Mirror neurons are theorized to be, according to some of the more heavily popularized literature these days, neurons which activate in the primate brain upon observation of another individual performing an action.
The most frequently cited experiments suggesting the presence and functionality of mirror neurons have involved macaque monkeys—these monkeys were fitted with electrodes which allowed scientists to observe particular activity patterns in neurons in the premotor cortex. The experiments sought to show a correlation between imitation, intention, and action that might shed light on the means by which primates (possibly including humans) may internally simulate the mental states of others. But did it succeed? Some might answer “yes”, and many since have attempted to correlate the mirror neuron experiment results with theories in autism research, since autism is commonly (though not necessarily accurately) associated with deficits in imitation, modeling, and empathy.
This discussion will attempt to explain the actual findings in monkey and human research associated with mirror neurons, and pose the argument that the mirror neuron studies being performed on human subjects do not necessarily imply for autism what much of contemporary popular science literature claims. That is, while mirror neuron studies may indeed offer valuable information about brain differences and the various ways in which minds process and react to certain stimuli, these studies do not actually prove that the observed differences between autistic and nonautistic behavior and cognition are explained by a “dysfunctional” mirror neuron system.
Additionally, many recent publications linking autism and mirror neurons exhibit much in the way of biased language, faulty initial assumptions, and poor experimental design, which could in the long run end up serving as a detriment to both the autistic population (e.g., through the perpetuation of ideas suggesting that autistics lack some essential element of personhood) and the field of neuroscience (since good science must work tirelessly to avoid the kinds of bias that stem from prejudice and ignorance, such as that which resulted in “scientific” racism, which is now widely considered to be pseudoscientific and therefore a blemish on the history of science).
The neurons focused on in the macaque experiments are located in what is called the F5 area of the brain, and are thought to be associated with certain hand and mouth movements. The paper Mirror neurons and the simulation theory of mind-reading, by Vittorio Gallese and Alvin Goldman, Trends In Cognitive Sciences - Vol. 2, No. 12, December 1998 explains the implications of the macaque experiment as follows:
These experiments showed that the activity of F5 neurons is correlated with specific hand and mouth motor acts and not with the execution of individual movements like contractions of individual muscle groups. What makes a movement into a motor act is the presence of a goal. This distinction is very important since it allows one to interpret the role of the motor system not just in terms of the control of the dynamic variables of movement (like joint torques, etc.), but rather as a possible candidate for the instantiation of mental states such as purpose or intention.
The most profound implication here, according to researchers, is that the neurons in question might provide valuable clues about goal-setting and intention in response to observed movements, and by extension, the ability of primates to model the mental states of others. While being aware that the macaques do not actually exhibit the sorts of behaviors generally associated with evidence of “theory of mind” in humans, nor tend toward imitating their peers, researchers nonetheless suspect that mirror neurons might still play a key role in human social communication. With regard to the possibility of mirror neurons existing in humans in the first place, Gallese and Goldman write:
Two lines of evidence strongly suggest that an action/observation matching system similar to that discovered in monkeys also exists in humans. The first refers to an elegant study by Fadiga et al.16 in which the excitability of the motor cortex of normal human subjects was tested by using Transcranic Magnetic Stimulation (TMS). The basic assumption underlying this experiment was the following. If the observation of actions activates the premotor cortex in humans, as it does in monkeys, this mirror effect should elicit an enhancement of the motor evoked potentials (MEPs) induced by TMS of the motor cortex, given its strong anatomical links to premotor areas. TMS was performed during four different conditions: observation of an experimenter grasping objects; observation of an experimenter doing aimless movements in the air with his arm; observation of objects; detection of the dimming of a small spot of light. The results of this study showed that during grasping observation MEPs recorded from the hand muscles markedly increased with respect to the other conditions, including the attention-demanding dimming detection task. Even more intriguing was the finding that the increase of excitability was present only in those muscles that subjects would use when actively performing the observed movements. This study provided for the first time evidence that humans have a mirror system similar to that in monkeys. Every time we are looking at someone performing an action, the same motor circuits that are recruited when we ourselves perform that action are concurrently activated.
