Treatment of Asperger Syndrome

Treatment of Asperger Syndrome

Asperger syndrome is considered an autism spectrum disorder that is characterized by impairments in social interaction and communication, as well as repetitive and restricted patterns of behaviors and interests, which manifest to a degree where the individuals with this disorder are still "high-functioning," and more able in the realms of various intelligences in comparison to those with autism (Toth & King, 2008). This disorder has been found to occur at a rate of 2.5 in every 10,000, while all autistic disorders occur at a rate of 60 in every 10,000 (Toth & King, 2008). There is a strong hereditary component to Asperger syndrome, as a study investigating family histories of one hundred males with Asperger syndrome determined that there was a history of autistic spectrum disorder in 50% of the sample, as well as pre-natal and peri-natal risk factors, including alcohol exposure, neonatal seizures, premature birth, and postnatal asphyxia, in one quarter of the sample (Toth & King, 2008). Asperger syndrome is sometimes used as a diagnosis for children with autism that do not present typical symptomatology and who instead of being distant or avoidant, often initiate social interactions (Toth & King, 2008). The criteria for a diagnosis of Asperger syndrome according to the DSM-IV-TR include cognitive ability that is intact as well as the absence of any early language delays.

Causes of Asperger syndrome include fetal abnormalities, as well as genetic and environmental factors (Toth & King, 2008). As far as genetic factors are concerned, some research has pointed to the possibility that genetic risk factors may be similar among different children, but the phenotypic expression of these factors, manifested as symptom severity, may vary based on different exposure to environmental risk factors (Toth & King, 2008). Research on individuals with Asperger syndrome has identified two loci on chromosomes 1 and 3 that are likely involved in the genetics surrounding autistic disorders, further pointing to Asperger Syndrome as a less severe form of autistic disorder rather than a completely separate disorder (Toth & King, 2008).

The neurobiological correlates of Asperger syndrome are not well understood, and further research is required in this area (McAlonan et al., 2002). However, there are certain characteristics of Asperger syndrome that point to specific biological factors involved in the manifestation and expression of the disorder. For example, individuals with Asperger syndrome commonly demonstrate a lack of interest in the human face, preferring inanimate objects instead (Schultz et al., in press). This characteristic results in negative effects with regard to developing healthy and successful interpersonal relationships (Schultz et al., in press). Anatomically, this lack of interest in faces may be associated with abnormalities in the activation in right inferior temporal gyri (Schultz et al., in press).

In particular, face recognition among individuals with Asperger syndrome and autism yielded increases in the activity in the right inferior temporal gyri and reduced right fusiform gyrus activation in comparison to controls, which may result from individuals with autism spectrum disorders processing faces in a different way than controls, or due to cognitive-perceptual disturbances present in individuals with autism and Asperger syndrome (Schultz et al., in press). Furthermore, other areas of the brain are also likely implicated in Asperger syndrome, as research has determined that the amygdala and surrounding structures of the limbic system are structurally abnormal in autistic spectrum disorders (Schultz et al., in press).

Research investigating autism and Asperger syndrome has indicated through brain imaging studies that there are differences in limbic circuits, areas implicated in sensorimotor gating, in these individuals (McAlonan et al., 2002). Impairment in gating due to differences in limbic circuits maybe be part of the cause behind the inability to inhibit repetitive actions, speech and thoughts among individuals with autism spectrum disorders (McAlonan et al., 2002). A study by McAlonan et al. (2002) showed that among individuals with Asperger Syndrome, sensorimotor gating is significantly impaired, possibly due to the demonstrated less grey-matter in cerebellar and fronto-striatal regions of the brain as well as vast differences in white matter in comparison with controls (McAlonan et al., 2002). Futhermore, Asperger syndrome is likely associated with various alterations in development of the brain (McAlonan et al., 2002).