Nonverbal autism

There is a growing body of tentative evidence indicating the amygdala's involvement in the development of autism. The amygdala theory of autism focuses on the importance of the amygdala in relation to social functioning and observes that autism is largely a severe impairment of social functioning. The amygdala is thought to be associated with the fight-or-flight response in animals and its activity is heavily correlated with fear in humans. Additionally, it has been heavily implicated in relation to social functioning in various animal studies. Evidence suggests an amygdala hyperactivity model may be more accurate than one comparing it to a lesion.[7]

Lesion studies have shown that amygdala damage results in severe social impairment among animal models. Vervet monkey mothers with amygdala lesions were shown to be much less caring with their young neglecting and even abusing them.[8] Rats with amygdala ablations become much more docile.[8] Monkeys with lesions to the anterior temporal lobe develop a disorder known as Klüver–Bucy syndrome, characterized by loss of fear, hypersexuality, hyperorality, and an inability to recognize visual objects (often, but not always).[8]

Evidence shows the amygdala accounts for the emotional, oral, and sexual abnormalities listed above.[8] These abnormalities coincide with several characteristics of the diagnostic guidelines for autism, at least passably for an animal model.

Post-mortem analysis of humans shows an increased neuronal density in the amygdala in autism compared to controls, indicating a potential linkage and supporting the hyperactivity model.[8]

Several studies presented subjects with ASD photographs of human eyes and had them report the emotional state of the person in the picture. A smaller amygdala was associated with increased response time but not decreased accuracy.[8] There was also significantly less amygdaloid activation in the brains of those with ASD than controls. Subjects compensated for this lack of amygdaloid activity with increased activation in the temporal lobe, and are associated with verbally labeling images.[7] This activity is thought to imply less usage of emotional/social cues to identify objects and rather more objective, factually based processing. One may extrapolate from this model that patients with autism may learn that a specific facial configuration represents an emotional state and what that emotional state implies socially, but they may not come to truly understand how that person feels. This supports a theory of mind deficit.

Studies conducted specifically on nonspeaking autistic individuals provide similar evidence. Brain studies have shown several amygdaloid impairments among those with ASD. The amygdala in those with nonspeaking autism have less volume compared to controls, contain a higher density of neurons suggesting hyperconnection, and show a negative correlation between amygdala size and impairment severity among subjects.[7]

Infantile autism is actually associated with an oversized amygdala, there are developmental theories as to how this may occur. Research on major depressive disorder has shown that excessive activation such as stress or fear leads to allostasis, or degeneration of the neurons involved in creating the phenomenon. Initial hypertrophy results in atrophy and reduction of brain size in the given region.[7] Over time, this occurs in patients with severe depression, and they develop a decreased amygdala size. Some scientists theorize that this is happening early during infancy in the autistic brain, accounting for the initial overgrowth and later observed size reduction.[7]

When eye tracking software is employed to record where subjects focus their visual attention on images of human faces, small amygdala volume is associated with decreased eye fixation.[7] Eyes are considered to be especially important for establishing human connection and conveying emotion, thus fixation on them is considered to be a crucial part of identifying people and emotions in a social setting.

In addition to a negative correlation to eye fixation studies showed a smaller amygdala was associated with impairment in nonverbal communication skills as well.[7] This suggests that the amygdala is critical in developing all types of communicative abilities, not just verbal. This suggests the amygdala may play a crucial role in relating to other humans in a way that allows for behavioral mimicry.

Among patients with nonspeaking ASD researchers could predict symptom severity based on amygdala activity. Those with the least amygdala activity had the most impaired nonspeaking communication abilities, those with the most activity had the strongest communication abilities.[7]

The development of language, similar to the development of most physical skills, relies heavily on mimicry of other humans.[7] ASDs are known to impair one's ability to focus on and relate with people possibly as a result of a damaged amygdala. Nonspeaking autistics will often be able to learn more basic communicative skills such as pointing to objects or selecting a picture from a list. These skills are far more simple and do not require the degree of personal connection needed for language development.

It is important to note that these studies must be considered with great caution. Cross-sectional study can only suggest so much about the pathology of a disorder. Further study, particular longitudinal study, are needed to gain a more complete understanding.[7] It is also important to recognize that most disorders arise from a complex interworking of the entire brain and restricting a theory to one subsystem would be a mistake, this theory merely suggests how the amygdala may be involved with develop of ASD and provides evidence to support an association.