To determine the effect of intravenous porcine secretin on autistic behaviours in children aged 2 to 7 years, the effects of secretin on (1) performance on a standardized language measure, and (2) autistic behaviours, as rated by parents and child development professionals was examined. Employing a randomized, double-blind, placebo-controlled design, 95 participants were assigned to one of two groups and administered a single dose of either secretin or placebo. A follow-up assessment was conducted 3 weeks after the injection. No significant differences in language or autistic behaviour measures were observed at the 3-week follow-up between the groups. Also, there was no significant difference in the proportion of individuals who improved by [ges ] 6 points on the language measure at follow-up. This study showed no significant effects of secretin on children with autism. Our results are consistent with a systematic review of randomized controlled trials evaluating the effect of secretin in children with autism.

This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population-based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association between birth defects and newborn encephalopathy was found with defects affecting 27.5% of children with encephalopathy and 4.3% of control children (odds ratio 8.55; 95% confidence interval 5.25 to 13.91; p<0.001). In 11.8% of infants with a birth defect the defect was not diagnosed until after the newborn period, illustrating one of the difficulties in attempting to exclude infants with birth defects from studies of newborn encephalopathy. The majority of defects (89%) were not specific anomalies of the CNS. In 36.8% of children with encephalopthy who had a birth defect, the defect was considered to be the probable cause of the encephalopathy. Infants with birth defects who had encephalopathy had a poorer prognosis than those without: they were twice as likely to die by the age of 2 years and three times more likely to have cerebral palsy. This study catalogues the spectrum of birth defects associated with newborn encephalopathy and illustrates the importance of their inclusion when investigating both the aetiology and outcome of this condition.

Neonatal cerebral white matter echolucencies predict visual resolution acuity deficits in very-low-birthweight (VLBW) infants. We examined maternal sociodemographic, lifestyle, intrapartum, infant birth/perinatal, and ocular motor/refractive characteristics to determine whether they accounted for this association in infants who were tested once between postnatal age 25 and 56 weeks (corrected for gestational age at birth). Cranial ultrasound scans were read by consensus to identify echolucency in a population of VLBW infants with no known ocular abnormalities. Visual resolution acuity was measured with the Acuity Card Procedure (ACP) in 14 infants with echolucency and compared with that of 81 VLBW infants born in the same hospitals with normal ultrasound scans. In time-oriented logistic regression models, echolucency remained a consistent predictor of abnormal visual resolution acuity after adjustment for covariates in three developmental periods (pre-, peri-, and postnatal). Odds ratios ranged from 19.3 (95% confidence interval, 4.5 to 82.2; p=0.001) to 10.4 (95% confidence interval, 1.3 to 81.9; p=0.03). Reduced visual resolution acuity in VLBW infants appears to be due to cerebral white matter damage.

Although cerebral palsy (CP) is the most common cause of motor deficiency in young children, it occurs in only 2 to 3 per 1000 live births. In order to monitor prevalence rates, especially within subgroups (birthweight, clinical type), it is necessary to study large populations. A network of CP surveys and registers was formed in 14 centres in eight countries across Europe. Differences in prevalence rates of CP in the centres prior to any work on harmonization of data are reported. The subsequent process to standardize the definition of CP, inclusion/exclusion criteria, classification, and description of children with CP is outlined. The consensus that was reached on these issues will make it possible to monitor trends in CP rate, to provide a framework for collaborative research, and a basis for services planning among European countries.

Twenty-five children (21 males, 4 females; mean age 4.8 years) with attention-deficit-hyperactivity disorder (ADHD) participated in this study in addition to 25 typically developing children (21 males, 4 females; mean age 4.9 years). Parental ratings of the preschool children and preschool child self-ratings were examined within the framework of three domains: behavioral disturbance, social competence, and familial environment. Compared to their typically developing peers, preschool children classified as having ADHD were rated by their parents as significantly more aggressive, more demanding of parental time, less socially skilled, less adaptable to change in routine, and as exhibiting more non-compliance. In contrast to these parental ratings, preschool children with ADHD perceived themselves as equally competent, and as socially accepted as their peers. Parents of preschool children with ADHD rated themselves as less competent parents, and as experiencing a restricted parenting role. Although parenting a preschool child with ADHD was viewed as stressful, the parents did not rate general family functioning to be adversely affected.

Inter- and intrahemispheric somatosensory functions were evaluated in blinded tests of 11 children with partial and complete agenesis of the corpus callosum (age range 2 years 8 months to 11 years 9 months) and compared with those of age- and sex-matched control individuals both normally developing and with neurological impairment. Tests included uni- and bimanual measures of stereognosis, haptic visual discrimination, kinaesthesis, and texture matching. Children with callosal absence displayed significant difficulties with many somatosensory functions, but most deficits were no greater than those of the children who had neurological dysfunction and an intact corpus callosum. Children with callosal absence, however, had significantly greater difficulty with bimanual texture matching, seemingly because this task required refined spatial interpretation of somatosensory input. Response times for the individuals with callosal absence were significantly greater than those for control participants with neurological impairment on several tasks in which overall accuracy of performance among groups did not significantly differ. These findings suggest that children with agenesis of the corpus callosum may have less efficient and slower processing capacity for certain types of somatosensory information. Possible compensatory mechanisms are discussed.

A 5-year-old boy with focal cortical dysplasia was referred to our hospital because of epileptic seizures. He showed mild weakness of the left hand without sensory disturbance. Brain MRI revealed extensive cortical dysplasia with pachygyria and microgyria around the right central sulcus. On EEG examination, interictal spikes were noted over the right fronto/centro/parietal region. A 37-channel magnetometer revealed that the sources of the spikes were in a small, restricted region of the normal frontal lobe adjacent to the dysplastic brain. Somatosensory evoked magnetic fields indicated that the location of the current source of N20 was in the same area. Our patient shows a unique case of plasticity and reorganization of the somatosensory function due to cortical dysplasia.

Subdural hemorrhage (SDH) detected postnatally in the newborn infant is usually related to trauma at the time of vaginal delivery. With improvement in obstetric methods, the incidence of this problem has declined. However, with advances in obstetric ultrasonography, it has been recognized that SDH may occur in utero before the onset of delivery. Intrauterine SDH remains a rare event. A review of the literature revealed only 32 cases to date (Tables I and II). Neonatal SDH is venous in origin and associated with trauma in most cases. Etiopathogenesis of neonatal SDH is explained by shearing of bridging veins or other venous structures caused by trauma. Instrumental delivery (forceps or vacuum extraction) causes distortion of the infant's cranium with elongation of the falx and angulation of the tentorium, leading to tearing of posterior fossa venous structures and bleeding into the subdural space. Rupture or tearing of large venous channels, such as the great vein of Galen, straight or transverse sinus or falx laceration with rupture of the sagittal sinus, result in accumulation of blood in both the supratentorial and infratentorial compartments. However, etiopathogenesis of intrauterine SDH is less certain. The fetus is usually well protected from direct abdominal trauma by maternal structures and amniotic fluid. Fetal intracranial vessels may be susceptible to shearing or acceleration/deceleration forces because of the following features: first, the head is large and neck muscles weak; this allows more rotational movement with angular acceleration. Second, the subarachnoid space is larger, allowing the brain to move within the cranium easily. Third, the fetal brain has a higher water content that increases its mass and allows it to develop more momentum when acceleration is applied. These unique conditions could make the fetus more susceptible to developing subdural hematomas and allow the development of subdural hematomas without obvious trauma.

This reply concerns the paper which may be found at http://www.journals.cambridge.org/abstract_S0012162200000670