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Impulsivity and Vulnerability to Psychopathology

Explore the historical aspects and conceptual issues surrounding impulsivity, including neurobiological theories, behavioral definitions, etiological formulations, and genetic influences. Understand how impulsivity relates to vulnerability to psychopathology.

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Impulsivity and Vulnerability to Psychopathology

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  1. Impulsivity and Vulnerability to Psychopathology Chapter 6 Emily Neuhaus and Theodore P. Beauchaine

  2. HISTORICAL CONTEXT • Early neurobiological theories of behavioral control focused on frontal regions of the brain. • Observations of altered behavior among those who suffered from traumatic brain injuries (i.e., Phineas Gage in 1814). • Vagotonia hypothesis • Eppinger and Hess (1915) describe vagotonia as an abnormal irritability of all or only a few autonomic nerves.

  3. HISTORICAL CONTEXT • Minimal brain dysfunction (MBD) • Children with an underlying neurological disturbance, as well as learning disabilities and other problems who may or may not have been exposed to the 1918 encephalitic infection. • DSM-III (1980) • That the category of MBD was dropped, and children with learning difficulties were distinguished officially from those with behavioral difficulties

  4. TERMINOLOGICAL AND CONCEPTUAL ISSUES • Lacks a consistent operational definition and a standard method of measurement • Operationalizing impulsivity • Definitions based on results from neuropsychological tests (i.e., Wisconsin Card Sorting Test) • Do not speak to the neural mechanisms underlying the construct • Models of disinhibition • Integrate multiple components of the trait, suggesting several alternative brain mechanisms that may be responsible for impulsive behavior.

  5. TERMINOLOGICAL AND CONCEPTUAL ISSUES • Behavioral Definitions • “Behavior that is socially inappropriate or maladaptive and is quickly emitted without forethought” (Oas, 1984, 1985). • Strengths include not ruling out cognitively mediated mechanisms, emphasizes disinhibition as a maladaptive trait, does not include causal assumptions regarding the etiology of disinhibition, allowing for both psychological and biological contributions. • DSM-IV (2000) • Attention-deficit/hyperactivity disorder (ADHD) • Taking action without forethought, failing to plan ahead, risk taking, novelty-seeking, sensation-seeking, over-rapid responding, and susceptibility to the pull of immediate rewards (Hirshfeld-Becker et al., 2002).

  6. ETIOLOGICAL FORMULATIONS • Heterogeneity in the Impulsivity Phenotype • Behavioral (phenotypic) expression of impulsivity may derive from several sources • Brain injuries, exposure to teratogens such as alcohol, early traumatic experiences including social deprivation, child abuse, and neglect, or genetic vulnerabilities that give rise to deficient executive control over behavior. • Neurobiological substrates of disinhibition • Give rise to individual differences in impulsivity that are temperamental, present very early in life, and emerge before ADHD can be diagnosed. • Are supported by voluminous literatures derived from both animal models and humans. • Confer vulnerability to externalizing disorders across the life span, particularly in the context of high-risk environments characterized by violence, trauma, and emotional lability.

  7. ETIOLOGICAL FORMULATIONS • Temperamental Impulsivity and Central Dopamine Functioning • Early theories (mostly animal studies on reinforcement motivation and substance dependence) • Electrical and pharmacological stimulation of dopaminergically mediated mesolimbic structures is reinforcing, such that trained animals will engage in prolonged periods of operant behaviors. • Neural activity increases within mesolimbic structures during both reward anticipation and reward-seeking behaviors, and following administration of DA agonists. • DA antagonists attenuate—and in extreme cases block—the rewarding properties of food, water, and stimulant drugs of abuse.

  8. ETIOLOGICAL FORMULATIONS • Evidence for reduced DA functioning as a neural substrate of impulsivity have led to a reformulation of first-generation models indicating: • Associations between low basal DA activity/blunted DA reactivity and a propensity to use DA agonist drugs of abuse. • Significant correlations between blunted DA responses to amphetamine administration and the personality trait of novelty seeking. • Recent neuroimaging studies indicating reduced striatal activity during reward tasks among children and adolescents with ADHD and CD.

