Neurological Impairment In Children Research Articles

Defining paediatric neurorehabilitation: You cannot improve what you cannot characterize.

Neurorehabilitation is the primary therapy for neurological impairment in children, yet its potential to achieve change remains incompletely understood and probably underestimated. Understanding 'the difference neurorehabilitation can make' against a background of neurological repair and recovery as well as ongoing neurological development is an enormous challenge, exacerbated to no small extent by the lack of a 'common currency' for the description and measurement of the neurorehabilitation services a child is receiving. This review addresses attempts to parse neurorehabilitation treatment content in theoretically and mechanistically valid ways that might help address this challenge.

Pre-term labour: A study on evaluation of causes and outcome.

Despite recent advances in medicine, the incidence of pre-term birth is increasing globally. Approximately 70% of neonatal deaths, 36% of infant deaths, and 25-50% of cases of neurological impairment in children can be attributed to pre-term births. Identification of risk factors in women, supervised obstetric care during pregnancy, female empowerment, and patient education are strategies to minimize the burden of preterm deliveries. A prospective cross-sectional study was conducted over a 1-year period among 658 women in the Department of Obstetrics and Gynecology, Pramukhswami Medical College, Anand, Gujarat. Detailed history, general, and obstetrical examinations were carried out. Maternal and foetal outcomes were noted. Statistical software STATA 14.2 was used for data analysis. The incidence of pre-term birth in our study was 34.95%. The incidence of late pre-term, very term, and extremely pre-term was 28.42%, 4.71%, and 1.82%, respectively. Pre-mature rupture of the membrane was observed among 20.34% of patients with late pre-term labour. IUGR was identified in 9.52% and 15.94% of the very and late pre-term births, respectively. A statistically significant difference was found in the 1 minute and 5 minute Apgar scores between pre-term babies and term babies. Pre-maturity is a huge health and financial burden in rural and semi-urban central Gujarat. Pre-mature rupture of membranes, previous MTP, extreme physical activity, and maternal anaemia were the major risk factors linked with pre-term labour. Poor neonatal outcomes like LBW, IUGR, and a low Apgar score were significantly associated with the babies delivered pre-mature in our study.

A Potential Mechanism of Neurological Impairment in Children With Infantile Spasm: Based on Microanatomic Structure Analysis Employing Voxel-Based Morphometry and Surface-Based Morphometry

BackgroundInfantile epileptic spasms syndrome (IESS) would accompany with severe neurological impairment. Our study aimed to explore the potential mechanism by employing voxel-based and surface-based morphometry to detect brain microwould accompany with severe neurological impairment. Our study aimed to explore the potential mechanism by employing voxel-based and surface-based morphometry to detect brain microanatomic structure alteration. MethodsThe IESS group had 21 males and 13 females (mean age: 17.7 ± 15.6 months), whereas the healthy controls group had 22 males and 10 females (mean age: 29.4 ± 18.7 months). High-resolution 3D T1WI was performed. Computational Anatomy Toolbox implemented in Statistical Parametric Mapping 12 was used to measure the gray matter and white matter volume, and the cortical thickness separately. Independent sample t test was used to assess between-group differences. IESS group was assessed using the Bayley Scales of Infant Development. ResultsThe IESS group showed a significantly decreased volume of gray matter in right middle temporal gyrus, inferior temporal gyrus, superior temporal gyrus, right fusiform, and bilateral precuneus (P < 0.001). There were no significant between-group differences with respect to white matter volume or cortical thickness (P > 0.001). The results of Bayley Scales of Infant Development showed that the Mental Development Index (MDI) and Psychomotor Development Index scores of children with IESS were almost concentrated in the range of <70. MDI score showed a positive correlation with gray matter reduction area in IESS group. ConclusionChildren with IESS had impaired cognitive and delayed motor development. And the decreased gray matter in the right temporal lobe, fusiform, and bilateral precuneus could be the potential anatomic basis for impaired function, such as hearing, visual, and language.

Uninstrumented fusion in cervical kyphosis due to neurofibromatosis type I: report of two paediatric cases.

