Oculomotor capture in ADHD.

It is generally thought that deficits in response inhibition form an important area of dysfunction in patients with attention-deficit/hyperactivity disorder (ADHD). However, recent research using visual search paradigms seems to suggest that these inhibitory deficits do not extend towards inhibiting irrelevant distractors. Using an oculomotor capture task, the present study investigated whether boys with ADHD and their nonaffected brothers are impaired in suppressing reflexive eye movements to a task-irrelevant onset distractor. Results showed that boys with ADHD had slower responses than controls, but were as accurate in their eye movements as controls. Nonaffected brothers showed similar problems in the speed of responding as their affected brothers, which might suggest that this deficit relates to a familial risk for developing the disorder. Importantly, all three groups were equally captured by the distractor, which shows that boys with ADHD and their brothers are not more distracted by the distractor than are controls. Saccade latency and the proportion of intrusive saccades were related to continuous dimensions of ADHD symptoms, which suggests that these deficits are not simply present or absent, but rather indicate that the severity of these deficits relate to the severity of ADHD. The finding that boys with ADHD (and their nonaffected brothers) did not have problems inhibiting irrelevant distractors contradicts a general response inhibition deficiency in ADHD, which may be explained by the relatively independency of working memory in this type of response inhibition.

The influence of growth hormone (GH) substitution on patient-reported outcomes and cognitive functions in GH-deficient patients: a meta-analysis.

OBJECTIVE: The influence of growth hormone (GH) replacement on patient-reported outcomes (i.e., quality of life, health status and well-being) and cognitive functioning in GH-deficient adults is controversial. DESIGN: We carried out a meta-analysis of clinical trials concerning the influence of GH substitution on patient-reported outcomes and cognitive functions (studies were selected from 1985 to 2004). The results of individual studies were combined in a series of meta-analyses using a random effects model. Effects of GH replacement in GH-deficient adults were compared to baseline and/or placebo. RESULTS: Fifteen studies on GH and patient-reported outcomes were included (830 patients, follow-up 3-50 months). Four of these studies also provided data on cognitive functions (85 patients, follow-up 6-12 months). Relative to baseline, GH treatment is found to have a large effect on patient-reported outcomes at 3 months, a medium effect at 6 months and a small effect at 12 months. With respect to the median treatment duration of 6 months placebo appears to be as effective as GH substitution. Cognitive functioning does not improve after 6 months of GH substitution, relative to baseline. CONCLUSION: This meta-analysis provides no evidence that GH improves patient-reported outcomes in GH-deficient patients. As the amount of cognitive data was too limited to allow for comparisons with placebo, from the present meta-analysis no conclusions can be drawn with respect to the impact of GH treatment on cognition.

Deficits in visuo-spatial working memory, inhibition and oculomotor control in boys with ADHD and their non-affected brothers.

Few studies have assessed visuo-spatial working memory and inhibition in attention-deficit/hyperactivity disorder (ADHD) by recording saccades and consequently little additional knowledge has been gathered on oculomotor functioning in ADHD. Moreover, this is the first study to report the performance of non-affected siblings of children with ADHD, which may shed light on the familiality of deficits. A total of 14 boys with ADHD, 18 non-affected brothers, and 15 control boys aged 7-14 years, were administered a memory-guided saccade task with delays of three and seven seconds. Familial deficits were found in accuracy of visuo-spatial working memory, percentage of anticipatory saccades, and tendency to overshoot saccades relative to controls. These findings suggest memory-guided saccade deficits may relate to a familial predisposition for ADHD.