In short: when human subjects in the TMS study observed other individuals moving, readings taken from their muscles seemed to reflect the sorts of muscular precursors to movements that would actually be required in order to perform the task being observed. Note that actual neurons in the human brain were not electrode-probed as they were in monkeys; hence, while the TMS experiments do seem to indicate that observing someone performing a task can result in pre-motor movement potential in the muscles, they do not “prove” the existence of mirror neurons. Nevertheless, it is not entirely farfetched to think that perhaps humans do have mirror neurons—the question is whether the performed experiments actually tell us anything about internal modeling of others’ minds or mental state (“mind reading”). Gallese and Goldman define mind reading as follows:
Mind-reading is the activity of representing specific mental states of others, for example, their perceptions, goals, beliefs, expectations, and the like. It is now agreed that all normal humans develop the capacity to represent mental states in others, a system of representation often called folk psychology. Whether non-human primates also deploy folk psychology is more controversial (see last section of this article), but it certainly has not been precluded. The hypothesis explored here is that MNs are part of – albeit perhaps a rudimentary part of – the folk psychologizing mechanism.
The leap from detected premotor muscular activity to the presumption of simulated mental states seems to be quite a large one indeed (and not necessarily an appropriate one). Continuing onward, Gallese and Goldman discuss the two basic theorized types of “human mind reading”, known as theory theory and simulation theory:
There is a large literature concerned with the nature of (human) mind-reading. Two types of approaches have dominated recent discussion: theory theory (TT) and simulation theory (ST) (Refs 20–22). The fundamental idea of TT is that ordinary people accomplish mind-reading by acquiring and deploying a commonsense theory of the mind, something akin to a scientific theory. Mental states attributed to other people are conceived of as unobservable, theoretical posits, invoked to explain and predict behavior in the same fashion that physicists appeal to electrons and quarks to predict and explain observable phenomena. On the standard presentation, the theory of mind possessed by ordinary people consists of a set of causal/explanatory laws that relate external stimuli to certain inner states (e.g. perceptions), certain inner states (e.g. desires and beliefs) to other inner states (e.g. decisions), and certain inner states (e.g. decisions) to behavior. This picture has been articulated by functionalist philosophers of mind23–26 as well as by developmental psychologists27,28. According to TT, attributing particular mental states to others arises from theoretical reasoning involving tacitly known causal laws. Much on this subject has been done by developmentalists, eager to determine how the mind-reading capacity is acquired in childhood29. Many interpret children’s changes in mind-reading skills as evidence in favor of TT because the skill changes are construed as manifestations of changes in theory30,31. Theory theorists differ among themselves as to whether theory of mind is acquired by a general-purpose scientizing algorithm32 or by the maturation of a domain specific module or set of modules33,34. This debate will not concern us here. ST arose partly from doubts about whether folk psychologizers really represent, even tacitly, the sorts of causal/explanatory laws that TT typically posits. ST suggests that attributors use their own mental mechanisms to calculate and predict the mental processes of others.
In other words, “theory theory” suggests a learning situation in which humans gradually come to understand how other people think through interacting, recording data about interactions, processing it, and coming up with various generalized and specialized notions of how others are likely to think and react in particular situations. Gallese and Goldman, however, suggest that theory theory might not be enough to fully explain apparent “mind reading” abilities in humans, and posit that “simulation theory” might actually be a more likely explanation for the apparent capacity people seem to have allowing them to accurately intuit what others think and feel. That is, rather than applying “scientific” algorithms to evaluate others’ behavior, people might have a more direct route to understanding the minds of others—a route that exists by virtue of “simulation hardware” such as mirror neurons. While it does not seem that “mirror neurons” or their activity would actually preclude theory theory from being true, the notion that perhaps people “simulate” the mental processes of others at least seems worth exploring.
However, when exploring the simulation theory hypothesis in conjunction with autism research, the common implication is that nonautistic people have the ability to internally represent the mental states of others, whereas autistic people do not—and that the mirror neuron experiments might constitute something approaching empirical evidence for this. Seeking to test this idea, researchers at UC San Diego performed the following experiment, as described in the April 2005 Science Daily article, Autism Linked To Mirror Neuron Dysfunction:
The UC San Diego team collected EEG data in 10 males with autism spectrum disorders who were considered “high-functioning” (defined as having age-appropriate verbal comprehension and production and IQs above 80) and 10 age- and gender-matched control subjects.
