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Slater, Rebeccah Louise Elizabeth Ann. "Cortical pain processing in the infant brain." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445109/.
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Premature infants are exposed to multiple invasive procedures as part of their essential medical care. It is not known, however, if nociceptive information is processed by the cortex at this age. The fundamental question to be addressed by this thesis is whether premature infants display cortical responses to noxious stimulation. This thesis describes a series of studies where the question of cortical pain processing is addressed by directly measuring cortical responses to noxious stimulation using near-infrared spectroscopy (NIRS) and electroencephalography (EEG). The NIRS results show that, following an acute noxious event, the contralateral somatosensory cortex is functionally activated in infants from 25 weeks postmenstrual age (PMA). Awake infants have a larger cortical response than asleep infants and, in the awake group, the size of the response increases with PMA. The magnitude of the haemodynamic response correlates with pain scores calculated using the premature infant pain profile (PIPP), although infants who do not display a change in facial expression can still process noxious stimuli at the cortical level. Latency to response is longest in the youngest infants using either the haemodynamic response or change in facial expression as an output measure. The underlying pain-related neuronal activity in the cortex has been investigated using EEG. Nociceptive-specific event related potentials have been observed in infants from 31-42 weeks PMA, with a recognisable N-P complex visible in the contralateral somatosensory cortex in 82% of studies. Noxious stimulation can evoke specific patterns of neural activity within the cortex of preterm and term infants that can be observed on a single-trial basis. The studies represent the first measurements of cortical activation in the immature preterm cortex following a noxious event. The fact that noxious information is transmitted to higher levels of the central nervous system highlights the importance of developing a systematic approach to reduce pain and improve analgesic strategies in this vulnerable population.
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Goksan, Sezgi. "Imaging nociceptive brain activity in the newborn infant." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:ea4d49fc-cf7e-4775-bb82-ddb3385cc2d9.
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In this thesis electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) are used to investigate the temporal and spatial patterns of noxious-evoked brain activity in newborn infants. EEG was used to investigate responses to graded intensities of experimental noxious stimulation, and evoked brain activity was compared with behavioural and spinal cord activity constituting common surrogate measures of pain in infants. Nociceptive-specific brain activity was elicited in response to all forces of experimental noxious stimulation (applied forces: 32 - 128 mN). In addition, the magnitude of the noxious-evoked response was positively correlated with the magnitude of reflex leg withdrawal, and this relationship was observed in the absence of changes in facial expression. As fMRI had not previously been used to investigate nociceptive processing in infants at 3 Tesla, initial experiments were conducted to optimise the acquisition parameters. The results from optimisation showed that an echo time of approximately 50 ms should be used in future fMRI studies in infants. Experiments conducted alongside this optimisation used fMRI to investigate the cortical and subcortical structures activated by experimental noxious stimulation (applied forces: 32 - 128 mN) in newborn infants (0 - 11 days old). This was compared with noxious-evoked brain activity in adults (applied forces: 32 - 512 mN). Experimental noxious stimulation evoked a widespread pattern of brain activity in newborn infants that overlapped with the network of brain regions activated by nociceptive processing in adults.
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Ambrose, Natalie Lauren. "Cell Death and Microglia in the Developing Brain." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/26157.
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Introduction: Sudden unexpected death in infancy (SUDI) is the leading cause of post-neonatal death in the developed world. SUDI has been sub-categorised into explained causes, such as motor vehicle accidents, drowning and known illness (eSUDI); or unexplained causes, which includes sudden infant death syndrome (SIDS) and undetermined causes of death. SIDS by definition is a diagnosis of exclusion, with the pathogenesis currently elusive with no clear pathological defining features. It has been shown that SIDS infants have multiple abnormalities within brainstem regions crucial to cardio-respiratory control with this proposed to contribute to their premature death, however the linking pathway(s) are yet to be identified. Thus, investigation of the neuropathological changes remains a critical pillar of SIDS research. Notably, increased cell death, beyond that required in normal physiological development, has been implicated in SIDS, with amassing evidence in the literature of apoptotic cell death in regions of the SIDS brain, most notably in the brainstem and hippocampus. To build upon this, this thesis aimed to extend the scope of brain regions examined in the context of cell death in eSUDI and SIDS cases. Furthermore, this thesis also focused on a new cell type of interest in SUDI, being microglia. The role of microglia in the context of central nervous system insult and disease is a rapidly evolving field of neuropathological research, however, to date, literature in the infant brain is limited (reviewed section 2.4.4). Overall, this thesis aimed to: firstly, examine the methods of classifying unexplained SUDI cases to standardise our dataset. Secondly, to investigate cell death marker expression, cell stress and apoptotic pathways, and microglia populations in the developing human brain, specifically to (i) identify variability amongst brain regions, (ii) variability between SUDI sub-groups, and (iii) the effects of intrinsic and extrinsic stimuli. Finally, to investigate the effects of intermittent hypercapnic hypoxia and nicotine exposure (two leading risk factor models of SIDS) in the developing piglet brain.
Methods: Both human (Chapters 3-6) and piglet (Chapter 7) brain tissue samples were utilised for this thesis. The primary method used was immunohistochemistry, with the distribution of cell death (active caspase-9, active caspase-3, TUNEL) and microglia (ionised calcium binding adaptor molecule-1 (Iba1), cluster of differentiation factor 68 (CD68) and human leukocyte antigen clone DR-DP-DQ (HLA)) marker expression explored amongst a broad range of brain regions. Human brain tissue was also investigated using a commercially available Cell Stress and Apoptosis Signalling Antibody Array to investigate 18 promoter, executioner, inhibitor and regulator proteins of the cell stress and apoptosis cascade.
Results: Of the SUDI cases collected 2008-2012, there was a high level of variation in the diagnostic classification of SIDS and undetermined, thus necessitating the convening of an expert panel to apply a standardised classification of unexplained SUDI, SIDS and its subgroups (Chapter 3). On examining the neurological tissue, regional heterogeneity in all cell death and microglia markers was observed within the developing infant brain. During the first year of life, less than 20% of all neurons are undergoing physiological apoptosis (Chapter 4), and microglia occupy less than 5% of the total area (Chapter 6) in any given brain region. Changes in SIDS brain tissue were region dependent, with the brainstem and amygdala identified as regions of interest in the context of cell death (Chapter 4); the temporal cortex in the context of promoters of cell stress and apoptosis (Chapter 5); and the hippocampus in regards to changes in microglial populations (Chapter 6). Changes predominated in SIDS II suggesting the observations are influenced by confounding risk factors. In the piglet brain, continuous nicotine exposure was not associated with any changes in microglia, however acute/sub-acute IHH mediated region-dependent changes, particularly in the hippocampus (Chapter 7).
Conclusion: The neuropathological findings from this work highlight that cell death and microglia markers are heterogeneously expressed in regions of the postnatal developing brain. Region-specific changes in the SIDS brain also have potential links to extrinsic stimuli, based on the findings in the piglet model. The brainstem, amygdala and broader temporal cortex are regions of interest in the context of SIDS and cell death, while the hippocampus is a region of interest in the context of microglia. This thesis provides a comprehensive analysis of microglial and cell death distribution and markers in the SIDS brain, contributing to our understanding of region-unique vulnerabilities. The results suggest new brain regions, and new markers of cell stress and apoptotic pathways, that can be targeted in future studies of the pathogenesis of SIDS.
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Williams, G. R. "Mapping touch and nociception in the human infant brain." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1398507/.
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Infants often experience clinically-essential painful procedures. The aim of this thesis was to measure, using functional magnetic resonance imaging (fMRI) and electroencephalography (EEG), activation patterns in the infant brain in response to noxious and non-noxious cutaneous stimulation. Using fMRI we assessed somatosensory and nociceptive circuitry in infants undergoing brush, three forces of von Frey, or pinprick stimulation of the foot. First we established optimum parameters and protocols specific for this study. Next, we characterised brain activity and somatotopy, and then considered modulation of activity related to stimulus intensity, stimulus modality, clinically-required sedation, age, and clinical background. Brain regions activated included primary and secondary somatosensory cortices, precuneus, insula, frontal, occipital, motor and cingulate cortices. Activations were somatotopic and di ered according to intensity, modality or clinical background. This is the first study to use fMRI to demonstrate brain activations in response to brush, von Frey hair and pinprick stimulation in human newborn infants. EEG recordings of lance in infants show a noxious-specific deflection at Cz which is not seen in adults undergoing experimental pain. To determine whether this di erence is due to age or stimulus modality we measured EEG activity to lance in healthy adult volunteers. Lance and innocuous tactile stimulations were applied to fifth finger beds, one of which was sensitised with mustard oil. Pain scores were recorded, and verbal descriptors were used to estimate peripheral fibre activation. EEG was compared to infant data collected in a previous study. Brain activity to lance in adults was di erent from control, and was modulated by sensitisation. EEG activity was related to pain score and verbal descriptors. The same stimulation initiated a distinct pattern of activity in infants which di ered from adults. This is the first study to characterise EEG responses to lance in adults, and to compare results with lance in newborn infants.
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Goodwin, James R. "Functional near-infrared spectroscopy of the adult and infant brain." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/99582/1/James_Goodwin_Thesis.pdf.
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The non-invasive technology, functional near-infrared spectroscopy (fNIRS) utilizes an array of channels consisting of sources and detectors positioned on the scalp to penetrate the head of adults and infants to measure brain activity. This thesis investigates the use of channels with short source-detector separations to reduce the interference of hemodynamics from the superficial layers. Results indicate such shallow measurements of the interferrant scalp hemodynamics can be subtracted from the deeper composite (superficial layers and cerebral) measurement to isolate and improve the brain signal. In addition, an optimized methodology was developed to acquire the best data yield for alert upright infants.
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Moukarzel, Sara. "The complexity of understanding human milk components and infant brain development." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/57297.
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Understanding which and how human milk components contribute to infant brain development is complicated in part by their large diversity, complex arrangement in the milk matrix and potential interaction in metabolism. This research addressed the importance of studying the composition of minor milk lipids and of exploring their relationship with non-lipid milk components in infant brain development. More specifically, the milk fat globule membrane (MFGM), a complex tri-layer of cholesterol, glycoproteins, and polar lipids including ethanolamine plasmalogens (Pls-PE), naturally emulsifies milk triacylglycerols but is not currently added to infant milk substitutes. Clinical evidence suggests MFGM plays a role in cognitive function. Whether MFGM directly affects the developing brain is unclear. Due to analytical challenges, little is known about the fatty acid composition of human MFGM lipids, particularly Pls-PE. Pls-PE may be enriched in long-chain polyunsaturated fatty acids (LC-PUFA) such as docosahexaenoic acid (DHA), an important neural lipid during development. Additionally, milk contains different forms of water-soluble choline (WSC) compounds (free choline, glycerophosphocholine, phosphocholine) for which distinct biological roles are unknown, although choline as a molecule per se is an important structural component of the brain and a precursor of the neurotransmitter acetylcholine. After developing an analytical method for separation and recovery of milk Pls-PE, the first study demonstrated both human and cow milk Pls-PE are enriched in LC-PUFA including DHA compared to other phospholipids. Milk Pls-PE DHA does not seem to vary with maternal DHA intake. Using artificially-reared infant rats, the second study showed that developmental brain phospholipids and metabolites differ between rats fed formula with or without MFGM, with a closer phospholipid composition to mother-reared rats in rats fed MFGM. By analyzing human preterm and term milk samples for WSC composition using mass spectrometry in the third study, we confirmed previous findings of the wide variability in WSC total content and composition in human milk and reported no significant association between individual WSC compounds. These studies provide new knowledge that milk contains novel components potentially relevant to the brain, and, while the mechanisms for improved cognition remain unclear, MFGM affects neonatal brain phospholipid composition.Land and Food Systems, Faculty of
Graduate
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Jamieson, Elizabeth Cherry. "Human brain lipid fatty acid composition in relation to infant diet." Thesis, Connect to e-thesis, 1998. http://theses.gla.ac.uk/981/.
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Thesis (Ph.D.) - University of Glasgow, 1998.Ph.D. thesis submitted to the Faculty of Medicine, University of Glasgow, 1998. Research carried out in the Departments of Pathological Biochemistry and Child Health, Royal Hospital for Sick Children, Yorkhill NHS Trust. Includes bibliographical references. Print version also available.
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Ball, Gareth. "Computational magnetic resonance image analysis of brain development in the preterm infant." Thesis, Imperial College London, 2011. https://kclpure.kcl.ac.uk/portal/en/theses/computational-magnetic-resonance-image-analysis-of-brain-development-in-the-preterm-infant(882d3802-c781-4171-8ce2-29ed1a8cc4d9).html.
