A preliminary report of the dopamine receptor D(4) and the dopamine transporter 1 gene polymorphism and its association with attention deficit hyperactivity disorder.

Attention deficit hyperactivity disorder (ADHD) is one of the most prevalent childhood-onset psychiatric syndromes affecting 5%-10% of school-age children worldwide. Distortions in the catecholaminergic system seem to be responsible for this condition. Within this system there are several candidate genes, the dopamine receptor D(4) (DRD4) and the dopamine transporter 1 (DAT1), with common polymorphism which might be associated with ADHD. We performed a family based association study with 36 trios and 19 parent proband pairs. All diagnoses were confirmed by the "Hypescheme" diagnostic computer program. In this study we did not observe an association of ADHD with DRD4 and DAT1 polymorphism neither by the haplotype relative risk (HRR) method nor by the transmission disequilibrium test (TdT) method. The odds ratio for the DRD4 7-allele was 1.01 and 0.94 for both statistical tests, respectively, and the respective odds ratio for the DAT1 6-allele were 0.91 and 0.88.

Information transmission defect identified and localized in language learning impaired children by means of electrophysiology.

Children with language processing deficits have various learning impairments and poor scholastic performance. In 3-10% of all children a specific language processing deficit can be identified by the Sound Connecting Sub-Test of the Illinois Test of Psycholinguistic-Abilities (SC-ITPA). These children among which we drew our index group (AS-Group) suffer from the disability to recognize isolated sounds as parts of words. Following linguistic terminology this is known as an auditory sequential sound processing deficit (ASSPD) Eighteen children (AS-Group) and 21 controls (C-Group) were subjected to mapped P300 evoked potential analyses of cortical response to acoustic stimulation in the oddball paradigm. The data presented here show that there exists significant relation between the P300 amplitude reduction and ASSPD. The P300 amplitude decrease measured in the AS-Group is due to a reduced information transmission in accordance with Johnson's Triarchic Model of the P300 Amplitude. The cerebral structures involved in poor language processing are localized at the left temporo-parietal cortex. This supports the hypothesis that the underlying neuronal defect of ASSPD is localized in the language center and not in the auditory pathway. The P300 amplitude may serve as electrophysiological tool to identify ASSPD and to quantify the degree of improvement in the course of specific therapy.