Impairment Of Cognitive Development Research Articles

Protective effects of docosahexaenoic acid supplementation on cognitive dysfunction and hippocampal synaptic plasticity impairment induced by early postnatal PM2.5 exposure in young rats.

PM2.5 exposure is a challenging environmental issue that is closely related to cognitive development impairment; however, currently, relevant means for prevention and treatment remain lacking. Herein, we determined the preventive effect of docosahexaenoic acid (DHA) supplementation on the neurodevelopmental toxicity induced by PM2.5 exposure. Neonatal rats were divided randomly into three groups: control, PM2.5, and DHA + PM2.5 groups. DHA could ameliorate PM2.5-induced learning and memory dysfunction, as well as reverse the impairment of hippocampal synaptic plasticity, evidenced by enhanced long-term potentiation, recovered synaptic ultrastructure, and increased expression of synaptic proteins. Moreover, DHA increased CREB phosphorylation and BDNF levels and attenuated neuroinflammation and oxidative stress, reflected by lower levels of IBA-1, IL-1β, and IL-6 and increased levels of SOD1 and Nrf2. In summary, our findings demonstrated that supplementation of DHA effectively mitigated the cognitive dysfunction and synaptic plasticity impairment induced by early postnatal exposure to PM2.5. These beneficial effects may be attributed to the upregulation of the CREB/BDNF signaling pathway, as well as the reduction of neuroinflammation and oxidative stress.

Electronic Devices’ Impairment of Cognitive Development in Children under Fourteen Years of Age

Electronic Devices’ Impairment of Cognitive Development in Children under Fourteen Years of Age

Leptin participation in the processes of nervous impulse transmission and its influence on the formation of neuro-mental development of children

Review of publications on the functional features of leptin in the central nervous system in children. The participation of leptin mechanisms in the transmission of nerve impulses, the effect of leptin on cognitive functions in children. The article reveals the general mechanisms of maturation of the central nervous system in children, the participation of leptin and leptin receptors in the formation of cognitive abilities in children. Possible interrelationships of impairments in cognitive development and lipid metabolism including obesity are revealed.

Development of a Vaccine against Human Cytomegalovirus: Advances, Barriers, and Implications for the Clinical Practice.

Human cytomegalovirus (hCMV) is one of the most common causes of congenital infection in the post-rubella era, representing a major public health concern. Although most cases are asymptomatic in the neonatal period, congenital CMV (cCMV) disease can result in permanent impairment of cognitive development and represents the leading cause of non-genetic sensorineural hearing loss. Moreover, even if hCMV mostly causes asymptomatic or pauci-symptomatic infections in immunocompetent hosts, it may lead to severe and life-threatening disease in immunocompromised patients. Since immunity reduces the severity of disease, in the last years, the development of an effective and safe hCMV vaccine has been of great interest to pharmacologic researchers. Both hCMV live vaccines—e.g., live-attenuated, chimeric, viral-based—and non-living ones—subunit, RNA-based, virus-like particles, plasmid-based DNA—have been investigated. Encouraging data are emerging from clinical trials, but a hCMV vaccine has not been licensed yet. Major difficulties in the development of a satisfactory vaccine include hCMV’s capacity to evade the immune response, unclear immune correlates for protection, low number of available animal models, and insufficient general awareness. Moreover, there is a need to determine which may be the best target populations for vaccine administration. The aim of the present paper is to examine the status of hCMV vaccines undergoing clinical trials and understand barriers limiting their development.

Concomitant procedures with early-onset scoliosis rib-based surgeries.

