Evoking subclinical hypomania as a potential autism treatment - a hypothesis based on an up-to-date literature review

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Maciej Świerczek Krzysztof Nesterowicz

Abstract

The growing number of children diagnosed with autism spectrum disorder (ASD) urges the scientific community to find a simple and cost-effective solution to this problem. Before 1990, the general population prevalence for autism was considered steady at 4–5/10,000 (1/2,000–1/2,500). However, recent studies on children in the United States have reported an ASD diagnosis in 1/91 3-17 year olds and 1/110 8 year olds.


A comprehensive literature review of over 700 articles on neurotransmitter levels and brain performance in autism and other psychiatric conditions was conducted to finally include 83 studies. The results of the search led us to the conclusion that autism is a state of the brain performance opposite in many aspects to mania (in particular hypomania), both behaviourally (in particular autism being characterized by social deficits and hypomania by hypersociability), neurochemically (e.g. low brain vasopressin, high cortisol in autism vs. high brain vasopressin, low cortisol in mania) and by activity of key brain areas (e.g. mirror neuron system, amygdala).


We hypothesize that instead of targeting separate neurotransmitter systems in autism, the focus should be on 'moving and locking' the brain into a subclinical hypomanic state when required. When in a subclinical hypomanic state, a patient's sociability (the key and most debilitating symptom of autism) should be massively improved. We have designed experiments which would test the above hypothesis.

Article Details

How to Cite
ŚWIERCZEK, Maciej; NESTEROWICZ, Krzysztof. Evoking subclinical hypomania as a potential autism treatment - a hypothesis based on an up-to-date literature review. Medical Research Archives, [S.l.], v. 6, n. 1, jan. 2018. ISSN 2375-1924. Available at: <https://journals.ke-i.org/index.php/mra/article/view/1644>. Date accessed: 21 may 2018. doi: https://doi.org/10.18103/mra.v6i1.1644.
Section
Review Articles

References

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