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Folic acid (FA) and vitamin B12 have been measured prospectively in 110 children that were under treatment with anticonvulsants. The control group consisted of 59 healthy children. A statistically significant difference in levels of serum FA and mean corpuscular volume (MCV) was observed between groups. Children under anticonvulsant treatment had lower serum FA levels and higher MCV. No significant difference was observed between the two groups in levels of serum vitamin B12. All children with serum FA levels lower than 3 ng/ml were given folate and no adverse side effects were observed due to treatment. Anticonvulsant drugs decrease serum FA levels; therefore, FA should be determined periodically in children under long-term anticonvulsant treatment.

We have evaluated, in a prospective study, the total and per unit area mass, measured in lumbar spine by Dual Photo-absorptiometry, in a group of 62 children on long-term anticonvulsant treatment. A second group of 58 normal children was used as a control. The total and per unit area bone mass increased with age, weight, height and bone maturity in all of the children studied. There were no significant differences found between the two groups. Children on multi-therapy and that were over six years of age showed statistically significantly less bone mass per area when compared th the control group (p less than 0.01). Phenobarbital, Carbamazepine and Valproic acid in monotherapy did not statistically diminish bone mass. Of these anticonvulsants, Phenobarbital was responsible for the most statistically significant decline in bone mass per area (p = 0.027). After six year of treatment, whether on mono-therapy or on poly-therapy, bone mass was lower with respect to the control series, although this was not statistically significant.

The authors give the results of a horizontal study made in the course of the work carried out during 1988 in the Developmental Follow-up Unit of the University Hospital "Virgen Macarena" of Seville, making emphasis on the psiconeurological pathology detected and its relation to the cause consultation. A total of 443 children were studied, this number being 77% of the cases under control up to that time. 82.2% of the children (N = 364) were normal on neurological examination, with normal I.Q. at the last control. However, 147 of these children (33.2% of the total) had shown some transient neuromotor abnormality over the follow-up period. Of the total, 17.8% (N = 79) showed one more of the following permanent sequelae: Defects of mental development 15% (N = 67), Motor sequelae 8.8% (N = 39), Sensorial deficits 5.6% (N = 25), Convulsions 3.6% (N = 16), Important behaviour disorders 0.5% (N = 2). The presence of motor sequelae had a significant correlation with: CNS defects (p less than 0.001), Metabolic changes in the neonatal period (p less than 0.005), Neonatal convulsions (p less than 0.005), Isquemic-anoxic syndrome (p less than 0.05). Deficits of mental development are associated significantly with: Polimalformative syndromes (p less than 0.001), CNS defects (p less than 0.001) and with neonatal convulsions (p less than 0.001). The neuromotor abnormalities detected (in order of frequency) were: Changes in muscle tone (32%), Motor retardation (31.8%). Changes in prehensive behaviour (22%), Changes in motility (21%). Retarded expressive conduct (14.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative assessments were made regarding the effects of prolonged administration of anticonvulsant drugs (phenobarbital, carbamazepine, valproate and polytherapy) on the different biochemical parameters related to phosphocalcium metabolism, in 98 children between 1 and 14 years. The most patent effect was on the levels of 25-Hydroxycholecalciferol which went down significantly (p = 0.0001) in children treated with phenobarbital (34.5 +/- 17 ng/ml) or polytherapy (28.4 +/- 18 ng/ml) in relation to those treated with carbamazepine (49.2 +/- 15 ng/ml) or valproate (43.1 +/- 15 ng/ml) and to control group (45.9 +/- 13 ng/ml). The alkaline phosphatase has been found significantly higher among those treated with phenobarbital, carbamazepine and polytherapy, evidencing significant differences in relation to those treated with valproate and to control group (p less than 0.05). For calcium, parathyroid hormone and osteocalcine levels no differences were found in the different drugs, nor with control group. Depending on the duration of treatment there was a significant reduction (p = 0.02) in the levels of 25-Hydroxycholecalciferol in children treated over 3 years, but no difference for calcium, phosphorous, alkaline phosphatase and PTH under this parameter.

The effects of prolonged administration of anticonvulsants were analyzed on different biochemical parameters related to phosphocalcium metabolism in 98 children aged 1 to 14, not affected by other chronic pathology, and to whom no Vitamin D nor other vitamin-mineral complexes had been administered. We take as reference a group of normal children studied during the same period. Determinations were accomplished with the usual chemical controls in our laboratory (autoanalysis of continuous flow, radioimmunoassay and colorimetric measurements) and the following mean levels were obtained for treated children: Calcium: 9.2 +/- 0.4 mg/dl, phosphorous: 3.5 +/- 1.9 mg/dl, alkaline phosphatase: 252 +/- 72 U/L, 25-Hydroxycholecalciferol: 35.6 +/- 18 ng/ml, Osteocalcine: 5.4 +/- 3.6 ng/ml, and parathyroid hormone: 0.4 +/- 0.1 ng/ml. These values differed significantly from those found in the control group for phosphorous, lower in children under treatment (p = 0.000), and the 25-Hydroxycholecalciferol was likewise lower (p = 0.000). In other way the mean levels of alkaline phosphatase were higher in treated children (p = 0.000). No significant differences were obtained for mean levels of calcium, parathyroid hormone and osteocalcine. These differences are maintained when distributing patients among different age groups. Solar radiation received by treated children during the months preceding the extraction, did not produce significant differences on 25-Hydroxycholecalciferol, with mean values that were similar at the end of summer (34 +/- 9 ng/ml) and the end of winter (36.6 +/- 18 ng/ml).

We evaluated annually the compliance of dietary restriction, weight, height, head circumference EEG and IQ score on 16 children with phenylketonuria comparing the children diagnosed early with those later. The compliance was good in children treated early and bad in the others. Height and head circumference was normal in all children and we found a tendency towards obesity in the older ones. The IQ score was lower than 80 in 77% of the children diagnosed later and in those the EEG showed slow basal activity in 55%.

The role of sleep and sleep deprivation as inducer of paroxysmal abnormalities in EEG was studies in 104 infants and children under 14 years of age. These children suffered from various types of seizures and of normal standard EEG. These children who suffered from seizures of epileptic origin, after sleep deprivation had an EEG that showed a paroxysmal activity of 70.91% of the cases (p less than 0.001). The forced lack of sleep and the sleep that follows were found to be equally important as activators of paroxysmal abnormalities. The method of activation was found to be efficient in both partial an generalized seizures. The paroxysmal abnormalities were noted as being greater in phase II sleep. The EEG in sleep deprivation can show paroxysmal abnormalities, in children with epileptic seizures, that were hidden from standard EEG.