Retrospective cohort study. To determine if additional procedures can be safely performed under the same anesthesia as early-onset scoliosis (EOS) rib-based surgeries. EOS patients with rib-based implants often require repeated invasive surgery to treat their spinal deformity, with associated risks of cognitive development impairment from multiple anesthetic exposures. Many of these patients have comorbidities that require additional procedures, possibly increasing the risk of adverse outcomes. We performed a retrospective review of EOS patients treated with rib-based implants with at least 2year follow up at a single institution. Patients were divided into two cohorts: Group A included patients who never had another procedure in conjunction with a rib-based implant insertion, expansion, and/or revision surgery throughout their treatment and Group B included patients who had at least one other procedure operate in conjunction with rib-based implant surgery. Univariate analysis was performed to compare demographics, surgical parameters, and incidence of complication between the two groups. A subanalysis of patients who experienced an infection requiring surgery in Group A and Group B was also performed to further analyze the impact of concomitant procedures. 147 EOS patients underwent rib-based growing instrumentation at our institution. 98 patients (Group A) did not have another procedure occur under the same anesthetic as a rib-based implant surgery and 49 patients (Group B) had another procedure performed in conjunction with a rib-based implant surgery. Gender, etiology, BMI, length of follow up and number of rib-based implant procedures were similar between both cohorts (p = 0.91, 0.24, 0.28, 0.91, 0.77, respectively). The total surgical and anesthesia time was significantly longer in the patients undergoing concomitant procedures (Group B) (p < 0.0001, p < 0.0001, respectively). Among the patients in Group B, Otolaryngology was the most common department adding surgical care, followed by non-spine orthopaedics and general surgery. Mircrolaryngoscopy and bronchoscopy were performed most often (24 procedures), followed by cerumen removal under anesthesia (22 procedures), ear tube insertion (19 procedures) and bronchoscopy (19 procedures). Infection requiring irrigation and debridement was the most common complication found in both cohorts. Although Group B had a significantly lower number of patients who experienced complications (p = 0.002), the complication rate per procedure was 14% in Group A and 16% in Group B. When performing a subanalysis on patients who experienced an infection requiring irrigation and debridement surgery among Group A (47 patients) and Group B (8 patients), gender, etiology, BMI, length of follow up, and number of rib-based implant procedures were similar (p = 0.71, 0.26, 0.06, 0.69, 0.84 and, respectively). The total surgical and anesthesia time were similar (p = 0.11 and 0.13, respectively). In addition, the number of irrigation and debridement surgeries needed to treat each infection even was similar between the two groups (p = 0.59). There was no difference in complication rate per procedure when other services operate in conjunction with rib-based implant surgery. III.

Cytomegalovirus infection in pregnancy – An update

Cytomegalovirus (CMV) is a ubiquitous DNA virus with a global seroprevalence of 83 %. It is the most common pathogen causing teratogenic congenital infection. It is therefore a major public health concern. Maternal infection is associated with congenital CMV (cCMV), the leading cause of non-genetic sensorineural hearing loss. cCMV also causes impairment of cognitive development and cerebral palsy. Transmission of CMV occurs through direct contact with bodily fluids such as saliva, urine or semen from someone who is actively shedding the virus. Transmission rates are higher after primary infection with the rate of transmission increasing with gestational age. Severe fetal effects are however more common when infection occurs before 20weeks. Past infection does not confer immunity to mother or protect the fetus. cCMV may present with cerebral or extracerebral abnormalities on ultrasound, fetal growth restriction and fetal loss. Diagnosis of primary maternal CMV in pregnancy should be based on seroconversion in pregnancy (de novo appearance of virus‐specific immunoglobulin G (IgG) in the serum of pregnant women who were previously seronegative) or on detection of specific immunoglobulin M (IgM) and IgG antibodies in association with low IgG avidity. Prenatal diagnosis of fetal CMV is imperfect and based on amniocentesis performed at least 8 weeks after presumed maternal infection and after 17 weeks of gestation. Hygiene information and education of pregnant women is currently the most effective strategy for prevention of CMV infection. The role of vaccines, antiviral drugs and immunoglobulins remains unproven.

Intestinal parasitic infections in children under five in the Central Hospital of Nampula, Northern Mozambique.

Intestinal parasites are known to cause infection in humans worldwide, with higher prevalence in low- and middle- incoming countries. Children are greatly affected leading to malnutrition and subsequently to physical and cognitive development impairment. Despite the scale and importance of this issue, there are few studies conducted in Mozambique concerning parasitic intestinal infections in hospitalized children. To our knowledge this is the first published report with data on this subject from Northern Mozambique. A cross-sectional study was conducted in 2012 and 2013 in 831 children, attending the Central Hospital of Nampula in Northern Mozambique. One single stool sample was obtained from each child. Socio-demographic and clinical data were also obtained. Parasitological analysis of feces was performed through direct examination and Ritchie concentration technique and Giardia duodenalis antigen detection by rapid immunochromatographic test. Modified Ziehl-Neelsen staining was used for coccidia detection. The global prevalence of pathogenic intestinal parasites was 31.6%. G. duodenalis (23.9%) was by far the most prevalent parasite followed by Strongyloides stercoralis (4.1%) and Cryptosporidium sp. (3.4%). Intestinal parasites were more frequent in older children (p = 0.005; aOR = 1.025). This work is one of the few published studies reporting intestinal parasites infection in hospitalized children. The percentage of children affected with G. duodenalis is higher than found in other studies in the African region. This highlights the need of particular attention being given to this intestinal protozoan and its resistance to water treatment, as well as to environmental health and personal hygiene.

