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.
In more general terms, our sense of being an integrated, embodied self seems to depend crucially on back- and-forth, echo-like “reverberation” between the brain and the rest of the body—and indeed, thanks to empathy, between the self and others. Indiscriminate scramblings of the connections between high-level sensory areas and the amygdala, and the resulting distortions to one’s salience landscape, could as part of the same process cause a disturbing loss of this sense of embodiment—of being a distinct, autonomous self anchored in a body and embedded in a society. Perhaps somatic self-stimulation is some children’s attempt to regain their embodiment by reviving and enhancing body-brain interactions while at the same time damping spuriously amplified autonomic signals. A subtle balance of such interactions may be crucial for the normal development of an integrated self, something we ordinarily take for granted as the axiomatic foundation of being a person. No wonder, then, that this very sense of being a person is profoundly disturbed in autism.
We have so far considered two candidate theories for explaining the bizarre symptoms of autism: the mirror- neuron dysfunction hypothesis and the idea of a distorted salience landscape. The rationale for proposing these theories is to provide unitary mechanisms for the bewildering array of seemingly unrelated symptoms that characterize the disorder. Of course, the two hypotheses are not necessarily mutually exclusive. Indeed, there are known connections between the mirror-neuron system and the limbic system. It is possible that distortions in limbic-sensory connections are what lead ultimately to a deranged mirror-neuron system. Clearly, we need more experiments to resolve these issues. Whatever the underlying mechanisms turn out to be, our results strongly suggest that children with autism have a dysfunctional mirror-neuron system that may help explain many features of the syndrome. Whether this dysfunction is caused by genes concerned with brain development or by genes that predispose to certain viruses (that in turn might predispose to seizures), or is due to something else entirely remains to be seen. Meanwhile, it might provide a useful jumping off point for future research into autism, so that someday we may find a way to “bring Steven back.”
Autism reminds us that the uniquely human sense of self is not an “airy nothing” without “habitation and a name.” Despite its vehement tendency to assert its privacy and independence, the self actually emerges from a reciprocity of interactions with others and with the body it is embedded in. When it withdraws from society and retreats from its own body it barely exists; at least not in the sense of a mature self that defines our existence as human beings. Indeed, autism could be regarded fundamentally as a disorder of self-consciousness, and if so, research on this disorder may help us understand the nature of consciousness itself.
CHAPTER 6
The Power of Babble: The Evolution of Language
—THOMAS HENRY HUXLEY
ON THE LONG FOURTH OF JULY WEEKEND OF 1999, I RECEIVED A phone call from John Hamdi, who had been a colleague of mine at Trinity College, Cambridge, nearly fifteen years earlier. We hadn’t been in contact and it was a pleasant surprise to hear his voice after such a long time. As we exchanged greetings, I smiled to myself, reminded of the many adventures we had shared during our student days. He was now a professor of orthopedic surgery in Bristol, he said. He had noticed a book I’d recently published.
“I know you are mainly involved in research these days,” he said, “but my father, who lives in La Jolla, has had a head injury from a skiing accident followed by a stroke. His right side is paralyzed, and I’d be grateful if you could take a look at him. I want to make sure he’s getting the best treatment available. I heard there’s a new rehab procedure which employs mirrors to help patients recover the use of a paralyzed arm. Do you know anything about this?”
A week later John’s father, Dr. Hamdi, was brought to my office by his wife. He had been a world-renowned professor of chemistry here at UC San Diego until his retirement three years earlier. About six months prior to my seeing him he sustained a skull fracture. In the emergency room at Scripps Clinic he was informed that a stroke,