Severe cervical kyphosis (CK) inneurofibromatosis type 1 (NF-1) is associated with a high risk for progression and neurologic impairment in children. We present our surgical technique and mid-term outcomes of uninstrumented anterior tibial strut grafting for severe CK secondary to NF-1. Case report. The Consensus-based Clinical Case Reporting Guideline Development (CARE) guidelines were followed. Two paediatric patients (8- and 3-year-old) presented with severe CK secondary to NF-1. A halo body jacket (HV) allowed the progressive distraction of the cervical spine, avoiding neurological compromise and deformity progression. Circumferential fusion was obtained with anterior tibial strut autograft and posterior onlay bone graft. Cervical spine fusion was successfully maintained at a minimum 4-year follow-up in both patients. In children with severe CK secondary to NF-1, cervical distraction and immobilisation with a HV followed by uninstrumented anterior tibial strut grafting and posterior bone grafting, provided spinal fusion and stability without increasing the risk of neurological injury and donor site morbidity. The reported surgical technique appears to be a valuable tool in thearmamentariumof the spinalsurgeon.

A follow up investigation of placental pathology, responsive parenting, and preschool children’s executive functioning and language development

ABSTRACT Despite documented effects linking underlying placental diseases and neurological impairments in children, little is known about the long-term effects of placental pathology on children’s neurocognitive outcomes. In addition, maternal responsivity, known to positively influence early postnatal cognitive development, may act to protect children from putative adverse effects of placental pathology. The current study is a follow up of medically healthy, term born, preschool age children, born with placental pathology. A sample of 118 children (45 comparison children with normal placental findings, 73 born with placental pathology) were followed when children were 3–4 years old. In comparison to children born to mothers with normal placentas, placental pathology was associated with poorer performance in the executive function involving cognitive flexibility, but not inhibitory control or receptive language. Maternal responsivity was observed to be marginally protective on the impact of placental pathology risk on cognitive flexibility, but this was not seen for either inhibitory control or receptive language.

Plasma GDNF levels in spinal dysraphism and its relation with neurological impairment in children: A point of care study

GDNF plays a crucial role in the stimulation of recovery, neuroplasticity and synaptic reorganization after spinal cord injury providing neuroprotection and neuroregeneration. Plasma GDNF levels are upregulated in cases of spina bifida owing to the intrauterine damage of the exposed spinal cord. Our aim was to compare the plasma GDNF levels in patients of spina bifida with non-spina bifida cases and assess the correlation with neurological impairment at one year of follow up. Single centre prospective analysis of cases of spina bifida from 2020 to 2022at presentation and after one year of follow up post-surgery. Cases with hernia and hydrocele without any other disorders were recruited into the control group. Plasma GDNF levels were assessed with immunoassay kits and compared with neurological involvement. 85 cases were included in the study. GDNF levels were elevated in cases compared to controls (mean 6.62 vs 1.76) with significant p value (<0.01). Same was observed for open and closed defects (mean 7.63 vs 4.86: p<0.01). At follow up of 52 cases post-surgery cases with neurogenic bladder with abnormal urodynamic studies, sphincter involvement and motor impairment had significantly elevated baseline levels of GDNF compared with those who did not have this neurological impairment (p<0.01). The neurotrophic factor up-regulation can reflect an endogenous attempt at neuroprotection against the biochemical and molecular cascades triggered by the spinal cord damage. This upregulation can be represented as important biochemical markers of severe spinal cord damage and can be associated with severity of spine injury in MMC patients. Our results are in keeping with these findings, that, there were increased levels of plasma GDNF levels in cases of spinal dysraphism compared to control population. Also, the type of lesion reflecting the severity whether a closed or an open dysraphism, showed significant difference in levels between them suggesting, yet again, more damage in open defect as expected. The levels were higher with involvement of bladder, sphincter and lower limb power. There is significant elevation of plasma GDNF levels in cases of spina bifida and this elevation is proportional to the degree of spinal damage and hence the neurological impairment. GDNF levels are a good predictor for assessing the severity of the lesion and thus the outcome in these cases. Additional prospective and long-term studies with a larger cohort are needed for a better understanding of neurotrophin pattern modulation in MMC.

Mesenchymal Stromal Cell Delivery Via Cardiopulmonary Bypass Provides Neuroprotection in a Juvenile Porcine Model

Oxidative/inflammatory stresses due to cardiopulmonary bypass (CPB) cause prolonged microglia activation and cortical dysmaturation, thereby contributing to neurodevelopmental impairments in children with congenital heart disease (CHD). This study found that delivery of mesenchymal stromal cells (MSCs) via CPB minimizes microglial activation and neuronal apoptosis, with subsequent improvement of cortical dysmaturation and behavioral alteration after neonatal cardiac surgery. Furthermore, transcriptomic analyses suggest that exosome-derived miRNAs may be the key drivers of suppressed apoptosis and STAT3-mediated microglial activation. Our findings demonstrate that MSC treatment during cardiac surgery has significant translational potential for improving cortical dysmaturation and neurological impairment in children with CHD.