Cytomegalovirus in Pregnancy

AbstractHuman cytomegalovirus is worldwide the most common pathogen causing teratogenic congenital infection. Maternal cytomegalovirus (CMV) infection is a serious health concern as it is associated with severe birth defects like sensori-neural hearing loss, impairment of cognitive development and cerebral palsy. It is acquired by contact with body fluids and by vertical transmission from mother to fetus. Transmission rates are particularly high after primary infection of women. Unlike rubella infection, past infection with CMV and seropositivity at the time of conception does not confer protection to the fetus. The rate of transmission increases with period of gestation but the severity is more when an infection is transmitted to fetus before 20 weeks gestation. Congenital CMV (cCMV) infection may present as cerebral or extracerebral ultrasound abnormalities, fetal growth restriction and fetal loss. Hearing loss is the most common long term sequelae of cCMV infection accounting for about 25–30% of all cases of hearing loss in children in the US. Immunoglobulin G avidity testing is used to better define the timing of the infection in the mother. Invasive testing and ultrasound aid in the diagnosis of fetal infection. Hygiene information to pregnant women for prevention of CMV infection is currently the most effective preventive strategy. The role of vaccines, antiviral drugs and immunoglobulins is still not proven.

Traffic-related air pollution and childhood obesity in an Italian birth cohort

BackgroundAir pollution is associated with several adverse health outcomes in children, such as respiratory illnesses and cognitive development impairment. There are suggestions of an effect of traffic-related air pollution on the occurrence of childhood obesity, but the results are not consistent. ObjectivesThe aim of the study is to analyse whether air pollution and vehicular traffic exposure, during the first four years of life, influence obesity- related measures among 4 and 8-year-old children from a prospective birth cohort in Rome. MethodsA cohort of newborns, enrolled in 2003–2004 within the GASPII project, was followed at 4 and 8 years of age with parental interviews and clinical examinations. Air pollution was assessed at residential address using Land Use Regression models (for NO2, NOx, PM10, PM2.5, PMcoarse, PM2.5 absorbance and one traffic variable (Total traffic load of all roads in a 100m buffer)). The outcomes under study were body mass index (BMI Z-scores according to WHO recommendations, considered both categorical and continuous) measured at 4 and 8 years, and, waist circumference, waist-to-hip ratio, total and HDL cholesterol measured at 8 years. The associations were evaluated through both cross-sectional and longitudinal approaches, using logistic regression models, Generalized Estimating Equation models (GEE) and linear regression models, as appropriate. Moreover, Inverse Probability Weighting (IPW) methodology was used to account for selection bias at enrolment and at follow-up. ResultsA total of 719 infants were enrolled and 581 (80.8%) and 499 (69.4%) were followed at 4 and 8 years, respectively. The prevalence of overweight/obesity was 9.3% and 36.9% at 4 and 8 years. No evidence of an association was found between vehicular traffic and being overweight/obese. Similarly, there was no evidence of an association between exposure to air pollutants and all other ponderal excess parameters. ConclusionsThe study shows no association between exposure to vehicular traffic and exposure to pollutants on obesity related parameters such as BMI, blood lipids and abdominal adiposity during childhood. Overall evidence of air pollution being obesogenic remains limited.

