Do Autistic Brains Grow At Faster Rates?

According to a recent study, the size of brain structures in adult autistic brains look very different than those seen in autistic children.

Wrong Planet takes an in-depth look at this fascinating scientific paper published in the journal Neuron.

Read on for the exclusive article!

Most research on the neurobiological mechanisms of autism has been examined in brains of postmortem young adults, roughly 10-20 years after the clinical onset of autism. But as more data are collected and new technologies such as MRIs are developed, a better understanding of how the autistic brain develops can be reached. Because autistic behaviors begin emerging as early as 9 months, this is a critical time period to research autistic neurobiology; yet, there is actually very little postmortem data and no MRI data on autistic brains prior to the age of 2-4 years old. Interestingly, much of the sparse postmortem data for this age range disagrees with anatomical data from older autistic brains.

Many regions of the brain that are thought to be involved with autism appear to be smaller in older autistic brains. Regions such as the hippocampus (involved in spatial learning and memory), amygdala (involved in emotional processing, learning and memory), cerebellum (variety of cognitive and motor functions), and frontal/temporal lobes (social and communicative functioning) all have been reported in various studies as having a decrease in size (and in some cases, these structures are deteriorated) which may correlate with dysfunction in the processes these structures are involved with. Relatively smaller structures are not a universal pattern in autistic brains (only some structures appear to be smaller) possibly because the brain does not develop and mature in a wholly synchronous manner, but rather in a “bottom-up” fashion, beginning with more posterior regions (such as basal ganglion at the brain stem) and then more anterior regions (such as frontal cortex) mature much later. This may explain why some structures that grow and mature much earlier, such as the occipital cortex, have not been reported as being significantly smaller in autistic brains. This kind of differential effect on the development of various brain structures suggests that timing is vital and thus research on autistic development during a more appropriate (earlier) time period is necessary.

As technology advances, more data can be collected on what the autistic brain looks like and how it functions in children. Surprisingly, current research is showing different results in the brains of autistic children compared to data collected in adults. The very same structures that appear smaller in adult autistic brains appear much larger and overgrown in autistic children. These findings support results of larger head circumference in young autistic patients. Head circumference is initially a good indicator of brain size, but during adolescence, cerebral spinal fluid begins to occupy an increasing amount of space in the skull relative to brain size. So, even though brains in autistic children have been found to have a 5-10% larger weight than non-autistic brains, there is only about a 1% difference found in some studies of adult autistic brains. Although the actual brain size of autistic patients seems to even out with non-autistic brains, the mechanisms for early overgrowth of some structures and then their subsequent growth-arrest or degeneration (resulting in relatively smaller structures) in the adult brain, is unknown.

How can research begin to explain the ramifications of this two-phase shift in brain structure development in autistics? Data are hard to collect at such a young age for many reasons. There are not that many post mortem studies on children 2-4 years old and younger, and while MRIs are the most informative and non-invasive method available for research; toddlers are less than cooperative for placing in MRI machines, which require patients to lay still for extended periods. One possibility for this direction of research is exploration of brain functioning during sleep. Current research is finding many higher cognitive pathways still function during sleep and can thus be monitored in peaceful sleeping babies.

Until these kinds of methodical issues are resolved, there can only be speculation as to what causes this initial overgrowth and recline in relative growth of brain structures thought to be involved in autism. One theory suggests that there are too many neurons and or glia, causing connectivity issues in frontal and temporal lobe regions (where overgrowth is found to be the highest). These regions, involved in social interactions and language, are still forming vital connections during the same time that autistic behaviors begin emerging. Can having abnormally large brain structures during this stage of development affect neural connections? Perhaps the substrate (brain tissue) is too dense for neurons to migrate properly to find their appropriate connections or perhaps they never reach their destination because they have too far to travel (in the bigger structures). Too little is known about the complexity of how neural networks communicate to make any real inferences about such shifts in neuron connectivity, but with the fast rate of improvement in the field of bioinformatics, computational neuroscience is becoming increasingly important with generating models for simulating neural networks.

Considerations for developmental aspects of autism are becoming ever more important. Even gene-association studies may be inconsistent because the genes that cause and regulate differential development may not be the same as those genes that respond to these differences later in life, making it hard to define a clear set of “autism” genes. This means, that genes found in autism studies may be identifying genes involved with secondary issues and are not finding genes that have to do with developing autism directly. Indeed, many genes identified thus far in autistic patients have to do with regulating cell death in the brain and may only be expressed secondarily in response to the overgrowth of particular brain structures. There are also other epigenetic processes that occur only during this early period of development that regulate gene expression without changing genetic code (ie-no mutations to find) which may also account for inconsistency between genetic studies. Hopefully, with this new emphasis for researching early developmental mechanisms in autism, new experimental research will elucidate how brain structures relate to our conscious experience and give a deeper sense of understanding and appreciating for our own brain and experiences.

Courchesne et al., 2007. Neuron 56:399-413.