Paediatric Society and Hyperinsulinism Charity National Surveys on CGM Access for Patients With Recurrent Hypoglycaemia.

Recurrent hypoglycemia can result in significant neurological impairments in children and continuous glucose monitoring (CGM) technology has been shown to reduce recurrent hypoglycemia in conditions such as type 1 diabetes. In the United Kingdom, CGM devices are currently only recommended by the National Institute of Clinical Excellence (NICE) for patients with diabetes and not for other diagnoses. To examine access to CGM technology for children and young people with recurrent hypoglycemia in the United Kingdom. In 2021, the British Society of Paediatric Endocrinology and Diabetes (BSPED) conducted a national health professional survey in England, Wales, Scotland, and Northern Ireland looking at CGM access to funding for children and young people with recurrent hypoglycemia, without the diagnosis of diabetes. The UK Children's Hyperinsulinism Charity (UK CHC) also conducted a national patient survey. Responses from BSPED were received from 55 units while the UK CHC received 69 responses from individual families, the largest response to a survey carried out by the charity. The results of the BSPED and UK CHC surveys found that funding streams for CGM were highly variable. Only 29% were able to access CGM for recurrent hypoglycemia and from these, 65% were self-funding CGM. Quality of life benefits were evident from the UK CHC survey on the utility of CGM in reducing worry, improving sleep, lessening the burden of frequently finger-pricking and reducing out-of-hours appointments as a result of hypoglycemia. Patient-reported utilization rates of blood glucose test strips per week were significantly reduced. BSPED and UK CHC national surveys support a call and a consideration for CGM access to be widened to patients who suffer from recurrent hypoglycemia such as those with hyperinsulinism or metabolic conditions. The prevention of recurrent hypoglycemia and improving quality of life for patients and carers remain a cornerstone management for people who suffer from frequent hypoglycemia. CGM education is critical to support its use and understand its limitations. Further research is warranted to determine the safety and efficacy of CGM in detection and reduction of hypoglycemic events, impact of hospital stay, and long-term neurological outcomes in those who suffer from recurrent hypoglceamia.

Hypothyroidism induces motor deficit via altered cerebellar HB-EGF/EGFR and autophagy.

Thyroid hormones (TH) are vital for brain functions, while TH deficiency, i.e. hypothyroidism, induces neurological impairment in children and adults. Cerebellar neuronal apoptosis and motor deficits are crucial events in hypothyroidism; however, the underlying mechanism is less-known. Using a methimazole-treated hypothyroidism rat model, we investigated cerebellar autophagy, growth factor, and apoptotic mechanisms that participate in motor functions. We first identified that methimazole up-regulated cerebellar autophagy, marked by enhanced LC3B-II, Beclin-1, ATG7, ATG5-12, p-AMPKα/AMPKα, and p62 degradation as well as reduced p-AKT/AKT, p-mTOR/mTOR, and p-ULK1/ULK1 in developing and young adult rats. We probed upstream effectors of this abnormal autophagy and detected a methimazole-induced reduction in cerebellar phospho-epidermal growth factor receptor (p-EGFR)/EGFR and heparin-binding EGF-like growth factor (HB-EGF). Here, while a thyroxine-induced TH replenishment alleviated autophagy process and restored HB-EGF/EGFR, HB-EGF treatment regulated AKT-mTOR and autophagy signaling in the cerebellum. Moreover, neurons of the rat cerebellum demonstrated this reduced HB-EGF-dependent increased autophagy in hypothyroidism. We further checked whether the above events were related to cerebellar neuronal apoptosis and motor functions. We detected that comparable to thyroxine, treatment with HB-EGF or autophagy inhibitor, 3-MA, reduced methimazole-induced decrease in Nissl staining and increase in c-Caspase-3 and TUNEL-+ve apoptotic count of cerebellar neurons. Additionally, 3-MA, HB-EGF, and thyroxine attenuated the methimazole-induced diminution in riding time on rota-rod and grip strength for the motor performance of rats. Overall, our study enlightens HB-EGF/EGFR-dependent autophagy mechanism as a key to cerebellar neuronal loss and functional impairments in developmental hypothyroidism, which may be inhibited by HB-EGF and 3-MA treatments, like thyroxine.

