However, the most obvious signs of autism, such as atypical social and language development, and restricted or repetitive behaviors and interests, often present themselves between the ages of two and three, and most children with ASD can be diagnosed in early childhood as a result.
[6] Research findings indicate that young children diagnosed with autism exhibit challenges in both initiating and responding to joint attention.
[8] These deficits in joint attention are observed consistently across various age groups, spanning from infancy to adolescence within the autism spectrum.
[9] In one study, researchers suggest that a displayed pattern of delays, absences, or a general impaired response to stimuli (hyporesponsiveness) and a fascination with intense or repetitive stimulation (sensory seeking) is more likely in nonspeaking autistic children, suggesting that both hyporesponsiveness and sensory seeking is related to poor communication outcomes in children with ASD.
[12] 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).
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.
[12] Several studies presented subjects with ASD photographs of human eyes and had them report the emotional state of the person in the picture.
The left amygdala[13] is critical in the involvement of processing mental state and emotional information from complex visual stimuli, particularly the eye region.
Instead, they exhibit greater reliance on temporal lobe structures, specialized for verbally labeling complex visual stimuli and processing faces and eyes.
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.
theorize that this is happening early during infancy in the autistic brain, accounting for the initial overgrowth and later observed size reduction.
In addition to a negative correlation to eye fixation studies showed a smaller amygdala was associated with impairment in nonverbal communication skills as well.
[14] The theory of mind in autism provides an explanation for pragmatic impairments in language and communication, attributing them to social deficits and their underlying neurocognitive mechanisms.
In contrast, the PDH suggests that grammatical impairments, encompassing syntax, morphology, and phonology, in individuals with autism can be predominantly attributed to abnormalities in the procedural memory system.
[3] The process of breaking down a syllable at a time and having it visually displayed and audibly available to the child can prompt them to imitate and create nonrandom and meaningful utterances.