An intriguing new hypothesis that seeks to explain all of the diverse psychological symptoms associated with autism. Here’s the abstract:
While significant advances have been made in identifying the neuronal structures and cells affected, a unifying theory that could explain the manifold autistic symptoms has still not emerged. Based on recent synaptic, cellular, molecular, microcircuit, and behavioral results obtained with the valproic acid (VPA) rat model of autism, we propose here a unifying hypothesis where the core pathology of the autistic brain is hyper-reactivity and hyper-plasticity of local neuronal circuits. Such excessive neuronal processing in circumscribed circuits is suggested to lead to hyper-perception, hyper-attention, and hyper-memory,which may lie at the heart of most autistic symptoms. In this view, the autistic spectrum are disorders of hyper-functionality, which turns debilitating, as opposed to disorders of hypo-functionality, as is often assumed. We discuss how excessive neuronal processing may render the world painfully intense when the neocortex is affected and even aversive when the amygdala is affected, leading to social and environmental withdrawal. Excessive neuronal learning is also hypothesized to rapidly lock down the individual into a small repertoire of secure behavioral routines that are obsessively repeated.
Of course, all of the usual caveats apply: this is just a hypothesis, the rat model is a crude approximation, etc, etc. And yet, there is something alluring about this paper’s complete inversion of the standard autistic model, as hypofunctionality is traded for hyperfunctionality. You can read the whole paper in the new Frontiers of Neuroscience, which is the coolest new journal I’ve seen in quite some time. I want to talk some more about the unique open access model of Frontiers, but that will have to wait until I’m not paying by the minute for internet access in a foreign country.