Plausibility of the combination of 17 α hydroxyprogesterone injection and Nifedipine versus Magnesium sulfate in the management of preterm labor, RCT

Background: Preterm birth is the leading cause of neonatal mortality and the most common reason for neonatal admission to the hospital. Although the causes of preterm labor are not well understood, the burden of preterm births is clear—preterm births account for approximately 70% of neonatal deaths and 36% of infant deaths as well as 25–50% of cases of long-term neurologic impairment in children. Objective: To compare the effectiveness of the tocolytic action of the standard protocol of Magnesium sulfate versus the combination of Nifedipine and 17 α hydroxyprogesterone injection in the term of acute tocolysis therapy on the perinatal outcome and to abrupt threatened preterm labor between 24 weeks to 33 weeks and 6 days. Patients and methods: A prospective randomized control trial study conducted at Zagazig Maternity Hospital, included 102 pregnant women who presented with threatened preterm labor at the Emergency Department of Zagazig University Maternity Hospital. The participants were divided into two groups, group (1) included 51 cases who received the standard protocol of Magnesium Sulfate: loading dose 4 g IV; maintenance 2 g/hr for 24 hrs.

Neurological impairment in children with acute liver failure following liver transplantation-A single-center experience.

Although overall survival of ALF has improved, neurological restoration after recovery from ALF may not always be satisfactory. The purpose of this study was to investigate the occurrence and possible causes of NI in children with ALF following LT. We retrospectively examined all children younger than 16years old with ALF who subsequently underwent LT at our center between January 2005 and December 2016. NI was assessed in December 2016 using the six-point Pediatric Cerebral Performance Category score and was defined as any increase in the score. There were 62 children with median age 10months (quartile range 5-34). The etiology of ALF was indeterminate in 47 children (75.8%). The median duration from admission to LT was 5.5days (quartile range 4-7), and 96.8% (60/62) received living donor LT. The overall survival was 83.9% (52/62) in a median follow-up period of 4.2years. Mild-to-moderate NI was observed in 23.1% (12/52) of the survivors. Possible causes of NI were underlying systemic disease (n=3), perioperative brain lesion (n=2), and unclassified (n=7). All seven patients with unclassified NI were less than 12months old. The unclassified NI causes were presumed to be ALF, its perioperative care, and the vulnerable infant brain. NI in children with ALF following LT was not rare and should be prevented. Further investigations are required to clarify the characteristics of the patients with unclassified NI.

Management and Outcome of Traumatic Intracerebral Hemorrhage in 79 Infants and Children from a Single Level 1 Trauma Center.

Objective: Traumatic brain injury is a leading form of pediatric trauma and a frequent cause of mortality and acquired neurological impairment in children. The aim of this study was to present the severity and outcomes of traumatic intracerebral bleeding in children and adolescence. Methods: Seventy-nine infants and children with intracerebral bleedings were treated between 1992 and 2020 at a single level 1 trauma center. Data regarding accident, treatment and outcomes were collected retrospectively. The Glasgow Outcome Scale was used to classify the outcome at hospital discharge and at follow-up visits. CT scans of the brain were classified according to the Rotterdam score. Results: In total, 41 (52%) patients with intracerebral bleedings were treated surgically, and 38 (48%) patients were treated conservatively; in 15% of the included patients, delayed surgery was necessary. Patients presenting multiple trauma (p < 0.04), higher ISS (p < 0.01), poor initial neurological status (p < 0.001) and a higher Rotterdamscore (p = 0.038) were significantly more often treated surgically. Eighty-three percent of patients were able to leave the hospital, and out of these patients, about 60% showed good recovery at the latest follow-up visit. Overall, 11 patients (14%) died. Conclusion: The findings in this study verified intracerebral bleeding as a rare but serious condition. Patients presenting with multiple traumas, higher initial ISS, poor initial neurological status and a higher Rotterdamscore were more likely treated by surgery. Trial registration: (researchregistry 2686).

Relationship Between Oxidative Stress, Tau Level and Antioxidant Mechanisms of the KEAP-1/NRF-2/HO-1 in Children with Hydrocephalus.