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Currently 7-8% of all babies born in the UK are born preterm and the incidence has increased significantly over the past two decades. Improving medical care has led to increased survival in those born prematurely; however, preterm infants carry a profound risk of severe neurological disabilities along with a spectrum of major deficits across several domains including cognition, attention, coordination and behaviour. These wide-ranging and long-term consequences represent a significant burden to health and education services, yet the aetiology of the most prevalent cognitive and behavioural disorders remain unclear. Magnetic resonance imaging provides the means to quantitatively assess cerebral growth and development and is being increasingly employed to study the developing preterm brain. Evidence from neonatal imaging studies has revealed a number of specific cerebral alterations present in the preterm population that appear to predict neurodevelopmental outcome in early childhood and include diffuse microstructural disturbances of the developing white matter and regional volumetric tissue losses. In addition, a number of perinatal risk factors have been identified that are associated with both preterm birth and altered cerebral development. This thesis aims to test the hypothesis that connectivity and growth of developing neural systems are adversely affected by prematurity at birth and additionally influenced by specific perinatal risk factors. This is achieved through the application of multi-subject, multi-modal MRI analysis to quantify tissue microstructure and volume alongside novel methods for defining regional connectivity in the developing preterm brain. Evidence is provided that suggests connected neural structures are disturbed in preterm infants resulting in a complex pattern of regional micro- and macrostructural alteration that is evident at term-equivalent age and potentiated by respiratory morbidity. This is convergent with current theories of the mechanisms underpinning preterm brain injury and provides further insight into the consequences of preterm birth on brain development.
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Rutherford, Mary. "Magnetic resonance imaging of hypoxic-ischaemic brain lesions in the term infant." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262817.
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Boström, Kristina. "The cognitive and neurodevelopmental benefits of breastfeeding: : Nutrition or parent-infant interaction." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-9656.
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Breastfeeding is encouraged exclusively until the infant is 6 months and then continuing up until the age of two years and further, as a supplement to solid food. Few infants get this opportunity even though positive effects have been seen. In recent days brain imaging techniques has begun to study the differences in brain development between breastfed and formula fed infants. In this essay methods for assessing the cognitive and neurodevelopmental aspect of breastfeeding aspects will be reviewed. The results found in this review suggest that breastfeeding has a benefit in the development of the brain and in addition a beneficial impact on the parents. This can be seen in faster development of crucial brain areas, better cognitive functions and better maternal sensitivity which in turn relates to a child’s better adjustment. However, it is not clear how these benefits develop, if it is due to breastfeeding or parental characteristics related to breastfeeding.
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Bauer, Christopher Edward. "Associations between Sleep, Infant Feeding Methods, Brain Development and Behavior| A Multimodal Approach to Assess Plasticity in the Brain." Thesis, West Virginia University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10259351.
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Purpose: Sleep-disordered breathing (SDB) is a spectrum disorder that is estimated to effect a significant proportion of the pediatric population (1-3% in USA). SDB is able to disrupt and fragment sleep through frequent arousals and intermittent hypoxia. In addition, the long term effects of SDB in pediatrics have been well-documented; decreases in intelligence quotient (IQ), executive function, school performance, and alertness have all been observed. Although surgical treatments can be quite effective, there are no widely accepted prophylactic measures to prevent SDB development. Recently, breastfeeding duration in infancy has been demonstrated to be correlated with reduced SDB (lower AHI, RAI, and higher SpO2), as well as increases in IQ, executive function, and school performance (independent of SDB). The overarching goal of this dissertation was to examine the potential effects of both breastfeeding duration and SDB severity on the neurological underpinnings associated with observed behavioral and cognitive deficits; namely, correlations with white matter structural volume and fractional anisotropy (FA) scores through diffusion tensor imaging (DTI). Here, I proposed a unique developmental hypothesis where breastfeeding may ultimately reduce SDB, enabling the preservation of rapid eye movement (REM) sleep, and leading to healthier neurological white matter development.
Method: Twenty-four children with SDB and 19 healthy controls were imaged using MR techniques. White matter volume was measured using the central 13 millimeters of the corpus callosum (CC). DTI of major white matter tracts was also conducted. The SDB group received neurocognitive testing to assess cognitive performance; the control group was assessed using real-world academic report cards. Finally, REM sleep was quantified in infants using overnight polysomnography (PSG), with SDB metrics and infant feeding method also measured. Results: There was no correlation between infant feeding methods and CC volume in either group, nor a significant differences between CC volumes in children with SDB versus those without. However, increased breastfeeding duration was correlated with increased left superior longitudinal fasciculus (LSLF) and left angular bundle (LAB) FA scores in healthy controls. In 8-9 month old infants, increased breastfeeding duration was also correlated with a reduced proportion of REM sleep (%TST), and children with exclusive breastfeeding had reduced SDB in infancy compared to children with any formula feeding. Finally, exclusively formula-fed infants were diagnosed with “primary snoring” more often than those with any amount of breastfeeding.
Conclusions: The findings in this dissertation revealed associations between breastfeeding, SDB, REM sleep, and white matter integrity in the brain. These results support the hypothesis that certain cognitive effects associated with SDB and infant feeding methods may have common underlying anatomical brain changes that subserve these observed phenomena.
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Nyström, Pär. "From Motion to Movements : Revelations by the Infant EEG." Doctoral thesis, Uppsala University, Department of Psychology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9067.
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The introduction of high density EEG (hd-EEG) nets for easy application on subjects of all ages has improved the possibilities to investigate the development of the infant neurophysiology. This dissertation consists of three studies (I – III) that investigate the visual motion system and mirror neuron system of the infant, and methodological sections that outline the bioelectrical background and the characteristics of the methods used.
Study I covers the maturation of cortical areas involved in motion perception in adults and infants using an ERP paradigm. Over three age groups (2, 3 and 5 month olds) the cortical activation increased dramatically. All infant groups showed significant activation when moving displays was contrasted to static displays on a video screen. The study shows that 5-month-old infants and older can be expected to process motion in a similar fashion as adults.
Study II covers the infant mirror neuron system (MNS). In adults the mu rhythm perturbations is considered a reliable measure of activation of the MNS. This study presented both a mu rhythm analysis and a ERP analysis to detect MNS activity in 6-month-olds and in adults. This study concludes that the infant MNS can be measured using ERPs and that the development of mu rhythm perturbations requires further study.
Study III focused on exploring the mu rhythm suppressions. 8-month-olds observed a live actor that performed goal directed reaches and non-goal directed hand movements. The results show robust mu rhythm perturbations time-locked to the grasping moment. The study concluded that the MNS activity is possible to evaluate by analysis of mu rhythm perturbations and that the MNS show mature characteristics at the age of 8 months.
In summary, Study 2 and 3 present new methods to investigate the infant mirror neuron system and shows that the infant MNS is active at 6 months of age. At 8 months of age the infant MNS show mature EEG responses to simple actions such as reaching. How the MNS development relates to the infants’ motor development, and how the MNS interacts with the development of social skills requires further studies that could benefit from the methods presented here.
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Khorsandi, Mehdi. "Brainstem Gangliosides in Suddden Infant Death Syndrome." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc504326/.
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Recent studies have shown that the Sudden Infant Death Syndrome (SIDS) is related to abnormal control of respiration (Ischemic degeneration of the brainstem may play an important role in altered respiratory control leading to death). In our studies we have examined brainstem ganglioside compositions in samples derived from SIDS victims and appropriate controls. Gangliosides are acidic glycosphingolipids that contain sialic acid. The high concentration of gangliosides in the central nervous system (CNS) implies that these lipids play an important role in CNS function. Some studies have indicated that gangliosides may function as receptor site determinants or modifiers, and in neural transmission. In our studies we used the Tettamanti, et al methodology to extract gangliosides, and High Performance Thin Layer Chromatography (HPTLC) and laser densitometry techniques for ganglioside analysis. The results of these analyses are being employed to establish lipid profile patterns to determine if there are significant variations in these lipid patterns between SIDS and control groups.
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MacFarlane, Hood Bruce. "Development of visual selective attention." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387062.
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Stets, Manuela. "Improving tools for the analysis of brain based measures of infant information processing." Thesis, Durham University, 2012. http://etheses.dur.ac.uk/6922/.
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While current methodological approaches to data-acquisition and -analysis used in ERP-studies have shown to be appropriate for adult populations, their applicability with infant populations is debatable. Many researchers agree that they are, in fact, unsuitable for infants. However, due to a lack of alternatives, traditional ways of data-collection and -analysis originally designed for adults are still used with developmental and clinical populations. The four studies reported in the current thesis propose novel approaches to methodological issues involved in infant ERP-studies. Limiting the number of artefact-free trials included in the average, Study 1 shows that fewer trials from earlier stages of a test-session can convey meaningful information and provide new insights into infant cognition. Additionally, it is shown that large amounts of usable data are often discarded in a traditional data-analysis. Study 2 aimed to provide a general overview on attrition in infant ERP-studies – which often seems to be accepted as a given among developmental psychologists – and to find underlying causes for attrition which may be based on study-design features that are common to all studies. The majority of investigated features did not impact attrition. Therefore, further factors outside the scope of the current consideration are responsible for an increase in attrition. Studies 3 and 4 built on the findings of the first two. Presenting infants with eight experimental conditions, Study 3 illustrates a novel approach to study-design which both yielded more data from individual participants and decreased attrition. Finally, using the data-analysis outlined in Study 1 on the data collected for Study 3, Study 4 both substantiates the claims made in Study 1 and provides further, previously unanticipated insights into infant cognition. These findings illustrate that more infant-suitable strategies for study-design and data-analysis are possible and that they can enhance our knowledge about infant cognitive processes.
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Salvan, Piergiorgio. "A neuroimaging study of the neural language network in the preterm infant brain." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/a-neuroimaging-study-of-the-neural-language-network-in-the-preterm-infant-brain(73f7259e-6d60-40b3-9c92-2cfbb00a2331).html.
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Language is uniquely human, and represents a fundamental feature of human cognition. However, whether the brain’s language network is already present around time of normal birth, or emerges in parallel with the behavioural development of this cognitive function during childhood, remains unclear. Preterm children are at increased risk for cognitive, language, and behavioural impairment. Studying preterm born infants at the time of normal birth therefore represents an opportunity to test hypotheses regarding the ontogeny of the language brain network, and to shed new light on how premature environmental exposure may affect the emergence of neurolinguistic architecture. Non-invasive in-vivo magnetic resonance imaging represents a powerful tool with which to study quantitatively the developing human brain. Previous neuroimaging studies have shown the presence around the time of normal birth of functional neural correlates of auditory speech processing, suggesting the presence of organized brain architecture at term. Current evidence also suggests that the human brain is particularly sensitive to developmental disruption occurring during the last trimester of gestation, with premature delivery having a long lasting signature on whole-brain architecture and later neurodevelopment. This thesis aims to 1) test the hypothesis that an adult-like brain language network is already present at the time of normal birth and is linked to cognitive performance at two years; 2) assess the effect of early environmental exposure linked to the degree of prematurity at birth in the relationship between brain and behaviour. Evidence is provided for the presence at term-equivalent age of adult-like functional/structural language brain features, linked to linguistic and cognitive abilities developed in early childhood, and independent of premature environmental exposure. This is consistent with the idea that neurolinguistic development is strongly constrained by brain maturation, and depends on the interplay between an initial genetic endowment, driving brain development, and interactions in a favourable socioeconomic environment.
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Bartocci, Marco. "Brain functional near infrared spectroscopy in human infants : cerebral cortical haemodynamics coupled to neuronal activation in response to sensory stimulation /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-034-6/.
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Morasch, Katherine Colona. "Explicit Memory and Brain-Electrical Activity in 10-month-old Infants." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/27065.
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One of the most intriguing and enduring issues in contemporary developmental cognitive neuroscience centers on the development of the ability to remember past experiences and the neural systems which support this capacity. Over the past 25 years, through methodological advancements and direct challenges to established assumptions, the focus of this developmental question has shifted to highlight the second half of the first year of life as the time when true explicit memory functionally emerges and begins to rapidly develop. The purpose of the following study was to test specific hypotheses regarding the biobehavioral development of explicit memory during infancy and present a new approach to studying the behavioral and physiological expression of this system. This study, which was guided by hypothesized neural substrates of this memory system, is the first direct investigation of continuous brain electrical activity during both the encoding and retrieval phases of explicit memory processing in infants. Memory-related differences in behavior and task-related brain activity in individual cortical areas were of particular interest.
The results of this study provided some support for the hypothesis that baseline-to-task changes in EEG power can distinguish between successful and unsuccessful ordered-recall memory. Specifically, decreases in brain-electrical activity relative to a baseline period were found at both frontal and temporal locations during stimulus encoding and retrieval for infants who failed the recall tests. However, either no change, or increases in EEG power at frontal and temporal sites was related to successful performance on this task. In addition, different patterns of brain-electrical activity were present for correct and incorrect responses from the same child.
