Autism: Asperger's Syndrome

Asperger's syndrome represents an autistic spectrum disorder that is primarily characterized by deficits in social reciprocity, diminished nonverbal communication skills, restricted or circumscribed interests, and repetitive and/or stereotyped behaviors. In comparison, autism is also associated with verbal language delays, whereas Asperger's syndrome is not. Asperger's syndrome was first described by Hans Asperger, a Viennese pediatrician, in 1944, who published a clinical description of a group of children who shared an unusual combination of developmental weakness and strengths. These children had severe social and communication abnormalities, restricted interests, motor delays, and clumsiness. Asperger initially named this syndrome autistic psychopathy (Miller & Ozonoff, 2000). However, although he noted the aforementioned deficits, this group of children acquired language at normal or earlier age and had normal intelligence and some specific strong abilities such as visuospatial skills and verbal abstraction abilities. In 1943, the child psychiatrist Leo Kanner published a description of a group of children with similar characteristics but with no mention of motor deficits as a core symptom of the syndrome.

NEUROPATHOLOGY/PATHOPHYSIOLOGY
The neuropathological basis of Asperger's syndrome remains unclear. Studies have assumed that Asperger's syndrome is part of the autism spectrum disorders, and the causes and mechanisms to explain the symptoms would be essentially the same and the differences would be attributable to the severity (Wicker et al., 2008). Overall, it is accepted that Asperger's syndrome is a polygenetic disorder, and several neurological findings of children with autism spectrum disorder have been described including deficits in intrahemispheric neural connectivity, reductions in the size of the corpus callosum, reductions in the inhibitory cortical activity, abnormal development of gray and white matter, increased activation in Wernicke's area, diminished activation in Broca's area during cognitive processing, decreased connectivity between the inferior frontal gyrus and the limbic system, and a significant deficit in the connectivity between the primary sensory cortex and the association cortex (Minshew & Williams, 2007). In summary, more recent findings support the hypothesis of Asperger's syndrome as a large-scale neural systems disorder in which deficits in cortical connectivity and abnormal balance between excitatory and inhibitory mechanisms might play the main role. For instance, one of the mechanisms that explain the social interaction impairment found in autism spectrum disorders is the deficit in emotional processing of face expressions. This weakness can be explained by the lack of neural connectivity (Wicker et al., 2008). Wicker et al. (2008) in a recent publication found that adults with autism spectrum disorder, when observing angry and happy faces, have an abnormally low activation of the areas involved in the processing of high-order emotional information: dorsomedial prefrontal cortex (DMPFC) and right ventrolateral prefrontal cortex. However, normal activity was found in the areas that are usually activated during perceptual analysis of facial features and expressions such as superior temporal sulcus and fusiform gyrus. This lack of synchrony in the activation of these areas and the deficit of signals from the amygdala to the DMPFC might explain the failure in relating the emotional features of faces with the initiation of socially appropriate behaviors.