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[Value of the Heidelberg Language Development Test in diagnosis of children with language development disorders].

Diagnosis of developmental speech and language disorders in accordance with the ICD-10 is to be based on the psychometric assessment of speech and language performance. In the present study the clinical validity of the Heidelberger Sprachentwicklungstest (HSET) for diagnosing expressive language disorders was assessed by comparing HSET subtest results for 92 children aged 4 to 10 years who had various speech and language disorders with the children's scores on another language test, a cognitive test and clinical findings. The HSET scores differed considerably from the clinical ratings of the severity of the language disturbance. The correlations between the HSET scores and the score on the other language test was also low. Although the correlations of the HSET scores with the performance IQ was low, the correlations with the verbal IQ were high. The implications of these findings for the use of the HSET in diagnosing children with language impairments are discussed.

Child↗

[Relationship between regulatory effects of serotonin and testosterone on the development of the LHRH producing system of the rat brain during the prenatal period of development].

We have performed radioimmunoassay of LHRH in rostral and septal-preoptic brain regions, as well as in mediobasal hypothalamus of male and female fetuses at day 21 of the prenatal period after the injection to pregnant females on days 11-20 of gestation of either p-chlorophenylalanine (PCPA) or of a combination of PCPA with ethane-1,2-dimethane sulfonate (EDS). Control animals received the injection of the same volume of physiological saline. In the control fetuses, both males and females, the level of LHRH in the rostral brain region was significantly lower than in the septal-preoptic region. The administration of PCPA increased the level of LHRH in the rostral brain region and decrease it in the septal-preoptic region, the effect being more prominent in males. When EDS was administered on the background of PCPA administration, sex-related differences in the level of LHRH in the studied brain regions were no longer present. It is proposed that serotonin stimulates migration of LHRH neurons in rostral-caudal direction, and this effect of serotonin is more significant in males, since it is potentiated by testosterone.

Animals↗

[Infants born with development disorders. What about the long-term statural development? What are the therapeutic possibilities?].

Intrauterine growth retardation (IUGR), defined as birth weight and/or length less than 3rd percentile (P) or less than-2 standard deviations (SD), concerns about 3% of newborns. About 85% born IUGR show spontaneous postnatal catch-up to a height > P3 or > -2 SD during the first two years of life. After the age of 4 year, the children without catch-up will remain short up to final height. Classical growth hormone (GH) deficiency usually does not seem responsible for the absence of catch-up in those children. A two-year GH therapy at supraphysiological doses increases growth velocity. The effect of this treatment on final height remains to be studied, as well as optimal treatment's modalities. Attention should be paid on the possible side-effects. Finally, the evaluation of the psychological impact of GH treatment will be critical.

Body Height↗

Motor stimulant effects of the adenosine A(2A) receptor antagonist SCH 58261 do not develop tolerance after repeated treatments in 6-hydroxydopamine-lesioned rats.

Several evidences indicate that the selective blockade of adenosine A(2A) receptors counteracts the motor activity impairment in experimental models of Parkinson's disease. In the present study, the effects of the adenosine A(2A) receptor antagonist, SCH 58261 (5-amino-7-(beta-phenylethyl)-2-(8-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine, were assessed following a repeated treatment schedule in the contralateral turning behavior rat model of Parkinson's disease. Unilateral lesions of the nigrostriatal pathway were induced by injecting 6-hydroxydopamine (6-OHDA) in medial forebrain bundle. Repeated administration of SCH 58261 was performed either alone (7 and 14 days repeated SCH 58261) or together with L-dopa (19 days repeated SCH 58261 plus L-dopa or L-dopa alone). After a 7- and 14-day repeated administration schedule, SCH 58261 (5 mg/kg) maintained its ability to potentiate the contralateral turning behavior induced by a subthreshold dose of L-dopa (2 mg/kg i.p.), showing no tolerance to its stimulant effects. SCH 58261 (5 mg/kg) plus L-dopa (3 mg/kg) or L-dopa (6 mg/kg) alone induced, at these dosages, the same number of contralateral turnings after the first administration. While chronic intermittent SCH 58261 plus L-dopa did not lead to a modified turning behavior during treatment, L-dopa alone produced a progressive increase in turning behavior intensity and duration. These results provide evidence that SCH 58261 retains its ability to potentiate L-dopa effects in a validated rat model of Parkinson's disease even after repeated treatments. Moreover, these results suggest that adenosine A(2A) blockade prevents the appearance of motor response alterations in L-dopa-treated rats, supporting the concept that A(2A) receptor antagonists have a therapeutic potential for the treatment of Parkinson's disease. Copyright 2001 Wiley-Liss, Inc.

Journal Article↗