Global Data on Autism Spectrum Disorders Prevalence: a Review of Facts, Fallacies and Limitations

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Global Data on Autism Spectrum Disorders Prevalence: a Review of Facts, Fallacies and Limitations Universal Journal of Clinical Medicine 5(2): 14-23, 2017 http://www.hrpub.org DOI: 10.13189/ujcm.2017.050202 Global Data on Autism Spectrum Disorders Prevalence: A Review of Facts, Fallacies and Limitations Onaolapo A Y1, Onaolapo O J2,* 1Behavioural Neuroscience/Neurobiology Unit, Department of Anatomy, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria 2Behavioural Neuroscience/Neuropharmacology Unit, Department of Pharmacology, Ladoke Akintola University of Technology, Osogbo, Osun State, Nigeria Copyright©2017 by authors, all rights reserved. Authors agree that this article remains permanently open access under the terms of the Creative Commons Attribution License 4.0 International License Abstract Autism spectrum disorders (ASDs) are a in the early to mid-1960s [2, 3], while the first range of neurodevelopmental disorders whose aetiologies hospital-based survey in sub-Saharan Africa was are largely unknown. In the past few decades, studies have conducted in five countries in the late 1970s [4]. Autism demonstrated that ASDs occur globally, and that the surveys have since become global, with different countries numbers of recorded cases are rising; however, conducting surveys to determine the prevalence and risk determining the true prevalence figures is still a major factors in their communities [1, 5], and thereby propose challenge, especially in developing nations. Also, subtle strategies to improve identification, diagnosis, differences in cultural norms might impede timely/accurate management as well as promote policy reforms that bring diagnosis and categorisation of patients. In this review, we awareness to the plight of the autistic child. examine the globally-available data on the prevalence of The term ‘Autism’ derives from the Greek word "autos", ASD and discuss some of the challenges of data acquisition, meaning "self”; and it was in the year 1911 that Eugen with reference to how these may impact the reliability of Bleuler first used the word autism in describing a symptom figures obtained. Some of the facts, fallacies and of schizophrenia. However, in 1943 and 1944 respectively, limitations relating to the presently-available figures are Leo Kanner (USA) and Hans Asperger (Germany) also highlighted. described individuals with social/emotional limitations and withdrawn behaviours. Kanner reported behavioural Keywords Neurodevelopment, Aetiology, Prevalence, aberrations such as poor social interaction, obsessiveness, Autism, Data stereotypic movement, and echolalia in the affected children. It was Kanner who first coined the term ‘infantile autism’ (earlier called Kanner’s syndrome) to describe his observations in this group of children who seemed 1. Introduction socially-isolated and withdrawn [6]; while Asperger named the condition he observed Asperger’s syndrome. Decades Epidemiology is not only concerned with patterns of of research will eventually reveal that both syndromes are disease occurrence within human populations, but it is also parts of a highly-variable spectrum of disorders. Autism concerned with the factors that determine or influence spectrum disorders (ASDs) are an array of development of disease, or maintenance of health. Over the neurodevelopmental disorders characterised by cognitive years, different study designs (surveillance, descriptive, and neurobehavioural deficits, whose underlying factors analytical, cohort, case-control and cross-sectional) have are genetic and/or neurobiological [7]. In the Diagnostic been employed in examining the relationships that may and Statistical Manual (DSM) III, autism debuted in 1980 exist between disease and disease determinants in defined as "infantile autism", which was replaced by the term human populations. Generally, epidemiological "Autistic Disorder" in 1987. In the DSM IV, it was referred investigations of neuropsychiatric diseases begin with to as pervasive developmental disorders (PDDs); and cross-sectional surveys, which help to determine the consisted of autistic disorder (autism), Asperger disorder, prevalence of the disease condition, patterns of risk factors, childhood disintegrative disorder, Rett syndrome, and as well as the possible correlates between disease and risk PDD-not otherwise specified (NOS). factors among representative samples [1]. The first Over the years, a lot has changed about our perception of epidemiological survey of autism was initiated in England ASDs, the perceived risk factors, core diagnostic criteria, Universal Journal of Clinical Medicine 5(2): 14-23, 2017 15 and even approaches to management. Presently, according the human brain (notably the cerebellum and cingulate to the DSM V, persistent