This study contributes to our understanding of the biobehavioral expression of infant explicit memory in three main ways. First, changes in both frontal and temporal lobe activity are directly involved in explicit memory processing both during event encoding as well as retrieval. Second, this work provides evidence of a developmentally appropriate and valid pattern of electrophysiology specific to explicit memory processing. Finally, this study bridges the gap between a classic behavioral task of infant memory (which has been conceptually linked to neuropsychological data) and current developmental cognitive neuroscience.Ph. D.
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Kendal-Reed, Martin Stuart. "Human infant olfaction : responses to food odours measured by brain electrical activity mapping (B.E.A.M.)." Thesis, University of Warwick, 1990. http://wrap.warwick.ac.uk/91144/.
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This thesis addresses the area of human infant olfaction, which has hitherto been a somewhat neglected area in psychology. A review of the available literature showed that a number of different experimental approaches to infant olfaction could be identified. It was concluded from this literature review that infants display a degree of olfactory competence in the weeks after birth. These previous findings are discussed in the light of a model concerned with odour significance. This model is systems-based and suggests an explanation for the apparent olfactory competence of human infants in the first weeks of life. It is argued that this may derive from pre-natal exposure to odorants and consequent acceleration of maturation in the foetal olfactory system. The experiments reported in this thesis concentrated on the cortical reactions of infants to a small range food odours. These reactions were plotted by means of a technique involving electro-encephalography. This technique involves a computerised imaging system which summarises cortical potentials from twenty-eight locations on the scalp and is known as Brain Electrical Activity Mapping (BEAM). It is believed that this is the first time that this method has been used to examine responses to odour in human infants. This study also involved the use of a special low ambient odour testing environment. A parallel study used respiratory plethysmography to test odour response. The major findings of the BEAM research are as follows: 1) The BEAM technique has been shown to be a practical method in the psychophysical measurement of cortical responses to odour in the human infant. 2) Human infants at the age of three months show a pattern of cortical activity in response to a small range of food odours. 3) There is evidence that a limited area of the infant brain is responding to these odours. It was argued that these findings lent some support to the model described above. However, similar findings to that of the BEAM work were not shown by the respiratory plethysmography study. This was explained by problems in data handling techniques. It was concluded that the BEAM method could be used to further knowledge in the area of infant olfactory response. Possible improvements to the experimental technique were discussed which would allow testing of infant response to maternal odour. Such future work could shed considerable light on the role of olfaction in the early infant-mother relationship.
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Young, Katherine S. "Adults' responses to infant vocalisations : a neurobehavioural investigation." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:6f91f1ae-0948-4b34-b45f-ee65ae421934.
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Infant vocalisations are uniquely salient sounds in the environment. They universally attract attention and compel the listener to respond with speed and care. They provide a wealth of information to parents about their infant’s needs and affective state. There is a scientific consensus that early parenting has a profound impact on child development. In particular, the sensitivity with which parents respond to their infant’s communicative cues has been shown to affect cognitive and socio-emotional outcomes. The mechanisms underlying such sensitivity are not well understood. In this thesis, adults’ sensitivity to infant cues will be considered in terms of two components, the ‘promptness’ and ‘appropriateness’ of responses, as originally conceptualised by Bell and Ainsworth (1972). Promptness of responses is considered in terms of adults’ ability to move with speed and effort after listening to infant vocalisations. Appropriateness, on the other hand, is considered in terms of adults’ ability to differentiate between functionally significant parameters in infant vocalisations. The effect of modifiable environmental factors on the promptness and appropriateness of responses is also investigated. Finally, a focused investigation of the brain basis of responses to infant vocalisations is presented. Overall, findings demonstrated that infant vocalisations undergo privileged, specialised processing in the adult brain. After hearing an infant cry, adults with and without depression were found to move with greater coordination and effort. Adults were also found to be attuned to subtle parameters in infant cries. This sensitivity was shown to be affected by two participant-level factors, depression and previous musical training. Furthermore, this sensitivity could be enhanced through intervention, as evidenced by findings from short-term, perceptual discrimination training. The notion of privileged processing of infant vocalisations is further supported by evidence of early discrimination of infant sounds in a survival-related subcortical brain structure. Future directions for this work include directly relating current experimental measures of adults’ responses to infant cues with parental sensitivity to infant communication during dynamic interactions. Translating current findings into applied settings would require an investigation of the effects of factors such as musical and perceptual training on sensitivity to infant cues in at-risk populations, such as mothers and fathers with depression. Lastly, an increased understanding of the brain basis of adults’ sensitivity to infant cues will provide insight into our greatest challenge: parenting our young.
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Ansari, Tahera Iqbal. "Stereological analysis of SIDS-linked micro-anatomical anomalies in specific regions of the brain, phrenic nerve and diaphragm." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266251.
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Pote, Inês. "Fetal and infant brain development in individuals with and without a familial risk of autism spectrum disorder." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/fetal-and-infant-brain-development-in-individuals-with-and-without-a-familial-risk-of-autism-spectrum-disorder(bc5caf2a-f0f4-47be-9699-ed2eb57ee934).html.
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There is currently very little known about early brain development; even less about how normal development may be disrupted in individuals genetically predisposed to neurodevelopmental conditions, including autism spectrum disorder (ASD). Hence, by using magnetic resonance imaging (MRI) to examine the structure and chemistry of the fetal, neonatal, and infant human brain, my intention was to provide further insight into early neurodevelopment. The additional focus on individuals with a familial risk of ASD, also aimed to detect any potential deviations from typical brain development that may be associated with an ASD risk status. The first experimental study of this thesis used MRI at 1.5T to reveal that the early environment – specifically, mother-infant interactions – is associated with variations in brain biology, within a sample of assumed-to-be typically developing individuals. Therefore, the next study, which compared brain volume in infants with and without a familial risk of ASD also incorporated measures of mother-infant interactions. In this second study, subcortical and cerebellar enlargements were identified in 4-6 month-old infants at risk of ASD, and larger volumes were associated with more autistic symptoms at 36 months. Within the high-risk group, a higher measure of maternal sensitivity was correlated with lower subcortical brain volumes. Next, to examine even earlier development and to estimate when differences between risk groups might first appear, fetuses and neonates with and without a familial risk of ASD were scanned using advanced MRI protocols at 3T. At both these timepoints, the cortex and cerebellum were identified as the fastest growing brain regions. In addition, fetuses at risk of ASD had smaller cortical volumes when compared to low-risk controls. Postnatally, within the first month of life, neonates at risk of ASD also had smaller intracranial and total brain volumes, as well as a smaller lentiform nucleus. Placed together with the infant findings, these studies suggest that an ASD genetic risk constrains brain growth in the perinatal period, but is associated with volumetric expansion of both subcortical and cerebellar regions in infancy. The subcortical region also appeared to be particularly affected by the abnormal growth trajectory of high-risk participants, as differences in this region were observed amongst high-risk individuals at both neonatal and infant timepoints. The subcortex was therefore selected as a region-of-interest in the final study, which mapped metabolic maturation from fetal to early postnatal life using magnetic resonance spectroscopy. In both low and high-risk groups, choline and myo-inositol decreased significantly with age, whilst N-acetylaspartate and creatine increased. In contrast, glutamate (measured as glutamate and glutamine; Glx) decreased from fetal to neonatal life, with a marked ‘dip’ around the time of birth before increasing in early infancy. The sample size at the 4-6 month timepoint also permitted an explicit comparison of low and high-risk infants, and because previous studies of older cohorts have linked glutamate abnormalities to ASD, Glx levels were compared between groups. The results showed, for the first time, that high-risk infants have significantly elevated levels of Glx at 4-6 months of age, when compared to low-risk controls. In conclusion, both the volume and biochemistry of the human brain undergoes rapid change in the late prenatal and early postnatal periods. Moreover, individuals with a familial risk of ASD already show differences in brain maturation from fetal life, including neurochemical pathways modulating the balance of neuronal excitation and inhibition. This is well before the onset of autistic symptoms, and therefore, has important implications for ASD in terms of risk (and resilience) pathways.
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Telford, Emma Jane. "The effect of preterm birth on white matter tracts and infant cognition." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/29557.
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Preterm birth (defined as birth before 37 weeks) is a leading cause of neurocognitive impairment in childhood, including difficulties in social cognition and executive function. Microstructural divergence from typical brain development in the preterm brain can be quantified using diffusion magnetic resonance imaging (dMRI) tractography during the neonatal period. The relationship between dMRI tractography metrics and later cognitive difficulties remains inconclusive. A general measure of white matter microstructure (gWM) offers a neural basis for cognitive processes in adults, however it remains unclear when gWM is first detectable in the developmental trajectory. Eye-tracking is a technique which assesses eye-gaze behaviour in response to visual stimuli, which permits inference about underlying cognitive processes, such as social cognition and executive function in infancy. The primary aims of this thesis were to test the hypotheses: dMRI tractography reveals significant differences in tract-average fractional anisotropy (FA) and mean diffusivity (MD) between preterm and term infants, and variance in tract-average FA and MD is shared across major tracts. Secondly, infants born preterm have altered social cognition and executive function compared to term born peers, assessed by eye-tracking and finally, neonatal MRI gWM is associated with cognitive function in infancy. Preterm (birth weight ≤ 1500g) and term infants (born ≥ 37 weeks’ post-menstrual age [PMA]) were recruited and underwent a MRI scan at term equivalent age (between 38 - 42 weeks’ PMA) and an eye-tracking assessment six to nine months later. Preterm infants were assessed at two years using the Bayley Scales of Infant and Toddler Development, Third Edition (BSID-III). dMRI tractography metrics were generated using probabilistic neighbourhood tractography (PNT) in eight pre-defined tracts-of-interest. Principal component analyses (PCA) were used to determine the correlations between the eight tracts-of-interest for four tract-averaged water diffusion parameters. dMRI metrics were compared to the eye-tracking performance and two year outcome data. Quantitative microstructural changes were identifiable within the preterm brain when compared to infants born at term. PCA revealed a single variable that accounts for nearly 50% of shared variance between tracts-of-interest, and all tracts showed positive loadings. Eye-tracking revealed group-wise differences in infant social cognition, attributable to preterm birth, but executive functions inferred from eye-tracking did not differ between groups. dMRI tractography metrics within the neonatal period did not relate to later outcome measures. This thesis shows that variance in dMRI parameters is substantially shared across white matter tracts of the developing brain and suggests that anatomical foundations of later intelligence are present by term equivalent age. Social cognition is altered by preterm birth, however social cognitive ability in infancy is independent of gWM.
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Morelen, Diana, and Michelle Moser. "Infant Mental Health and Diversity: Working Through the Lens of Development, Relationships, and Culture." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7693.
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Oquendo, Javier. "Elemental Analysis of Brainstem in Victims of Sudden Infant Death Syndrome." Thesis, University of North Texas, 1988. https://digital.library.unt.edu/ark:/67531/metadc500370/.
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A brainstem-related abnormality in respiratory control appears to be one of the most compelling mechanisms for sudden infant death syndrome (SIDS). The elements calcium, copper, iron, potassium, magnesium, sodium, phosphorus, sulfur, and zinc were analyzed by inductively coupled plasma atomic emission spectroscopy in the brainstem of 30 infants who died from SIDS and 10 infants who died from other causes (control). No differences were found between SIDS and control for any element except for more calcium in the SIDS group. A multivariate analysis of the data failed to group the majority of SIDS and control subjects in different clusters. Further research is required to determine the biological significance of the higher calcium found in the SIDS group.,
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Andersen, Danielle Louise. "Development of neurotransmitter receptors in the human brain and vulnerability to perinatal asphyxia and sudden infant death syndrome /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17412.pdf.
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Ng, Sze May. "Thyroid function in the extremely premature infant : effects on brain, growth and interactions with the hypothalmic-pituitary-adrenal axis." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533971.
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Vivekanandarajah, Arunnjah. "Cigarette smoke exposure and hypoxic effects on the expression of nicotinic acetylcholine receptors and apoptosis in the developing brain." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/16735.
