The neurobiology of autism: Theoretical applications
Section snippets
Etiology of autism
The etiology of ASDs is complex and has been associated with genes, neurological pathways, neurotransmitters, and environmental influences. Although etiologies have not been firmly established in the majority of cases, it is of interest to review possible causal factors to understand the incidence and prevalence of the spectrum of outcomes.
Weak central coherence model
The weak central coherence (WCC) model, originally proposed by Frith and Happé (1994), asserts that autism is characterized by a cognitive bias towards local processing over global processing. As a result, individuals with autism fail to automatically use context to aid in understanding their environment. Evidence for this theory includes the enhanced performance of individuals with autism on block design tasks, embedded-figures tasks, and several illusions that involve the influence of context
Cerebellum: function
While the cerebellum is known to regulate sequenced movement, research in the past few decades has emphasized the importance of the cerebellum in a wide variety of psychological functions (for reviews see Katz and Steinmetz, 2002, Schmahmann, 1997). Some of these functions include: procedural learning, emotion, thought, and attention (Allen and Courchesne, 2003, Courchesne et al., 1995). In particular, it appears to be implicated in attention shifting (Iarocci & McDonald, 2006). The cerebellum
Frontal lobe: function
The frontal lobe is central to many functions that may be implicated in autism. The prefrontal cortex is involved in executive functioning with respect to working memory, inhibition, planning, organization, set shifting, cognitive flexibility, orienting, and disengaging attention, all of which appear to be deficient among individuals with ASDs (Hughes et al., 1994, Ozonoff et al., 1991). Also, 40–70% of individuals with ASDs exhibit higher order cognitive impairment, suggesting that the frontal
Temporal lobe: function
The functions of the temporal lobe are numerous and include audition, memory, and object perception, as well as functions that may be affected in individuals with autism. The temporal lobe is associated with receptive language, particularly because it includes Wernickes's area (Wernicke, 1874). The temporal lobe also appears to be involved in many of the functions that can be considered part of social cognition: joint attention, action observation, and empathy (Schultz, 2005). Finally, it
Other brain regions
Converging evidence suggests that deficits in parts of the cerebellum, frontal lobes, and temporal lobes are implicated in the development of ASDs; however, reviews of the literature suggest that impairments in several other brain areas may also be involved. Parts of the parietal lobe may be implicated in deficits in the mirror neuron system of individuals with autism, particularly in challenges with action imitation (Hadjikhani et al., 2006, Williams et al., 2006; for reviews see Oberman and
Models
With a better understanding of some of the neural mechanisms underlying autism, it is now possible to re-evaluate the major theories of autism, in light of this research (summarized in Table 2).
The weak central coherence model predicts deficits in the cerebellum, and possibly in the frontal lobes and the corpus callosum among individuals with ASDs. A substantial amount of research implicates the cerebellum and the frontal lobes, while fewer studies implicate the corpus callosum. The theory of
Challenges in research
One of the major challenges in autism research is the heterogeneity of the causes, symptoms, severity, and labels for the disorder. Descriptions of samples range from “pure” autism, through ASD, and pervasive developmental disorder (PDD), which encompasses a large range of deficits. This range makes it difficult to generalize across studies in which the samples may be quite different (Bebko et al., 2008). In addition, co-morbidities such as cognitive impairment, seizure disorders, and
Future directions
Based on the previous section, it is clear that there are gaps in the autism research literature. With regard to the issue of age, research should continue to examine at-risk children (siblings of individuals with autism) longitudinally, tracking their neurological development from shortly after birth to see if they develop autism. Given the challenges of running fMRI and PET research with younger children, more EEG/ERP studies need to be conducted with infants and young children because these
Acknowledgement
Schroeder was supported during the preparation of this manuscript as a trainee through the Canadian Institutes of Health Research-National Alliance for Autism Research (CIHR-NAAR) Autism Spectrum Disorders Strategic Training Program (PI:JHH) & Canadian Institutes of Health Research-Canadian Graduate Scholarship. Cappadocia was supported through Social Sciences and Humanities Research Council and Ontario Graduate Scholarship. Bebko and Desrocher were each supported through Canadian Institutes of
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Autism diagnosis and screening: Factors to consider in differential diagnosis
2012, Research in Autism Spectrum DisordersCitation Excerpt :We argue that with respect to the assessment and diagnosis of autism, no such gold standard exists, nor is one particular measure likely to emerge in the foreseeable future. Also, despite the notion that autism has a neurodevelopmental cause, diagnosis is at this point based solely on observable behaviors (Brown, Ouellette-Kuntz, Hunter, & Kelley, 2010; Clifford, Hudry, Brown, Pasco, & Charman, 2010; Nydén et al., 2010a, 2010b; Schroeder et al., 2010). As a result, diagnosis is typically accomplished through observation of the child, interview of one or more caregivers, typically involving one or more tests of core symptoms of autism with established reliability and validity, and review of client history.
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2011, Brain ResearchCitation Excerpt :There is increasing evidence that multiple aetiologies may converge to disrupt the development and function of several brain systems that are implicated in the social and non-social behaviours that define ASDs (Happé and Ronald, 2008; Schroeder et al., 2010), including the frontal and temporal neocortex, the caudate, and the cerebellum (Abrahams and Geschwind, 2010).