Neonatal sepsis as a risk factor for neurodevelopmental changes in preterm infants with very low birth weight

Objectiveto evaluate neonatal sepsis as a risk factor for abnormal neuromotor and cognitive development in very low birth weight preterm infants at 12 months of corrected age. Methodsthis was a prospective cohort study that followed the neuromotor and cognitive development of 194 very low birth weight preterm infants discharged from a public neonatal intensive care unit. The Bayley Scale of Infant Development (second edition) at 12 months of corrected age was used. The outcomes were the results of the clinical/neurological evaluation and the scores of the psychomotor development index (PDI) and mental development index (MDI) of the Bayley Scale of Infant Development II. The association between neonatal sepsis and neuromotor development and between neonatal sepsis and cognitive development was verified by logistic regression analysis. Resultsmean birth weight was 1,119g (SD: 247) and mean gestational age was 29 weeks and 6 days (SD: 2). Approximately 44.3% (n=86) of the infants had neonatal sepsis and 40.7% (n=79) had abnormal neuromotor development and/or abnormal psychomotor development index (PDI<85) at 12 months of corrected age. On the mental scale, 76 (39.1%) children presented abnormal cognitive development (MDI<85). Children with neonatal sepsis were 2.5 times more likely to develop changes in neuromotor development (OR: 2.50; CI: 1.23-5.10). There was no association between neonatal sepsis and cognitive development impairment. Conclusionneonatal sepsis was an independent risk factor for neuromotor development impairment at 12 months of corrected age, but not for mental development impairment.

Neonatal sepsis as a risk factor for neurodevelopmental changes in preterm infants with very low birth weight

Objectiveto evaluate neonatal sepsis as a risk factor for abnormal neuromotor and cognitive development in very low birth weight preterm infants at 12 months of corrected age. Methodsthis was a prospective cohort study that followed the neuromotor and cognitive development of 194 very low birth weight preterm infants discharged from a public neonatal intensive care unit. The Bayley Scale of Infant Development (second edition) at 12 months of corrected age was used. The outcomes were the results of the clinical/neurological evaluation and the scores of the psychomotor development index (PDI) and mental development index (MDI) of the Bayley Scale of Infant Development II. The association between neonatal sepsis and neuromotor development and between neonatal sepsis and cognitive development was verified by logistic regression analysis. Resultsmean birth weight was 1,119g (SD: 247) and mean gestational age was 29 weeks and 6 days (SD: 2). Approximately 44.3%(n=86) of the infants had neonatal sepsis and 40.7% (n=79) had abnormal neuromotor development and/or abnormal psychomotor development index (PDI < 85) at 12 months of corrected age. On the mental scale, 76 (39.1%) children presented abnormal cognitive development (MDI<85). Children with neonatal sepsis were 2.5 times more likely to develop changes in neuromotor development (OR: 2.50; CI: 1.23‐5.10). There was no association between neonatal sepsis and cognitive development impairment. Conclusionneonatal sepsis was an independent risk factor for neuromotor development impairment at 12 months of corrected age, but not for mental development impairment.

The link between noise perception and quality of life in South Australia.

Environmental noise is a significant risk factor for a range of short- and long-term adverse health outcomes such as annoyance, cognitive development impairment, sleep disturbance, cardiovascular effects, and psychiatric problems. The aim of this study was to gather standardized quality of life (QOL) data hitherto rarely correlated with noise annoyance by source category. To provide an evidence-base for environmental noise policy development, a representative state-based survey was undertaken in South Australia (SA). A total of 3015 face-to-face interviews were conducted, using a questionnaire addressing noise sources, distances to busy roads and standardized measures of perceived annoyance and QOL. Population weighted descriptive survey and regression analysis. The most common sources of noise annoyances were road transport (27.7%, using a Likert scale, aggregating "little" to "extreme" annoyance), neighbors (22.0%), construction noise (10.0%), air conditioner noise (5.8%), rail transport noise (4.7%), and industry (3.9%). Using the QOL instrument, all eight health dimensions were significantly decreased for those reporting high noise annoyance ("very much" to "extreme") in relation to road transport and neighbors compared to those reporting low annoyance ("none" to "moderate") from these sources. Noise annoyance is common in the SA general population, and the evidence for a strong association with QOL reinforces the need for environmental noise management at a population basis.

Functional Implications of an Early Exposure to General Anesthesia: Are We Changing the Behavior of Our Children?

