Table of Contents<\/b><\/p>\n [\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column][vc_single_image image=”4393″ img_size=”full”][vc_column_text single_style=””]<\/p>\n Figure 1. Atypical Pattern of Connectivity in Autism Spectrum Disorder (ASD):<\/b> Atypical patterns of connectivity in ASD derive from abnormalities in the density, distribution, and cellular construction of grey and white matter<\/b> in the brain. (i) Hyper-connectivity<\/b> occurs, where these abnormalities consist of unusually dense<\/i><\/b> growth of neurons and their projections. (ii) Hypo-connectivity<\/b> occurs, where these abnormalities consist of unusually sparse<\/i><\/b> growth of neurons, their projections, and\/or their supporting glial cells. Both hyper- and hypo-connectivity have critical effects on behavior.<\/p>\n [\/vc_column_text][vc_custom_heading text=”Introduction” use_theme_fonts=”yes” el_id=”introduction”][vc_column_text single_style=””]Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition that affects 1 in 36 children aged 8 years (\u2248 4% of boys and 1% of girls)<\/b> in the United States. Diagnosis is explicitly based on the presence of characteristic behavioral impairments (i.e., early-onset difficulties in social communication and unusually restricted, repetitive behaviors and interests) that emerge in the second year of life and thus is not typically made until 3 to 4 years of age. Current studies of early brain and behavior development have provided valuable new insights into the nature of this condition. Most importantly, autism-specific brain imaging features have been identified as early as six months of age, and age-specific brain and behavioral changes have been revealed across the first two years of life, highlighting the developmental nature of ASD [1].[\/vc_column_text][vc_custom_heading text=”What is Known” use_theme_fonts=”yes” el_id=”blog-scroll-point-1″][vc_column_text single_style=””]<\/p>\n 1. Brain Size and Volume:<\/strong><\/p>\n One of the most consistent findings from early studies of brain development is that people with ASD show an abnormal pattern of growth and decline, both in overall size, and also in volume (Figure 2; Box \u2013 1)<\/b>. Specifically:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n The Postnatal Brain is an Unfinished Project!<\/i><\/strong><\/p>\n At birth, the human brain weighs on average about 350 g – that is about a third of the average adult brain, which weighs about 1,300 to 1,400 g [4]. In fact, the postnatal (after-birth) brain is an unfinished project. That is why the baby at birth has been described aptly as an \u2018external fetus,\u2019<\/b> which confers a sense of the vulnerability and the dependency of the baby.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n An enormous amount of development will take place during the initial few years of life. It has been suggested that the brain increases in volume by 100% in the first year of life (Figure 2)<\/b>. However even after infancy the project is not finished. The brain continues to grow, mature, and change in structure and function until we are at the end of our 20s, i.e., around adolescence.<\/p>\n [\/vc_column_text][vc_single_image image=”4392″ img_size=”full” el_class=”p-m-left-20″][vc_column_text single_style=””]<\/p>\n Figure 2. Measurement of Head Circumference, or Occipital Frontal Circumference (OFC)<\/b>, is a reflection of head growth and is a useful tool in tracking and monitoring childhood growth and development. Both in overall size, and also in volume, the brains of individuals with ASD show an abnormal pattern of growth and decline.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Connecting up the Brain<\/i><\/strong><\/p>\n Even though most neurons are generated while we are still in the womb, the connections of these neuronal cells, known as synaptogenesis, occur postnatally. And most importantly, this occurs at different rates in different regions of the brain<\/b>. As the connections in the head develop, consequently the size of the head itself requires to grow. As a result, it expands by about 14 cm on average during the first two years of life<\/b> outside the womb and then by an additional 7 cm during early childhood and adolescence<\/b> [5] (Figure 2)<\/b>.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Box-1<\/b><\/p>\n The Postnatal Brain is an Unfinished Project!<\/b><\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 2. Brain Connectivity:<\/strong><\/p>\n In general, it is recognized that the set of behaviors that define or commonly present in ASD are associated with abnormal brain connectivity (Figure 1)<\/b>. In recent decades, several seminal studies have demonstrated anomalous brain connectivity to be of central importance for an understanding of the brain bases of autism, and its role as the major structural as well as functional anomaly in the brain of people with ASD is not contested anymore.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Atypical patterns of connectivity in ASD derive from abnormalities in the density, distribution, and cellular construction of grey and white matter in the brain, leading to either hyper-connectivity or hypo-connectivity (Figure 1)<\/b>.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Both hyper- and hypo-connectivity have critical effects on behavior. For example:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Even though the existence and significance of abnormal brain connectivity in ASD is no more in doubt, there remain certain uncertainties concerning the atypical patterns of connectivity, for example:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 3. Cerebral Cortex Abnormalities:<\/strong><\/p>\n There is clear evidence implicating atypicality in the density of grey and white matter in individuals with ASD [7]. This evidence derives (a)<\/b> partly from studies of the exterior surfaces of the brain<\/b> and (b)<\/b> partly from studies of the cellular structure of cortical regions.