To account for some of the secondary symptoms of autism—hypersensitivity, avoidance of eye contact, aversion to certain sounds, and so on—researchers have developed the salience landscape theory. In a typical child, sensory information is relayed to the amygdala, the gateway to the emotion-regulating limbic system. Using input from stored knowledge, the amygdala determines how the child should respond emotionally to each stimulus, creating a salience landscape of the child's environment. In children with autism, though, the connections between the sensory areas and the amygdala may be altered, resulting in extreme emotional responses to trivial events and objects.
ficulty understanding metaphors, just like people with autism. These results suggest that cross-domain mapping may have originally developed to aid primates in complex motor tasks such as grasping tree branches (which requires the rapid assimilation of visual, auditory and touch information) but eventually evolved into an ability to create metaphors. Mirror neurons allowed humans to reach for the stars, instead of mere peanuts.
Can the Mirrors Be Repaired?
the discovery of mirror neuron deficiencies in people with autism opens up new approaches to diagnosing and treating the disorder. For example, physicians could use the lack of mu-wave suppression (or perhaps the failure to mimic a mother sticking out her tongue) as a diagnostic tool to identify children with autism in early infancy, so that the currently available behavioral therapies can be started as quickly as possible. Timely intervention is critical; the behavioral therapies are much less effective if begun after autism's main symptoms appear (typically between ages two and four).
An even more intriguing possibility would be to use biofeedback to treat autism or at least alleviate its symptoms. Doctors could monitor the mu waves of a child with autism and display them on a screen in front of the patient. If the child's mirror neuron functions are dormant rather than completely lost, it may be possible for him or her to revive this ability by learning—through trial and error and visual feedback—how to suppress the mu waves on the screen. Our colleague Pineda is pursuing this approach, and his preliminary results look promising. Such therapies, though, should supplement rather than replace the traditional behavioral-training techniques.
Another novel therapeutic approach might rely on correcting chemical imbalances that disable the mirror neurons in individuals with autism. Our group (including students Mikhi Horvath and Mary Vertinsky) has suggested that specialized neuromodulators may enhance the activity of mirror neurons involved in emotional responses. According to this hypothesis, the partial depletion of such chemicals could explain the lack of emotional empathy seen in autism, and therefore researchers should look for compounds that stimulate the release of the neuromodulators or mimic their effects on mirror neurons. One candidate for investigation is MDMA, better known as ecstasy, which has been shown to foster emotional closeness and communication. It is possible that researchers may be able to modify the compound to develop a safe, effective treatment that could alleviate at least some of au-tism's symptoms.
Such treatments, however, may offer only partial relief, because other symptoms of autism cannot be explained by the mirror neuron hypothesis—for example, repetitive motions such as rocking to and fro, avoidance of eye contact, hypersensitivity, and aversion to certain sounds. In an attempt to determine how these secondary symptoms might arise, our lab group (in collaboration with William Hirstein of Elmhurst College and Portia Iversen of Cure Autism Now, a nonprofit foundation based in Los Angeles) has developed what we call the salience landscape theory.
When a person looks at the world, he or she is confronted with an overwhelming amount of sensory information— sights, sounds, smells, and so on. After being processed in the brain's sensory areas, the information is relayed to the amygdala, which acts as a portal to the emotion-regulating limbic system. Using input from the individual's stored knowledge, the amygdala determines how the person should respond emotionally—for example, with fear (at the sight of a burglar), lust (on seeing a lover) or indifference (when facing something trivial). Messages cascade from the amygdala to the rest of the limbic system and eventually reach the autonomic nervous system, which prepares the body for action. If the person is confronting a burglar, for example, his heart rate will rise and his body will sweat to dissipate the heat from muscular exertion. The autonomic arousal, in turn, feeds back into the brain, amplifying the emotional response. Over time, the amygdala creates a salience landscape, a map that details the emotional significance of everything in the individual's environment.
Our group decided to explore the possibility that children with autism have a distorted salience landscape, perhaps because of altered connections between the cortical areas that process sensory input and the amygdala or between the limbic structures and the frontal lobes that regulate the resulting behavior. As a result of these abnormal connections, any trivial event or object could set off an extreme emotional response—an auto-nomic storm—in the child's mind. This hypothesis would explain why children with autism tend to avoid eye contact and any other novel sensation that might trigger an upheaval. The distorted perceptions of emotional significance might also explain why many children with autism become intensely preoccupied with trifles such as train schedules while expressing no interest at all in things that most children find fascinating.
We found some support for our hypothesis when we monitored autonomic responses in a group of 37 children with autism by measuring the increase in their skin conductance caused by sweating. In contrast with the control subjects, the children with autism had a higher overall level of autonomic arousal. Although they became agitated when exposed to trivial objects and events, they often ignored stimuli that triggered expected responses in the control group.
But how could a child's salience landscape become so distorted? Investigators have found that nearly one third of children with autism have had temporal lobe epilepsy in infancy, and the proportion may be much higher given that many epileptic seizures go undetected. Caused by repeated random volleys of nerve impulses traversing the limbic system, these seizures could eventually scramble the connections between the visual cortex and the amygdala, indiscriminately enhancing some links and diminishing others. In adults, temporal lobe epilepsy results in florid emotional disturbances but does not radically affect cognition; in infants, however, the seizures may lead to a more profound disability. And, like autism, the risk of temporal lobe epilepsy in infancy appears to be influenced by both genetic and environmental factors. Some genes, for example, could make a child more susceptible to viral infections, which could in turn predispose the child to seizures.
Our findings on autonomic responses may help explain the old clinical observation that high fever sometimes temporarily alleviates the symptoms of autism. The autonomic nervous system is involved in controlling body temperature; because fever and the emotional upheavals of autism appear to be regu-
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