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Neuropsychological functioning in stimulant-naive boys with hyperkinetic disorder

Published online by Cambridge University Press:  01 April 2005

SINEAD M. RHODES
Affiliation:
Division of Pathology and Neuroscience, University of Dundee, UK
DAVID R. COGHILL
Affiliation:
Division of Pathology and Neuroscience, University of Dundee, UK
KEITH MATTHEWS
Affiliation:
Division of Pathology and Neuroscience, University of Dundee, UK

Abstract

Background. Although children with hyperkinetic disorder and/or attention deficit hyperactivity disorder (ADHD) show disordered executive neuropsychological functioning, the nature of these changes remains controversial. Additionally, impairments in non-executive neuropsychological functioning have been relatively unexplored. Here, the authors describe the neuropsychological functioning of a sample of stimulant drug-naive boys with hyperkinetic disorder on a battery of neuropsychological tasks sensitive to impairments of both executive and non-executive functions.

Method. Seventy-five stimulant drug-naive boys meeting diagnostic criteria for ICD-10 hyperkinetic disorder were compared with 70 healthy developing controls matched for age but not IQ on computerized tests of neuropsychological functioning from the Cambridge Neuropsychological Test Automated Battery (CANTAB) and a Go/No-Go inhibition task.

Results. Boys with hyperkinetic disorder exhibited impairments on tasks with a prominent executive component – working memory, planning, strategy formation, attentional set-shifting and on a reaction time task. However, they were also impaired on tasks without prominent executive components – pattern and spatial recognition, spatial span, delayed matching to sample and paired associates learning. Contrary to predictions, no impairment was observed on the Go/No-Go inhibition task.

Conclusions. Medication-naive boys with hyperkinetic disorder displayed a broad range of neuropsychological impairments. Deficits were demonstrated on tasks with and without prominent executive components. Impairments were not confined to tasks dependent upon frontostriatal functioning, cannot wholly be explained by deficits in inhibitory control, nor can they be attributed to intelligence or previous exposure to stimulant medication.

Type
Original Articles
Copyright
© 2005 Cambridge University Press

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