Marta Colombo

INTELLECTUAL AND PHYSICAL OUTCOME OF CHILDREN UNDERNOURISHED IN EARLY LIFE IS INFLUENCED BY LATER ENVIRONMENTAL CONDITIONS

Thirty‐five schoolchildren who share a common history of early undernutrition and who were reared after recovery by adoptive families (16), in institutional care (eight) or by their biological families (11) were assessed for physical and intellectual outcome. The adopted children had mean normal weight and height for age, but the children from institutions were significantly shorter. Adopted children had mean Full‐scale, Verbal and Performance IQs in the normal ranges, with significant differences from the other two groups, mainly for the Verbal subscale. These results emphasize that the growth and development of early‐undernourished children are not irreversibly fixed by the acute illness, but are highly sensitive and modifiable by early and stable environmental improvement.

Dendritic development in neocortex of infants with early postnatal life undernutrition

The structure of large pyramidal cells from layer V of the motor cortex of undernourished and well-nourished infants was studied to determine the effects of postnatal nutrition on cortical dendritic development. In undernourished infants, the arborization and span of the basilar dendrites were decreased in comparison to controls. These findings indicated that undernutrition experienced during the first months of postnatal life could affect the growth of pyramidal cells, especially the formation of basilar dendrites.

Dendritic development in the neocortex of adult rats following a maintained prenatal and/or early postnatal life undernutrition

The Golgi-Cox method was used to study the maturation of the large pyramidal cells of the Vth cortical layer in three groups of adult rats: one subjected to undernutrition during the first month of life, another throughout the first 2 mth of life, and the last one during gestation and the suckling period. The main alterations consist of a decrease in the number and span of dendritic basilar processes of large pyramidal cells. In animals malnourished during prenatal life and the suckling period the reduction of the basal dendritic arborization was more apparent. It is postulated that the vulnerable period for the basal dendritic development occupies the period from the end of pregnancy until the first 3 wk of postnatal life in the rat (suckling period). Noxious influences acting during this phase induce sequelae that cannot be reversed by subsequent refeeding. A maintained nutritional insult during prenatal and early postnatal life induces the most severe changes in dendritic arborizations, compared to those resulting from a prolonged postnatal malnutrition.

Histological maturation of the neocortex in phenylketonuric rats

The histological maturation of pyramidal cells from the deeper layer of the neocortex was studied in phenylketonuric rats. The main alterations consist of a decrease in the number of span and dendritic basilar processes of large pyramidal cells, and changes in the structural organization of the cerebral cortex. It is postulated that high levels of phenylalanine induced immediately after birth disturb profoundly the process of neuronal maturation in the neocortex of the rat brain, probably with long-term effects.

Dendritic development in the neocortex of adult rats subjected to postnatal malnutrition

The Golgi-Cox method was used to study the maturation of the large pyramidal cells of the Vth cortical layer in two groups of adult rats, one subjected to early postnatal malnutrition and another malnourished only during the second month of life. The main alterations were observed in the pyramidal cells of cortical layer V of rats malnourished during the first month of life. They consist of a decrease in the number and span of dendritic basilar processes. In animals malnourished during the second month of life, the number and span of basilar dendritic processes in pyramidal cells of layer V, were normal. It is postulated that early postnatal malnutrition induced immediately after birth, profoundly disturbs the process of neuronal maturation in the neocortex of the rat brain, probably with permanent effects.

Follow‐up of Severely Undernourished Infants

SIR-Grantham-McGregor and colleagues (DMCN, 24, 321) point out that undernourished infants were markedly below normal in psychomotor abilities on admission to hospital, and that they never catch up with the performance of control infants. Secondly, they observed that social background did not predict the change in developmental quotient (DQ). In our own experience of treating patients with severe undernutrition early in life, we have found somewhat similar results’’ *. However, using the Bayley scales and other local instruments, we have found that psychomotor performance, severely depressed before treatment, showed a marked recovery after 160 days of impatient treatment. We also found that a mean DQ ofO. 59 f 0 17 before treatment had increased to 0 79 k 0. 14 upon discharge from Nutritional Recovery Centres (NRC). Moreover, some 10 per cent of patients, despite their undernutrition, had nearly normal psychomotor performance on admission to NRC (Table I). This could be attributable to differences in environmental sensorimotor stimulation, according to the children’s sociocultural backgrounds. Grantham-McGregor and colleagues reported a DQ of 72.1 f 15.0 on admission to hospital, andit is likely that some ofthose patients had normal psychomotor performance. We wish to stress this point because over the last two decades of research in this field there has been an over-emphasis on the association between undernutrition and mental performance. In our own studies, growth measures such as weight for age, height for age and head circumference for age have explained only 23 per cent of variance in psychomotor performance, and according to other authors3. there are non-nutritional factors which could explain the rest of the variance. We think that, among the biological risk factors,

Propionic acidaemia : two cases in Chile

Case 1 F.D.S., male, birth weight 2980g. At the second day of life he presented hypoglycaemia and 24 h later developed metabolic acidosis. At the 6th day of life he had vomiting, hypotonia and hyperreflexia that progressed to seizures and coma. Blood analyses showed metabolic acidosis and hyperammonaemia. The diagnosis of propionic acidaemia was confirmed by the study of organic acids in urine by gas chromatography, which showed large increases in the excretion of lactic, 3-hydroxypropionic, and methylcitric acids and in propiony!glycine, with a slight increase in 3-hydroxyisovaleric acid. A low protein, hypercaloric diet (1 g protein/kg per day, 200cal/kg per day) was started at the 10th day of life. Although severely undernourished, with treatment he recovered weight and height. At 5 months he had a psychomotor development of 3 months. One month later he had a bronchopneumonia and a severe metabolic imbalance and died. Case 2 J.G.F., 9-year-old boy. This boy developed normally until the age of 3 months, when he started vomiting, became severely hypotonic and started to present psychomotor delay. The diagnosis of propionic acidaemia was made at 16 months of age using gas chromatography (large increases in 3-hydroxypropionic, 3-hydroxyisovaleric and methylcitric acids and in propionylglycine). The treatment (a low protein, hypercaloric diet) was started at the age of diagnosis with 1 g protein/kg/day and 150 cal/kg per day. His physical development is normal and he has a borderline intelligence quotient.