Biomedical subjects

Leo de Sonneville

Publications and source records attributed to Leo de Sonneville.

4 recordsLinked to original sources

PubMed2005

Motor flexibility problems as a marker for genetic susceptibility to attention-deficit/hyperactivity disorder.

BACKGROUND: Since many children with attention-deficit/hyperactivity disorder (ADHD) have fine visuomotor problems that are already evident at a young age, motor dysfunctioning is investigated in family-genetic perspective. We hypothesized that if fine motor problems may be a marker for genetic susceptibility to ADHD, nonaffected siblings of ADHD probands would experience motor problems similar to those of their ADHD siblings. METHODS: Twenty-five carefully phenotyped ADHD probands with a family history of ADHD, their nonaffected siblings (n = 25), and 48 normal control subjects (aged 6 to 17) completed a motor fluency task and a motor flexibility task. The motor fluency task involved completion of a familiar, automatized trajectory, whereas the motor flexibility task required continuous adjustment of movement to complete an unpredictable random trajectory. RESULTS: On the motor fluency task, the performance of the nonaffected children was significantly better than that of the ADHD probands; strikingly, on the motor flexibility task, they performed as well as their ADHD siblings. CONCLUSIONS: Nonaffected siblings experience complex motor problems similar to their ADHD siblings but only in nonautomatized movements that require controlled processing. The results suggest that higher-order controlled motor deficits in ADHD may be associated with genetic susceptibility for ADHD.

Adolescent↗

PubMed2003

A paced visual serial addition test for fMRI.

BACKGROUND AND PURPOSE: The Paced Auditory Serial Attention Task (PASAT) is an attention and information processing task used in patients with diffuse brain disorders, like cerebral trauma and multiple sclerosis (MS). Based on the PASAT we used a adapted version of the test to assess several cognitive functions with fMRI. In this study we investigated the activation pattern on a group and individual level and upon parametric stimulation. METHODS: Nine young, healthy, right-handed subjects (mean age 24 years) were studied. The test contrasts an adding-and-memory stage with a control stage in a block design, at two different speeds. Group average maps (random effects analysis, p=0.05) were created to identify the brain areas subserving this task. For each area found active in the group map, the percentage of individuals showing activation in that same anatomical area was calculated. RESULTS: Group activation was localized in the superior and inferior parietal lobe bilaterally, the superior frontal gyrus bilaterally, the left medial frontal gyrus, the left inferior frontal gyrus and adjacent part of the insula, the anterior part of the cingulate gyrus and some cerebellar areas. For the main activated areas, 78-100% of the individual subjects showed activation in that same area. Contrasting the low speed with the high speed condition yielded activation with a considerable individual variation. CONCLUSION: The group mean activated areas were located mainly in the frontal and parietal lobes and those areas were also activated in the majority of the subjects, indicating limited inter-individual variation, rendering this test suitable for clinical applications in a variety of neurological disorders.

Adult↗

PubMed2003

Deficient response inhibition as a cognitive endophenotype of ADHD.

OBJECTIVE: To investigate whether a deficient response inhibition is a cognitive endophenotype of attention-deficit/hyperactivity disorder (ADHD). The authors hypothesized that nonaffected siblings of ADHD probands would have a response inhibition between that of ADHD probands and normal controls, although they resembled the controls at a behavioral level. METHOD: Participants were 25 ADHD probands with a family history of ADHD, their nonaffected siblings (n = 25), and 48 normal controls matched for age and IQ. All participants were between 6 and 17 years of age. The nonaffected siblings were compared with their ADHD siblings and with controls on measures reflecting different types of response inhibition. RESULTS: The nonaffected siblings had results similar to those of the ADHD probands, who differed from the controls on all inhibition measures (p <.05). CONCLUSIONS: Siblings of ADHD probands, while not behaviorally expressing the disorder, have ADHD-associated deficits in response inhibition. This suggests that subtyping based on measures of response inhibition can help identify genetic susceptibility to ADHD. Children with a genetic vulnerability to ADHD may have hidden cognitive deficits in the absence of manifest behavioral symptoms. Therefore, they should be monitored to detect possible learning problems.

Adolescent↗

PubMed2002

Inhibition of prepotent responding and attentional flexibility in treated phenylketonuria.

Inhibition of prepotent responding and attentional flexibility were assessed in 58 early and continuously treated phenylketonuria (PKU) patients and 69 controls, age 7 to 14 years. A computerized task was used requiring participants to process consecutive stimuli according to various attentional sets. Analysis of error rate suggested poorer inhibition of prepotent responding in PKU patients compared with controls. No influence of concurrent plasma phenylalanine (phe) was shown, neither in the younger (age < 11 years) nor in the older participants (age > or = 11 years). Analysis of error rate provided strong evidence for poorer attentional flexibility in PKU patients compared with controls. The difference between attentional flexibility in controls and PKU patients could mainly be attributed to younger PKU patients, with concurrent phe levels higher than 360 micromol/L. Younger PKU patients with phe levels below 360 micromol/L performed at the same level as age-matched controls. Performance of PKU patients was strongly associated with phe levels in age periods during the first 10 years of life, which are characterized by a strong development of executive functioning (ages 2-7 and age 9). High phe levels during these age periods could delay development of inhibitory control and attentional flexibility. With regard to treatment, analyses with lifetime and concurrent phe levels support strict dietary control throughout the first decade of life, after which the phe-restricted diet can be relaxed. However, based on the evidence that development of specific executive functions continues until approximately age 12, it is recommended to maintain phe levels below 360 micromol/L throughout early adolescence.

Adolescent↗