To be an autistic child means, with variable degrees of severity, to be incapable to establish meaningful social communications and bonds, to establish visual contact with the world of others, to share attention with the others, to be incapable to imitate others’ behavior or to understand others’ intentions, emotions, and sensations.

—Vittorio Gallese, 2006

Autism spectrum disorders are complex and highly variable with a poorly understood cause. There is a very large literature and much debate on possible genetic and environmental causes and an equally large literature attempting to sharpen the diagnosis, identify diagnostic markers, differentiate subtypes of the spectrum, and characterize the source of the variability among affected individuals. Many questions remain unanswered. What causes autism? Why is the incidence increasing? Is it one or many disorders? Why are males more likely to be affected? Are there effective treatments? One could write an entire book on the ins and outs of autism and indeed several such books already exist.

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Here my focus is more circumscribed. I restrict the discussion to the behavioral symptoms of autism and (neuro)cognitive models for explaining those symptoms. I highlight two of the most influential hypotheses, the broken mirror theory and the broken mentalizing theory (or broken theory of mind theory—I use the terms interchangeably). Further, I have no intention of providing a thorough review of the host of experiments that have investigated the range of abilities and disabilities in autism or even provide much depth in my discussion of the cognitive theories themselves. Please consult any of the many primary sources for a broader view.

Instead I have two main goals. One is to address the basic mirror neuron-based account of autism because the theory has been rather influential and a lot is at stake given how many lives autism touches. The other goal is to highlight an alternative perspective on autism in the same way that (I hope) I’ve been able to highlight alternative perspectives on mirror neuron function, embodied cognition, and imitation. Specifically, I’m going to suggest the possibility that the dominant neurocognitive theories of autism, which assume that behavioral deficits result from lack of or diminished social sensitivity, have it wrong and in fact have it backward.

What Can We Infer from Behavior?

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“Deficit theories” of dysfunction are reasonable and intuitive. If an individual fails to respond normally to sound, it’s a good bet that the person has a diminished capacity to process and hear sound. He simply isn’t capable of perceiving the signal. Likewise, if another individual fails to respond normally to social stimulation, it’s a reasonable bet that the person has a diminished capacity to process social information. But consider the following thought experiment. Imagine you had a stadium rock concert–type sound system hooked up to your living room television and you attempted to watch the evening news with the sound cranked up all the way. Most likely, you would cover your ears and quickly leave. If you forced yourself to stay, you would run into at least one of three problems as you tried to listen and watch. One, the physical pain would be so extreme that you wouldn’t be able to concentrate on the message. Two, attempts to dampen the sound and ease the pain, say by sticking your fingers in your ears, would filter out many of the fine details you need to hear normally. You would perceive less well. Three, if you did manage to listen, the extreme volume would excite so many nerve fibers that it would drown out the details of the signal itself and again you would miss many things. Excess can be as detrimental to normal function as paucity.

Consider also the behavioral patterns of two hypothetical individuals. Owen frequents the park or the beach, hiking, biking, swimming, or sailing. He’s an outdoor kind of guy with the tan and sun-bleached blond hair to prove it. Ethan, on the other hand, is usually found indoors. He spends his spare time reading, composing, working out at the gym, or enjoying the occasional indoor paintball battle. Ethan’s closet contains a rack of long-sleeve shirts and a clutch of wide-brimmed hats hanging on hooks right next to his basket of SPF 70 sunblocks, just in case he does find himself outdoors. Of the two, which is the sun lover? Owen, right? Not necessarily. Ethan could very well crave the warmth and brilliance of the sun, but can’t satisfy his desire because he is excessively sensitive to it, while Owen may be indifferent to whether it is bright and sunny or cool and overcast; as long as he’s on his bike or boat he’s happy.

We can play the same game with food-related behavior. Owen’s diet does not include any dairy products, whereas Ethan’s staples are pizza and milkshakes. Is it safe to assume that Ethan likes dairy more than Owen? No. This could be true, but it is also quite possible that Owen loves cheese and ice cream, more so than Ethan in fact, but is lactose intolerant.

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Behavior does not automatically reveal its cause and can be misleading. We must keep this in mind as we consider the behavioral phenotype associated with autism and the standard interpretations of it.