  9. GENETICS AND HERITABILITY • Behavioral Genetics of Impulsivity • Impulsivity is among the most highly heritable of all behavioral traits. • However, a common genetic vulnerability can result in divergent multifinal outcomes depending on environmental experience. • Molecular Genetics of Impulsivity • A significant linkage for ADHD on Chromosome 16, however, no specific gene has yet been identified through linkage analysis. • A small but significant role for the DRD4 gene, which codes for DA receptors located throughout the central and peripheral nervous systems linked to impulsivity.

  10. IMPULSIVITY AND VULNERABILITY TO PSYCHOPATHOLOGY • Behavioral Inhibition • This term refers to a general tendency to be wary in novel situations, to be slow to warm up, and to avoid overly stimulating environments. • A person who is temperamentally impulsive due to a heritable DA deficiency may be protected from severe psychopathology ifhe or she is also high on behavioral inhibition. • Environmental Risk • Parenting • Parents of impulsive and aggressive children are more negative, lax, verbose, and overreactive in their discipline practices than the parents of control children (Arnold, O’Leary, Wolff, & Acker, 1993; Barkley, Karlsson, & Pollard, 1985).

  11. IMPULSIVITY AND VULNERABILITY TO PSYCHOPATHOLOGY • Child abuse and neglect • Although the direction of effects is unclear, maltreated children are more impulsive than nonmaltreated children and histories of abuse are associated with higher levels of externalizing symptoms among children with ADHD (Briscoe-Smith & Hinshaw, 2006; Famularo, Kinscherff, & Fenton, 1992). • Neighborhood effects • Impulsive children who are reared in high-risk neighborhoods (typically defined by such factors as low socioeconomic status, high rates of violence and criminality, and low community involvement) are more prone to engage in antisocial behavior than impulsive children reared in low-risk neighborhoods (Meier, Slutske, Arndt, & Cadoret, 2008).

  12. IMPULSIVITY AND VULNERABILITY TO PSYCHOPATHOLOGY • Epigenetic and Other Experience-Dependent Effects • Epigenetic effects • Brain-derived neurotrophic factor (BDNF), which is involved in the differentiation of DA neurons in developing mesolimbic structures and has been implicated in the pathogenesis of impulsivity, may be susceptible to paternallymediated epigenetic effects (Kent et al., 2005). • Animal studies suggest that prenatal exposure to synthetic glucocorticoids leads to overactivity and ADHD-like behaviors, suggesting that such exposure may influence the “programming” of nascent DA systems (Kapoor, Petropoulos, & Matthews, 2007). • Brain tissue from spontaneously hypertensive rats exposed to polychlorinated biphenyls (PCBs) evidenced differences in mRNA, suggesting an epigenetic effect of PCB on gene expression (DasBanerjee et al., 2008).

  13. IMPULSIVITY AND VULNERABILITY TO PSYCHOPATHOLOGY • Neural plasticity • Examples of experience-dependent changes occur in several neural systems including mesolimbic DA structures: • Male rats that were exposed repeatedly to more dominant males in a stress-inducing paradigm. • Repeated episodes of maternal separation early in the lives of rat pups. • Stimulant use. • Implications for Learning • Alterations in DA responding that arise from genetic, epigenetic, and experience-dependent effects are likely to influence the efficiency of knowledge acquisition by: • Sensation-seeking tendencies that reduce motivation for learning mundane information. • Reduced efficacy of associative learning due to dampened activation of mesolimbic structures. • Compromised executive functioning.

  14. SYNTHESIS AND FUTURE DIRECTIONS • In the worst cases, impulsive children are reared by impulsive parents who, in addition to conferring genetic liability, transmit risk through inconsistent and stressful caretaking during infancy, child maltreatment, and coercive, labile parenting (Beauchaine et al., 2011). • Further accumulation of risk may occur via exposure to violence in high-risk neighborhoods, early escalation of substance use, low motivation, and learning difficulties. • In contrast, an impulsive child who is reared in a maximally protective environment faces few or none of these additional risk factors, and may develop both psychological and biological resilience given enriched educational experiences and competent parenting that teaches strong emotion regulation skills.

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