The Tell-Tale Brain: A Neuroscientist's Quest for What Makes Us Human

If salience landscape theory is on the right track, one would expect to find abnormalities in visual pathway 3 of autistic brains. Pathway 3 not only projects to the amygdala, but it routes through the superior temporal sulcus, which—along with its neighboring region, the insula—is rich in mirror neurons. In the insula, mirror neurons have been shown to be involved in perceiving as well as expressing certain emotions—like disgust, including social and moral disgust—in an empathetic manner. Thus damage to these areas, or perhaps a deficiency of mirror neurons within them, might not only distort the salience landscape, but also diminish empathy, social interaction, imitation, and pretend play.

As an added bonus, salience landscape theory may also explain two other quirky aspects of autism that have always been puzzling. First, some parents report that their child’s autistic symptoms are temporarily relieved by a bout of high fever. Fever is ordinarily caused by certain bacterial toxins that act on temperature-regulating mechanisms in the hypothalamus in the base of your brain. Again, this is part of pathway 3. I realized that it may not be coincidental that certain dysfunctional behaviors such as tantrums originate in networks that neighbor the hypothalamus. Thus the fever might have a “spillover” effect that happens to dampen activity at one of the bottlenecks of the feedback loop that generates those autonomic-arousal storms and their associated tantrums. This is a highly speculative explanation but it’s better than none at all, and if it pans out it could provide another basis for intervention. For example, there might be some way to safely dampen the feedback loop artificially. A damped circuit might be better than a malfunctioning one, especially if it could get a kid like Steven to engage even just a little bit more with his mother. For example, one could give him high fever harmlessly by injecting denatured malarial parasites; repeated injections of such pyrogens (fever-inducing substances) might help “reset” the circuit and alleviate symptoms permanently.

Second, children with autism often repeatedly bang and beat themselves. This behavior is called somatic self-stimulation. In terms of our theory, we would suggest that this leads to a damping of the autonomic-arousal storms that the child suffers from. Indeed, our research team has found that such self-stimulation not only has a calming effect but leads to a measurable reduction in GSR. This suggests a possible symptomatic therapy for autism: One could have a portable device for monitoring GSR that then feeds back to a body stimulation device which the child wears under his clothing. Whether such a device would prove practical in a day-to-day setting remains to be seen; it is being tested by my postdoctoral colleague Bill Hirstein.

The to-and-fro rocking behavior of some autistic children may serve a similar purpose. We know it likely stimulates the vestibular system (sense of balance), and we know that balance-related information splits at some point to travel down pathway 3, especially to the insula. Thus repetitive rocking might provide the same kind of damping that self-beating does. More speculatively, it might help anchor the self in the body, providing coherence to an otherwise chaotic world, as I’ll describe in a moment.

Aside from possible mirror-neuron deficiency, what other factors might account for the distorted salience landscapes through which many autistic people seem to view the world? It is well documented that there are genetic predispositions to autism. But less well known is the fact that nearly a third of children with autism have had temporal lobe epilepsy (TLE) in infancy. (The proportion could be much higher if we include clinically undetected complex partial seizures.) In adults TLE manifests as florid emotional disturbances, but because their brains are fully mature, it does not appear to lead to deep-seated cognitive distortions. But less is known about what TLE does to a developing brain. TLE seizures are caused by repeated random volleys of nerve impulses coursing through the limbic system. If they occur frequently in a very young brain, they might lead, through a process of synapse enhancement called kindling, to selective but widespread, indiscriminate enhancement (or sometimes effacement) of the connections between the amygdala and the high-level visual, auditory, and somatosensory cortices. This could account both for the frequent false alarms set off by trivial or mundane sights and otherwise neutral sounds, and conversely for the failure to react to socially salient information, which are so characteristic of autism.