Autism: The Clinical Perspective

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) characterizes Autism Spectrum Disorder (ASD) by two classes of behavior:

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A. Persistent deficits in social communication and social interaction across multiple contexts, including (1) deficits in social-emotional reciprocity such as reduced sharing of interests or emotions and failure to initiate or respond to social interactions; (2) deficits in nonverbal communicative behaviors used for social interaction, such as abnormalities in eye contact and body language or deficits in understanding and use of gestures, and lack of facial expressions and nonverbal communication; (3) deficits in developing, maintaining, and understanding relationships, such as difficulties adjusting behavior to suit various social contexts, making friends, and absence of interest in peers. B. Restricted, repetitive patterns of behavior, interests, or activities, including (1) stereotypes or repetitive motor movements, use of objects, or speech; (2) insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior; (3) highly restricted, fixated interests that are abnormal in intensity or focus; (4) hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment.

The DSM-V further allows for degrees of severity in the behavioral symptoms and allows for variants with and without accompanying intellectual impairment, and with and without accompanying language impairment, thus defining the spectrum.

For our purposes here, we note that the diagnostic criteria for ASD all but assume a deficit theory—“Persistent deficits in social communication”—and underscore the possibility of “hyporeactivity to sensory input.” There is a widespread view that autistic individuals are less sensitive to pain because their reactions to painful events, such as a blood draw, are often less dramatic than a typical child’s. A recent study took a closer look at autistic individuals’ pain reactivity and came to a rather different conclusion. Seventy-three children and adolescents with autism were studied along with 115 controls while they underwent a blood draw. Behavioral pain reactivity to the needle prick was rated by a nurse and a child psychiatrist, who were present during the procedure. Overall the autistic group showed a reduced behavioral response to pain, consistent with popular belief. However, the team also measured the children’s heart rate and blood serum levels of a stress hormone (β-endorphin). Autistic subjects showed a greater heart-rate response to the needle prick and had a higher concentration of β-endorphin than controls. The authors conclude, “The results suggest strongly that prior reports of reduced pain sensitivity in autism are related to a different mode of pain expression rather than to an insensitivity” (emphasis mine). Again: Behavior does not automatically reveal its cause.

Autism: The Cognitive Perspective

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In terms of cognitively oriented research, autistic individuals appear to lack the ability to, or at least have difficulty with, understanding the goals and intentions behind others actions, reading others’ emotions, empathizing, sharing attention with others (pointing out objects of interest or orienting to what others are attending to), recognizing faces, and imitating others. Certainly, there is ample evidence that autistic individuals can perform abnormally on tests of such abilities.

Many of these deficits include the kinds of things that a theory of mind should enable, like understanding the intentions of others, empathizing, and sharing attention. Accordingly, one prominent cognitive account of autism is that affected individuals lack a theory of mind, the ability to “mentalize.” Psychologist Simon Baron-Cohen has termed the condition mindblindness. It’s a reasonable theory: if someone performs poorly on tests that are designed to assess, say, intention understanding, then it is a good bet that the mental module underlying such an ability is broken.

Interestingly, mirror neuron codiscoverer Vittorio Gallese considers this theory “totally untenable,” citing as a key bit of evidence a single case study “carried out on a patient who suffered a focal bilateral lesion of the anterior cingulate cortex (ACC), previously identified as the candidate site for the Theory of Mind Module, [who] showed no evidence of mind reading deficits.” Gallese proposes his own theory:

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My hypothesis is that these deficits, like those observed in the related Asperger Syndrome, are to be ascribed to a deficit or malfunctioning of “intentional attunement” because of a malfunctioning of embodied simulation mechanisms, in turn produced by a dysfunction of the mirror neuron systems.

Intentional attunement is a fancy term for the ability to tune into the intentions of others, effectively a new label for the mentalizing idea. But Gallese goes further and claims that deficits in mentalizing are not a result of damage to a special-purpose theory of mind neural module, but to a more basic simulation mechanism that is dependent on mirror neurons. This is the broken mirror theory of autism that has been put forward by several authors.

We should apply Gallese’s lesion-based argument and note that hundreds of patients with Broca’s aphasia and/or limb apraxia, who often have lesions that disrupt motor ability and destroy the mirror system, are not reported as being autistic. By Gallese’s own logic, one would think that such a fact would render his theory “totally untenable,” but the broken mirror hypothesis has proven highly influential nonetheless.

