Hans<unk>  described common traits among his patients' family members, especially fathers, and research supports this observation and suggests a genetic contribution to<unk> . Although no specific genetic factor has yet been identified, multiple factors are believed to play a role in the expression of autism, given the variability in symptoms seen in children. Evidence for a genetic link is that AS tends to run in families where more family members have limited behavioral symptoms similar to AS (for example, some problems with social interaction, or with language and reading skills). Most behavioral genetic research suggests that all autism spectrum disorders have shared genetic mechanisms, but AS may have a stronger genetic component than autism. There may be shared genes in which particular alleles make an individual vulnerable, and varying combinations result in differing severity and symptoms in each person with AS. A few ASD cases have been linked to exposure to teratogens (agents that cause birth defects) during the first eight weeks from conception. Although this does not exclude the possibility that ASD can be initiated or affected later, it is strong evidence that ASD arises very early in development. Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation. Mechanism Functional magnetic resonance imaging provides some evidence for mirror neuron theory.<unk>  appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized effects. Although the specific underpinnings of AS or factors that distinguish it from other ASDs are unknown, and no clear pathology common to individuals with AS has emerged, it is still possible that AS's mechanism is separate from other ASDs. Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception. Abnormal fetal development may affect the final structure and connectivity of the brain, resulting in altered neural circuits controlling thought and behavior. Several theories of mechanism are available; none are likely to provide a complete explanation. General-processing theories One general-processing theory is weak central coherence theory, which hypothesizes that a limited ability to see the big picture underlies the central disturbance in ASD. A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals. Mirror neuron system (MNS) theory The mirror neuron system (MNS) theory hypothesizes that alterations to the development of the MNS interfere with imitation and lead to<unk> 's core feature of social impairment. One study found that activation is delayed in the core circuit for imitation in individuals with AS. This theory maps well to social cognition theories like the theory of mind, which hypothesizes that autistic behavior arises from impairments in ascribing mental states to oneself and others; or hyper-systemizing, which hypothesizes that autistic individuals can systematize internal operation to handle internal events but are less effective at empathizing when handling events generated by other agents.
Asperger syndrome
Hyperacusis
Zellweger syndrome
Avoidant personality disorder
Scheie syndrome
High-functioning autism
Rett syndrome
Zellweger spectrum disorders