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Introduction: Cigarette smoke exposure (CSE) during pregnancy and postpartum poses a significant threat to the infant’s health, such as respiratory and ear infections, cognitive deficits, as well as an increased risk for sudden infant death syndrome (SIDS). Nicotine, the major neurotoxic agent from cigarette smoke induces its action by binding to nicotinic acetylcholine receptors (nAChRs) with one downstream consequence being increased cell death (apoptosis). Further, recent studies on the structural abnormalities in the SIDS hippocampus interested us to study the proinflammatory cytokine, IL-1b. The objectives of the thesis were to determine the alterations in expression of nAChRs and apoptotic markers (active caspase-3 (Casp-3) and TUNEL) in the hippocampus and brainstem following: a) CSE in mice, b) postnatal nicotine exposure alone or in combination with c) intermittent hypercapnic hypoxia (IHH) (acute vs repeated) in piglets, and d) in the human infant hippocampus and determine any changes according to the diagnosis of SIDS, and the presence of the risk factors of CSE and prone sleeping. Methods: nAChR subunits and IL-1b expression were determined using single immunohistochemistry (IHC), apoptotic makers (Casp-3 and TUNEL) were determined using double IHC labelling on formalin fixed paraffin embedded tissue. Results: Pre- into post-natal CSE led to alterations in nAChR subunits with simultaneous changes in apoptotic markers in mice, postnatal nicotine affected the nAChRs more severely in the brainstem than hippocampus with predominant changes being for the a3 and b1 subunits, which were also more sensitive to pre- into post-natal CSE. Repeated IHH induced much more alterations in nAChRs (predominantly the a2b2 complex) than acute IHH in both the hippocampus and brainstem medulla. SIDS infants exhibited higher TUNEL in the subiculum which was associated with CSE, higher IL-1b in the CA1 region which was associated with prone sleeping position, and lower a7 expression in the dentate gyrus and CA4. Conclusion: Alterations in the expression of nAChR subunits due to CSE, nicotine and hypoxia, are evident in the developing hippocampus and brainstem, and were associated with increased apoptosis in a region specific manner. These results provide an indication of the mechanism(s) via which CSE to an infant affects the nAChRs in the brain and the need to continue with the health campaign advising against CSE.
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Riedel, Anett [Verfasser], and Anna Katharina [Akademischer Betreuer] Braun. ""Differential metabolic recruitment of cognitive, emotional and modulatory brain regions in infant and adolescent rats undergoing two-way active avoidance training" / Anett Riedel. Betreuer: Anna Katharina Braun." Magdeburg : Universitätsbibliothek, 2011. http://d-nb.info/1047561808/34.
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Missana, Manuela [Verfasser], and Tobias [Akademischer Betreuer] Grossmann. "Infant Processing of Emotional Faces and Bodies: Insights from Event-related Potentials and Asymmetrical Frontal Brain Activity / Manuela Missana ; Betreuer: Tobias Grossmann." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://d-nb.info/118050271X/34.
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Paradiso, Beatrice. "The brain beating and heart breathing: a unifying theory of the neuro- cardiac- respiratory control in infant and adult sudden unexpected deaths." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3427309.
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Background: Sudden Infant Death Syndrome (SIDS) is characterized by the death of an infant that cannot be explained, despite a systematic case examination, including death scene investigation, autopsy and review of the clinical history.
Nowadays, Sudden Unexpected Infant Death (SUID) is a wide-ranging concept used to describe any sudden and unexpected death, whether explained or unexplained, including SIDS, which occurs during the first year of life. Several differing and sometimes contradictory hypotheses of the underlying mechanisms of SIDS have been proposed. The most reliable seems to be the “triple risk hypothesis”. Based on this theory, unexpected infant deaths might arise as a consequence of the combination of three factors coming together: a vulnerable infant, a vulnerable phase of development and a final insult occurring in this
window of vulnerability. Recently, a unified neuropathological theory contributes to describing SIDS. According to this, serotonergic neurons play a crucial homeostatic function in the cardiorespiratory brainstem centres. A high incidence
of morphological abnormalities and biochemical defects of serotoninergic neurotransmission have been reported in the brainstem of SIDS victims. This brain region includes the main nuclei and structures that coordinate the vital activities, such as cardiovascular function and breathing, perinatal and after birth.
Nevertheless, evidence suggests likely genomic complexity and a degree of overlap among SIDS, Sudden Intrauterine Death (SIUD), Sudden Cardiac Death (SCD) and Sudden Unexpected Death in Epilepsy (SUDEP). In SUDEP, which has clinical parallels with SIDS, alterations to medullary serotoninergic neural
populations and autonomic dysregulation have been shown too.
Molecular profiling of SUDEP cases and the investigation of genetic models have directed to the identification of putative SUDEP genes of which most are ion channel active along the neurocardiac, neuroautonomic, and neurorespiratory pathway. Concurrently, anomalous time- activation, transcription or regional expression of candidate neuro-cardiac-respiratory genes implicated for SUDEP, could be similarly involved in other unexpected sudden deaths. A small but significant proportion of infants who die suddenly and unexpectedly have been shown on postmortem genetic testing to have Developmental Serotonopathies, Cardiac Channelopathies and Autonomic Nervous System Dysregulation, with considerable implications for surviving and future family members. This has led to the demonstration that neuro-cardiac genes are expressed in both tissues (brain and heart) and recently in the respiratory system.
Aim: Despite their decreasing incidence, SIDS and SUDEP are still important causes of death. There are many nuclei in the cardio and respiratory centres of the brain involved in unexpected and sudden deaths. Cardiac, sympathetic, and respiratory motor activities can be viewed as a unified rhythm controlled by
brainstem neural circuits for effective and efficient gas exchange. We aim to describe abnormalities in these nuclei, in part because robust molecular or functional examination of these nuclei has not been carefully performed. We intend to perform detailed functional mapping of these brainstem nuclei.
Specifically, the cardiorespiratory and cardioventilatory coupling can be understood as a unified vital rhythm controlled by brainstem neural circuits. By cardiorespiratory coupling, we mean the Respiratory Sinus Arrhythmia (RSA) that is characterized by a heart rate (HR) increasing during inspiration and an HR
decrease during expiration. Conversely, Cardioventilatory coupling (CVC) is considered the influence of heartbeats and arterial pulse pressure on respiration with the tendency for the next inspiration to start at a preferred latency after the last heartbeat in expiration. We hypothesized that these two reflex systems are not separate, but constitute an integrated network. We defined this last concept as "unifying theory". By studying all the maps of the cardiorespiratory nuclei of the Literature, we integrated this concept into a reworking map of brainstem nuclei
that could also explain the gasping and blocking cardiorespiratory of sudden deaths. The theory of a unique, unifying cardiorespiratory network, it has been
recently demonstrated in some cases of arrhythmia, in some cases of SUDEP with striking systolic hypotensive changes and in some cases of SIDS too.
Material and Methods: We investigated articles, reviews indexed in PubMed describing putative neuro-cardiac-respiratory genes and cardiorespiratory, and
cardioventilatory coupling theories. Specifically, we evaluated cardiorespiratory brainstem nuclei and whole brains of fetal, infant and adult autopsies respectively to detect congenital errors in the cerebral development or malformations, but also
to identify the “normal” or “dysplastic” brainstem centres.
Results: Based on the Literature, we identified a brain-heart gene mapping and a scheme of cardiorespiratory brainstem nuclei network. Contemporary, we collected a large pool of fetal brain malformations and cardiorespiratory nuclei
dysgenesis both in infants both in adult sudden deaths. We found dysgenesia, agenesia and hypoplasia of brainstem nuclei associated with SIDS cases, compared with post-mortem infant control cases. However, the arcuate nucleus
showed insignificant inter-variations regarding adults autoptic cases.
Discussion: Many intrinsic and extrinsic factors increase fetal, perinatal, infant, and adult sudden death susceptibility. The final common pathway for SIDS and
SUDEP involves a failure to arouse and autoresuscitate in response to environmental challenge. The different risk factors, among these a prone position, can directly alter the function of cardiorespiratory nuclei and impair the ability of this network to coordinate cardiorespiratory–cardioventilatory coupling.
Conclusions: Neuropathological analysis of the infant brainstem and neuro-cardiac-respiratory gene mapping represents a good tool to infer on the final events of SIDS and SUDEP, although nothing it is clear regarding the role of adult cardiorespiratory centres. An integrated study of postmortem neuropathology and molecular autopsies could help to understand the network of
this beating-breathing-thinking unit.
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Sacchi, Chiara. "Child development following fetal adversities. From neural to interactive processes of socio-emotional vulnerability in Intrauterine Growth Restricted infants." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422842.
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Recent years have witnessed a proliferation of contributions on antenatal growth vulnerabilities and the long-term consequences on neurodevelopment and health outcomes. Knowing the pre- and perinatal factors exposing neurodevelopment and behavioral growth would benefit early clinical decision making and timely interventions. The present doctoral thesis organizes a series of studies within the field of clinical developmental psychology investigating a model of the fetal origin of neurodevelopment. Specifically, the study of Intrauterine Growth Restriction (IUGR) is the doorway and the keystone for exploring the role of antenatal adversity in founding developmental cascades of effects drifting biobehavioral trajectories towards at-risk outcomes.
The IUGR describes a set of nutritional anomalies affecting fetal maturation and exposing to high risk the post-natal growth. Most of the approaches investigating such adversity address urgent medical questions on etiopathology, fetal management and long-term prediction of health and mental health outcomes. The downside of this displacement is that the focus on the postnatal experience of the social and relational world in infants and children with IUGR is largely left behind. This issue clouds the comprehension of the relationship between antenatal and postnatal influences and further, of the complexity necessary to properly describe IUGR developmental trajectories. In the attempt to bring this lens to the observation of neuro and behavioral development following IUGR and to connect antenatal growth with the postnatal experiences, we designed a series of studies aimed at expanding the comprehension of the putative neuro-behavioral mechanisms linking growth restriction to later outcomes. Besides, achieving this goal would lay the ground for further exploring the potential routes of reversing mechanisms, thus aspiring in being clinically informative.
The studies presented in this thesis are embedded in an integrated theoretical framework and a multimethod approach where child development results from multiple and transactional processes involving the interdependency of biological and environmental influences. Specifically, Chapter 1 describes a meta-analytic study ascertaining the effect of growth restriction on cognitive outcome and intellectual risk across childhood. Our findings robustly reveal that across infancy, childhood and middle-childhood individuals with Intrauterine Growth Restriction have systematically lower cognitive scores, increased borderline intellectual functioning and intellectual risk, compared to appropriate for gestational age (AGA) peers. Consistent results are reported for IUGR samples with either antenatal diagnosis or at-birth identification, as well as for comparisons within the study of preterm and term-born groups.
Chapter 2 presents a cohort study investigating grey matter volumes around the time of birth in very preterm (VTP) IUGR and AGA newborns. Findings prove extensive alterations in brain volumes characterizing IUGR perinatal brain development. Additionally, the study identifies IUGR VPT cognitive and motor performances in toddlerhood as significantly lower than the ones of AGA VPT peers. Interestingly, perinatal volumetric alterations did not exert a predictive role on such outcomes, opening at the presence of further processes involved in these developmental trajectories.
In line with this hypothesis, Chapter 3 presents the rationale and methods of a longitudinal case-control study investigating social and emotion processing in IUGR term-born infants, as putative neural and behavioral mechanisms translating antenatal vulnerability into atypical developmental outcomes. Extracted from this study, Chapter 4 reports on behavioral differences in between IUGR and AGA term-born infants during mother-infant interactions and on later cognitive outcomes. Preliminary findings suggest IUGR peculiar patterns of mother and infant interactive behaviors, with significantly lower levels of maternal structuring at 4 months and reduced infant’s responsiveness at 9 months. Also, they confirm later IUGR cognitive and motor risk as evaluated at 12 months of age.
Finally, considering such mother-infant interactive vulnerability, Chapter 5 proposes the application of a pediatric video-feedback intervention to support parents of a Small for Gestational Age (SGA; birth weight below the 10th centile) newborn. Findings for this family allow to observe that the intervention holds parental worries about infant’s physical growth and sustains their mentalization abilities to recognizing his communicative skills and progressively identifying the self- and emotional regulatory abilities.
Overall, our findings point out that fetal adversity, as described by IUGR, is a significant risk factor interesting child neurodevelopment, early exposing the brain and behavioral growth and parent-infant relational experiences. The studies proposed show the significance of observing multilevel processes and mechanisms that compose the crucial steps of a developmental cascade of cognitive and behavioral risk in order to understand the complexity of IUGR development. Consequently, in order to ameliorate the developmental outcomes of these children, constant and synergic research efforts should be directed to integrate different perspectives of study, explore the neighboring biobehavioral processes and to develop empirically-driven interventions targeting the processes of highest plasticity in IUGR development.
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Doverhag, Christina. "Inflammatory mechanisms in experimental neonatal brain injury and in a clinical study of preterm birth : involvement of galectin-3 and free radical formation /." Göteborg : Perinatal Center, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, 2010. http://hdl.handle.net/2077/21479.
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Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2010.Härtill 3 uppsatser. På spikbladet med titel : Inflammation in experimental neonatal brain injury and in a clinical study of preterm birth : involvement of galectin-3 and free radical formation.
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Weber, Ashley M. "Oxytocin: Biomarker of Affiliation and Neurodevelopment in Premature Infants." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461182484.
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Wilkinson, Dominic James Clifford. "Ethical issues in the use of magnetic resonance imaging of the brain in newborn infants with hypoxic-ischaemic encephalopathy : neuroimaging and decision-making for brain injured newborns." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:d61e4318-3568-4310-bf92-c7d70f2cb3da.