Hydrocephalus is a complex neurologic disorder that has a widespread impact on the central nervous system and a multifactor disease which affects the CSF dynamics and causes severe neurological impairments in children. The pathophysiology of hydrocephalus is not fully understood. However, increasing evidence suggests that oxidative stress may be an important factor in the pathogenesis of hydrocephalus. The purpose of this study is to investigate the relationship of the KEAP-1/NRF-2/HO-1 pathway, one of the main regulators of the antioxidant system in the hydrocephalus pathology, on oxidative stress and tau protein level. The study included 32 patients with hydrocephalus and 32 healthy controls. KEAP-1, NRF-2, HO-1, TAU, and MPO levels are measured using ELISA method TAS, TOS, and Total THIOL colorimetric method. KEAP-1, TAS, and Total THIOL levels were found significantly lowerer in the hydrocephalus group than in the control group. Nevertheless, it was identified that in the hydrocephalus group that the NRF-2, HO-1, TAU, MPO, TOS, and OSI levels were significantly elevated. In conclusion, although the KEAP-1/NRF-2/HO-1 pathway is activated in patients with hydrocephalus, it is identified that the antioxidant defense system is insufficient and ultimately leads to elevated oxidative stress. The elevation in the tau level may be an indicator of oxidative stress induced neurodegenerative damage.

Thermal Index for early non-invasive assessment of brain injury in newborns treated with therapeutic hypothermia: preliminary report

Perinatal asphyxia (PA) is the 3rd most common cause of neonatal death and one of the most common causes of severe neurological impairments in children. Current tools and measurements mainly based on the analysis of clinical evaluation and laboratory and electrophysiological tests do not give consistent data allowing to predict the severity of hypoxic-ischemic encephalopathy (HIE) until a magnetic resonance imaging (MRI) score is performed. The aim of this work is to evaluate the usefulness of the new index, called Thermal Index (TI) in the assessment of the degree of brain damage in newborns in the course of therapeutic hypothermia (TH) due to PA. This was a prospective, observational, pilot study which did not require any changes in the applicable procedures. Analysis has been applied to six newborn babies treated with TH in Neonatal/Paediatric ICU in University Hospital in Opole in 2018 due to PA. They all met criteria for TH according to the current recommendations. Brain MRI was performed after the end of TH when the children were brought back to normal temperature, with the use of a 1.5 T scanner, using T1-, T2-weighted images, fluid-attenuated inversion recovery (FLAIR), inversion recovery (IR), susceptibility-weighted imaging (SWI), and diffusion-weighted imaging (DWI). The images were assessed using MRI score according to the scoring system proposed by Weeke et al. The Thermal Index assessing endogenous heat production was calculated according to the formula proposed in this paper. A high, statistically significant positive correlation was found between MRI scores and TI values (0.98; p = 0.0003) in the 1st hour of therapy. High correlation with MRI assessment, the non-invasiveness of measurements and the availability of results within the first few hours of treatment, allow authors to propose the Thermal Index as a tool for early evaluating of the brain injury in newborns treated with TH. Further research is required to confirm the usefulness of the proposed method.

Abstract 16738: Association Between First and Second Trimester Maternal Screening Biochemistry, Ultrasound, and Fetal Brain Growth in Presence of Fetal or Maternal Congenital Heart Disease

Introduction: Newer research has highlighted significant neurological impairments in children and adults with congenital heart disease (CHD). The more severe the heart defect, the higher the neurologic impairment. Pregnancies complicated by fetal or maternal CHD carry a higher risk of placental abnormalities. We studied the association between pregnancy hormonal levels and fetal head and body growth. Hypothesis: Placental dysfunction in pregnancies with fetal or maternal CHD alters pregnancy hormonal levels affecting fetal brain and somatic growth. Methods: We performed a retrospective case-control study on pregnant women (year 2010-2019) at the University of Iowa. Only women with first and/or second trimester prenatal screening (ultrasound and blood test) were included. Pregnancies with fetal chromosomal abnormalities, multiple gestation, maternal diabetes, smoking, or hypertension were excluded. Pregnancies were either healthy controls (n=36), women with CHD (MCHD; n=26), or fetus with CHD (FCHD; n=23). Pregnancy hormonal levels, ultrasound findings, and fetal/neonatal growth percentiles and/or z-scores data were analyzed. Results: Women with CHD were younger (p=0.004) with increased fetal nuchal translucency (p=0.003) compared to controls. Women in MCHD (p=0.02) and FCHD (p=0.02) group delivered earlier than controls. FCHD had significantly lower pregnancy associated plasma protein-A (PAPP-A) levels than controls (p=0.04). The groups had no difference in the second trimester fetal head circumference (HC) and femur length. FCHD group had significantly smaller HC percentile (p=0.03) and z-scores (p=0.03) at birth than controls. Both FCHD and MCHD had smaller birth weight and length compared to controls. However, only FCHD group demonstrated significantly lower HC to birth weight ratio (p=0.01). The controls had a positive correlation between human chorionic gonadotropin level and head circumference z-score at birth (r=0.34;p=0.053). Conclusions: Pregnant women with CHD have increased fetal nuchal translucency and deliver at earlier gestational age. Women with fetal CHD have smaller neonatal head and body size at birth with associated low PAPP-A level early in their pregnancy probably related to placental dysfunction.

