Autism is a developmental neurobiological disorder that manifests itself during the first three or four years of life and lasts throughout a person’s lifetime. Although each autistic syndrome is different in its symptomatology, this disorder is characterized by two common features: 1) persistent deficits in social communication and interaction across multiple contexts, and 2) restricted, repetitive patterns of behavior, interests, or activities (Volden, 2017).
Autism primarily involves behavioral deficits. However, numerous research studies have shown that the problem begins during prenatal brain development. Below, the most recent lines of research on the neurobiological causes leading to this disorder will be described.
1. Autism and brain volume. Researchers have found a correlation between the degree of excess brain growthand the severity of autism symptoms. Studies conducted using structural magnetic resonance imaging have specifically demonstrated that brain overgrowth starts in the first year of life, if not sooner (Amaral et al., 2017; Kessler, Seymour, & Rippon, 2016). Although the cause of this excessive brain growth is currently unknown, the new datarepresent great progress for the early diagnosis and treatment of autism.
2. Autism and abnormal organization of the cerebral cortex. From the first months of gestation, the cerebral cortexis organized into various areas that differ from one another. However, it has been observed that this differentiation does not occur in the same way in children with this disorder. Researchers, utilizing a tomography procedure, examined the postmortem tissue from children with autism and without this, all between the ages of 2 and 15 years. Clusters of disorganized brain cells were discovered in the prefrontal cortex, a brain region strongly associated withcommunication and social interaction (Sanz-Cortes, Egana-Ugrinovic, Zupan, Figueras, & Gratacos, 2014). Other subsequent studies have supported this finding, with defective neuronal development during the second and third trimesters of pregnancy, beingone of the possible causes.
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3. Autism and amygdalahypoactivation. The amygdala is the brain structure responsible for emotional processing. The amygdala’s role in emotion is so important that individuals with amygdala damage are incapable of recognizing other people’s emotions, expressing their own emotions, or even naming these emotions. Previous studies utilizing a functional magnetic resonance imaging procedure show hypoactivation in the amygdala of children diagnosed with autism during emotion recognition tasks in comparison with the level of activation in age-matched controls(Barnea-Goraly et al., 2014). Other authors found certain morphological and sensory differences between the amygdala of children with autism and those without this(Kiefer et al., 2017).
4. Autism and slow functional brain development. Although no conclusive data exist, researchers have found that areas of the brain implicated in communication and social interaction grow and develop more slowly in boys with autism than in non-autistic boys (Ameis and Catani, 2015; Washington et al., 2014). This would explain the inability of these children to form emotional ties and to relate to their environment.
As observed in this post, there are numerous theories aimed at explaining autism. This multitude of hypotheses is due to the wide range of symptoms manifested by autism itself and to the complexity of the disorder. Nevertheless, future lines of research support the first two proposals for they are encouraging, and may lead to a better understanding of autism and its prevention and intervention during a person’s lifetimeby professional psychologists and neuropsychologists, among others.
Amaral, D. G., Li, D., Libero, L., Solomon, M., Van de Water, J., Mastergeorge, A., … Nordahl, C.W. (2017). In Pursuit of Neurophenotypes: The Consequences of Having Autism and a Big Brain. Atism Research: Official Journal of the International Society for Autism Research,10(5), 711-722.
Ameis, S. H. y Catani, M. (2015). Altered white matter connectivity as a neural substrate for social impairment in Atism Spectrum Disorder. Cortex, 62, 158-181.
Barnea-Goraly, N., Frazier, T. W., Piacenza, L., Minshew, N. J.,Keshavan, M. S., Reiss, A. L., &Hardan, A. Y. (2014). A preliminary longitudinal volumetric MRI study of amygdala and hippocampal volumes in atism. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 48, 124-128.
Kessler, K., Seymour, R. A., & Rippon, G. (2016). Brain oscillations and connectivity in autism spectrum disorders (ASD): new approaches to methodology, measurement and modelling. Neuroscience &Biobehavioral Reviews, 71, 601-620.
Kiefer, C., Kryza-Lacombe, M., Cole, K., Lord, C., Monk, C., & Wiggins, J. L. (2017). 126-Irritability and Amygdala-Ventral Prefrontal Cortex Connectivity in Children with High Functioning Autism Spectrum Disorder. Biological Psychiatry, 81(10), 53-58.
Sanz-Cortes, M., Egana-Ugrinovic, G., Zupan, R., Figueras, F., &Gratacos, E. (2014). Brainstem and cerebellar differences and their association with neurobehavior in term small-for-gestational-age fetuses assessed by fetal MRI. American journal of obstetrics and gynecology, 210(5), 452-459.
Volden, J. (2017). Autism Spectrum Disorder. California: Springer International Publishing.
Washington, S. D., Gordon, E. M., Brar, J., Warburton, S., Sawyer, A. T., Wolfe, A., … Gaillard, W. D. (2014). Dysmaturation of the default mode network in autim. Human brain mapping, 35(4), 1284-1296.
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