The intense world syndrome – an alternative hypothesis for autism

Abstract

Autism is a devastating neurodevelopmental disorder with a polygenetic predisposition that seems to be triggered by multiple environmental factors during embryonic and/or early postnatal life. 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. We further discuss the key autistic neuropathologies and several of the main theories of autism and re-interpret them in the light of the hypothesized Intense World Syndrome. Keywords: autism, microcircuit, connectivity, plasticity, neocortex, amygdala, valproic acid INTRODUCTIONAutism as a syndrome was first described by Leo Kanner, a child psychologist, in 1943. His initial description, based on 11 case studies emphasized ". . .an innate inability to form the usual, biologically provided affective contact with other people." For a long time, autism was thought to be a consequence of bad parenting and the "refrigerator mother" theory (Bettelheim, 1967) lasted from the 1950s well beyond the 1970s. Bernard Rimland (Rimland, 1964) and Michael Rutter (Rutter, 1968) established empirically that the parents of autistic children were not different in their parenting from the parents of non-autistic controls and helped building a case for a neurobiological basis of autism. Autism is now recognized as a neurodevelopmental disorder manifesting within the first 3 years after birth and progressively worsening in the course of life. The core symptoms are impairments of sociability, communicative skills and imagination, together with stereotypic behaviors and repetitive tendencies (DSM-IV, 1994). At the cognitive level, all autistic children seem to display some form of abnormality in perception, attention, and memory (Ben Shalom, 2003;Dakin and Frith, 2005;Sanders et al., 2007).Genetic analyses have revealed that autism is a polygenetic disorder where any one or more set of genes can predispose toward, but no one gene has been...

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“…El análisis a partir de estos instrumentos y el surgimiento de nuevos enfoques que consideran el TEA como un "Síndrome del Mundo Intenso" (Markram, Rinaldi y Markram, 2007) han permitido obtener una nueva visión sobre las anomalías en el procesamiento sensorial. Así, si bien es cierto que en algunos casos estas anomalías pueden ser disfuncionales, autores como Bogdashina (2007) consideran que en otros casos se trata de "superhabilidades" a las que las personas sin TEA no tienen acceso.…”

Synaptic and Intrinsic Balancing during Postnatal Development in Rat Pups Exposed to Valproic Acidin Utero

“…On the one hand, neocortical slices taken from young VPA animals are hyper-reactive when subjected to strong electrical stimulation (Rinaldi et al, 2008b). On the other hand, young VPA animals are not at any greater danger of epileptic seizure than their control counterparts, and most of the reported behavioral effects of prenatal VPA exposure on rodents are mild (for review, see Markram et al, 2007).…”

The Empathy Imbalance Hypothesis of Autism: A Theoretical Approach to Cognitive and Emotional Empathy in Autistic Development

“…the neural foundation of an ee surfeit could be a hyperresponsive amygdala activated by the subcortical pathway and insufficiently down-regulated by cortical activity (due to ce deficits). Markram, rinaldi, and Markram (2007) introduced the "intense world" hypothesis of autism and paid particular attention to the role of the amygdala. they argued, on the basis of neurophysiological findings in a rodent model of autism, that the disorder involves hyperreactivity and hyperplasticity of local neuronal circuits.…”