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Results for “developmental disorders”

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PubMed1982

Stimulant drug effects in developmental disorders and hyperactivity--toward a resolution of disparate findings.

An attempt is made to integrate data from a variety of clinical populations and from the animal literature. Evidence is presented suggesting that mentally retarded and autistic children generally show a poor response to stimulant medication, whereas hyperactive and normal children respond beneficially. Cognitive research in mentally retarded and autistic children is reviewed, and it is suggested that both diagnostic groups suffer from attentional difficulties, the mechanisms of which may be very similar. The literature on stimulant-induced stereotypy in animals is discussed, with emphasis on the clinical implications for autism and mental retardation. An attentional model is proposed to account for type of therapeutic response to stimulant medication. This is followed by a possible method for testing the model and by specific predictions relating to subject characteristics and response.

Amphetamines↗
PubMed1989

[[Klippel-Trenaunay syndrome--an embryonic developmental disorder. A case report with reference to the orthodontic symptoms].

The Klippel-Trenaunay syndrome is a disturbance in the development of the mesodermal and ectodermal tissues occurring in utero. It is characterized by the clinical triad of unilateral soft tissue and bone hypertrophy, varicosities and hemangiomas. For dentists the orofacial manifestations of the syndrome are interesting: unilateral hypertrophy of the maxilla and mandible, mandibular joint and alveolar processes and tooth germs. In addition, the gingival margins are thickened, eruption is premature and there is marked facial asymmetry.

Angiomatosis↗
PubMed1991

[Osteotomies for treating developmental disorders of the neurocranium and visceral cranium].

Craniofacial deformities are primarily caused by premature synostosis of cranial sutures. Depending on the involved sutures, typical deformities of the neuro- and visceral cranium are produced. They result in severe functional and aesthetic disturbances. Several osteotomies, which do not only make an aesthetic improvement possible but a correction of severe malfunction, are available for therapy. Preoperative planning and postoperative treatment require the combination of orthodontics and maxillofacial surgery.

Craniosynostoses↗
PubMed2004

A social adjustment enhancement intervention for high functioning autism, Asperger's syndrome, and pervasive developmental disorder NOS.

This paper reports the findings of a 20-week social adjustment enhancement curriculum for boys aged 8-12. The curriculum was designed to address three areas hypothesized to be deficient in persons with HFA, AS, and PDDNOS: emotion recognition and understanding; theory of mind; and executive functions/real life type problem solving. Parents attended a semi-structured concurrent psychoeducational training meeting during children's sessions. Statistically significant improvements in facial expression recognition, and problem solving were reported for intervention group children compared to waiting list control group children. For the intervention group (the only group for whom data were available), older and less cognitively able boy's scores on a depression inventory decreased significantly more than younger children's. Mother's depression scores tended to decrease and there were significant reductions in child problem behaviors reported. Results are discussed in the context of individual differences in participant cognitive levels and profiles, symptom severity, and affect-related variables.

Adjustment Disorders↗
PubMed1989

Neurogenesis of the basal forebrain in euploid and trisomy 16 mice: an animal model for developmental disorders in Down syndrome.

The neurogenesis and early histochemical differentiation of the basal forebrain in trisomy 16 fetal mice and their euploid littermates were examined by combining [3H]thymidine autoradiography with acetylcholinesterase histochemistry. Neurons of the basal forebrain were being born between embryonic day 11 and 15 in both chromosomally normal (euploid) and aneuploid mice. In euploid littermate controls, neurogenesis proceeded along a caudal to rostral gradient with the peak on embryonic day 11 for caudal portions and embryonic day 13 for rostral portions of the basal forebrain. In contrast, in trisomy 16 mice, rostral sections exhibited a peak of neurogenesis on embryonic day 11, 2 days earlier than in their euploid littermate controls. Hypocellularity of the basal forebrain region was noted in trisomy 16 mice; particularly dramatic was the reduction of the population of cells that expressed acetylcholinesterase. This reduction in cell number in the trisomics was not accompanied by a reduction in cell size or by a dramatic change in the distribution of residual neurons when compared to that of euploid littermate controls. Since trisomy 16 mice do not survive the perinatal period, we examined the pattern of acetylcholinesterase expression in normal C57B1/6J mice from embryonic day 16 to postnatal day 5 to determine the postnatal disposition of these neurons. Already at embryonic day 16, fibers staining for acetylcholinesterase penetrated the striatal anlage, in their course towards targets in the cerebral cortices. By postnatal day 5, the previously expansive distribution of basal forebrain neurons had become consolidated in a more ventral and rostral position by the extensive outgrowth of the striatal neurons, a pattern resembling that seen in adult animals.

Acetylcholinesterase↗
PubMed1993

Neurological development during toddling age in normal children and children at risk of developmental disorders.

Toddling age (1.5-4 years) is a period in which the quality rather than the quantity of motor functions changes. We examined 305 normal and 43 so called 'risk' children with an examination technique which concentrates on observations of motor functions (grasping, sitting, crawling, standing and walking) in a standardized free field situation. Examples of the changes during toddling age are presented such as the decrease of yoke movements (i.e. shoulder movements during reaching), the increase of trunk motility, of variability of speed during crawling, narrowing of gait width, and an increased ability to avoid objects on the floor and to show maneuverability during walking. All changes occurred in the normal children between the ages of 2 and 3 years. They reflect a 'transformation' of neural functions. Many of the 'risk' children show qualitatively different motor behaviour, which is interpreted as non-optimal and which can be an early sign of neurological impairment. The transformation in neural functions is discussed in terms of neuroanatomical changes during toddling age.

Aging↗