Part of the appeal of the broken mirror theory is that it accounts for high-level social deficits in terms of a basic neural mechanism that covers much cognitive ground. Mirror neurons support language, imitation, theory of mind, empathy, intention or goal understanding, and the ability to read others’ emotions. All of these are impaired in autism, therefore autism can be traced back to a deficit in the mirror neuron system. Of course, if mirror neurons don’t support any of these functions, as I’ve argued at length in this book, then the inferential chain that leads to the broken mirror hypothesis falls apart. Based on the arguments put forward in earlier chapters, it follows that the broken mirror theory of autism is itself totally untenable.

I arrive at this conclusion by unraveling the foundational assumptions underlying mirror neuron function. Others have attacked the broken mirror theory from another direction. Cognitive neuroscientist Antonia Hamilton has carefully reviewed the predictions of the theory against available experimental data regarding autistic individuals’ behavior. She comes to the same conclusion: autism is not caused by broken mirrors. Hamilton’s argument boils down to the fact that autistic individuals simply don’t exhibit the behavioral profiles that the broken mirror theory predicts. For example, while it is true that some studies found that autistic individuals perform more poorly on tests of the imitation of meaningless actions, other studies found that they can imitate goal- or object-oriented actions quite effectively. And there is also good evidence for preserved action recognition ability in autism. In one study, Hamilton and her colleagues asked autistic children to match pictures of different hand postures to drawings of actions (such as ironing a shirt) in which the hands of the actor were not depicted. The autistic group outperformed the control group of nonautistic children. These abilities should be impaired according to the broken mirror theory.

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Psychologist Morton Ann Gernsbacher also reviewed the relevant empirical evidence and reinforced Hamilton’s assessment. She writes that a number of studies “are unanimous in demonstrating that autistic individuals of all ages are perfectly able to understand the intentionality of their own actions and of other humans’ actions; there is neither ‘incapacity’ nor impairment in understanding of the intentions of action.” Gernsbacher also raises serious concerns regarding the neuroimaging data argued to reveal dysfunction of the mirror system in autism. She points to two studies that reported abnormal mirror neuron activity in autistic subjects in 2005 and 2006. The studies were highly publicized in outlets like The New York Times, Scientific American, and NOVA, yet, Gernsbacher notes, their results failed to replicate (could not be reproduced in subsequent studies) and some subsequent studies reported no difference between autistic and control groups.

Psychologist Cecelia Heyes also argues against the broken mirror hypothesis. Her argument centers on imitation, which according to the broken mirror claim should be severely impaired in autism. Heyes rejects the commonly accepted notion that autistic individuals have a fundamental deficit in imitation. Her argument is that standard tests of imitation are not direct assessments of imitation ability because of their cognitive complexity. In typical tasks, participants are asked to “do this” while some action is modeled, which requires conscious inferences about what specifically is being asked, sustained attention, working memory to remember the sequence of movements, and the motivation to comply. To get around these issues, Heyes and colleagues measured automatic imitation (unconscious mimicry) by asking autistic participants to open or close their hand as quickly as possible when they saw a stimulus hand start to move. The team wanted to know whether autistic individuals would show a movement compatibility effect: faster response times when the perceived action matched the required response. This is precisely what they found, indicating that autistic individuals are quite capable of associating perceived and executed actions.

Overall, and despite the hoopla surrounding the broken mirror theory of autism in the popular press, there is a growing consensus that the scientific evidence does not support the claim.

What about the broken mentalizing theory? The strongest argument for a theory of mind deficit in autism comes from the false-belief task, a classic behavioral assay for the ability to mentalize. In the standard version, one puppet, call her Sally, places a desirable item such as a piece of chocolate in a basket and then leaves the scene. Another puppet, Anne, then enters and moves the object to a nearby box. Sally then returns and the subject, who had been watching the drama, is asked to predict where Sally will look for her object. The key bit is that in order to get it right, the observer has to recognize that Sally believes that the object is still in the basket even though it is not. If the subject predicts that Sally will look in the basket, this means that he or she knows that behavior is caused not by the environment alone (where the object is, in fact) but by people’s beliefs about the world, that is, mental states. The false-belief task is argued to be, therefore, a litmus test for the presence of theory of mind.

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Four-year-old children pass the false-belief test but children younger than four usually fail, as do autistic children and autistic adults (more often than controls, anyway). From this it is typically concluded that autistic people and nonautistic children under the age of four lack a theory of mind.