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Infants with hypoxic-ischaemic encephalopathy (birth asphyxia) have a high risk of death or disability. Those with poor prognosis are sometimes allowed to die after withdrawal of intensive care. In recent years, doctors have used new types of brain scan, magnetic resonance imaging (MRI), to predict the type and severity of impairment if the infant survives and to help with such decisions. In this thesis, I analyse the issues arising from the use of MRI for prognostication and decision-making in newborn infants. I argue that previous prognostic research has been hampered by a failure to identify and focus on the most important practical question and that this contributes to uncertainty in practice. I outline recommendations for improving research. I then look at existing guidelines about withdrawal of life-sustaining treatment. I identify several problems with these guidelines; they are vague and fail to provide practical guidance, they provide little or no genuine scope for parental involvement in decisions, and they give no weight to the interests of others. I argue that parental interests should be given some weight in decisions for newborn infants. I develop a new model of decision-making that, using the concept of a Restricted Life, attempts to set out clearly the boundaries of parental discretion in decision-making. I argue that where infants are predicted to have severe cognitive or very severe physical impairment parents should be permitted to request either withdrawal or continuation of treatment. I justify this model on the basis of overlapping interests, (prognostic, experiential and moral) uncertainty, asymmetrical harms, and the burden of care. In the conclusion, I set out a guideline for the use of MRI in newborn infants with hypoxic-ischaemic encephalopathy. I suggest that this guideline would provide a more robust, coherent and practical basis for decision-making in newborn intensive care.
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Machaalani, Rita. "Brainstem pathology in SIDS and in a comparative piglet model." University of Sydney. Medicine, 2003. http://hdl.handle.net/2123/605.
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This thesis tests the hypothesis that increased neuronal cell death in SIDS infants is related to the ability of risk factors, such as prone sleeping, to expose infants to intermittent hypercapnic hypoxia (IHH). Based on the hypothesis that the NMDA system is linked to neuronal death, by way of excitotoxicity, correlations were also sought between cell death and changes in NMDA receptor (NR1) expression in brainstem nuclei controlling cardiorespiratory function. The first aim of this study was to verify that increased neuronal cell death occurs in SIDS infants. To verify a piglet model of SIDS risk factors, brainstem changes were examined in piglets exposed to IHH, and comparisons were made to changes seen in SIDS infants. The NMDA receptor was characterised in controls for both the human infant and the piglet groups. Comparisons of neuronal changes were made with SIDS infants, and piglets exposed to IHH. Non-radioactive in-situ hybridisation and immunohistochemistry were performed on formalin fixed and paraffin embedded brainstem tissue to identify markers of cell death (caspase-3, active caspase-3, and TUNEL), and to examine NR1 mRNA and protein expressions. Staining was quantified using computerised image analysis software. Eight nuclei from the brainstem medulla (caudal in piglets, and mid in infants), and two nuclei from the rostral pons (infants) were studied. The first dataset included human infants aged 1-6 months with a diagnosis of SIDS (n=15) or non-SIDS (n=10). The second dataset comprised developing piglets aged 13-14 days, with controls (n=6), against those exposed to IHH for 2 (n=6) or 4 (n=5) days. Increased neuronal cell death was not verified in the SIDS infants, but abnormalities in NR1 expression were present in selected nuclei of the medulla. Piglets exposed to IHH had increased neuronal cell death and changes in NR1 in selected nuclei of the medulla. There was also a positive correlation between increased cell death and high NR1 levels. Preliminary data showed that SIDS infants who usually slept prone had some differences in NR1 compared to those who did not usually sleep prone. From these findings, it was concluded that IHH may underlie the abnormalities in NMDA receptor expression that are present in the brainstem of SIDS infants. Although IHH can induce an increase in neuronal cell death, its significance in the aetiology of SIDS is not known. In piglets, IHH induced cell death correlated with high NMDA expression in some brainstem nuclei, supporting the hypothesis that excitotoxicity may be involved in the mechanism for cell death. Moreover, this thesis presents for the first time, �preliminary pathological proof� of an association between prone sleeping and abnormal NMDA receptor expression in SIDS infants.
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Kaukola, T. (Tuula). "Perinatal brain damage in very preterm infants:prenatal inflammation and neurologic outcome in children born term and preterm." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514278402.
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Abstract Despite improvements in peri- and neonatal care and an increase in the overall survival of very preterm infants, the incidence of neurologic sequelae has remained high. The pathogenesis of many brain imaging findings, such as white matter damage, WMD, is poorly understood. The factors predisposing to brain damage differ between term and preterm infants. More detailed information is needed of how brain imaging correlates with neurodevelopmental impairment after the neonatal period. The present study investigated the pre- and perinatal factors leading to brain damage and their effects on neurologic and neurodevelopmental outcome in very preterm children. We also analyzed the differences in umbilical cord serum cytokines in term and preterm children with cerebral palsy, CP. Furthermore, the correlations between the findings on diffusion-weighted imaging, DWI, measurements in brainstem auditory evoked potentials, and neurodevelopmental outcome were assessed. We demonstrated that pregnancies complicated by combined histologic chorioamnionitis and placental insufficiency independently predicted abnormal neurologic outcome at 2 years of corrected age. WMD additively predicted poor outcome. Isolated fetal inflammatory response, umbilical cord serum acute phase cytokines (IL-1α, IL-1β, IL-6, IL-8, TNF-α), did not associate with neurologic outcome in either term or preterm children. Instead, a cluster of cytokines different from acute phase cytokines were related to CP, and the protein profile differed between term and preterm children. Disturbed hemodynamics during the pre- and perinatal period affected outcome in very preterm infants. In severe placental insufficiency, fetal cardiac compromise associated with suboptimal neurodevelopmental outcome at 1 year of corrected age. In addition, several clinical factors characterising cardiorespiratory status after birth associated with abnormal neurologic outcome at 2 years of corrected age. We found the apparent diffusion coefficient, ADC, a quantitative measurement of water diffusion, in pons to correlate with the conduction rate of impulses travelling through the auditory tract. We also demonstrated a high value of ADC in corona radiata to associate with poor outcome in gross motor and eye-hand coordination skills at 2 years of corrected age. Both pre- and perinatal factors associate with later outcome in very preterm infants. An isolated fetal inflammatory response does not predict neurologic outcome. Findings on DWI in specific brain regions predict abnormal neurodevelopmental outcomeTiivistelmä Huolimatta vastasyntyneisyyskauden parantuneista hoitotuloksista ja että yhä useampi hyvin ennenaikaisena syntynyt lapsi jää eloon, heidän neurologisen vammautuneisuuden ilmaantuvuus on edelleen korkea. Monien aivojen kuvantamislöydösten, kuten valkean aineen vaurion, syntymekanismit tunnetaan huonosti. Aivojen vaurioitumiselle altistavat tekijät eroavat täysiaikaisena ja ennenaikaisena syntyneillä lapsilla. Tarvitaan myös aiempaa yksityiskohtaisempaa tietoa aivojen kuvantamislöydösten merkityksestä lasten vastasyntyneisyyskauden jälkeiseen kehitykseen. Tässä tutkimuksessa selvitettiin raskauden- ja syntymänaikaisia tekijöitä, jotka vaikuttavat aivojen vaurioitumiseen hyvin ennenaikaisena syntyneillä lapsilla sekä näiden tekijöiden merkitystä lasten neurologiseen kehitykseen. Tarkastelimme myös napaveren seerumin välittäjäaineiden, sytokiinien, eroavuuksia täysiaikaisena ja ennenaikaisena syntyneillä CP-lapsilla. Lisäksi selvitimme diffuusiomagneettitutkimus- ja aivorunkoherätevastelöydösten sekä neurologisen kehityksen välisiä yhteyksiä. Tämän tutkimuksen mukaan kohdunsisäinen tulehdus ja istukan vajaatoiminta yhtä aikaa esiintyessään ovat poikkeavan neurologisen kehityksen itsenäisiä riskitekijöitä lapsilla 2 vuoden korjatussa iässä tutkittuna. Valkoisen aivoaineen vaurio edelleen lisäsi näiden lasten huonon neurologisen kehityksen ennustetta. Raskauden kestosta riippumatta, sikiön tulehdusvastetta kuvaavat napaveren akuutin vaiheen tulehdusvälittäjäaineet (IL-1α, IL-1β, IL-6, IL-8, TNF- α) eivät vaikuttaneet lapsen neurologiseen kehitykseen. Sen sijaan, CP-lasten napaverestä löytyi erityinen joukko ei-akuutin vaiheen välittäjäaineita. Nämä valkuaisaineet erosivat toisistaan täysiaikaisena ja ennenaikaisena syntyneillä CP-lapsilla. Raskauden- ja syntymänaikaiset verenkierron häiriöt vaikuttivat hyvin ennenaikaisena syntyneiden lasten myöhempään kehitykseen. Vaikeassa istukan vajaatoiminassa sikiön sydämen toiminnan heikkeneminen liittyi lapsen suboptimaaliin neurologiseen kehitykseen 1 vuoden korjatussa iässä tutkittuna. Lisäksi useat syntymänjälkeiset keuhkojen ja verenkierron tilaa kuvaavat kliiniset tekijät liittyivät lapsen poikkeavaan neurologiseen kehitykseen 2 vuoden korjatussa iässä tutkittuna. Tutkimuksemme mukaan, veden diffuusiota määrällisesti kuvaava diffuusiokerroin, ADC, aivosillasta mitattuna, liittyi impulssien johtumisnopeutueen kuuloradastossa. Lisäksi korkea ADC-arvo aivojen sepelviuhkassa liittyi karkean motoriikan ja silmä-käsi-yhteistyötaitojen huonoon kehitykseen 2 vuoden korjatussa iässä tutkittuna. Sekä raskauden- että syntymänaikaiset tekijät vaikuttavat hyvin ennenaikaisena syntyneiden lasten myöhempään kehitykseen. Yksittäinen sikiön tulehdusvaste ei ennakoi lapsen neurologista kehitystä. Tiettyjen aivoalueiden diffuusiokuvantamislöydökset ennustavat lapsen poikkeavaa neurologista kehitystä
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Leonardo, Christopher C. "The Role of Extracellular Matrix and Matrix-Degrading Proteases in Neonatal Hypoxic-Ischemic Injury." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002587.
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Russell, Dana J. "Human Cranial Growth and Shape Change: Are Fetal Rates and Morphologies Extended Throughout the First Year of Life?" Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/anthro_theses/43.
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Selection for increased encephalization in humans necessitated extensive brain growth after birth. To estimate changes in rates of growth and corresponding shape changes during gestation and infancy, chord and arc distances were obtained from the frontal, parietal, and occipital bones of 44 human fetuses, neonates, and infants (one year old and younger). Rates of growth in chord and arc measurements were calculated and compared using linear regression of log-transformed variables, followed by ANCOVA. Curvature of bone lengths and widths were estimated by chord/arc indices. Fetal rates of cranial growth were significantly slower while the fetal frontal and occipital bones were significantly more curved than those of infants. Fetal rates of cranial growth decrease during the first six postnatal months, in conjunction with rapid changes in shape, except for parietal superior-inferior height where bossing of the bone is similar in fetuses and neonates.
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Charton, Elise. "Lait humain vs. préparation pour nourrissons : digestibilité des protéines et impact sur l’axe microbiote-intestin-cerveau." Electronic Thesis or Diss., Rennes, Agrocampus Ouest, 2023. http://www.theses.fr/2023NSARB368.