Zika Virus Infection Promotes Local Inflammation, Cell Adhesion Molecule Upregulation, and Leukocyte Recruitment at the Blood-Brain Barrier.

The blood-brain barrier (BBB) largely prevents toxins and pathogens from accessing the brain. Some viruses have the ability to cross this barrier and replicate in the central nervous system (CNS). Zika virus (ZIKV) was responsible in 2015 to 2016 for a major epidemic in South America and was associated in some cases with neurological impairments. Here, we characterized some of the mechanisms behind its neuroinvasion using an innovative in vitro human BBB model. ZIKV efficiently replicated, was released on the BBB parenchyma side, and triggered subtle modulation of BBB integrity as well as an upregulation of inflammatory and cell adhesion molecules (CAMs), which in turn favored leukocyte recruitment. Finally, we showed that ZIKV-infected mouse models displayed similar CAM upregulation and that soluble CAMs were increased in plasma samples from ZIKV-infected patients. Our observations suggest a complex interplay between ZIKV and the BBB, which may trigger local inflammation, leukocyte recruitment, and possible cerebral vasculature impairment.IMPORTANCE Zika virus (ZIKV) can be associated with neurological impairment in children and adults. To reach the central nervous system, viruses have to cross the blood-brain barrier (BBB), a multicellular system allowing a tight separation between the bloodstream and the brain. Here, we show that ZIKV infects cells of the BBB and triggers a subtle change in its permeability. Moreover, ZIKV infection leads to the production of inflammatory molecules known to modulate BBB integrity and participate in immune cell attraction. The virus also led to the upregulation of cellular adhesion molecules (CAMs), which in turn favored immune cell binding to the BBB and potentially increased infiltration into the brain. These results were also observed in a mouse model of ZIKV infection. Furthermore, plasma samples from ZIKV-infected patients displayed an increase in CAMs, suggesting that this mechanism could be involved in neuroinflammation triggered by ZIKV.

Regulation of Thyroid-disrupting Chemicals to Protect the Developing Brain.

Synthetic chemicals with endocrine disrupting properties are pervasive in the environment and are present in the bodies of humans and wildlife. As thyroid hormones (THs) control normal brain development, and maternal hypothyroxinemia is associated with neurological impairments in children, chemicals that interfere with TH signaling are of considerable concern for children's health. However, identifying thyroid-disrupting chemicals (TDCs) in vivo is largely based on measuring serum tetraiodothyronine in rats, which may be inadequate to assess TDCs with disparate mechanisms of action and insufficient to evaluate the potential neurotoxicity of TDCs. In this review 2 neurodevelopmental processes that are dependent on TH action are highlighted, neuronal migration and maturation of gamma amino butyric acid-ergic interneurons. We discuss how interruption of these processes by TDCs may contribute to abnormal brain circuitry following developmental TH insufficiency. Finally, we identify issues in evaluating the developmental neurotoxicity of TDCs and the strengths and limitations of current approaches designed to regulate them. It is clear that an enhanced understanding of how THs affect brain development will lead to refined toxicity testing, reducing uncertainty and improving our ability to protect children's health.

Management and outcome of traumatic subdural hematoma in 47infants and children from asingle center.