Paradoxically, these facts immediately raise problems for the idea that the behavioral symptoms of autism are caused fundamentally by a broken theory of mind module. For one, as Yale psychologist Paul Bloom points out, three-year-old children, who cannot pass the false-belief test, do not behave as if they are autistic. In fact, autism is often diagnosed well before the child’s fourth birthday, an age at which autistic and nonautistic children are indistinguishable in terms of performance on such tests of theory of mind. Another problem is that a nontrivial proportion of autistics and many higher-functioning individuals on the autism spectrum can pass the false-belief task, but still exhibit the social difficulties that define the spectrum disorder. There must be something beyond a theory of mind deficit, as mea- sured by the false-belief task, at the core of autism.

The false-belief task itself may be part of the problem. Gernsbacher noted that success on the task depends in large part on language ability: to get the answer right, you have to understand the question you are being asked. Given that autistic individuals have language problems, it is not surprising that they fail the false-belief task. Bloom has similar qualms about the task and even articulated two reasons for abandoning it altogether as a measure of theory of mind. His first reason is that the task is too cognitively demanding and therefore isn’t tapping into just theory of mind. Similar to Heyes’s argument regarding imitation tasks, Bloom notes that the false-belief task places significant demands on the ability to suppress salient but misleading information for correct task performance (like where the object actually resides), and so on. In support of his claim, he points to evidence that with simplified versions of the test, kids younger than four can get it right. His second reason is that theory of mind is required for other tasks that children even younger than two years old typically pass. We already encountered one example in the previous chapter: toddlers often imitate the intended rather than the actual action: if an experimenter attempts to operate a toy but fails, children imitate the intent, not the failures, demonstrating that very young children understand intentions. Bloom cites several more examples.

Though not extensive, there is some evidence that, as with children younger than four years old, simplifying the theory of mind task reveals the capacity to mentalize in autism. One task involves a doll that favors a snack that the participant dislikes. The child is then asked to predict which snack the doll will choose to eat. Autistic children who fail the standard false-belief task can often pass the simplified task.

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So neither the broken mirror nor the broken mentalizing theory hold up well to the empirical facts regarding the abilities and deficits in autism. Antonia Hamilton concludes her review of the literature:

Neither a low-level theory (the broken mirror theory) nor a high-level theory (the broad mentalising theory) can fully account for the current data. It is likely that future theories will need to be more subtle and to distinguish between different types of mirror neuron system and different types of mentalising. Thus, blanket statements about deficits in “the mirror neuron system” or “mentalising” in autism will no longer be sufficient.

I agree that neither theory is satisfactory, but I’m not convinced that more subtle distinctions between types of mirror system or theory of mind operations will fare better. The problem, I suspect, is hidden in the fact that all of this discussion still centers on ideas about what is lacking in autism. Autistic people have no mirror system or no theory of mind or no empathy or no ability to process social information. These are deficiency or hypofunction theories; a good first guess, but not the only possibility. And given that they haven’t had all that much success, maybe it’s time to focus some research effort on a theory based on excess or hypersensitivity. Perhaps autistics don’t experience a socially numbed world but rather a socially intense world.

The Intense World Syndrome

In fact, Henry Markram, Tania Rinaldi, and Kamila Markram proposed such a theory in a 2007 article aptly titled, “The Intense World Syndrome—An Alternative Hypothesis for Autism.” The theory is grounded, oddly enough, in a rat model of autism. I say “oddly enough” because autism has traditionally been considered a uniquely human disorder, with defining symptoms showing up in high-level social and language domains. But it turns out that rats who are exposed prenatally to valproic acid—a compound used in human medications to control seizures and bipolar disorders—develop some key features of autism both neurally and behaviorally, including loss of cerebellar neurons, abnormalities in the serotonergic system, decreased social interactions, increased repetitive behaviors, enhanced anxiety, motor abnormalities, and sensory hypersensitivity. Curiously, the prevalence of autism in humans who are prenatally exposed to valproic acid through maternal use of the medication is substantially higher (one estimate is 11–100 times) than in the general population.

Some of the symptoms listed above—increased anxiety, sensory hypersensitivity—don’t regularly surface in the debates over broken this or broken that theories of autism, and for good reason: the theories have little to say about them. How do you end up with hypersensitivity to sensory stimulation in a syndrome caused by a broken theory of mind module? But these symptoms are fairly typical of autistic individuals and something that we should seek to explain. As we’ll see, hyperfunction accounts have a natural explanation.

