In Hui Ye's presentation on axonal blockage, we spoke about the the success of microscopic magnetic coils in axons which can reversibly prevent axon depolarization(Ye,2020). There are several neurological conditions in which brain regions are abnormally activated, causing divergent behavior. Some examples include: cerebellar ataxia which may result from excessive long term alcohol use, where the cerebellum becomes deficient in inhibiting and refining movement coming from the motor cortex, hyperactivation of the nucleus accumbens and amygdala in those suffering from PTSD, and exaggerated activation of the amygdala in autistic individuals when making eye contact(Liberzon,1999) (Hadjikhani,2018). These hyperactivation neurodivergent conditions lead to exaggerated and uncoordinated movement in those with damaged cerebellums, excessive fear and panic in non-life threatening contexts for PTSD patients, and abnormal anxiety reactions in autistic individuals during standard social interactions, such as making eye contact.
Face processing in humans and other social species have been shown to be vital for effective social interaction and communication. It is so innate in humans, that neurotypical infants instinctually make eye contact and recognize facial expressions such as smiles; this recognition is often evident behaviorally in "appropriate" mirroring actions in infants: if you smile, they often smile! These facial interactions activate the limbic system and fusiform face area (FFA) without previous exposure or training. This activation indicates that facial expression-mediated communication is innate and has an evolutionary purpose. During adolescence, continued social interaction develops the facial recognition site and the "social brain," allowing for typical social interaction(Hadjikhani,2018). In autistic infants, there appears to be divergent networks in facial processing, especially when it comes to eye contact. Eye contact appears to abnormally activate the amygdala in autistic individuals - the fear processing center of the brain. This means that autistic individuals have an innate anxiety reaction when the the eye contact centers of the brain, the medial prefrontal cortex and orbitofrontal cortex, are activated (Hadjikhani,2018). Since these interactions are subconsciously anxiety-inducing, throughout adolescence autistic individuals avoid eye contact and face-reading social interaction. The result of this is an underdeveloped social brain throughout the lifetime
Abnormal brain network connections such as in autism may be treatable if the anxiety reaction is mitigated early in development. This would allow for eye contact in autistic individuals to no longer be subconsciously avoided, causing the social brain to undergo neurotypical development. These magnetic coils mentioned by Hui Ye may be effective in blocking the frontal cortex region from communicating with fear-processing networks by preventing the exaggerated depolarization of the connecting white matter tracts. to the extent that they do in autism. It should not block all communication with the amygdala, as complete severance of one network from another will almost certainly detrimental affects. Instead, perhaps some of the white matter tract should be blocked to stop the exaggerated anxiety activation in autistic individuals. The next problem is finding where exactly the tract is located that connects these networks. Since autism expresses itself on a spectrum, it is likely the wiring is not uniform in location and extent, therefore complicating this potential procedure. Further, this needs to be tested on animal models first. Can we use animal models to mimic autism effectively? This is a strong lead in treating autism treatment, but there are a lot of variables to address as well.
References:
Liberzon, I., Taylor, S. F., Amdur, R., Jung, T. D., Chamberlain, K. R., Minoshima, S., Koeppe, R. A., & Fig, L. M. (1999). Brain activation in PTSD in response to trauma-related stimuli. Biological psychiatry, 45(7), 817–826. https://doi.org/10.1016/s0006-3223(98)00246-7
Skach, J., Conway, C., Barrett, L., & Ye, H. (2020). Axonal blockage with microscopic magnetic stimulation. Scientific reports, 10(1), 18030. https://doi.org/10.1038/s41598-020-74891-3
Hadjikhani, N., Åsberg Johnels, J., Lassalle, A., Zürcher, N. R., Hippolyte, L., Gillberg, C., Lemonnier, E., & Ben-Ari, Y. (2018). Bumetanide for autism: more eye contact, less amygdala activation. Scientific reports, 8(1), 3602. https://doi.org/10.1038/s41598-018-21958-x
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