The development of conditioned blocking and monoamine metabolism in children with attention-deficit-hyperactivity disorder or complex tics and healthy controls: an exploratory analysis.

Conditioned blocking (CB) measures the transient suppression of learning that a new stimulus, added during learning, has the same consequences as the conditioned stimulus already present. Normal CB increases between the age of 8 and 20 years (Oades, R.D., Roepcke, B. and Schepker, R., A. test of conditioned blocking and its development in childhood and adolescence: relationship to personality and monoamine metabolism, Dev. Neuropsychol., 12 (1996) 207-230). In the present study CB development is compared between healthy children (CN), children with attention deficit (ADHD) and those with complex tics or Tourette's syndrome (TS) with mean ages of 10-11 years. All children needed fewer learning trials with increasing age: the ADHD group showed a slight impairment. Only controls improved CB with increasing age. A trend for worse CB in the TS than the other groups was significant for those over 11 years. While ADHD children over 11 years showed less CB than controls, younger ADHD children showed more. A correlational analysis of the status of monoamine metabolism in 24 h urine samples showed a positive relationship for CB with dopamine metabolism in controls and TS children, but a negative relationship in ADHD children. In contrast, increases of serotonin metabolism were negatively related to CB in TS but positively in ADHD patients. In conclusion, when selective information processing abilities reflected by CB start to develop at puberty-onset, there is a relative worsening in ADHD patients. But TS patients show an impairment independent of age. Changes in the balance between dopamine and serotonin systems may contribute to normal and abnormal cognitive development.

[Pathogenesis of hyperkinesis in children]. / O patogeneze giperkinezov u detei.

Pheylalanine metabolism was studied in 56 children with various forms of hyperkinesias. It was found that in the development of slow and fast hyperkinesias a certain role belongs to dihydroxyphenylalanine (DOPA). It is probable, that in patients with Turett's syndrome the synthesis of DOPA is increased while in patients the excretion of phenylacetylglutamine was found to be disturbed: it was decreased in the patients with the fast and increased in the children with the slow hyperkinesias. Phenylalanine load led to a lowering of the DOPA level in the patients with Turett's syndrome; an intensification of the synthesis of phenylacetylglutamine and diminution of the intensity of hyperkinesias. L-glutamine load resulted in detoxication of the toxic phenylalanine metabolites which inhibited the DOPA synthesis, as well as in a short-time increase in the phenylacetylglutamine excretion and a moderation of tonic hyperkinesias that manifested by athetosis and dystonia. All this points out that in the development of various forms of hyperkinesias a certain role belongs to amino acid metabolites.