BackgroundPrevious reports indicate the presence of histological abnormalities in the brains of individuals with autism spectrum disorders (ASD) suggestive of a dysplastic process. In this study we identified areas of abnormal cortical thinning within the cerebral cortex of ASD individuals and examined the same for neuronal morphometric abnormalities by using computerized image analysis.ResultsThe study analyzed celloidin-embedded and Nissl-stained serial full coronal brain sections of 7 autistic (ADI-R diagnosed) and 7 age/sex-matched neurotypicals. Sections were scanned and manually segmented before implementing an algorithm using Laplace’s equation to measure cortical width. Identified areas were then subjected to analysis for neuronal morphometry. Results of our study indicate the presence within our ASD population of circumscribed foci of diminished cortical width that varied among affected individuals both in terms of location and overall size with the frontal lobes being particularly involved. Spatial statistic indicated a reduction in size of neurons within affected areas. Granulometry confirmed the presence of smaller pyramidal cells and suggested a concomitant reduction in the total number of interneurons.ConclusionsThe neuropathology is consistent with a diagnosis of focal cortical dysplasia (FCD). Results from the medical literature (e.g., heterotopias) and our own study suggest that the genesis of this cortical malformation seemingly resides in the heterochronic divisions of periventricular germinal cells. The end result is that during corticogenesis radially migrating neuroblasts (future pyramidal cells) are desynchronized in their development from those that follow a tangential route (interneurons). The possible presence of a pathological mechanism in common among different conditions expressing an autism-like phenotype argue in favor of considering ASD a “sequence” rather than a syndrome. Focal cortical dysplasias in ASD may serve to explain the high prevalence of seizures and sensory abnormalities in this patient population.

Autism spectrum conditions (ASC) and the delayed development of object permanence is often not questioned, and is rarely understood. The following paper attempts to explore this idea and suggests reasons for why such development is delayed and the possibility that certain difficult behaviours seen in children with ASC are less likely to be connected to having poor theory of mind and more connected to lacking generalized concepts of object permanence.

Poor Theory of Mind (ToM) (or difficulties imputing mental states to self and others) [1], (See also [2-5]) is often blamed for certain responses and behaviour in autism. However, the Theory of Mind Task Battery requires an understanding of language, the use of cognitive skills, as well as the child's motivation and attention to complete. All of these factors are either weak or underdeveloped in individuals with autism suggesting that this is not the best means to measure one's understanding that other people have their own thoughts, plans, beliefs, or point of view. Behaviours like strong defiance, insistence on sameness, fear associated with sudden change and severe anxiety may be related to difficulties seeing beyond the 'now' [6]. This paper suggests that some of the stress and anxiety in the autism population may actually be due to delayed object permanence (OP) (knowing something may still exist even if it is out of sight), which can appear as poor ToM. This delay in establishing OP is governed by single focused attention. For more information on this concept see: Lawson, W. (2011) The passionate mind, JKP:London. Although ToM and OP are defined differently, this paper aims to show the relationship between them and how one concept can influence the other using examples in everyday life to illustrate how poor OP is associated with single focused attention, which detracts from the bigger picture.

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MRI studies on abnormal brain development are dependent on the quality, quantity, and type of normative development data available for comparison. Limitations affecting previous studies on normative development include small sample sizes, lack of demographic representation, heterogeneous subject populations, and inadequate longitudinal data. The National Institutes of Health Pediatric MRI Data Repository (NIHPD) for normative development was designed to address the aforementioned issues in reliability measures of control subjects for comparison studies. The subjects were recruited from six Pediatric Study Centers nationwide to create the largest, non-biased, longitudinal database of the developing brain. Using the NIHPD, we applied a 3D shape analysis method involving spherical harmonics to identify the cortical surface complexity of 396 subjects (210 female; 186 male) between the ages of 4.8 y and 22.3 y. MRI data had been obtained at one, two, or three time points approximately two years apart. A total of 144 participants (79 female; 65 male) provided MRI data from all time points. Our results confirm a direct correlation between cortical complexity and age in both males and females. Additionally, within the examined age range, females displayed consistently and significantly greater cortical complexity than males. Findings suggest that the underlying neural circuitry within male and female brains is different, possibly explaining observations of sexual dimorphism in social interaction, communication, and higher cognitive processes.