The EEG data was analyzed for mu rhythm suppression. Mu rhythm, a human brain-wave pattern, is suppressed or blocked when the brain is engaged in doing, seeing or imagining action, and correlates with the activity of the mirror neuron system. In most people, the mu wave is suppressed both in response to their own movement and to observing the movement of others.
Subjects were tested while they moved their own hands and while they watched videos of visual white noise (baseline), of bouncing balls (non-biologic motion) and of a moving hand.
As expected, mu wave suppression was recorded in the control subjects both when they moved and when they watched another human move. In other words, their mirror neuron systems acted normally. The mirror neurons of the subjects with autism spectrum disorders, however, responded anomalously—only to their own movement.
Upon first reading, the description of this experiment probably sounds fairly straightforward. But examining it for a moment from a more critical perspective, all this experiment really tells us is that autistic brains seem to respond differently to a particular kind of stimulus (in a particular environment). It does not actually prove that autistic brains are actually “dysfunctional” to begin with; it merely demonstrates an observation of difference in functionality between autistic and nonautistic cognition. Nor is any attempt made to explain why mu waves might not be suppressed in autistics when those subjects viewed the moving hand—it could be that the autistic subjects were simply processing the data in their environment differently. Of course, there is certainly nothing unscientific (or unethical) about noting these differences in reaction pattern and functionality between autistic and nonautistic brains, however, there is plenty to scrutinize when conclusions such as the following (from the same Science Daily article as quoted above) are drawn:
“The findings provide evidence that individuals with autism have a dysfunctional mirror neuron system, which may contribute to many of their impairments—especially those that involve comprehending and responding appropriately to others’ behavior,” said Lindsay Oberman, first author of the paper and UCSD doctoral student working in the labs of senior authors V.S. Ramachandran, director of the Center for Brain and Cognition, and Jaime Pineda, director of the Cognitive Neuroscience Laboratory.
While it is certainly not ridiculous to theorize that the mu wave experiment might carry implications that could explain autistic differences in processing, it must be acknowledged that the experiment does not actually “prove” any sort of correlation between mirror neurons and a person’s ability to comprehend others’ behavior or “respond appropriately”. There might be any number of reasons why autistics might not seem to comprehend others’ behavior or respond appropriately to it, none of which necessarily have anything to do with mirror neuron activity or lack thereof. Not to mention the fact that what comprises an “appropriate response” is subjective and culturally variable; in many Asian cultures, for instance, it is considered rude for people to make direct eye contact with their workplace superiors, and for children to make eye contact with adults.
And if one applies “theory theory” here (as opposed to simulation theory), the apparent disconnect between autistic and nonautistic patterns of relating and interacting comes into much sharper focus, since over time a typically-developing person will learn that other people have minds “like them” (because nonautistic people are more numerous), whereas an autistic person might be more likely to continue to see the minds of others as mysterious. Perhaps the lack of mu wave suppression in autistics observing a hand motion reflects the fact that autistics do not automatically make the kinds of assumptions that nonautistic people do about others in their vicinity. Perhaps it reflects the fact that autistic brains are “using” mu wave activity to accomplish cognitive functions not being tested for by the experiment described above. Or perhaps it reflects something else entirely—we really won’t know until more experiments are performed.
But what about the “bottom line” here? After all, autistics do seem to demonstrated reduced comprehension of the behavior of others, in addition to difficulties in imitation and an observed lack of “appropriate” (i.e., typical) responses to particular behaviors on the part of others, cultural variability notwithstanding. Isn’t it just “grasping at straws” (politically correct straws, no less) to suggest that nothing concrete can be drawn from mirror neuron studies? Not hardly. In all these studies claiming an association between “broken mirror neurons” and autism, there is a distinct lack of any serious exploration of the ability (or lack thereof) of nonautistic people to understand autistic people. Clearly, there is a communication breakdown here (between autistics and nonautistic), but not one that can be neatly and succinctly explained by suggesting that autistics are “broken”. If mirror neurons can theoretically be said to indicate an ability to simulate others’ mental states and understand their feelings and motivations, then why are autistics so commonly described as “mysterious” and/or “otherworldly”? Why don’t nonautistic people seem able to internally simulate the mental states of autistics? Have any experiments been performed in this regard at all? What seems to be happening here is that people are having tremendous difficulty accepting the heterogeneity of humanity and proposing instead that “human-ness” is dependent upon one’s possession of certain typical, majority traits—meaning that people who lack these traits are not merely different, but less than, limited, and perhaps not even people to begin with.
