Childhood psychosocial development and fatal injuries in Gauteng, South Africa.

BACKGROUND: In South Africa, injuries are the third leading cause of death and disability. Children are especially susceptible to unintentional injuries, especially pedestrian injuries, burns and drowning. Injury risk is informed by children's exposure to adverse environmental circumstances, and individual capacities dependent on developmental maturity. Boys are at greater risk than girls. This study investigates the incidence of fatal childhood injuries as well as sex differences across psychosocial development stages. METHODS: Data on fatal injuries in Gauteng, South Africa's most populous province, were obtained from the National Injury Mortality Surveillance System. The analysis drew on Erikson's psychosocial theory of development which was used to create meaningful age groups. Age-specific population data from the 2011 Census were used to calculate rates, and significant differences were determined through the generation of risk ratios and confidence intervals. RESULTS: There were 5404 fatal injuries among children in Gauteng from 2008 to 2011. The average age of victims was 8.9 years, and the majority male (65.6%). In infancy, the mortality rates for all injuries and non-traffic unintentional injuries were significantly higher than for the other age groups. Burns were the most common cause of death in infancy and early childhood. Pedestrian injuries accounted for a third of mortality in preschool and school age, and homicide rates were significantly higher in adolescence than in the other developmental stages. For injuries in general, boys had significantly higher mortality rates than girls in all age groups except preschool. The only instance where the mortality rate for girls was significantly higher than for boys was for adolescent ingestion poisoning suicides. CONCLUSIONS: The exposure to environmental and social risks is differentially moderated with maturing age and levels of autonomy. The sex of the child also informs risk. The nature of these risks is important when considering child injury prevention strategies.

Maternal postpartum depression and infant social withdrawal among human immunodeficiency virus (HIV) positive mother-infant dyads.

Maternal postpartum depression poses significant risks for mother-child interaction and long-term infant outcomes. Human immunodeficiency virus (HIV) status has also been implicated in the development of postpartum depression, but the association between maternal depression and infant social behavior in the context of HIV infection has not been fully investigated. First, we examined the relationship between maternal postpartum depression and infant social withdrawal at 10-12 months of age in HIV-infected mothers and infants. Second, we ascertained whether infant social withdrawal could be significantly predicted by maternal postpartum depression. The sample consisted of 83 HIV-infected mother-infant dyads. Mothers were assessed for postpartum depression with the Edinburgh Postnatal Depression Scale (EPDS), and infant social withdrawal behavior was rated using the Modified Alarm Distress Baby Scale (m-ADBB). 42.2% of the mothers scored above the cut-off point for depression on the EPDS, and a third of infants (31%) were socially withdrawn. Notably, maternal depression did not predict infant social withdrawal as measured by the m-ADBB. Infant social withdrawal was also not significantly associated with failure to thrive or gender. These preliminary findings need further investigation with respect to the impact on long-term neurodevelopmental and behavioral outcomes.

The pathogenic and progressive features of chronic human hippocampal epilepsy.

To design useful experimental models of epilepsy, it is necessary to clearly understand the known clinical-pathologic features of the disease process. Studies of mesial temporal lobe epilepsy (MTLE) patients have identified several distinctive clinical and pathophysiologic characteristics and many of these can be analyzed in experimental models. For example, patients with typical MTLE have medical histories that often contain an initial precipitating injury (IPI), are likely to have hippocampal sclerosis in the surgical specimen, and have better seizure outcomes than patients with typical idiopathic temporal seizures (i.e. cryptogenic). Hippocampal from children as young as age 1 year with IPI histories also demonstrate neuron damage similar to adults with hippocampal sclerosis. Compared to IPI patients without seizures (i.e. trauma, hypoxia, etc.), IPI cases with severe seizures showed younger ages at the IPI, shorter latent periods, and longer durations of habitual MTLE. Hippocampal damage is often bilateral, however, the epileptogenic side shows hippocampal sclerosis and the opposite side usually shows only mild neuron losses. Moreover, MTLE patients show declines in hippocampal neuron densities with very long histories of habitual seizures (15 to 20 years), however, the additional neuron loss adds to the template of hippocampal sclerosis and occurs in limited subfields (granule cells, CA1 and prosubiculum). Hippocampal axon and synaptic reorganization is another pathologic feature of MTLE, and involves granule cell mossy fibers and axons immunoreactive for neuropeptide upsilon, somatostatin, and glutamate decarboxylase (which synthesizes GABA). Finally, MTLE patients with hippocampal sclerosis show increased granule cell mRNA levels for brain derived neurotropic factor, nerve growth factor, and neurotrophin-3 that correlate with mossy fiber sprouting or with declines in Ammon's horn neuron densities. Taken together, our data support the following concepts: (1) The pathogenesis of MTLE is associated with IPI histories that probably injure the hippocampus at some time prior to habitual seizure onsets, (2) most of the damage seems to occur with the IPI, (3) there can be additional neuron loss associated with long histories, (4) another pathologic feature of MTLE is axon reorganization of surviving fascia dentata and hippocampal neurons, and (5) reorganized axon circuits probably contribute to seizure or propagation.