The existence of a rat model makes it possible to explore, in substantial detail, the neural bases of an autistic-like phenotype. The Markrams and their team did precisely that. They focused on three brain regions, the somatosensory cortex, the prefrontal cortex, and the amygdala. Somatosensory cortex is well developed and extensively studied in rodents and so provides a good model for sensory systems. They assessed prefrontal cortex as a means to sample a higher-order cortical processing system. And they studied the amygdala due to its known role in emotional processes and to assess neural function in a nonneocortical network. Here’s the highlight reel version of what their work showed.

They determined that local neuronal networks in the three brain regions tested in rats are hyperreactive. They demonstrated this by broadly stimulating, in vitro, a small patch of rat brain tissue (less than one millimeter square) and recording the response from individual neurons embedded within that patch. The broad stimulation activates both the recorded cell itself as well as its local network. The response, therefore, reflects not only direct stimulation but also indirect network stimulation via the cell’s neighbors. In animals treated with valproic acid, the neuronal response to network stimulation was greater than in control animals. In fact, it was about twice as strong in the two cortical regions. Interestingly, this is not due to the intrinsic hyperreactivity of the cells themselves. If a single cell is stimulated rather than its network, hyporesponsivity occurs: more stimulation is required to make the cell fire. So it is not the neurons themselves that are hyperexcitable, it’s the networks. The driving force behind the micro network–level hyperreactivity appears to be the direct connections between neurons. Valproic acid–treated animals exhibit a 50 percent increase in the number of direct connections between neurons within a local circuit.

Further, the Markrams and their team found that neural networks in valproic acid–treated rats are also hyperplastic. It has been known since the 1960s that if two connected neurons are stimulated simultaneously for a period of time, the subsequent response to stimulation of the two-cell network is enhanced for quite a long time afterward compared to baseline. This is long-term potentiation (or LTP) and it is thought to be an important cellular mechanism in learning and memory. The LTP effect doubled in valproic acid– treated animals compared to control rats in all three brain regions studied, showing that this form of plasticity is enhanced. Network connectivity plasticity is also enhanced. When connectivity patterns between neurons in local and expanded networks were examined before and after widespread and prolonged (overnight) activation of the entire network, valproic acid–treated rats exhibited an increase in the rate of rewiring, mostly evident in the nonlocal networks, compared to controls. This hyperplasticity seems to have behavioral consequences: treated rats have an exaggerated fear learning response—response to a tone that had previously been paired with a mild electric shock—that is stronger, generalizes more readily, and persists longer than in control animals.

Given these kinds of neural changes in the rat model of autism, a plausible story can be told about the neural basis of the range of autistic behaviors. Hyperabilities, such as increased sensory sensitivity or memory in specialized domains, can be explained by hyperreactivity and hyperplasticity of neural circuits. Hyporesponse to social stimuli can be explained in terms of the emotional intensity of the signal, which triggers anxiety and avoidance responses, which means less information is acquired in individual social situations and over time reduced opportunities to learn in the social domain. Theory of mind performance would also be expected to suffer with a hyperactive response to social signals—even if there is no fundamental deficit in mentalizing—because of increased anxiety when interacting with others and/or because avoidance behavior decreases the amount of information perceived or learned. Repetitive behaviors can be viewed as a coping mechanism aimed at regulating the child’s intense world. Motor deficits can be explained by hyperexcitability of the response to sensory stimulation, which has motor consequences, as we’ve discussed, or from hyperreactivity of motor systems themselves. And because language is at some levels a sensorimotor task and at other levels a highly social behavior, abnormalities in the sensorimotor or social domains can be expected to affect language.

All of this is interesting—suggestive even—but how relevant is it, really, to autism? That’s a fair question. At this stage, all we really have is circumstantial evidence in the form of parallels between human autism and the valproic acid–treated rat model. Ultimately, the proof of the pudding is in the eating. If therapies or preventative measures can be developed in the rat model that actually prove useful in humans, or if the same neural changes could be unambiguously demonstrated in humans, then we have a decent pudding.