<\/b><\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Studies utilizing measures of the exterior surfaces of the brain<\/b> have shown abnormalities in all of the following:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Nonetheless, the precise anomalies of cortical surface area, thickness, and gyrification that have been reported are numerous and varied, because the groups studied have differed in age, gender, and functioning levels of ASD.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Studies of the cellular structure of the minicolumns<\/b> of grey and white matter in the cerebral cortex of individuals with ASD also reliably show abnormalities [8]. The consensus in the literature findings is that:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 4. Cerebellar Abnormalities:<\/strong><\/p>\n Structural magnetic resonance imaging (sMRI) and post-mortem studies reveal that the grey matter in the cerebellum is decreased<\/i><\/b> relative to the neurotypical brain. In the cerebellum, the most significant finding that has been demonstrated and stood the test of time is, reduction in the number of Purkinje cells<\/b> [9]. Considering the role of Purkinje cells in the inhibitory control of neural activity, reduced inhibition deriving from cerebellar abnormalities has consequently disruptive effects not only on motor behavior, but also on cognitive, affective, as well as sensory behaviors.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 5. Abnormal Circuitry:<\/strong><\/p>\n The region of cortical and subcortical structures within which<\/i><\/b>, or between which<\/i><\/b>, abnormalities of grey and white matter are most consistently observed, are predictably, those that are components of widely distributed brain circuits subserving behaviors that are aberrant in people with ASD [10].<\/p>\n [\/vc_column_text][vc_column_text single_style=””]Circuits with likely or potential relevance to autism include, what are termed:[\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_custom_heading text=”Methods of Research into Brain Structure in Individuals with ASD” use_theme_fonts=”yes” el_id=”blog-scroll-point-2″][vc_column_text single_style=””]Brain structure can be studied at various levels, ranging from, for example:<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][vc_column_text single_style=””]Consequently, there are correspondingly several different methods of probing brain structure, as follows [11-12].[\/vc_column_text][vc_column_text single_style=””]<\/p>\n 1. Post-Mortem or Autopsies Studies: <\/strong><\/p>\n Invaluable for systematic examination at both macroscopic and microscopic levels of analysis, having the advantage that structural examination can be extended over a prolonged period. However, the disadvantage is that small numbers of cases are available, prone to be older individuals or individuals with multiple disorders that may have affected the brain.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 2. Animal Models: <\/strong><\/p>\n Involve lesioning specific areas of the brain, usually for e.g., the mouse or rat. As well as assessing subsequently the effects on the animal\u2019s behavioral pattern.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 3. Insights from Syndromic Forms of ASD: <\/strong><\/p>\n Various forms of syndromic ASD can reveal abnormalities of likely relevance to autism, for instance, both Fragile-X syndrome<\/i><\/b> and Turner syndrome<\/i><\/b> involve structural abnormalities within the limbic system of the brain. While autistic traits in individuals with tuberous sclerosis<\/i><\/b> are associated with malformations of temporal lobe cortex.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 4. Computerized (Axial) Tomography (CT\/CAT Scan<\/i>): Often called CT scans, used ideally in hospitals and other clinical settings, especially for diagnosis purposes, for e.g., brain tumors and hemorrhaging. Uses X-rays; this allows for multiple sequential X-rays to be taken and the computer is then used to build up a three-dimensional (3D) image of the brain. Applicable for examining bony tissue, but undesirable because of radiation risks. Notably, passing X-rays through healthy individuals, and in particular healthy children, even if such procedures are necessary for diagnosis.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 5. Diffusion Tensor Imaging (DTI<\/i>): <\/strong><\/p>\n Also known as diffusion MRI<\/i><\/b>, is a relatively new technique based around the process of diffusion, i.e., moving of the molecules, and is used to detect changes in diffusion of water molecules in both grey and white matter in the brain. Thus, this method of brain imaging is particularly suited for examining brain tissue at a more microscopic level than can be achieved with the standard form of sMRI.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n 6. Structural Magnetic Resonance Imaging (sMRI\/MRIs<\/i>): <\/strong><\/p>\n [\/vc_column_text][vc_single_image image=”4391″ img_size=”full” el_class=”p-m-left-20″][vc_column_text single_style=””]<\/p>\n Figure 3. Picturing the Brain: (i)<\/b> Developments in brain imaging have revolutionized the way we can study the brain. (ii) Structural MRI (sMRI)<\/b> allows for repeated images<\/i><\/b> to be made of the same brain and so can show how<\/i><\/b> the structure changes over time. (iii) Functional MRI (fMRI)<\/b> is good at showing us where<\/i><\/b> things are in the brain and what<\/i><\/b> they are doing, but it is not so good at showing us when<\/i><\/b> they are happening. Thus, neuroimaging techniques allow us to visualize brain activity.