Contextual abnormalities of saccadic inhibition in children with attention deficit hyperactivity disorder.
Abnormalities of executive function are observed consistently in children with attention-deficit hyperactivity disorder (ADHD), and it is hypothesised that these arise because of disruption to a behavioural inhibition system. Executive and inhibitory functions were compared between unmedicated and medicated children with ADHD (combined type), age-matched healthy children and healthy adults. Executive functions were measured using a test of spatial working memory shown previously to be sensitive to ADHD and to stimulant medication. Inhibitory functions were measured using an ocular motor paradigm that required individuals to use task context to control the release of fixation. Context was set according to the probability that a target would appear at either of the two locations. In one block, targets appeared on 80% of trials. In the other block, targets appeared on 20% of trials. The ability to control the release of fixation was inferred from the fixation offset effect (FOE), or the difference in saccade latency when the current fixation is offset 200 ms prior to the onset of the saccade target (gap condition), compared with when there is no offset (overlap condition). Although the healthy children made more errors on the spatial working memory task than the healthy adults, there was no difference between the two groups in their ability to control fixation using context. Both showed a larger FOE when target probability was low. As expected, the unmedicated ADHD group made more errors on the spatial working memory test than the healthy children, although spatial working memory performance was normal in the medicated ADHD group. However, both the unmedicated and medicated ADHD groups were unable to modulate the FOE according to context, and this was due to their inability to voluntarily inhibit saccades when there was a low target probability. These data suggest that the context-based modulation of fixation release is not controlled by the same systems that control executive function. Furthermore, deficits in executive function and inhibitory control appear independent in children with ADHD.
Cairney
S
S
The Neurophysiology nd Neurovisual Research Unit, Mental Health Research Institute of Victoria, Parkville, Victoria, Australia 3052. sheree@neuro.mhri.edu.au
Maruff
P
P
Vance
A
A
Barnett
R
R
Luk
E
E
Currie
J
J
D001289:Attention Deficit Disorder with Hyperactivity / Q000503:physiopathology*; D000697:Central Nervous System Stimulants / Q000627:therapeutic use; D002648:Child; D003463:Cues; D005260:Female; D005403:Fixation, Ocular / Q000502:physiology*; D005625:Frontal Lobe / Q000033:anatomy & histology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008569:Memory Disorders / Q000209:etiology / Q000503:physiopathology*; D008570:Memory, Short-Term / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology*; D009434:Neural Pathways / Q000033:anatomy & histology / Q000503:physiopathology; D015835:Ocular Motility Disorders / Q000209:etiology / Q000503:physiopathology*; D011597:Psychomotor Performance / Q000502:physiology; D011930:Reaction Time / Q000502:physiology; D012438:Saccades / Q000502:physiology*
D000697:Central Nervous System Stimulants