Researchers at the University of Montreal conducted a fresh analysis of autism research including cognition, genetics, and brain imaging has shed new insight to potential causes of autism and also why it can present so differently in different people. The team of researchers, led by Laurent Mottron, developed a new model they dubbed, “Trigger-Threshold-Target.”
While there are as many theories on the potential causes of autism as there are researchers, the premise for this particular study is that autism is a genetically induced plastic reaction. The term “brain plasticity” refers to the brain’s ability to adapt by responding and remodeling itself. In the Trigger-Threshold-Target model, the “trigger” is a set of genetic mutations that enhance brain plasticity. The individuals’ threshold for brain plasticity then determines whether the result will be autism with intellectual disability, autism without intellectual disability, or intellectual disability without autism. This model confirmed that much like a blind person will develop a heightened sense of smell and hearing, autistic brains develop a heighted ability to process different kinds of information. The result is a brain that scans the environment for the type of information it prefers, while ignoring the materials it doesn’t. “One of the consequences of our new model will be to focus early childhood intervention on developing the particular strengths of the child’s brain, rather than exclusively trying to correct missing behaviors, a practice that may be a waste of a once in a lifetime opportunity,” explains Mottron.
The team of academics developed their model by reexamining research that measured brain activity in animals implanted with genetic mutations associated with autism while undertaking perceptual tasks. Those studies revealed that most of those mutations increased brain plasticity, or the brain’s ability to create connections when processing new information. They also reexamined established evidence that present in autism is an altered balance between the processing of social and non-social information. “The Trigger-Threshold-Target model,” explains Mottron, “builds a bridge between these two series of facts, using the neuro cognitive effects of sensory deprivation to resolve the missing link between them.”
Mottron’s team concluded that the different superiorities in perception or language present in different subgroups of autistic people indicate that an autistic infant’s brain is adapting to information the same way a blind or deaf infant’s brain does. Because their brains are unable to process a certain type of stimuli, their brains develop their other senses to compensate, just as autistic brains enhance their brain plasticity with heighted activity, connectivity, and structural modifications in the perceptive areas of the brain. The different parts of the brain that host this increased plasticity become the “target” and develop as the autistic individual’s particular strengths or weaknesses.
“Speech and social impairment in some autistic toddlers may not be the result of a primary brain dysfunction of the mechanisms related to these abilities, but the result of their early neglect,” Mottron said. “Our model suggests that the autistic superior perceptual processing compete with speech learning because neural resources are oriented towards the perceptual dimensions of language, neglecting its linguistic dimensions. Alternatively, for other subgroups of autistic people, known as Asperger, it’s speech that’s overdeveloped. In both cases, the overdeveloped function outcompetes social cognition for brain resources, resulting in a late development of social skills.”
This model also provides new insight into why some autistic people have intellectual disabilities while others do not. They believe this is the result of the underlying mutation altering the brain cell networking function. Rather than simply triggering an enhanced normal plastic reaction, those mutations trigger a reaction that does not occur in non-autistic brains. If brain cell networking is functioning normally, the only change is in the allocation of resources.
Mottron and his team conclude that the implications should influence the methods employed in early intervention. They believe that rather than focusing on each child’s particular difficulties or deficits, they should encourage the compensational strengths of that child to allow them to receive a broader spectrum on information that their brains are individually designed to processes. “Most early intervention programs adopt a restorative approach by working on aspects like social interest. However this focus may monopolize resources in favor of material that the child process with more difficulties, Mottron said. “We believe that early intervention for autistic children should take inspiration from the experience of congenitally deaf children, whose early exposure to sign language has a hugely positive effect on their language abilities. Interventions should therefore focus on identifying and harnessing the autistic child’s strengths, like written language.”