Catecholamines in Attention Deficit Disorders

J Millichap

doi:10.15844/pedneurbriefs-10-3-1

Author:

J Gordon Millichap

Northwestern University Feinberg School of Medicine, US

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Abstract

How to Cite: Millichap, J.G., 1996. Catecholamines in Attention Deficit Disorders. Pediatric Neurology Briefs, 10(3), pp.17–18. DOI: http://doi.org/10.15844/pedneurbriefs-10-3-1

A multistage hypothesis emphasizing the interaction of norepinephrine (NE), epinephrine (EPI), and dopamine in the modulation of attention and impulse control is presented by the Department of Psychiatry, University of Texas Health Science Center, San Antonio, TX. A neurochemical deficit in ADHD is frequently proposed, and a “catecholamine hypothesis” is supported by the effectiveness of stimulant medications which act as dopaminergic and noradrenergic agonists. The noradrenergic system consists of 1) a central NE system and 2) a peripheral NE system. Dextroamphetamine and methylphenidate which block the reuptake of NE lead to increases in plasma NE and urinary EPI in children with ADHD. The anterior cingulate and frontal lobe connections which govern inhibitory control of visual attention are influenced by both dopamine and noradrenergic systems. The frontal lobes are normally rich in dopamine, and patients with medio-orbital prefrontal lesions who are characteristically impulsive, having deficits in inhibitory control, may show presynaptic dopamine deficiencies. ADHD has been explained as “a primary deficit in inhibitory control.” Stimulants enhance available dopamine at central synapses, suggesting a “dopamine hypothesis” for ADHD. A multistage hypothesis for ADHD involving interacting catecholamine systems is proposed. [1]

COMMENT. No single neurotransmitter imbalance is the answer to ADHD, and the interaction of all three appears to play a role in the control of impulse and attention.

Deficits in selective and sustained attention processes in early treated children with phenylketonuria were correlated with serum phenylalanine concentration in a study of 20 patient with normal IQ at the Department of Paediatrics, University of Munster, Germany [2]. These attention deficits probably resulted from impairment of frontal lobe function and could probably be avoided by a stricter dietary control of the PKU. Phenylalanine inhibits the synthesis of dopamine and serotonin as well as the uptake of tyrosine and tryptophan.

References

Pliszka, SR, McCracken, JT and Maas, JW (1996). Catecholamines in attention-deficit hyperactivity disorder: current perspectives. J Am Acad Child Adolesc Psychiatry Mar 199635(3): 264–72, DOI: https://doi.org/10.1097/00004583-199603000-00006 [PubMed]

Weglage, J, Pietsch, M, Funders, B, Koch, HG and Ullrich, K (1996). Deficits in selective and sustained attention processes in early treated children with phenylketonuria--result of impaired frontal lobe functions?. Eur J Pediatr Mar 1996155(3): 200–4, DOI: https://doi.org/10.1007/BF01953938 [PubMed]

[CIT0001] Pliszka, SR, McCracken, JT and Maas, JW (1996). Catecholamines in attention-deficit hyperactivity disorder: current perspectives. J Am Acad Child Adolesc Psychiatry Mar 199635(3): 264–72, DOI: https://doi.org/10.1097/00004583-199603000-00006 [PubMed]

[CIT0002] Weglage, J, Pietsch, M, Funders, B, Koch, HG and Ullrich, K (1996). Deficits in selective and sustained attention processes in early treated children with phenylketonuria--result of impaired frontal lobe functions?. Eur J Pediatr Mar 1996155(3): 200–4, DOI: https://doi.org/10.1007/BF01953938 [PubMed]

Reading: Catecholamines in Attention Deficit Disorders

Attention Deficit Disorders

Catecholamines in Attention Deficit Disorders

Author:

J Gordon Millichap

Northwestern University Feinberg School of Medicine, US

X close

Abstract

References