SummaryBackgroundTraumatic brain injury (TBI) is a frequent cause of mortality and acquired neurological impairment in children. It is hypothesized, that with the adequate treatment of SDH in children and adolescence, excellent clinical and functional outcomes can be achieved. The aim of this study was to present the severity and outcome of traumatic SDH in children and adolescence as well as to analyze differences between patients treated surgically and conservatively.MethodsIn this study 47 infants and children with a subdural hematoma (SDH) were treated between 1992 and 2010 at a single level-one trauma center. Data regarding accident, treatment and outcomes were collected retrospectively. To classify the outcomes the Glasgow outcome scale (GOS) scores at hospital discharge and at follow-up visits were used. Severity of SDH was classified according to the Rotterdam score.ResultsIn total, 47 cases were treated (21 surgically, 26 conservatively), with 10 patients needing delayed surgery. Overall, 89% of the patients were able to leave hospital, 5 patients died, 2 patients (5%) within 24 h, another 2 (5%) after 48 h and 1 (2%) within 7 days. In 25 patients (53%) a good recovery was recorded at the last follow-up visit. Outcome was mainly influenced by the following factors: age, severity of TBI, and neurological status. Overall, in 70% good clinical and neurological outcomes could be achieved.ConclusionThe results of this study confirmed that pediatric SDH is a rare, but serious condition. Despite a poor prognosis, most patients could be treated with good outcomes, given that the choice of treatment is correct.Trial registrationResearch registry 2686Electronic supplementary materialThe online version of this article (10.1007/s00508-020-01648-3) contains supplementary material, which is available to authorized users.

Behavioral and Biochemical Features of the Course and Surgical Treatment of Experimental Obstructive Hydrocephalus in Young Rats

Introduction: Hydrocephalus is a multifactorial disease, affecting the dynamics of cerebrospinal fluid (CSF) and leading to severe neurological impairment in children; in spite of the recent advances in hydrocephalus research, it has many physiopathological aspects that still remain poorly understood, especially after treatment. Objectives: To analyze the clinical, radiological, histopathological, and biochemical aspects of kaolin-induced hydrocephalus in an experimental model, both in the acute phase and after shunt treatment, by means of behavioral tests, magnetic resonance imaging (MRI) scans, histopathological studies, and level of inflammatory interleukins in the CSF. Methods: Seven-day-old Wistar rats were used and subdivided into three subgroups: treated hydrocephalic (n = 24), untreated hydrocephalic (n = 17), and controls (n = 5). The hydrocephalic groups underwent cisternal injection of 15% kaolin for induction of hydrocephalus at 7 days of age. The treated group was submitted to a ventricular-subcutaneous shunt (VSCS) 1 week after induction. All animals were euthanized at 21 days of age. They underwent motor function and memory testing as well as brain MRI scans. Histopathological analysis for glial fibrillary acidic protein and Ki-67 was done, and CSF was collected for measurement of IL-1β, IL-6, and TNF-α. Results: The average time to reach the water maze platform was highest in the untreated hydrocephalic group. The magnetization transfer rates were 37.21 and 33.76 before and after shunting, respectively. The mean astrocyte counts were 2.45, 1.36, and 90.5 for shunted, untreated, and control animals, respectively. The mean CSF IL-1β concentrations were 62.3 and 249.6 pg/mL, the average IL-6 levels were 104.2 and 364.7 pg/mL, and the average TNF-α values were 4.9 and 170.5 pg/mL for the treated hydrocephalic group and the untreated group, respectively. Conclusions: Pups treated with a CSF shunt showed better performance on memory tests. VSCS did not revert demyelination caused by hydrocephalus. Likewise, reactive astrocytosis and cell proliferation over the germinal matrix were not reversed after shunting. Hydrocephalic animals had raised levels of inflammatory interleukins, which returned to normal after treatment.

Mercury Levels in Women and Children from Interior Villages in Suriname, South America.

Natural sources of mercury, historical gold mining, and contemporary artisanal and small-scale gold mining (ASGM) activities have led to mercury contamination in Suriname. Our primary objective was to evaluate mercury levels in hair of women and children from interior villages in Suriname where mercury levels in fish are elevated. We also estimated blood levels of mercury using an established mathematical conversion to facilitate comparison with other biomonitoring programs in the United States. Estimated levels of mercury in the blood of participants from Suriname were significantly higher than those in women from a heavy marine fish-consuming population in southeast Louisiana and estimates of the US national average. This includes women from Surinamese villages well upstream of ASGM activities. Since residents in these areas rely heavily on local fish, this is likely the source of their exposure to mercury. The levels in hair are similar to those seen in women from longitudinal studies finding neurological impairments in children exposed pre- and postnatally. Additional biomonitoring and neurodevelopmental assessments are warranted in these areas, as well as other areas of the Suriname. Mercury levels in hair (Suriname) and blood (southeast LA USA) were determined using cold vapor atomic absorption spectroscopy (CVAAS).