But even if we don’t have a perfect pudding in the end, the rat model of autism is nonetheless useful for our purposes here because it essentially demonstrates proof that autism-like symptoms can emerge from a hyperreactive system. It doesn’t have to be the case that abnormal performance on this or that task is a result of depressed neural function. The Markrams make this point eloquently in connection with previous work on the link between amygdala dysfunction and autism. It is worth an extended quote (citations removed):

The very first animal model of autism was based on lesioning the amygdala and studying the effects on social behavior and hierarchy, implying that the lack of amygdala activity may explain the lack of social interactions or social intelligence in autism. This view dominated the research performed on the role of the amygdala in autism. Parallels were drawn between amygdala lesioned patients and autistic subjects, functional magnet[ic] resonance imaging (fMRI) studies revealing an insufficiently activating amygdala in autistic subjects were associated with deficits in interpreting other people’s state of minds and feelings. However, the opposite could also be true and lead to similar symptoms: rather than being hypo-active or not sufficiently responding, the amygdala could be overly reactive in autism. Consequently, autistic people could be processing too much emotionally relevant information, including enhanced fear and anxiety processing. The outcome could be a similar one to a not sufficiently active amygdala: withdrawal and decreased social interaction due to an enhanced stress-response and socio-emotional overflow. Indeed, as described below our studies on [valproic acid]-treated rat offspring indicate that the amygdala is hyper-reactive, hyper-plastic, and generates enhanced anxiety and fear processing. In accordance with this, more recent fMRI studies as well reveal amygdaloid hyperactivation in autism.

This kind of effect—hyper-responsivity leading to avoidance— is observed regularly and uncontroversially in the sensory domain. Autistic individuals often cover their ears when even moderately loud sounds are present in the environment and exhibit other forms of avoidance behavior. As with the rock concert sound system example at the beginning of this chapter, if an autistic person failed to get information out of moderately loud sounds or simply left the room, we wouldn’t say that he or she had a diminished capacity to hear the sound. The response is more readily explained as an increased sensitivity to sensory stimulation. As autistic author Temple Grandin said in a radio interview, “How is a person going to socialize if their ears are so sensitive that just being at a restaurant is like being inside the speaker at a rock ‘n’ roll concert and it’s hurting their ears?” Good question.

Do You See What I See?

One other indicator of hypersensitivity is staring us in the face, literally. Autistic individuals seem to perceive less in facial expressions than nonautistic individuals, and the part of the brain that is partial to faces, the fusiform face area, responds less well in autistic folks. The first-pass (and most popular) interpretation of these findings: autistic people can’t read faces because their neural face area is poorly developed. A research team in Pittsburgh scanned Temple Grandin while she was watching pictures of faces and nonface scenes and found exactly this result. Grandin described her experience in the scanner while lecturing at UC Davis’s MIND institute in 2008 (CAPS indicate emphasis in Grandin’s phrasing):

Now [researcher] Nancy Minshew did another brain scan and she found I was more interested in THINGS than I was in looking at pictures of people. . . . She starts showing me all these weird videos of people, airplanes flying over the Grand Canyon, bridges and apples and all kinds of objects. And I’m looking at this [thinking] where did she get this 1970s video? How many copyright violations do we have on this video? Why was I looking at the THINGS? Because the THINGS told me more information about where the tapes came from. And I was trying to figure out what the experiment was all about.

If all you did was analyze the brain scans it would look like Grandin’s face area is dysfunctional. But, it is clear from her recounting of the experience that she was attending more to the nonface pictures, which could easily produce the observed results even if her fusiform face area (FFA) were perfectly normal (attention modulates the neural response). You are wondering whether the reason why she was more attentive to the nonface pictures is because her face area is dysfunctional in the first place. It’s possible, and it is the standard explanation of both the brain response pattern and Grandin’s behavior, which is more object- than face-oriented. It’s not the only possibility, though! It could be, for example, that her FFA is hyperreactive, which leads her to avoid attending to faces, which results in more attention paid to nonface objects, which leads to the observed imaging result. Or maybe she’s just smart enough to recognize that the THINGS tell you more information, as she noted, in the context of the problem she had tasked herself with during the study, to figure out the goals of the experiment.