There is a rapidly growing body of animal and clinical evidence suggesting that the exposure to anesthetics and sedatives during the critical stages of brain development results in long-lasting (perhaps permanent) impairment in cognitive development in a variety of mammalian species. With improved understanding of the mechanisms responsible for behavioral outcomes of anesthesia-induced developmental neurotoxicity, there is hope for development of protective strategies that will enable safe use of anesthesia in the youngest members of our society. Here, I review presently available evidence regarding anesthesia-induced neurocognitive and social behavioral impairments and possible strategies for preventing them. I also review limited and somewhat controversial evidence that examines the effects of nociception and surgical stimulation on anesthesia--induced developmental neurotoxicity.

Retraction notice to “THE EFFECT OF MATERNAL INFECTION ON COGNITIVE DEVELOPMENT AND HIPPOCAMPUS NEURONAL APOPTOSIS, PROLIFERATION AND DIFFERENTIATION IN THE NEONATAL RATS” [Neuroscience 246 (2013) 422–434

Many epidemiological reports stated a strong association between maternal infection and development of cerebral palsy, which is a major cause of cognitive impairment. The pathophysiological mechanism of intrauterine inflammation is complex. Recently, it was demonstrated that inflammation has a modulating effect on adult neurogenesis. In this study, we discovered the effect of maternal infection to hippocampal neuronal apoptosis, proliferation and differentiation, and cognitive development in the developing brains of neonatal rats. Morris water maze test was used to assess learning and memory. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to determine neuronal apoptosis, immunostaining was conducted to assess neurogenesis, and Western blot for extracellular signal-regulated kinase (ERK), cyclic AMP responsive element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Results demonstrated that maternal infection increased neuronal apoptosis and significantly impaired spatial learning and memory ability. Maternal infection significantly increased cell proliferation, accompanied by an increased expression of ERK (P3-P7), CREB (P3-P7) and BDNF (P3). On P28, there was no significant difference of cell survival and differentiation in two groups. These results suggest that variation in ERK activity and subsequent expression of its downstream targets, including CREB and BDNF might contribute, at least partially, to modulation of inflammation related cell proliferation, survival and differentiation. Maternal infection increased hippocampal neuronal apoptosis and affected cell proliferation and differentiation in neonatal rats, which may be regarded as an etiological factor in cognitive development impairment.

Concomitant Plasmodium falciparum and intestinal helminth infections in a rural community of southern Côte d’lvoire

Background Despite efforts to control the disease, malaria is still threatening the life of millions of people in sub-Saharan Africa [1]. In addition the distribution of malaria often overlaps in space with so called neglected tropical diseases (NTDs). People in endemic areas can therefore host more than one parasite species infection at the same time, hence making polyparasitism a common phenomenon [2-4]. The consequences of these diseases are manifold and can include impairment of cognitive development and anemia, school aged-children and pregnant women representing the most vulnerable groups with particular risk of morbidity [4-6]. In Cote d’lvoire, these diseases are widely prevalent but vary in their spatial distribution and present different patterns of associations. Risk factors such as distance to water bodies and socio-economic status have been identified among the underlying causes for this heterogeneity [7,8] As a result of this heterogenous occurrence of multi-parasite infections related morbidity and burden due to polyparasitism will vary as well between areas. For control activities decision making usually takes place at global and/or national level but for integrated, cost-effective and sustainable control efforts better understanding of co-infection dynamics at different spatial scales are urgently needed. The main goal of this study was therefore to describe the pattern of concomitant infections with Plasmodium and intestinal helminths in a rural setting in southern Cote d’lvoire.

