Dr. Beecroft: Presenting a synopsis of the current thinking around autism etiology and treatment

The science behind an autism diagnosis and its treatment is changing very rapidly, which is a good thing for our members, according to Dr. William Beecroft, medical director of behavioral health at Blue Cross Blue Shield of Michigan. Based on collateral research on precision psychiatry and neuroscience, this column explores the current, predominant hypothesis of the etiology of autism.

We’ve known for many years that neonates, when born, have an overabundance of neurons and neural junctions in the brain — the most that they will ever have in their lives. Autistic children have even more, although the reason is currently unknown. We also know that the major neural pathways that link parts of the brain start out with a variable density of these neurons and junctions. When mapped to areas of the brain that mitigate and drive the symptoms of autism we see, they directly relate to those symptoms.

For example, the pathway to the Fusiform Gyrus (occipital lobe), which is related to facial recognition, is hypoactive in some autistic individuals, contributing to social difficulties interacting with others, especially strangers. Other connections and pathways such as the pathway to the temporal parietal lobe (which is linked to social cognition) is dysfunctional with many individuals as well as the path to the orbital frontal cortex, which has a role in social behavioral as well. Having poor function in these areas at the same time then drives the social difficulties many individuals exhibit.

These pathways may have either too many or not enough neurons and neural connections. If the pathway has too many, the behaviors mitigated by that pathway are accentuated. Those with not enough are deficit in the behaviors controlled by those areas of the brain. I have only provided three pathways involved in common behavioral symptomology, but there are other pathways involved as well. The observed behaviors and symptoms are a combination of the variable factors in multiple pathways and modify each other due to feedback loops in the brain.

The way the brain works then is to naturally “prune” the excess neurons in pathways where there is too much activity and not change or modestly “grow” additional neurons and junctions in pathways that do not have enough activity. This process is referred to as the brain being “plastic” and having over time the ability to strengthen weak pathways and slow down ones that are too active. This “plasticity” is more pronounced in younger children and decreases over the lifespan.

This is where Applied Behavior Analysis, known as ABA, comes in. As a combination of learning theory and behavior modification, ABA works by increasing the strength of the pathways, which will then improve (as much as possible) the behavior that are a deficit for the individual. The other pathways that are too active can be slowed by not giving positive reinforcement for the negative behaviors that are desired to be “extinguished” or “mitigated.” Both processes are a natural occurrence of pruning of the excess neurons and not decreasing or slightly increasing the neurons in the hypoactive pathways. 

This is like habit modification and learning in general. You practice things you want to remember, which results in having faster recall. Those things you want to forget or habits you want to lose aren’t rewarded. It takes much longer to extinguish a habit or behavior than learn a new one. The key to successful change, though, is consistent and repetitive reward for positive change and no reward for negative attributes. This is where working in a team with clear communication of even minute changes is important for all people who interact with the individual. 

Once the behaviors have been brought to their best ability, there needs to be a period of trial and error with less frequent rewards to capitalize on the gains made to the process outlined above.

This combination of the science behind the process and improving the consistency in the process offers significant hope for improvement in function to the best of that individual’s capacity.

References:

• NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. Grabrucker AM, editor. Autism Spectrum Disorders [Internet]. Brisbane (AU): Exon Publications; 2021 Aug20. doi: 10.36255/exonpublications.autismspectrumdisorders.2021.diagnosis Chapter 2 Autism Spectrum Disorders: Diagnosis and Treatment Ronan Lordan, Cristiano Storni, and Chiara Alessia De Benedictis.

• Determining Associations Between Intervention Amount and Outcomes for Young Autistic Children a Meta-Analysis. Micheal Sandbank, PhD; James E. Pustejovsky, PhD; Kristen Bottema-Beutel, PhD; Nicolette Caldwell, PhD; Jacob I. Feldman, PhD; Shannon Crowley LaPoint, PhD; TiffanyWoynaroski, PhD, CCC-SLP

• Neurodevelopmental Hypothesis about the Etiology of Autism Spectrum Disorders Toshio Inui 1 *, Shinichiro Kumagaya2 and Masako Myowa-Yamakoshi 3 1Department of Psychology, Otemon Gakuin University, Osaka, Japan, 2Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan, 3Graduate School of Education, Kyoto University, Kyoto, Japan Huttenlocher, P.R.

• Synaptic density in human frontal cortex - developmental changes and effects of aging Brain Res. 1979; 163:195-205
  Children with Autism Have Extra Synapses in Brain | Columbia University Irving Medical Center