Poor response inhibition: At the nexus between substance abuse and attention deficit/hyperactivity disorder

Stephanie M. Groman, Alex S. James, J. David Jentsch

Research output: Contribution to journalReview articlepeer-review

99 Scopus citations

Abstract

The co-morbidity between attention deficit hyperactivity disorder (ADHD) and substance abuse and dependence disorders may have multiple causes and consequences. In this review, we will describe neurobehavioral, genetic and animal model studies that support the notion that a common, genetically determined failure of response inhibition function is an endophenotype for both disorders. Through an impairment in the ability to cognitively control pre-potent behaviors, subjects can exhibit a collection of ADHD-like traits (impulsivity and hyperactivity), as well as susceptibility for the initiation of drug taking and its ultimate progression to an inflexible, uncontrollable form. At the neural level, dysfunction within circuitry that includes the ventrolateral frontal and cingulate cortices, as well as in associated basal ganglia zones, contributes to a common pattern of behavioral impairment, explaining aspects of co-morbidity. Animal models of substance abuse/dependence and ADHD that exhibit deficits in response inhibition have substantiated the role of this endophenotype in both disorders and their co-morbidity and should provide a testing ground for interventions targeting it. New directions for research that will further explore this hypothesis and begin to reveal the underlying biological mechanisms will be proposed.

Original languageEnglish (US)
Pages (from-to)690-698
Number of pages9
JournalNeuroscience and Biobehavioral Reviews
Volume33
Issue number5
DOIs
StatePublished - May 2009
Externally publishedYes

Bibliographical note

Funding Information:
Preparation of this review was supported, in part, by USPHS grants P50-MH077248, P20-DA022539 and RL1-MH083270.

Keywords

  • Animal models
  • Cognitive control
  • Dopamine
  • Impulsivity
  • Norepinephrine
  • Prefrontal cortex

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