Pediatric Anesthesia Neurotoxicity

Through the years, care of millions of premature infants and young children has resulted in numerous exposures to a variety of anesthetic and sedative agents. These agents, designed to achieve the substantial depth of neuronal inhibition required for complete loss of consciousness and insensitivity to pain, are often a necessary component of successful treatment. However, data collected in animal models over the past decade suggest that general anesthetics damage developing neurons. Emerging animal and human data also suggest an association between early exposure to general anesthesia and long-term impairment of cognitive development. Consequently, the prudence of administering anesthesia to this population is now being scrutinized. Because general anesthesia cannot often be avoided when young children are diagnosed with conditions requiring surgery, or undergo time in intensive care units, the scientific community is focused on gaining a thorough understanding of the mechanisms of action so that we may take full advantage of the beneficial effects of anesthetics and sedatives without potentially devastating neurotoxic outcomes. A distinctive panel of speakers convened during SmartTots: Pediatric Anesthesia Neurotoxicity, a session at the 2011 International Anesthesia Research Society Annual Meeting, to provide an overview of 2 important lines of research. One focused on improving our knowledge of the cellular mechanisms operational in anesthetic-induced developmental neurotoxicity, and another focused on advancing our understanding of anesthesia-related neurobehavioral sequelae in mammalian species exposed to anesthesia during critical stages of brain development. Laszlo Vutskits, MD, PhD, University Hospitals of Geneva and Head, Neuroscience-oriented Anesthesia Research Group, University of Geneva, Switzerland, offered insight into recent experimental work demonstrating that general anesthetics have a major impact on the formation and elimination of synaptic contacts between neurons. The purpose of this presentation, “Beyond Toxicity: General Anesthetics and Synaptogenesis,” was to address (1) major neurodevelopmental events taking place during the brain growth spurt with a special emphasis on synaptogenesis, (2) the role of neural activity during neural network formation, and (3) how general anesthetics, being powerful modulators of neural activity, influence physiological patterns of synaptogenesis in a developmental stage–dependent manner. Vutskits reviewed basic neurobiological doctrines related to the brain growth spurt and recent observations suggesting that general anesthetics might stand as powerful regulators of synaptogenesis and thereby neural plasticity. Vutskits provided the following conclusions: (1) neural activity has a fundamental role during the assembly of the central nervous system; (2) functional properties of developing neural networks are fundamentally different between the early and late stage of the growth spurt, thus emphasizing the need for probing multiple time points; and (3) general anesthetics can rapidly induce developmental stage–dependent, persistent changes in synapse densities. Functional implications and significance of these conclusions remain unclear. Greg Stratmann, MD, PhD, Associate Professor of Clinical Anesthesia and Perioperative Care at the University of California, San Francisco, presented his research investigating whether anesthesia-induced cognitive decline is treatable. During his presentation, Stratmann discussed a conceptual framework of the neurocognitive deficit that may be caused by anesthesia in infancy, the concepts of prevention and treatment of anesthesia-induced neurocognitive decline, and the efficacy of an intervention designed to treat anesthesia-induced neurocognitive decline in rats. Stratmann reviewed his model for environmental enrichment and discussed his findings that the ill effects of anesthesia on brain function, which are apparent later in life, can be overcome when environmental enrichment is instituted up to 3 weeks after exposure to sevoflurane. These findings support the concept that harnessing the brain’s natural ability to adapt to functional demands can modify the course of anesthesia-induced cognitive decline in rats. He emphasized the need to understand if, and how, anesthesia changes brain function both in animals and in humans. Stratmann cautioned that clinical practice should not be changed until we are certain that a change is From the Departments of Anesthesiology and Neuroscience, University of Virginia Health System, Charlottesville, Virginia. Accepted for publication August 10, 2011. Supported by SmartTots. Conflict of Interest: See Disclosures at the end of the article. Reprints will not be available from the author. Address correspondence to Vesna Jevtovic-Todorovic, MD, PhD, MBA, University of Virginia Health System, Medical School/Steele Wing, PO Box 800710, Charlottesville, VA 22908. Address e-mail to VJ3W@hscmail. mcc.virginia.edu Copyright © 2011 International Anesthesia Research Society DOI: 10.1213/ANE.0b013e3182326622

Neuropsychological development in children with Dravet syndrome

Aim of this study is to report a detailed profile of neuropsychological development in children with Dravet syndrome. Twelve children with Dravet syndrome were longitudinally assessed using a detailed clinical and neuropsychological evaluation. Six had typical features of severe myoclonic epilepsy in infancy (SMEI) whereas the other six resulted borderline. All twelve underwent serial neuropsychological assessments with neurodevelopmental scales and further assessment of specific cognitive abilities. Our results reported an apparent normal development before disease onset, a general evolution in two main stages, more active the first one and with a general trend towards a clinical stabilization afterwards. The onset of cognitive decline was generally later than what is reported in other series; furthermore, the impairment of cognitive development is less severe, especially in borderline cases. As to specific cognitive competence, attention, visual motor integration, visual perception as well as executive functions are the most impaired abilities; language appears less involved, with a predominance of phonological defects. In our cohort the global development of patients appear less affected than in previous studies. Furthermore, our study points out an impairment of several specific cognitive skills even in patients with a developmental quotient apparently in the normal range. Language and other cognitive skill impairment such as attention, visuo-spatial organization, working memory and executive function appear consistent with what is usually found in cerebellar disorders.