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Une majorité de nourrissons reçoivent encore aujourd’hui des préparations pour nourrissons (PPN), fabriquées à base de lait bovin et soumises à de nombreux traitements technologiques. Ces substituts ont pour but de mimer au mieux le lait humain (LH). Cependant, malgré l’évolution des PPNs, des différences persistent entre le LH et les PPNs en termes de composition et structure, et effets sur le développement et la santé à court et long termes du nourrisson et adulte en devenir. L’objectif de ce travail était de comprendre comment la nature de l’alimentation infantile, LH vs. PPN, modulait la digestibilité protéique et, plus globalement, comment elle influençait l’axe microbiote intestin-cerveau. Deux modèles du nourrisson humain ont été utilisés et comparés, le mini-porc Yucatan entre 16 et 21 jours de vie, et un modèle de digestion in vitro dynamique paramétré pour mimer le nourrisson à terme. Les contenus digestifs et tissus ont ensuite été analysés via des approches métagénomique (microbiote), histologique et de perméabilité ex vivo (physiologie intestinale), d’expression génique et de métabolomique ciblée (intestin, cerveau et plasma). Les résultats ont montré que la digestibilité de l’azote total et dans une moindre mesure, celle de certains acides aminés (Lys, Phe, Thr, Val, Ala, Pro et Ser) différaient entre LH et PPN. Les deux modèles de digestion (in vivo et in vitro) étudiés ont conduit à des résultats similaires en termes de déstructuration des aliments et du taux de protéines intactes résiduelles en phase gastrique. Le modèle de digestion in vitro dynamique utilisé ici est donc un bon outil de prédiction de la digestion in vivo. L’axe microbiote-intestin-cerveau et notamment la composition du microbiote, ainsi que le métabolisme du tryptophane, malgré une digestibilité similaire entre aliments, étaient modulés différemment par le LH et la PPN. L’augmentation de la permeabilité intestinale, bien que modérée, était associée à un renforcement du système immunitaire mucosal avec le LH. Ces modifications sont associées à des changements d’expression génique (fonctions barrière et endocrine, récepteurs aux AGV) aux niveaux hypothalamique et striatal, et de profils métaboliques principalement aux niveaux hippocampique et plasmatique. Certains composants présents dans le LH (ex.: oligosaccharides, azote non protéique tel que l’urée, consortium bactérien) et absent dans la PPN peuvent expliquer ces résultats. La supplémentation des PPNs en ces composants bioactifs et/ou la modulation de la fraction protéique pourraient être des leviers pour l’optimisation des PPNsNowadays, a high rate of infants is still being fed infant formulas (IF) based on cow milk and subjected to several technological treatments. These substitutes aim to mimic as close as possible the human milk (HM). Despite of IF improvement, differences still exist between HM and IF in terms of composition and structure, and effects on health in infancy, and later on in adulthood. The objective of this work was to understand how the infant food modulated the dietary nitrogen digestibility and, in overall, how it shaped the microbiota-gut-brain axis. Two infant models were used and compared, the 16 to 21-day-old mini-piglet Yucatan and an in vitro dynamic digestion model parametered with term infant digestive conditions. Digestive contents and tissues were then analyzed using metagenomic (microbiota), histological and ex vivo permeability (intestinal physiology) approaches, gene expression and targeted-metabolomic approaches (intestine, brain and plasma). The results showed that the digestibility of nitrogen and at least extent, that of a few amino acids (Lys, Phe, Thr, Val, Ala, Pro and Ser) were different between HM and IF. The two digestion models (in vivo and in vitro) led to similar observations in terms of meal deconstruction and proteolysis, showing that the in vitro dynamic digestion model is a good proxy of the in vivo digestion regarding digestion kinetics. The microbiota-gut-brain axis, notably regarding the colonic microbial composition and the tryptophan metabolism, which digestibility was similar between infant foods, were differently modulated by HM and IF. The increase of the intestinal permeability, though moderately, was associated with a boost of the intestinal immune system and changes in gene expression (barrier and endocrine functions, volatile fatty acids receptors) at hypothalamic and striatal levels and with changes in hippocampal and plasma metabolomic profiles. Some components present in HM (e.g.: oligosaccharides, non-protein nitrogen such as urea, bacteria consortia) and absent in IF can explain the discrepancies observed. IF-supplementation with these bioactive components and/or with the modulation of the protein profile would be of interest for further investigation
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Cainelli, Elisa. "Brain electrophysiological development in premature infants." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423450.
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Background. Improvements in postnatal care provided in neonatal intensive care units have resulted in increasing survive percentage of children born at the limits of viability. A large number of premature infants experienced major impairment and/or minor neurodevelopmental disabilities, such as cognitive, psychiatric and motor disorders. The etiology of these developmental deficits still remains not completely understood, but they may be the result of neonatal brain injury as well of interruption of the normal process of brain maturation that occurs during the last trimester of pregnancy, a critical period of prenatal ontogenesis.
Prediction of the outcome of individual preterm infants is difficult. Although a premature infant may be asymptomatic for abnormal clinical signs, he may exhibit subtle alterations in brain activity which often remain unrecognized. A neurophysiologic evaluation of brain activity in the third trimester of gestation would probably be of great benefit for early detection of pathological processes or subclinical alterations. Electroencephalogram and cortical auditory evoked potentials turned out to be simple and useful techniques in evaluation of brain maturation.
Aims. We conducted cross-sectional and longitudinal investigations at early crucial phases of development (35 and 40 weeks post-conception) in order to identify differences in cerebral activity between premature infants born at different gestational ages and full-term neonates, using electroencephalogram (EEG) at rest and cortical auditory evoked potentials (CAEP). We further aimed to correlate the neonatal data with later neurodevelopment.
Methods. The research is divided into three studies: Study 1: EEG spectral activity was recorded at 35 post-conception weeks in 40 premature infants and compared between groups of infants born at different gestational age (“extremely low gestational age”, ELGA: 23–27+6, ‘‘very low gestational age’’, VLGA: 28–31+6 and “low gestational age”, LGA: 34-35). The results were correlated with behavioral developmental scores obtained at 12 months corrected age from 20 infants. Study 2: a subgroup of 10 infants of Study 1 repeated the EEG recording at 40 post-conception age. EEG spectral activity of this subgroup was compared longitudinally and further the activity recorded at 40 GA were compared with those of a group of 10 full-term infants. Study 3: CAEP were recorded in active sleep at 35 post-conception weeks in response to an auditory stimulation in 36 premature infants and compared between groups of infants born at different gestational age (ELGA, VLGA, LGA). The results were correlated with behavioral developmental scores obtained at 12 months corrected age from 20 infants.
Methodology Study 1 and 2. Electrical brain activity was recorded for 40 minutes on 5 bipolar channels. Data were transformed into the frequency domain using a Fast Fourier Transform algorithm. Frequency spectrum was divided into the following bands: δ (0.5-4 Hz, comprising δ1 0.5-1 Hz and δ2 1-4 Hz), θ (4-8 Hz), α (8-13 Hz) and β (13-20 Hz). Statistical analysis were performed on absolute and relative power values only on central sites (C3-C4, C3-T3, C4-T4).
Methodology Study 3. 1000 Hz (paradigm 1) and 500 Hz (paradigm 2) auditory stimulations were performed on continuous EEG recording. Design consisted of 300 tones for each paradigm. Inter-stimulus interval randomly varied between 600 and 900 ms; 12 monopolar channels were recorded, referenced to the bilateral linked ear lobes. 600 ms epochs were divided for statistical analysis in time windows of 100 ms. Statistical analysis were performed only on central sites (Fz, Cz).
Results. Study 1. On C3-C4, relative spectral power values differed significantly between ELGA and LGA groups. Infants born at lower gestational ages had a higher amount of power in the δ and a lower amount of α and β spectral power. The preliminary data on those infants attaining 12 months of corrected age showed that higher amount of δ and a lower amount of β and α resulted associated with poor relational skills and personal self autonomies. Study 2. At 40 post-conception age, premature infants showed on C3-C4 a decrease in δ activity and a mild, not significant, increase in higher frequencies; no significant differences in spectral power values were found with full-term neonates. Study 3. In response to 1000 Hz tones no waveforms became evident on Fz in ELGA infants, while LGA presented a wide and slow positive response; the groups differed significantly. VLGA’s grand average waveform resembled that of LGA group, but characterized by a high variability. Responses to 500 Hz resulted highly variable and not reliable.
Conclusions. We found early subtle brain electrical alterations in premature infants experiencing different developmental pathways, suggesting a different cortical organization; these differences seem to be associated with later development. The potential of neurophysiological methodologies is to provide a useful indicator of good prognosis or poor developmental outcomes.Premesse. Gli avanzamenti tecnologici che negli ultimi decenni hanno caratterizzato le cure perinatali e le tecniche di terapia intensiva neonatale hanno permesso la sopravvivenza di una percentuale sempre maggiore di neonati prematuri nati ad età gestazionali sempre più basse, ai limiti della sopravvivenza. Eppure, studi sullo sviluppo a breve e lungo termine hanno dimostrato che molti neonati prematuri riportano esiti maggiori e/o disordini evolutivi minori, come deficit cognitivi e neuropsicologici, disturbi psichiatrici/comportamentali e motori. La causa di tali disordini dello sviluppo rimane poco chiara, ma può essere il risultato di sofferenza cerebrale in epoca neonatale come anche dell’interruzione del normale processo di sviluppo che avviene nel terzo trimestre di gravidanza, un periodo estremamente critico per la maturazione cerebrale. Predire come sarà lo sviluppo di un neonato prematuro rimane attualmente molto difficile. Infatti, sebbene un neonato possa essere asintomatico per segni clinici indicativi di una condizione patologica in atto, possono essere presenti alterazioni subcliniche del funzionamento cerebrale che spesso non vengono riconosciute. Una valutazione neurofisiologica dell’attività cerebrale nel neonato prematuro può probabilmente essere di grande utilità nel precoce riconoscimento di processi patologici o di alterazioni subcliniche. L’elettroencefalogramma (EEG) e i potenziali evocati uditivi corticali (CAEP) si sono dimostrati tecniche semplici e valide nel valutare la maturazione cerebrale. Obiettivi dello studio. Abbiamo condotto delle valutazioni neurofisiologiche trasversali e longitudinali in due fasi precoci e cruciali dello sviluppo (35 e 40 settimane postconcezionali) allo scopo di identificare differenze nell’attività elettrica cerebrale fra prematuri nati ad età gestazionali diverse e neonati a termine, usando EEG a riposo e i CAEP. Tali indagini in epoca neonatale sono state poi correlate con lo sviluppo comportamentale a distanza. Metodi. La ricerca è stata articolata in tre studi: Studio 1: è stata eseguita l’analisi spettrale dell’EEG registrato a 35 settimane postconcezionali in 40 neonati prematuri; tale attività è stata comparata fra gruppi di neonati nati ad età gestazionali diverse (estremi prematuri, ELGA: 23–27+6, veri prematuri, VLGA: 28–31+6 e prematuri, LGA: 34-35). I risultati ottenuti in epoca neonatale sono stati correlati con l’indice di sviluppo comportamentale ottenuto ai 12 mesi di età corretta nei primi 20 bambini che hanno raggiunto tale età. Studio 2: un sottogruppo di 10 neonati dello Studio 1 ha ripetuto la registrazione EEG a 40 settimane postconcezionali; la potenza spettrale ottenuta dalle registrazioni EEG a 35 e 40 settimane postconcezionali è stata cofrontata longitudinalmente; successivamente l’attività spettrale ottenuta alle 40 settimane postconcezionali è stata confrontata con quella di 10 neonati a termine alla nascita. Studio 3: i CAEP sono stati registrati in sonno attivo a 35 settimane postconcezionali in 36 prematuri e comparati fra gruppi di neonati nati ad età gestazionali diverse (ELGA, VLGA, LGA). I risultati sono stati correlati con l’indice di sviluppo comportamentale ottenuto ai 12 mesi di età corretta nei primi 20 bambini che hanno raggiunto quest’età. Metodologia Studio 1 e 2. L’attività elettrica cerebrale è stata registrata per 40 minuti su 5 canali bipolari. I dati ottenuti sono stati trasformati nel dominio delle frequenze utilizzando una trasformazione Fast Fourier. Lo spettro di frequenza è stato diviso nelle seguenti bande: δ (0.5-4 Hz, composto da δ1 0.5-1 Hz e δ2 1-4 Hz), θ (4-8 Hz), α (8-13 Hz) e β (13-20 Hz). Le analisi statistiche sono state eseguite sui valori di potenza assoluti e relativi ottenute solo dai siti centrali (C3-C4, C3-T3, C4-T4). Metodologia Studio 3. Durante la registrazione continua dell’EEG i neonati sono stati stimolati con treni di toni a 1000 Hz (paradigma 1) e a 500 Hz (paradigma 2). Il disegno sperimentale prevedeva 300 toni per ciascun paradigma. L’intervallo inter-stimolo variava in maniera casuale fra 600 e 900 ms; sono stati registrati 12 canali monopolari, riferiti bilateralmente ai lobi degli orecchi. Le epoche di 600 ms sono state divise per l’analisi statistica in finestre temporali di 100 ms. Le analisi statistiche sono state eseguite solo sui siti centrali (Fz, Cz). Risultati. Studio 1. In C3-C4, i valori di potenza spettrale relativa differivano significativamente fra i gruppi di ELGA e LGA. I neonati nati alle età gestazionali più basse avevano una maggiore potenza relativa in δ e una minore in α e β. La correlazione di questi dati con lo sviluppo comportamentale dei primi bambini che hanno raggiunto i 12 mesi di età corretta ha mostrato come alte percentuali di potenza in δ e basse in β e α fossero associate ad abilità relazionali più povere ed autonomie personali meno mature. Studio 2. A 40 settimane postconcezionali i prematuri hanno mostrato in C3-C4 una riduzione di potenza δ relativa e un lieve, non significativo, aumento di potenza nelle alte frequenze; non sono state trovate differenze significative rispetto i neonati a termine. Studio 3. Nel paradigma a 1000 Hz non è stato possibile rilevare nessuna risposta ai suoni nei neonati ELGA, mentre nei LGA in Fz era evidente una lenta ed ampia onda positiva; la grande media dei due gruppi differiva significativamente in Fz. La grande media dei neonati VLGA assomigliava a quella dei LGA, ma era caratterizzata da un’alta variabilità. Le risposte a toni di 500 Hz sono risultate troppo variabili e non riproducibili. Conclusioni. Confrontando neonati prematuri che hanno sperimentato linee di sviluppo differenti, abbiamo trovato delle differenze sottili nell’attività elettrica cerebrale che suggeriscono un’alterazione dell’organizzazione corticale. Tali differenze sembrano inoltre associate allo sviluppo comportamentale nel primo anno di vita. Questi risultati suggeriscono che le tecniche neurofisiologiche possano essere molto utili nella prognosi dei neonati prematuri.
