfunction in the “brain reward cascade,” a complex interaction among neurotransmitters (primarily dopaminergic and opioidergic). Individuals with a family history of alcoholism or other addictions may be born with a deficiency in the ability to produce or use these neurotransmitters. Exposure to prolonged periods of stress and alcohol or other substances also can lead to a corruption of the brain reward cascade function. We evaluated the potential association of four variants of dopaminergic candidate genes in RDS (dopamine D1 receptor gene [DRD1]; dopamine D2 receptor gene [DRD2]; dopamine transporter gene [DAT1]; dopamine beta-hydroxylase gene [DBH]). Methodology: We genotyped an experimental group of 55 subjects derived from up to five generations of two independent multiple-affected families compared to rigorously screened control subjects (e.g., N = 30 super controls for DRD2 gene polymorphisms). Data related to RDS behaviors were collected on these subjects plus 13 deceased family members. Results: Among the genotyped family members, the DRD2 Taq1 and the DAT1 10/10 alleles were significantly (at least p < 0.015) more often found in the RDS families vs. controls. The TaqA1 allele occurred in 100% of Family A individuals (N = 32) and 47.8% of Family B subjects (11 of 23). No significant differences were found between the experimental and control positive rates for the other variants. Conclusions: Although our sample size was limited, and linkage analysis is necessary, the results support the putative role of dopaminergic polymorphisms in RDS behaviors. This study shows the importance of a nonspecific RDS phenotype and informs an understanding of how evaluating single subset behaviors of RDS may lead to spurious results. Utilization of a nonspecific “reward” phenotype may be a paradigm shift in future association and linkage studies involving dopaminergic polymorphisms and other neurotransmitter gene candidates.

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Generational Association Studies of Dopaminergic Genes in Reward Deficiency Syndrome (RDS) Subjects: Selecting Appropriate Phenotypes for Reward Dependence Behaviors

Publisher Summary This chapter discusses the assessment and treatment for attention deficit or hyperactivity disorders The chapter defines Attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) is a lifelong disorder that affects, perhaps, as high as 10% of the population, depending on which review article one reads and how it is classified and characterized ADD/ADHD overlaps with other disorders and presents in three main forms: inattentive, hyperactive-impulsive, and combined, according to the DSM-IV An older term, hyperkinesis, is still used at times to represent attention deficit with hyperactivity The overlap of both ADD/ADHD and specific learning disabilities (LDs) is as high as 70% In some cases, ADD/ADHD and LD overlap with conduct problems The attention deficit disorder without hyperactivity is sometimes referred to as ADD-, according to Barkley's (1990) classification The attention deficit disorder with hyperactivity, ADD +, also overlaps with learning disabilities, but is more concurrent with oppositional defiant disorder (ODD) and conduct disorder (CD) This chapter summarizes that although ADD/ADHD is express in terms of poor educational achievements, inappropriate emotional behavior, and all of the problems seen in terms of compliance, academics, etc, the problem is not a primary emotional disorder, an educational disorder, or a behavioral disorder; it is neurological This means that ADD/ADHD is reflected in the way the child, adolescent, or adult processes information, which is, in turn, affecting how the individual perceives the world and therefore responds to it

Judith O. Lubar

Papers

Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors.

Electroencephalographic biofeedback of SMR and beta for treatment of attention deficit disorders in a clinical setting.

Generational Association Studies of Dopaminergic Genes in Reward Deficiency Syndrome (RDS) Subjects: Selecting Appropriate Phenotypes for Reward Dependence Behaviors

Neurofeedback Assessment and Treatment for Attention Deficit/Hyperactivity Disorders