Lawrence T. Taft

Developmental changes in overflow in normal and aberrantly functioning children

Overflow involuntary movement in a resting extremity when the contralateral extremity is performing a voluntary movement was measured in normal and aberrantly functioning children. After 9 years of age, normal children showed a marked decrease in overflow movements. In contrast, subjects with evidence of CNS abnormalities have an increased amount of observed overflow and a significant delay in the capacity to inhibit such movements voluntarily. The excessive overflow noted in neurologically abnormal children is not wholly accounted for by mental subnormality, or by delayed neurological maturation, but appears to be an indication of a damaged brain.

The Genetic Relationship of Progressive Muscular Dystrophy (Duchenne Type) and Mental Retardation

Two hundred and eleven patients with progressive muscular dystrophy (pmd) of the Duchenne type were identified in 135 separate families. The overall incidence of mental retardation in the 211 patients was 20.9 per cent. There was no evidence of a similar increase in the incidence of mental defect among non‐dystrophic siblings.

The Care and Management of the Child with Muscular Dystrophy

The partf of the paediatrician in the care and management of the child with muscular dysti ophy is initially one of diagnosing the disorder and informing the parents, and later of involvement in the long‐term psychological and social consequences for the child and the family. The author discusses the problems which are likely to arise in the initial stages of counselling and treatment, and those which may present as the child grows older.

PARENTS OF AUTISTIC CHILDREN

is affected), cleidocranial dysostosis (which may also show skull bossing, open cranial sutures, wormian bones, proptosis and delayed dentition, but in which there is no increased bone density and the inheritance is autosomal dominant), progressive diaphysial dysplasia (Englemann’s disease, in which there is poor muscle development, sometimes hepatosplenomegaly, and progressive sclerotic changes in the diaphyses of the long bones, vertebrae and pelvis, with spontaneous amelioration of symptoms when growth ceases ; its variant, Ribbing’s disease, usually appears at puberty, is accompanied by pain, is nonprogressive and is confined to the lower limbs), idiopathic non-familial acro-osteolysis (in which dwarfism, absence of frontal sinuses and frequent wormian bones occur, but in which there may be pain and tenderness over the terminal phalanges, and progressive osteolytic changes are seen on X-ray), and hypervitaminosis D. Amid the many confusing varieties of bony disorders, this condition should not be difficult to diagnose on the infrequent occasions when it appears.

CONGENITAL SENSORY NEUROPATHY

On the other hand, its metabolism is stimulated by phenobarbitone through enzyme facilitation, so that the addition of this drug to phenytoin may lower. the effective blood level. Yet another metabolic hazard which has recently come to light is the effect of anticonvulsants upon vitamin D utilization. Phenituride (Benuride), primidone, phenytoin and phenobarbitone (in that order of importance) have,all been shown to cause lowering of serum calcium and a rise in alkaline phosphatase, even sometimes producing osteomalacia.’“ Much remains to be clarified in this difficult fieid. of study, but more and more evidence is accumulating which should at least ma‘ke us stop and think what we are doing to children when we prescribe heavy doses of anti-epileptic drugs for a long time.