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Camargos, Ana Cristina Resende. "Biomarcadores neuroend?crino-inflamat?rios, estado redox e desenvolvimento infantil de crian?as com sobrepeso e obesidade entre seis e 24 meses de idade." UFVJM, 2016. http://acervo.ufvjm.edu.br/jspui/handle/1/1177.
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A obesidade infantil ? considerada um dos maiores problemas de sa?de p?blica do mundo. Estudos demonstram altera??o do padr?o de secre??o de adipocinas, cortisol e do fator neurotr?fico derivado do c?rebro (BDNF), bem como inflama??o cl?nica cr?nica sublimiar e desequil?brio redox em crian?as com sobrepeso e obesidade na idade escolar. Al?m disso, o excesso de peso tamb?m est? associado a reduzido desenvolvimento cognitivo e motor. Apesar da literatura indicar que os primeiros 24 meses de vida representam um per?odo importante para o desenvolvimento da obesidade infantil, n?o existem evid?ncias se crian?as com sobrepeso e obesidade nesta faixa et?ria j? apresentam altera??es em par?metros neuroend?crino-inflamat?rios, com poss?vel impacto no desenvolvimento infantil. Dessa forma, os objetivos deste estudo foram: 1) analisar as concentra??es plasm?ticas de adipocinas e BDNF, as concentra??es s?ricas de cortisol e o estado redox de crian?as com sobrepeso/obesidade entre seis e 24 meses de idade; 2) avaliar o desenvolvimento cognitivo e motor de crian?as com sobrepeso/obesidade entre seis e 24 meses de idade e; 3) verificar associa??es entre os biomarcadores avaliados com o desenvolvimento cognitivo e motor nessa faixa et?ria. Foi realizado um estudo transversal com crian?as com sobrepeso/obesidade e eutr?ficas entre seis e 24 meses de idade, cadastradas nas Estrat?gias de Sa?de da Fam?lia. As concentra??es plasm?ticas de leptina, adiponectina, resistina, receptores sol?veis do fator de necrose tumoral 1 e 2 (sTNFR1 e sTNFR1), BDNF e as concentra??es s?ricas de cortisol foram mensuradas pelo m?todo ELISA. As quimiocinas foram mensuradas pela t?cnica cytometric bead arrays e o estado redox foi determinado por meio da detec??o das concentra??es de subst?ncias reativas ao ?cido tiobarbit?rico (TBARS), da atividade das enzimas catalase (CAT) e super?xido dismutase (SOD) e da habilidade de redu??o do ferro (FRAP). O desenvolvimento infantil foi avaliado por meio do instrumento Bayley Scales of Infant and Toddler Development, 3? edi??o (Bayley-III). Foi utilizado teste t para amostras independentes para comparar os grupos e correla??o de Pearson ou Spearman para verificar a associa??o entre as vari?veis. Al?m disso, foi utilizado um modelo de regress?o linear m?ltipla stepwise para verificar a associa??o entre os biomarcardores selecionados com o desenvolvimento cognitivo e motor. As concentra??es plasm?ticas de leptina (p=0,0001), adiponectina (p=0,0007), BDNF (p=0,003) e as concentra??es s?ricas de cortisol (p=0,048) foram significativamente superiores no grupo de crian?as com sobrepeso/obesidade. Em contrapartida, as crian?as deste grupo apresentaram menores concentra??es de TBARS (p=0,004) e menor atividade das enzimas antioxidantes CAT (p=0,045) e SOD (p=0,02). N?o foram encontradas diferen?as significativas nas concentra??es de quimiocinas, sTNFR1, sTNFR2, resistina e FRAP entre os grupos (p>0,05). Al?m disso, as crian?as do grupo sobrepeso/obesidade apresentaram menores escores de desenvolvimento cognitivo (p=0,03) e motor (p=0,04). Foi ainda encontrada associa??o significativa entre as concentra??es plasm?ticas de leptina e sTNFR1 com o escore composto cognitivo (p=0,001) e das concentra??es plasm?ticas de sTNFR1 com o escore composto motor (p=0,003). Todos esses resultados apontaram a presen?a de altera??es neuroend?crino-inflamat?rias em crian?as com sobrepeso/obesidade entre seis e 24 meses de idade. Al?m disso, embora a maior parte das crian?as com sobrepeso/obesidade apresentem desenvolvimento infantil dentro dos limites de normalidade, evidencia-se pior desempenho cognitivo e motor. Por fim, foi demonstrado que maiores concentra??es de sTNFR1 e menores concentra??es de leptina foram associadas com melhores desfechos de desenvolvimento infantil nessa faixa et?ria.
Tese (Doutorado) ? Programa Multic?ntrico de P?s-Gradua??o em Ci?ncias Fisiol?gicas, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2016.
Childhood obesity is one of the world?s most serious public health issues. Studies have demonstrated dysregulated secretion pattern of adipokines, cortisol, brain-derived neurotrophic factor (BDNF), as well as chronic low-grade inflammation and redox imbalance in school-age overweight or obese children. Overweight/obese infants also had lower cognitive and motor development scores. Although the literature points out that the first 24 months of life represent an important period for the development of childhood obesity, it is not known whether overweight/obese infants in this age interval present alterations in neuroendocrine inflammatory parameters, with possible impact on child development. Then, the objectives of this study were: 1) to analyze the plasmatic levels of adipokines and BDNF, serum cortisol and redox status in overweight/obese infants between 6 and 24 months of age; 2) to evaluate the cognitive and motor development in overweight/obese infants between 6 and 24 months of age and; 3) to verify the association of the biomarkers evaluated with cognitive and motor development in this age interval. A cross-sectional study was conducted with infants with overweight/obesity and normal-weight between 6 and 24 months enrolled in Family Health Strategies. Plasma leptin, adiponectin, resistin, BDNF, soluble tumour necrosis factor receptors 1 and 2 (sTNFR1, sTNFR2), and serum cortisol levels were measured using conventional ELISA kits. Plasma chemokines were measured using the cytometric bead arrays kit, and oxidative stress was assessed by thiobarbituric acid reactive substances (TBARS) concentration, enzymes catalase (CAT) and dismutase superoxide (SOD) activity, as well by ferric reducing antioxidant power (FRAP). Infant development was performed using the Bayley Scales of Infant and Toddler Development, 3rd edition (Bayley-III). A t test for independent samples was performed to compare the groups and Pearson and Spearman correlation was used to verify the association between parameters. Multiple linear stepwise regression models were utilized to verify the association between the biomarkers selected and cognitive and motor composite scores. Plasma levels of leptin (p=0.0001), adiponectin (p=0.0007), BDNF (p=0.003) and serum cortisol (p=0.048) were significantly higher in overweight/obese infants. In contrast, concentration of TBARS (p=0.004), CAT (p=0.045) and SOD activity (p=0.02) were lower in overweight/obese infants. There were no differences in the levels of chemokines, sTNFR1, sTNFR2, resistin and FRAP between groups (p>0.05). Moreover, overweight/obese infants had lower cognitive (p=0.03) and motor (p=0.04) development scores than normal-weight infants. A significant association of plasma leptin and sTNFR1 levels with cognitive composite scores (p=0.001) were found and plasma sTNFR1 levels were associated with motor composite scores (p=0.003). All these results point out neuroendocrine inflammatory response changes in overweight/obese infants between 6 and 24 months. Moreover, although most of overweight/obese infants have presented cognitive and motor development within normal limits, there is evidence of worse cognitive and motor performance. Finally, high sTNFR1 and low leptin levels were associated with increase developmental outcomes in infants in this age interval.
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Angrisani, Rosanna Mariangela Giaffredo. "Estudo eletrofisiológico longitudinal da via auditiva em lactentes nascidos pequenos para a idade gestacional." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5170/tde-12022014-162325/.
Full textAbstract:
A adequação do peso ao nascimento é um fator de risco para atrasos de desenvolvimento. Dentre outras causas de morbidade e mortalidade, encontra-se a prematuridade e a Restrição de Crescimento Intrauterino (RCIU). O termo \"Pequeno para a Idade Gestacional\" (PIG) é utilizado muitas vezes, como indicador de RCIU, cujo feto pode ter sido submetido a agravos em diferentes momentos da gestação. A literatura aponta o PIG como risco para atraso no desenvolvimento neuropsicomotor, incluindo a linguagem. Objetivo: Acompanhar a maturação da via auditiva em lactentes nascidos PIG, comparando-os aos lactentes nascidos Adequados para Idade Gestacional (AIG) a termo e pré-termo, por meio do estudo das respostas do PEATE por estímulo click e tone burst (TB) nos seis primeiros meses de vida. Método: Estudo longitudinal, observacional de caráter multicêntrico. Foram avaliados 172 lactentes nascidos PIG e AIG, a termo e pré-termo, nos períodos neonatal, aos três e aos seis meses, por meio do PEATE com estímulo tipo click e tone burst em 0,5 kHz e 1 kHz, a 80dBnNA. Resultados: no período neonatal, os RN T/PIG não se diferenciaram dos RN T/AIG quanto às respostas do PEATE, o mesmo ocorrendo entre PT/PIG e PT/AIG. Ao se comparar o grupo T e PT/PIG, observou-se diferença entre as latências das ondas III, V e intervalos interpicos (Itpc) I-III e I-V, com latências maiores nos PT/PIG; não foram evidenciadas diferenças com TB nas frequências avaliadas. Na comparação do grupo T e PT/AIG, observou-se diferença entre as latências das ondas III, V e nos Itpc III-V e I-V e latências maiores nos PT/AIG. Não houve diferenças no TB nas frequências avaliadas. Aos três meses, não houve diferenças entre os T/PIG e T/AIG; na comparação PT/PIG e PT/AIG, houve diferenças no Itpc III-V, com latência menor no grupo PT/PIG. Não houve diferenças entre T/PIG e PT/PIG; o grupo AIG mostrou diferença entre T e PT nas latências da onda V e Itpc I-V. Na terceira coleta, aos seis meses, os T/PIG e T/AIG evidenciaram diferenças significativas entre as latências da onda III e Itpc I-III, o mesmo não ocorrendo quando se comparou PT/PIG e PT/AIG, os quais se diferenciaram somente no Itpc III-V. Ao se comparar T/PIG e PT/PIG, verificou-se diferenças relevantes somente no TB 0,5 kHz. Conclusão: Os achados do presente estudo permitiram concluir que o processo maturacional da via auditiva em lactentes nascidos PIG ocorre em diferente velocidade quando comparado ao de lactentes AIG; os PIG têm maturação acelerada, principalmente nos três primeiros meses, caracterizando desta forma um período de recuperação do ponto de vista da audição; a prematuridade influencia mais a maturação do sistema nervoso auditivo central que o fator peso ao nascer no período neonatal; a maturação ocorreu no sentido caudo-rostral nos dois grupos. O PEATE com TB em 0,5 kHz e em 1 kHz evidenciou o processo maturacional, porém não de modo tão detalhado quanto o fez com o estímulo tipo click. As crianças PIG devem ser monitoradas até pelo menos os três anos de idadeThe appropriateness of weight at birth is a risk factor for developmental delays. Prematurity and intrauterine growth restriction (IUGR) are among other causes of morbidity and mortality. The term \"small for gestational age\" (SGA) is often used as an indicator of IUGR, when the fetus may have been subjected to restrictions at different periods of pregnancy. The literature points SGA as a risk for neuropsychological developmental delay, including language. Objective: to monitor the maturation of the auditory pathway in SGA infants, comparing to term and preterm appropriate for gestational age (AGA) infants, through the analysis of the ABR responses to click and tone burst stimulus in the first six months of life. Method: A longitudinal, observational and multicenter study was conducted. A total of 172 SGA and AGA infants, term and preterm, were evaluated in the neonatal period and at three and six months of age through the ABR with click and tone burst stimulus with 0.5 kHz and 1 kHz at 80dBHL. Results: in the neonatal period, the term SGA infants did not differ from term AGA infants for ABR responses. The same was observed between preterm SGA and preterm AGA infants. When comparing the term and preterm SGA groups, there was a difference between the latencies of waves III, V and interpeak intervals (lTPI) I-III and I-V, with longer latencies in preterm SGA; there were no differences with the tone burst stimuli in the analyzed frequencies. When comparing the AGA term and preterm groups, differences were observed on latencies of waves III, V and ITPI III-V and I-V, with longer latencies for preterm infants. There were no differences in the frequencies evaluated with the tone burst stimuli. At three months of age, there were no differences between the term SGA and AGA; when comparing preterm SGA and AGA, differences were found for ITPI III-V, with shorter latencies in preterm SGA. SGA term and preterm infants did not differ; there were differences between term and preterm AGA in latencies of wave V and ITPI I-V. In the third data collection, at six months of age, term SGA and AGA infants significantly differed on latencies of wave III and ITPI I-III, which did not occur when comparing preterm SGA and AGA infants, who differed only regarding ITPI III-V. Significant differences were only observed when comparing term and preterm SGA infants regarding the tone burst stimuli at 0.5 kHz. Conclusion: The findings of this study showed that the maturational process of the auditory pathway in SGA infants occurs at different speed when compared to AGA infants; SGA infants have accelerated maturation, especially in the first three months of age, thus characterizing a recovery period from the hearing standpoint; in the neonatal period, the maturation of the central auditory nervous system is more influenced by prematurity than birth weight; maturation occurred in caudo-rostral direction in the two groups. The ABR with tone burst at 0.5 kHz and 1 kHz evidenced maturational process, but not in such detail as with the click stimuli. The SGA infants should be monitored until at least three years of age
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Pandit, Anand. "Modelling whole-brain structural connectivity in preterm infants." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18060.
