A preliminary investigation of 4 to 11-year-old children's knowledge and understanding of stress

Objective. To examine children's knowledge, understanding and experience of stress from 4 to 11 years of age across four age groups (4–5, 6–7, 8–9, and 10–11 years old). Methods. A semi-structured interview format was used to elicit information from 50 children about their understanding and experience of stress. Results. Most children were able to define stress, with older children providing more complex responses. Many children had indirect and/or personal experience of stress. Younger children were more likely than older children to report that there was nothing people could do to stop stress; children reported using both adaptive and maladaptive coping strategies to deal with stress. Conclusion. Some young children have a basic understanding of stress and many have experience of stress; both understanding and experience develop with age. Practice Implications. The research has potential implications for provider-patient communication, particularly within preventative health education and clinically within the field of childhood post-traumatic stress disorder (PTSD).

Being there:a qualitative interview study with fathers present during the resuscitation of their baby at delivery

Objective: To explore fathers' experiences of the resuscitation of their baby at delivery. Design: A descriptive, retrospective design using tape-recorded semistructured interviews with fathers present during the resuscitation of their baby at delivery. Fathers described what happened, their interactions with healthcare professionals, their feelings at the time and afterwards. Setting: Participants were recruited from a large teaching hospital in the UK. Participants: A purposive sample of 20 fathers whose baby required resuscitation at delivery. Results: Participant responses were analysed using thematic analysis. Four broad themes were identified: 'preparation', 'knowing what happened', 'his response' and 'impact on him'. Fathers had no difficulty recalling their emotions during the resuscitation. These feelings remained vivid and were mostly negative. Most fathers wanted to go to their baby during the resuscitation but did not do so. They felt they should stay with their partner, did not want to impede the resuscitation or felt they were not 'allowed' to go to their baby. The fathers' position in the room and the extent to which they were focusing on their partner had an impact on their recollection of what happened. Fathers had no opportunity to discuss the resuscitation with healthcare professionals afterwards. Several fathers felt they had not yet recovered from the experience and a few had symptoms synonymous with post-traumatic stress disorder. Conclusion: This is the first study to specifically explore fathers' experiences of newborn resuscitation. The findings should inform healthcare education, policy development and the provision of support to fathers.

Ethosuximide modifies network excitability in the rat entorhinal cortex via an increase in GABA release

Ethosuximide is the drug of choice for treating generalized absence seizures, but its mechanism of action is still a matter of debate. It has long been thought to act by disrupting a thalamic focus via blockade of T-type channels and, thus, generation of spike-wave activity in thalamocortical pathways. However, there is now good evidence that generalized absence seizures may be initiated at a cortical focus and that ethosuximide may target this focus. In the present study we have looked at the effect ethosuximide on glutamate and GABA release at synapses in the rat entorhinal cortex in vitro, using two experimental approaches. Whole-cell patch-clamp studies revealed an increase in spontaneous GABA release by ethosuximide concurrent with no change in glutamate release. This was reflected in studies that estimated global background inhibition and excitation from intracellularly recorded membrane potential fluctuations, where there was a substantial rise in the ratio of network inhibition to excitation, and a concurrent decrease in excitability of neurones embedded in this network. These studies suggest that, in addition to well-characterised effects on ion channels, ethosuximide may directly elevate synaptic inhibition in the cortex and that this could contribute to its anti-absence effects. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.

Neuropsychiatric manifestations in inflammatory neuropathies:a systematic review

We conducted a systematic literature review on psychological and behavioral comorbidities in patients with inflammatory neuropathies. In Guillain-Barré syndrome (GBS), psychotic symptoms are reported during early stages in 30% of patients. Typical associations include mechanical ventilation, autonomic dysfunction, inability to communicate, and severe weakness. Anxiety and depression are frequent comorbidities. Anxiety may increase post-hospital admissions and be a predictor of mechanical ventilation. Post-traumatic stress disorder may affect up to 20% of ventilated patients. Sleep disturbances are common in early-stage GBS, affecting up to 50% of patients. In chronic inflammatory demyelinating polyradiculoneuropathy, memory and quality of sleep may be impaired. An independent link between depression and pre-treatment upper limb disability and ascites was reported in POEMS (Polyneuropathy, Organomegaly, Endocrinopathy, M-protein, Skin) syndrome, with an association with early death. Hematological treatment of POEMS appears effective on depression. Published literature on psychological/behavioral manifestations in inflammatory neuropathies remains scarce, and further research is needed. This article is protected by copyright. All rights reserved.

Preeclampsia : an accelerator–brake defect disorder

Life's perfect partnership starts with the placenta. If we get this right, we have the best chance of healthy life. In preeclampsia, we have a failing placenta. Preeclampsia kills one pregnant woman every minute and the life expectancy of those who survive is greatly reduced. Preeclampsia is treated roughly the same way it was when Thomas Edison was making the first silent movie. Globally, millions of women risk death to give birth each year and almost 300,000 lose their lives in this process. Over half a million babies around the world die each year as a consequence of preeclampsia. Despite decades of research, we lack pharmacological agents to treat it. Maternal endothelial dysfunction is a central phenomenon responsible for the clinical signs of preeclampsia. In the late nineties, we discovered that vascular endothelial growth factor (VEGF) stimulated nitric oxide release. This led us to suggest that preeclampsia arises due to the loss of VEGF activity, possibly due to a rise in soluble Flt-1 (sFlt-1), the natural antagonist of VEGF. Researchers have shown that high sFlt-1 elicits preeclampsia-like signs in pregnant rats and sFlt-1 increases before the clinical signs of preeclampsia in pregnant women. We demonstrated that removing or reducing this culprit protein from preeclamptic placenta restored the angiogenic balance. Heme oxygenase-1 (HO-1 or Hmox1) that generates carbon monoxide (CO), biliverdin (rapidly converted to bilirubin) and iron is cytoprotective. We showed that the Hmox1/CO pathway prevents human placental injury caused by pro-inflammatory cytokines and suppresses sFlt-1 and soluble endoglin release, factors responsible for preeclampsia phenotypes. The other key enzyme we identified is the hydrogen sulfide generating cystathionine-gamma-lyase (CSE or Cth). These are the only two enzyme systems shown to suppress sFlt-1 and to act as protective pathways against preeclampsia phenotypes in animal models. We also showed that when hydrogen sulfide restores placental vasculature, it also improves lagging fetal growth. These molecules act as the inhibitor systems in pregnancy and when they fail, this triggers preeclampsia. Discovering that statins induce these enzymes led us to an RCT to develop a low-cost therapy (StAmP Trial) to prevent or treat preeclampsia. If you think of pregnancy as a car then preeclampsia is an accelerator–brake defect disorder. Inflammation, oxidative stress and an imbalance in the angiogenic milieu fuel the ‘accelerator’. It is the failure in the braking systems (the endogenous protective pathway) that results in the ‘accelerator’ going out of control until the system crashes, manifesting itself as preeclampsia.