Literature DB >> 16209748

A dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/impulsive and combined subtypes.

Terje Sagvolden1, Espen Borgå Johansen, Heidi Aase, Vivienne Ann Russell.   

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to "inhibit" responses ("disinhibition"). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological "soft signs," and a "failure to inhibit" responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns.

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Year:  2005        PMID: 16209748     DOI: 10.1017/S0140525X05000075

Source DB:  PubMed          Journal:  Behav Brain Sci        ISSN: 0140-525X            Impact factor:   12.579


  268 in total

1.  Home environment: association with hyperactivity/impulsivity in children with ADHD and their non-ADHD siblings.

Authors:  A Mulligan; R Anney; L Butler; M O'Regan; T Richardson; E M Tulewicz; M Fitzgerald; M Gill
Journal:  Child Care Health Dev       Date:  2011-12-14       Impact factor: 2.508

Review 2.  From reinforcement learning models to psychiatric and neurological disorders.

Authors:  Tiago V Maia; Michael J Frank
Journal:  Nat Neurosci       Date:  2011-02       Impact factor: 24.884

3.  DAT1 and COMT effects on delay discounting and trait impulsivity in male adolescents with attention deficit/hyperactivity disorder and healthy controls.

Authors:  Yannis Paloyelis; Philip Asherson; Mitul A Mehta; Stephen V Faraone; Jonna Kuntsi
Journal:  Neuropsychopharmacology       Date:  2010-08-25       Impact factor: 7.853

4.  Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder.

Authors:  Yannis Paloyelis; Mitul A Mehta; Stephen V Faraone; Philip Asherson; Jonna Kuntsi
Journal:  J Am Acad Child Adolesc Psychiatry       Date:  2012-06-05       Impact factor: 8.829

5.  The dopamine receptor D4 gene (DRD4) moderates family environmental effects on ADHD.

Authors:  Michelle M Martel; Molly Nikolas; Katherine Jernigan; Karen Friderici; Irwin Waldman; Joel T Nigg
Journal:  J Abnorm Child Psychol       Date:  2011-01

6.  Ventromedian forebrain dysgenesis follows early prenatal ethanol exposure in mice.

Authors:  Elizabeth A Godin; Deborah B Dehart; Scott E Parnell; Shonagh K O'Leary-Moore; Kathleen K Sulik
Journal:  Neurotoxicol Teratol       Date:  2010-11-11       Impact factor: 3.763

7.  Aberrant glutamate signaling in the prefrontal cortex and striatum of the spontaneously hypertensive rat model of attention-deficit/hyperactivity disorder.

Authors:  Erin M Miller; Francois Pomerleau; Peter Huettl; Greg A Gerhardt; Paul E A Glaser
Journal:  Psychopharmacology (Berl)       Date:  2014-02-28       Impact factor: 4.530

8.  Preliminary evidence for reduced posterror reaction time slowing in hyperactive/inattentive preschool children.

Authors:  Olga G Berwid; Jeffrey M Halperin; Ray Johnson; David J Marks
Journal:  Child Neuropsychol       Date:  2013-02-06       Impact factor: 2.500

Review 9.  Cognitive neuroscience of Attention Deficit Hyperactivity Disorder: current status and working hypotheses.

Authors:  Chandan J Vaidya; Melanie Stollstorff
Journal:  Dev Disabil Res Rev       Date:  2008

Review 10.  Membrane transporters as mediators of synaptic dopamine dynamics: implications for disease.

Authors:  Kelly M Lohr; Shababa T Masoud; Ali Salahpour; Gary W Miller
Journal:  Eur J Neurosci       Date:  2016-09-02       Impact factor: 3.386

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