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Magnetic resonance imaging provides much better means of allowing us to image the brains of healthy children and adults as such without the attendant health risks, which gives sMRI its main advantage over CAT scanning. Uses a machine-generated magnetic field, which resonates in ways that can be used to build up a detailed 3D image of brain structure. sMRI also gives a much clearer picture of the brain; and it can differentiate grey matter and white matter in the brain (Figure 3)<\/b>.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Most of all, this technology has also enabled us for repeated scanning of the same brain and so rendered us the ability to visualize how they develop over a span of time (Figure 3)<\/b>. However, the scanning machine is noisy and claustrophobic, and the individual being examined has to keep still for a longer period of time. This clearly poses a problem with children because most pediatric MRI studies require the ASD individual to lie still for between 5 to 20 minutes. As everyone who works with children will tell you, getting them to lie still even for a few reasonably short periods of time can be extremely difficult!<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Besides, the use of the machine is expensive. For all these reasons, studies of individuals with ASD tend to include small numbers of participants, and the fact that few studies include very young or low-functioning individuals unless sedated.<\/p>\n [\/vc_column_text][vc_custom_heading text=”Conclusion” use_theme_fonts=”yes” el_id=”conclusion”][vc_column_text single_style=””]<\/p>\n In an infant, the presence of abnormal crossing of cranial growth parameters by head measurements (i.e., an actual measurement out of the normal range) raises the possibilities of a developing central nervous system disorder. As a result, one of the possible disorders in both \u2018macrocephaly\u2019 (large head) and \u2018microcephaly\u2019 (small head) is a disease entity of the autistic syndrome.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n It is widely accepted there exists abnormal connectivity within and between various brain regions and structures. Both hyper- and hypo-connectivity occur, and it is usually thought that hyper-connectivity within local networks is associated with isolated peaks of ability, and while hypo-connectivity between more widely distributed regions or networks is associated with autism-related behavioral anomalies or impairments. Meaning that the autistic brain is not wired up normally.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n Anomalous connectivity in the brains of individuals with ASD probably results from abnormalities in the density of grey matter and\/or white matter in specific brain regions or structures, i.e., occasionally too much, and sometimes too little. Moreover, abnormalities may vary with age, gender, and complexity of an individual\u2019s autism-related problems.<\/p>\n [\/vc_column_text][vc_column_text single_style=””]<\/p>\n The developments in brain imaging techniques completely revolutionized the way in which we can study the brain by enabling us to produce images of it in vivo, that is within the living body.<\/p>\n [\/vc_column_text][vc_column_text single_style=”” el_class=”blog-banner-section”]<\/p>\n Folate (vitamin B9) is very important for your child\u2019s brain development!<\/p>\n During pregnancy, it helps prevent neural tube defects and plays a big role in forming a normal and healthy baby\u2019s brain and spinal cord. Folate also helps cells divide and assists in both DNA and RNA synthesis.<\/p>\n Emerging research suggests that the presence of FRAAs negatively impacts folate transport into the brain.<\/p>\n Yes, there is a test – The Folate Receptor Antibody Test (FRAT\u00ae<\/sup>) has emerged as a diagnostic tool for detecting the presence of FRAAs.<\/p>\n It is important to screen at an early age or as soon as possible as there may be corrective measures available. Please consult your physician for further information.<\/p>\n To request a test kit, click on the button below.<\/p>\n Request Now<\/a><\/p>\n<\/div>\n<\/div>\n [\/vc_column_text][vc_column_text single_style=”” el_class=”text-gray-23″]For information on autism monitoring, screening and testing please read our blog<\/a>.[\/vc_column_text][\/vc_column][\/vc_row][vc_row el_id=”references”][vc_column][vc_custom_heading text=”References” use_theme_fonts=”yes”][vc_column_text single_style=””]<\/p>\n [\/vc_column_text][\/vc_column][\/vc_row]<\/p>\n","protected":false},"excerpt":{"rendered":" Figure 1. Atypical Pattern of Connectivity in Autism Spectrum Disorder (ASD): Atypical patterns of connectivity in ASD…<\/p>\n","protected":false},"author":3,"featured_media":4393,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[71,64],"tags":[],"yoast_head":"\n\n
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\n<\/strong><\/p>\nDid You Know? Folate Receptor Autoantibodies (FRAAs) may impede proper folate transport.<\/h4>\n
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Is there a test for identifying Folate Receptor Autoantibodies (FRAAs)?<\/h4>\n
![\"FRAT](\"https:\/\/autism.fratnow.com\/blog\/wp-content\/uploads\/2023\/12\/frat-mascot-image.webp\")
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\nhttps:\/\/policy.bristoluniversitypress.co.uk\/child-development-and-the-brain-1<\/a><\/li>\n<\/ol>\n