What is autism and how does it affect the brain?

Autism is a neurobiological developmental disorder appearing in the first three to four years and persisting across the lifespan, marked by persistent deficits in social interaction and communication and by restrictive, repetitive behaviors or interests.

What neurobiological causes lead to autism?

Multiple neurobiological factors are implicated, including altered fetal neural development, abnormal cortical organization, atypical brain growth, and limbic system differences, suggesting interacting prenatal and early postnatal mechanisms rather than a single cause.

How does excessive brain volume relate to autism?

MRI studies link accelerated brain growth in infancy with greater autism symptom severity; excessive brain volume often begins in the first year and may support earlier diagnosis and targeted interventions.

How is the cerebral cortex organized differently in autism?

Research shows disorganized cortical regions and misplaced cells, especially in the prefrontal cortex related to social and communication functions, possibly originating during the second and third trimesters of gestation.

What role does the amygdala play in autism?

The amygdala often shows reduced activation and morphological differences in autistic individuals, which can impair emotion recognition and processing during social tasks as shown by fMRI studies.

Does functional brain development slow in autism?

Some studies indicate slower maturation of brain areas for communication and social interaction in autism, which may hinder affective bonding and inform the timing of early interventions, though evidence remains preliminary.

Autism and the Brain: Neurobiological Causes of Autism

The Murcian Association of Neuroscience explains the relationship between autism and the brain and the neurobiological causes that lead to autism.

Introduction: autism and the brain

Autism is a neurobiological developmental disorder that manifests during the first three or four years of life. Furthermore, it is a disorder that persists throughout the lifespan. Although each autistic syndrome differs in its symptomatology, two factors are common to this disorder:

The child presents persistent deficits in social interaction and communication
They have restrictive and repetitive patterns of behavior, interests, or activities (Volden, 2017).

Neurobiological causes

Autism involves mainly behavioral deficits; however, numerous studies have shown that the problem begins in the neural development of the fetus. Below, the most recent lines of research on the neurobiological causes that lead to this disorder are described.

Autism and brain volume

First, some researchers have found a relationship between the degree of excessive brain growth and the severity of autism symptoms. Indeed, structural and magnetic resonance studies have shown that excessive brain growth in children with autism begins during the first year of life, or even earlier (Amaral et al., 2017; Kessler, Seymour and Rippon, 2016). Although the cause of this accelerated growth is unknown at present, these findings represent a major advance for early diagnosis and treatment of autism.

Autism and abnormal organization of the cerebral cortex

Second, we have the cerebral cortex, which tends to organize into differentiated regions from the first months of fetal gestation. However, it has been observed that this differentiation does not occur in the same way in children with autism. One study compared the brain organization of deceased children diagnosed with autism with others without the diagnosis using a tomographic technique. In that study, both groups were between the ages of 2 and 15. As a result, it was shown that the brains of children with autism had disorganized areas, with misplaced cells in the prefrontal cortex closely related to communication and social interaction (Sanz-Cortes, Egana-Ugrinovic, Zupan, Figueras and Gratacos, 2014). Subsequent studies have supported this finding, one possible cause being abnormal neural development during the second and third trimesters of gestation.

Autism and amygdala hypoactivation

Indeed, the amygdala is the brain structure responsible for emotional processing. Its emotional function is such that when the amygdala is damaged the person is unable to recognize emotions in others, to express them, or even to name them. Some pioneering studies using functional magnetic resonance imaging demonstrated that the amygdala of children diagnosed with autism had a lower functional level when they performed an emotion recognition task, compared to the activation level of same-age children without the diagnosis (Barnea-Goraly et al., 2014). Other authors also found certain morphological and sensitivity differences between the functionality of the amygdala of a child with autism and that of one without the diagnosis (Kiefer et al., 2017).

Autism and slowing of functional brain development

Although there are not yet conclusive data, some studies have found that the brain areas involved in communication and social interaction grow and become functional more slowly in children with autism than in children without the disorder (Ameis and Catani, 2015; Washington et al., 2014). This would explain these children’s inability to form affective bonds and to relate to other people and to their environment.

As can be seen in this post, there are numerous theories that attempt to explain autism. Certainly, this multitude of hypotheses is due to the variety of symptoms that the disorder itself presents and to the complexity that autism encompasses. Nevertheless, future lines of research support the first two proposals, which is encouraging, and will allow psychologists and neuropsychologists, among others, to better understand autism and its prevention and intervention throughout the lifespan.

Bibliography

Amaral, D. G., Li, D., Libero, L., Solomon, M., Van de Water, J., Mastergeorge, A., … y Wu Nordahl, C. (2017). In pursuit of neurophenotypes: The consequences of having autism and a big brain. 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 Autism Spectrum Disorder. Cortex, 62, 158-181.
Barnea-Goraly, N., Frazier, T. W., Piacenza, L., Minshew, N. J., Keshavan, M. S., Reiss, A. L. y Hardan, A. Y. (2014). A preliminary longitudinal volumetric MRI study of amygdala and hippocampal volumes in autism. Progress in Neuro Psychopharmacology and Biological Psychiatry, 48, 124-128.
Kessler, K., Seymour, R. A. y 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. y 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. y 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., … y Gaillard, W. D. (2014). Dysmaturation of the default mode network in autism. Human brain mapping, 35(4), 1284-1296.