Developing brain and general anesthesia -- is there a cause for concern?

Skilled management of sick premature babies and very young children has resulted in numerous exposures of their brains to a variety of anesthetic agents designed to achieve the substantial depth of neuronal inhibition required for complete loss of consciousness and insensitivity to pain. Unfortunately, our recent animal findings suggest that commonly used general anesthetics are damaging to developing neurons and cause significant neuronal deletion in vulnerable brain regions. In addition, emerging animal and human data suggest an association between early exposure to general anesthesia and long-term impairment of cognitive development. Consequently, the prudence of frequent anesthesia exposure of this population is now being scrutinized. It is important to note that on the basis of currently available information, there are still considerable differences of opinion regarding the clinical relevance of the animal findings. Since there is insufficient evidence establishing a clear association between animal and human findings, it would be premature to suggest major changes in current clinical practice.

Executive functioning impairments in premature children: Implications for neuropsychological research and classroom intervention.

Event Abstract Back to Event Executive functioning impairments in premature children: Implications for neuropsychological research and classroom intervention. Ashlee R. Loughan1* and Lauren A. Serpati2 1 Walden University, College of Social and Behavioral Sciences School of Psychology, United States 2 George Mason University, College of Education and Human Development, United States The premature birth rate has increased by 30 percent since the 1980’s, resulting in more than 500 thousand premature births annually [4]. Research indicates that preterm infants are at risk for persistent impairments in cognitive development [5],[6]. These impairments include executive functioning (EF) deficits, which subsequently result in learning challenges during the school years [1],[3]. Along with EF deficits, preterm birth also effects the structural development of the brain [2]. Recent MRI studies have linked prematurity with structural brain abnormalities including ventricular enlargement; white matter damage; thinning of the corpus callosum; delayed myelination; smaller basal ganglia, amygdala, and corpus collosum; along with decreased hippocampal formation [2],[5]. Educational research additionally reveals that most low birth weight children will at some point in their academic career receive special education services if not provided continuous assistance. As a result, an investigation identifying the relationship between EF deficits and the underpinning brain irregularities in preterm children is proposed. Determining the cognitive challenges of premature children at a young age is essential for their success in both school and beyond. More investigations correlating brain region impairments to EF may assist in predicting later cognitive obstacles. Thus, detecting precise abnormalities from birth might enhance psychologist and educator abilities to effectively develop early treatment interventions in those challenged by EF demands during the academic years. Researchers in both the fields of education and neuroscience are urged to inform themselves about this high-risk, yet marginally understood group, so that clinicians, teachers, and service providers can look to the future and effectively manage the EF deficits observed by this population in school settings.

The unacknowledged impact of chronic schistosomiasis

To summarize new knowledge on the range of disease due to chronic schistosomiasis and examine the debilitating burden of both light and heavy infection; to outline goals of disease prevention, including current age-targeted strategies and more extended programmes aimed at preventing transmission. A systematic search of 2004-2007 papers via PUBMED and related databases using 'schistosom' and disability- or treatment-related subject headings. Reports were independently reviewed for inclusion. Sixty-eight papers met review objectives. These suggest new evidence for a causative link between schistosome infection, antiparasite inflammation, and risk for anaemia, growth stunting and undernutrition in affected populations, as well as exacerbation of co-infections and impairment of cognitive development and work capacity. Formal quality-of-life assessment defines a significant 9.5-24% disability with the most aggressive schistosome species, Schistosoma japonicum. Schistosomiasis represents a serious but under-recognized disease burden for many developing countries. Infection (and not intensity of infection) should be considered the defining feature of morbidity formation. Links between infection and long-term disabilities reduce the chances of combating rural poverty. Changes in our appreciation of schistosomiasis-related disease burden means it is no longer appropriate to leave infected persons untreated, and newer approaches to control should focus on preventing transmission.