At least one study has confirmed that alternative explanations of the face processing “dysfunctions” in autism may be on the right track. Autistic and nonautistic individuals were scanned using fMRI while they looked at pictures of faces that were either emotionally neutral or emotionally charged. Crucially, using eye-tracking technology, the researchers also monitored which parts of the images their participants were looking at during the experiment. Overall, autistic participants activated their fusiform face region less vigorously than nonautistic controls, replicating previous work. But the eye-tracking data showed that this was simply because they spent less time looking at the most informative region of the faces, the eyes. In fact, when the researchers looked at fusiform activation as a function of time spent fixating on the eyes in the photos, they found a strong positive correlation in the autistic group. This means that the autistic brain is responding quite well to face stimuli, if one takes into account the amount of time spent looking at them.

Again we might ask the same question we asked previously, why aren’t autistic individuals looking at the most informative region of a face in the first place? If it’s not a general face processing deficit, maybe it is a facial emotion processing deficit that limits their ability to detect information in the eyes. According to this view, the face processing system in general is working OK, reflected by the activation in the FFA when autistics actually look at faces, but because autistic people can’t process the emotion in them, they don’t spend as much time looking at the critical regions compared to controls. As before, this is a possible interpretation. But again, it’s not the only interpretation. An alternative is that autistics don’t look at the eyes as much because of a hyperactive response to emotional information, which is particularly evident in the eyes. And consistent with this alternative possibility, the same study reported that amygdala activation was stronger in the autistic compared to the nonautistic group while looking at faces.

Also consistent with the alternative, emotional hyperreactivity hypothesis are statements from autistic individuals themselves. Here’s a sample gleaned from a paper covering face processing in autism: It’s painful for me to look at other people’s faces. Other people’s eyes and mouths are especially hard for me to look at.

My lack of eye contact sometimes makes people, especially my teachers and professors, think that I’m not paying attention to them.

—Matthew Ward, student, University of Wisconsin

Eyes are very intense and show emotions. It can feel creepy to be searched with the eyes. Some autistic people don’t even look at the eyes of actors or news reporters on television.

—Jasmine Lee O’Neill, author

For all my life, my brothers and everyone up ’til very recently, have been trying to make me look at them straight in the face. And that is about the hardest thing that I, as an autistic person, can do, because it’s like hypnosis. And you’re looking at each other square in the eye, and it’s very draining.

—Lars Perner, professor, San Diego State University

These are revealing statements for two reasons. First, they provide a clear indication of an intact theory of mind in these individuals (“my lack of eye contact . . . makes people . . . think that . . .”). And second, active avoidance of eye contact provides just as much evidence for sensitivity to the information contained therein as does active engagement of eye contact. If you can’t recognize that there is information in the eyes, why avoid them?

* * *

Autism remains poorly understood on all levels. I’m not trying to suggest that I have the answers. We do know a few things though. We know that the broken mirror hypothesis does not fare well in light of empirical facts. Autistic individuals do not exhibit the range of deficits that the theory predicts and more importantly in my mind, mirror neurons do not support the kind of abilities that are affected in autism. The broken mentalizing theory doesn’t do much better given that there are significant concerns about the tasks that are typically used to assess theory of mind, the fact that performance on such tasks does not reliably distinguish autistic from nonautistic individuals, and the fact that a broken mentalizing account only addresses one aspect of the overall picture in autism. The intense world theory shows some promise. The range of data we’ve considered in this chapter more than justifies ramping up the investigation of this theory in the “human model” of autism.

* * *

An aside: Just because someone doesn’t make eye contact, slinks away from social interaction, or appears overly obsessed with THINGS, doesn’t necessarily mean that he or she can’t read emotions, is asocial, or lacks empathy. Conversely, just because another person is engaging, gregarious, and charismatic doesn’t mean he or she has achieved the platonic social ideal. Sociopaths, for example, sometimes exhibit just these features; serial murderer Ted Bundy is a famous example.

In the wake of the recent rash of shootings in Aurora, Newtown, and elsewhere there has been an unfortunate implied or explicit link made between autism and antisocial behavior. The link is easy to make under standard assumptions about the disorder, particularly high-functioning autistic individuals who are described as being not like us, an enigma, or lacking in empathy. They’ve been deemed robotic and alien, even likened to nonhuman animals, rendering the ingredients for the classic Hollywood demon. Experts repeatedly and correctly point out, however, that there is no causal link between autism and violence, nor between autism and sociopathic behavior.

Excerpted from "The Myth of Mirror Neurons: The Real Neuroscience of Communication and Cognition" by Gregory Hickok. Copyright © 2014 by Gregory Hickok. With permission of the publisher, W. W. Norton & Company, Inc. All rights reserved.