deficits in social communication/ gyrus) in autistic children) [15]. social interaction and a restricted/repetitive (stereotypical) The cause(s) of the above-mentioned pathological patterns of behaviour, interests or activities; which must be changes are traceable to both genetics and the environment. present in the early developmental period(but might not The heterogeneity of ASD is not only reflected in its become obvious until social demands exceed limited behavioural manifestations, but also in the genetic basis, as capacity), cause clinically significant impairment (in social, many candidate ASD genes have been studied or occupational or other important areas of current implicated [16]. Also, while studies may differ in terms of functioning) and must not be better explained by their conclusions regarding the degree of involvement of intellectual disability or global developmental delay, are genetics, it is generally accepted that genetics plays a the core criteria for the diagnosis of ASD [8]. DSM 5 also crucial role in ASD. Presently, candidate genes that have makes provision for differential diagnosis such as ‘social been implicated in ASD include those that encode for communication disorder’. Level of severity of symptoms neural adhesion molecules, ion channels, scaffold proteins, {3 levels given for both social communication/social protein kinases, receptor/carrier proteins, signaling interaction, and restricted/repetitive (stereotypical) patterns modulator molecules, and circadian relevant proteins [17]. of behaviour} determines the degree of supportive care Environmental factors that had been linked to needed, with level 3 severity requiring very substantial ASD-associated neuroinflammation and immune support. Apart from the core symptoms, patients often have dysfunction include early-life exposure to various co-morbid psychiatric and behavioural manifestations like xenobiotics including heavy metals such as lead, mercury self-injury, aggression, impulsivity, hyperactivity, anxiety and aluminium [18]. The Ethyl mercury compound and mood symptoms; all of which may worsen the overall (Thimerosal) is a bacteriostatic agent that was a component prognosis, stress the caregivers, and further complicate of a number of childhood vaccines in Western nations. The management. Recently, results from epidemiological possibility of its involvement in ASD led to its removal surveys indicate that the global prevalence of ASDs is on from many vaccines meant for children; and while it must the rise; although data from sub-Saharan Africa and a be noted that this was not accompanied by a sharp decline number of other developing countries still show numbers in ASD prevalence, its continued use in vaccines given to that are generally lower than those from the developed pregnant women further complicates the picture [18]. The countries [9-11]. Whether this reflects an absolute low use of aluminium(Al) as an adjuvant in many vaccines has prevalence, deficits in diagnostic skills, mal-adaptation of continued, due to the fact that Al salts help to stimulate the diagnostic criteria as it relates to cultural differences in immune system to yield adequate antibody titres [19]. behaviour, or under-sampling is still being studied. However, there is abundant scientific literature on the The aetiology of ASD is still being studied, and despite neurotoxic effects of Al; and its ability to adversely affect years of research, a complete understanding of the both the immune and the nervous systems, hence making it causative factors is still elusive; and while it is now known a plausible risk factor for triggering ASD [18]. Al’s ability that genetics may plays a big role in ASD, a rapidly to alter neuronal gene expression can also affect the increasing prevalence suggests a bigger role of response of neurons to environmental insults such as toxins environmental factors. [18]. The presence and abundance of environmental risk Generally, abnormalities in neural connectivity factors may be a major determinant of geographical involving synapses, tracts and neuronal communication via variations in the true prevalence figures of ASD; however, neurotransmitters are key pathological features of the brain the wide variety of candidate environmental risk factors in autism [12]. Neurodevelopmental defects in synapse makes matching environmental factors to prevalence a formation/elimination and changes in ratios of challenging task. inhibitory/excitatory synapses leads to defective local and There have also been reports suggesting that some of the long range connectivity [12]. An active neuroinflammatory behavioural characteristics of “autistic” children in process involving the cerebral cortex and the cerebellum; developing countries differ, when compared to those in with associated loss of cerebellar Purkinje cells, marked developed
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