Full textAbstract:
Premature birth is a major issue for neurological health. Advances in medical care have led to a decrease in neonatal mortality; however, morbidity in preterm survivors remains substantial and neurocognitive issues, particularly involving cognition, language and behaviour are prevalent. Cerebral white matter injury is common in preterm-born infants and is associated with neurocognitive impairments. By identifying the pattern of connectivity changes in the brain following premature birth a more comprehensive understanding of the neurobiology underlying these deficits could be obtained. Whole-brain macrostructural connectivity was characterised in a group of preterm-born children, and the influence of age and prematurity was explored using a data-driven analysis of diffusion magnetic resonance imaging data. An age-adapted framework, combining anatomical and tissue segmentations with probabilistic diffusion tractography, was used to derive connectivity matrices, weighted by mean tract anisotropy: a measure of connective certainty and strength. In a sparsified, group-consistent connectivity matrix, a novel feature selection method comprising Lasso regression and stability selection was used to identify connections whose mean anisotropy was related to age at imaging or delivery. As hypothesised, older children were found to have greater connectivity in tracts involving frontal or temporal lobe structures. Increasing prematurity at birth was related to widespread, bilateral reductions in connectivity in all cortical lobes and several sub-cortical structures, consistent with previous histological and neuroimaging data. Results were robust to both increasing sparsity and the removal of subjects with serial imaging in the cohort. The pattern of white matter damage elicited in these results may be responsible for the neurocognitive impairments observed. This thesis presents a scalable, data-driven method, which could detect contrasting effects of development and prematurity in a sparse model of infant whole-brain structural connectivity. The approach can be used to evaluate connectivity in ever-increasing detail and undertake iterative discovery of the macroconnectome with increasing precision.
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VanMeenen, Kirsten M. "Brain electrical activity in infants of depressed and anxious mothers." College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2587.
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Thesis (Ph. D.) -- University of Maryland, College Park, 2005.Thesis research directed by: Human Development. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Jary, Sally Louise. "Assessing neurodevelopmental outcome in infants with severe perinatal brain injury." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.665148.
Full textAbstract:
Historically the evaluation and reporting of neurodevelopmental outcomes following perinatal brain injury have been limited to good outcome/poor outcome or disabled/not disabled. More infants are surviving and new treatments to protect the brain require careful testing. Sensitive measures of evaluating developmental outcome in infants with the poorest outcome are required. The aims of this thesis are to describe developmental measures widely used; to examine data arising from a key developmental measure in two groups of children with perinatal brain injury; to use the data to quantify the abilities of even the most severely affected and to compare these findings with neuroimaging in infants with Post Haemorrhagic Ventricular Dilatation (PHVD); and to compare findings of two different editions of the key measure in a group of infants with Neonatal Encephalopathy (NE). Formal assessment at 2 years using the Bayley Scales of Infant Development (Bayley-2) confirmed wide-ranging, but frequently poor outcome, in infants with PHVD. Bayley Developmental Quotients (DQ), used in preference to conventional Bayley-2 Index scores, were found to differentiate between grades of functional ability and disability, even in the most severely delayed infants. Bayley DQ correlated strongly with parenchymal lesion area measured on neonatal cranial ultrasound scans but increasing ventricular size was not associated with reductions in Bayley DQ in infants with preceding grade 3 IVH. Cerebral, thalamic and cerebellar brain volumes from MRI scanning at term age were found to be significantly affected in this cohort. Smaller brain volumes were associated with decreasing Bayley DQ and with motor development in particular. These findings have the potential to enhance the precision of outcome prediction in infants with PVHD which may be of use to clinicians in informing early direction of care and in providing information to families about developmental challenges facing their baby. Comparative study of Bayley-2 scores with revised Bayley Scales of Infant and Toddler Development (Bayley-3) in infants with NE, found higher than expected Bayley-3 scores particularly in those with severe delay. Increased Bayley-3 cut-off thresholds for severe disability are recommended when comparing outcomes using different versions of the test.
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Boynewicz, Kara, Suzann Campbell, Whitney Cole, Laura Zawacki, April Clark, Dipti Kale, and S. Madhavan. "Behavior During Tethered Kicking in Infants with Periventricular Brain Injury." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/8358.
Full text
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Campbell, Suzann K., Whitney Cole, Kara Boynewicz, Laura Zawacki, April Clark, Deborah Spira-Gaebler, Raye-Anne DeRegnier, et al. "Behavior During Tethered Kicking in Infants with Periventricular Brain Injury." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/8360.
Full textAbstract:
Purpose: To describe behavior of children with periventricular brain injury (PBI) in a tethered-kicking intervention.
Methods: Sixteen infants with PBI were randomly assigned to exercise or no-training in a longitudinal pilot study. Frequencies of leg movements and interlimb coordination were described from videos at 2 and 4 months' corrected age (CA).
Results: Eight of the 13 children (62%) with longitudinal data increased the frequency of leg movements while tethered to a mobile between 2 and 4 months' CA. Movement frequency was correlated with scores on the Test of Infant Motor Performance, but no differences between experimental groups were found. Children with typical development at 12 months' CA increased the proportion of leg movements that were synchronous between 2 and 4 months, as did a child with cerebral palsy in the experimental group.
Conclusions: The tethered-kicking intervention facilitates movement in infants with PBI, but effects on development remain to be demonstrated.
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Grau, Olivares Marta. "Neuropsychological and structural brain correlates of lacunar infarcts." Doctoral thesis, Universitat de Barcelona, 2008. http://hdl.handle.net/10803/2714.
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L’infart cerebral és la segona causa de mort, així com d’incapacitació a nivell mundial (Di Carlo et al.,2000), essent responsable de múltiples seqüeles físiques i cognitives, incloent la demència. L’infart cerebral es caracteritza per una simptomatologia neurològica focal i sobtada en consonància amb la localització topogràfica de la lesió cerebral, un cop s’han exclòs altres possibles causes. La demència vascular (DV) històricament s’ha basat en el model de demència multi-infart (Erkinjuntti et al.,2002), tot i que cada vegada hi ha una major evidència de que diferents patologies vasculars (malaltia vascular subcortical de petit vas o infarts llacunars), així com infarts corticals, poden contribuir a desenvolupar-la (Hachinski et al.,1974; Esiri et al.,1997; Rockwood et al.,1999; Erkinjuntti et al.,1999; Pohjasvaara et al.,2000; Ballard et al.,2000). L’objectiu d’aquesta recerca és l’estudi del perfil neuropsicològic i dels dèficits cognitius associats a la malaltia vascular cerebral de petit vas (infarts llacunars i lesions de la substància blanca), així com l’evolució d’aquests pacients després de 2 anys d’haver patit l’event vascular. Aquest tema mereix especial interès perque la malaltia vascular subcortical de petit vas és una de les causes més comunes de demència vascular (DV), i el fet de poder conèixer el seu estat prodròmic i poder previndre els principals factors de risc, ens podrien fer possible el desenvolupament d’estratègies preventives. Aquesta àrea d’estudi també mereix atenció perque s’han fet molts estudis sobre l’evolució i les seqüeles cognitives en els infarts isquèmics de gran vas, però no hi ha gaire evidència sobre l’efecte d’un primer ILL i l’evolució a llarg terme d’aquests pacients. Finalment, no hi ha estudis a la literatura sobre el perfil neuropsicològic de les diferents síndromes llacunars (segons Miller-Fisher) i la seva evolució a llarg terme.
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Kiseleva, Anna. "L’efficience inverse de l'influence de l'odeur maternelle sur la catégorisation des visages chez le nourrisson." Electronic Thesis or Diss., Bourgogne Franche-Comté, 2023. http://www.theses.fr/2023UBFCK082.
Full textAbstract:
Cette thèse examine comment le principe de l'efficience inverse peut être appliqué à l'interaction olfacto-visuelle sur le développement du nourrisson en utilisant une stimulation périodique visuelle rapide (FPVS) avec une approche de marquage fréquentiel en électroencéphalographie (EEG). En particulier, nous avons essayé de confirmer ce principe en nous basant sur le développement de la vision pendant la première année de la vie (étude 1) et une demande visuelle différente à un âge donné (études 2 et 3) car il a été montré que la perception visuelle du nourrisson peut être facilitée par la réception de signaux olfactifs.Nous avons observé qu'un effet de facilitation de l'odeur maternelle sur la catégorisation des visages diminue progressivement avec la maturation du système visuel entre 4 et 12 mois (étude 1), montrant un compromis développemental entre la vision et l'olfaction. Cela suggère que la force de l’effet de l’odeur est liée à celle de la réponse aux visages, ici à partir de stimuli visuels complexes. Ainsi, dans l'étude 2 manipulant la demande visuelle (en simplifiant les stimuli) chez des nourrissons de 4 mois, nous avons trouvé une réponse sélective aux visages plus forte dans ce cas associé à une réduction de l'effet de l’odeur. Enfin, tenant compte de la catégorisation des visages plus efficace dans le cerveau des enfants de 12 mois en raison du développement visuel, dans l’étude 3 nous avons au contraire augmenté la demande visuelle en accélérant la vitesse de présentation des images. Cette fois, une réponse sélective des visages plus faible a été observée, mais l'effet d'odeur n'a pas augmenté, mais plutôt réduit, la réponse, suggérant une surcharge sensorielle.Dans l'ensemble, ce travail de thèse démontre pour la première fois l'application du principe d'efficience inverse à l'olfaction au cours du développement sensoriel. La réponse sélective au visage plus forte (en raison du niveau de maturation suffisant de la vision ou de la diminution de la demande visuelle) conduit à l'interaction olfactive-visuelle la plus faible (c'est-à-dire la facilitation intersensorielle), cependant la faible réponse sélective des visages n'est pas toujours liée à un plus fort effet de l'odeur: seulement quand le système visuel n'est pas suffisamment développé au début de la vieThis thesis examines how the inverse effectiveness principle can be applied to the olfactory-to-visual interaction during infant development using fast periodic visual stimulation (FPVS) with a frequency-tagging approach in scalp electroencephalography (EEG). In particular, we have tried to confirm this principle based on the developmental improvement of vision (Study 1) and different visual demand at a given age (Study 2 and 3) as it was shown that infant visual perception can be facilitated by the reception of odor cues.We observed that a facilitation effect of maternal body odor on rapid face categorization gradually declines with the progressive maturation of the visual system from 4 to 12 months (Study 1), showing a developmental trade-off between vision and olfaction. This suggests that the strength of the odor effect is linked to the strength of the face-selective response, elicited here using quite complex naturalistic stimuli. Thus, in Study 2, we manipulated visual demand (i.e., simplifying the stimuli) in 4 month-old infants and found a stronger face-selective response in the less demanding categorization that led to the suppression of the odor effect. Taking in account the effective face categorization in 12-month-old brain linked with visual development, in Study 3, we instead increased visual demand by doubling the image presentation rate. As expected, a weaker face-selective response was measured, however the odor effect did not increase but rather reduced the response, suggesting a sensory overload.Overall, this dissertation demonstrates for the first time the application of the inverse effectiveness principle to olfaction during perceptual development, through Study 1 and 2. The stronger face-selective response (due to the sufficient maturation level of vision or decreased visual demand) leads to the weakest olfactory-to visual interaction (i.e. intersensory facilitation), however the low face-selective response not always links to the enhanced odor effect: only when visual system is not enough developed in the early infancy