Archiv - Dezember 2009

Mapping Attention-Deficit/Hyperactivity Disorder from Childhood to Adolescence-No Neurophysiologic Evidence for a Developmental Lag of Attention but Some for Inhibition.

Mirko Doehnert1,2, Daniel Brandeis1,3,4, Katrin Imhof1, Renate Drechsler1 and Hans-Christoph Steinhausen1,5,6

1 Department of Child and Adolescent Psychiatry, University of Zurich, Zurich, Switzerland
2 Department of Child and Adolescent Psychiatry, University of Leipzig, Germany
3 Center for Integrative Human Physiology, University of Zürich, Switzerland
4 Department of Child and Adolescent Psychiatry and Psychotherapy, Central, Institute of Mental Health, Mannheim, Germany
5 Aalborg Psychiatric Hospital, Aarhus University Hospital, Aalborg, Denmark
6 Clinical Child and Adolescent Psychology, University of Basel, Switzerland

Biol Psychiatry. 2009 Oct 5. [Epub ahead of print]

Abstract

Background

The role of a developmental lag for deficits of higher brain functions in attention-deficit/hyperactivity disorder (ADHD) has not yet been tested in longitudinal studies. We examined the development of neurophysiological markers of attention (Cue P300; contingent negative variation [CNV]) and inhibition (NoGo P300) in ADHD and control groups from childhood to adolescence for support of the developmental lag hypothesis of ADHD.

Methods

ADHD ( n = 28/3 girls) and control ( n = 22/5 girls) subjects were assessed at baseline (Time 1; ADHD age 10.8 ± 1.8 years, controls 10.4 ± 1.1 years) and at two follow-up examinations (Time 2 after 1.2 years, Time 3 after 2.5 years). Event-related potential maps were recorded during a cued Continuous Performance Test (CPT) at all assessments and analyzed using scalp and source (sLORETA) measures.

Results

CPT performance showed common effects of ADHD and younger age, consistent with (but not specific to) developmental lag. The NoGo P300 developed earlier and became stronger in control subjects than in the ADHD group, again consistent with an initial developmental lag. In contrast, the attenuation of the Cue P300 and the CNV with ADHD at all assessments was opposite to the enhancement with younger age and thus inconsistent with developmental lag. The sLORETA source localization also differed between ADHD and developmental effects.

Conclusions

These results provide strong evidence for multiple and persistent neural processing deficits in ADHD. They do not support the developmental lag hypothesis for attentional dysfunction in ADHD despite partial evidence that developmental lag contributes to inhibitory brain dysfunction during early adolescence.

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