It seems quite premature to read too much into “mirror neuron” studies. Particularly when noting the heavily biased, exclusionary language that appears in many popular articles on autism these days. For example, consider the article Scientists Say Everyone Can Read Minds, by Ker Than, LiveScience, April 27, 2005, which states:
Empathy allows us to feel the emotions of others, to identify and understand their feelings and motives and see things from their perspective. How we generate empathy remains a subject of intense debate in cognitive science.
Some scientists now believe they may have finally discovered its root. We’re all essentially mind readers, they say.
The author goes on to relate:
“Mirror neurons suggest that we pretend to be in another person’s mental shoes,” says Marco Iacoboni, a neuroscientist at the University of California, Los Angeles School of Medicine. “In fact, with mirror neurons we do not have to pretend, we practically are in another person’s mind.”
Since their discovery, mirror neurons have been implicated in a broad range of phenomena, including certain mental disorders. Mirror neurons may help cognitive scientists explain how children develop a theory of mind (ToM), which is a child’s understanding that others have minds similar to their own. Doing so may help shed light on autism, in which this type of understanding is often missing.
What is wrong with this picture? Well, let’s start with the title. If “everyone” can read minds, and autistics cannot, then by this definition, autistics cannot be included in the group inclusive of, well, everyone. While this might seem to be a picky point, imagine for a moment that an article were published with a title like, “Scientists Say Everyone Has a Uterus”. Clearly, this title excludes an entire category of people from the “everyone” designation—that is, males of the species. So regardless of whether autistics can or cannot “read minds” in the manner suggested in the article, the title itself is still problematic. Moving onward, we see that the word “empathy” appears in the first quote. Merriam-Webster’s dictionary offers the following definition of empathy:
Main Entry: em·pa·thy
Etymology: Greek empatheia, literally, passion, from empathEs emotional, from em- + pathos feelings, emotion—more at PATHOS
1 : the imaginative projection of a subjective state into an object so that the object appears to be infused with it
2 : the action of understanding, being aware of, being sensitive to, and vicariously experiencing the feelings, thoughts, and experience of another of either the past or present without having the feelings, thoughts, and experience fully communicated in an objectively explicit manner; also : the capacity for this
The second definition above seems to be the one referred to in the LiveScience article quoted above—that is, empathy is what allows “us” (again, that “us who are not autistic”) to see things from someone else’s perspective. It also, according to the article, allows us to “feel the emotions of others”. To posit that autistics are incapable of feeling the emotions of others is to make a huge and very dangerous leap into speculation.
To make the fallacious nature of this speculation clearer, imagine that you have been given a drug which has “re-mapped” the physical appearance of your emotional manifestations. For instance, now instead of smiling when you are happy, you are compelled to run in circles. Instead of crying or brooding when you are sad, you are compelled to play with rubber bands. Instead of laughing when you are amused, you stick your tongue out. It would not be appropriate in this scenario for someone to come along and accuse you of not being able to feel happiness, sadness, or amusement simply because you were not smiling, crying, or laughing when they would have done those things. It might be understandable for such an observer to assume you weren’t feeling the emotions in question, but it would not be correct. And heuristics are only as good as their ability to provide accurate data; if an heuristic fails to provide accurate data, then it is time to develop a better one.
If neurology is to truly get to the bottom of the mysteries of brain differences (and all brains are mysterious, not just autistic ones!), techniques for assessing subjective emotions must be developed that well exceed what we presently have available. We cannot continue to rely on “folk psychology” or superficial assumptions based on observed behaviors the way many people still seem to be doing; clearly, human cognitive variety has proven that sort of technique to be far less than adequate.
Another example of problematically biased language being used in conjunction with commentary on “mirror neurons” is found in the November 2006 Scientific American article entitled, Broken Mirrors: A Theory of Autism by Vilayanur S. Ramachandran and Lindsay M. Oberman. This article sets up the reader with a melodramatic title and continues from there:
At first glance you might not notice anything odd on meeting a young boy with autism. But if you try to talk to him, it will quickly become obvious that something is seriously wrong. He may not make eye contact with you; instead he may avoid your gaze and fidget, rock his body to and fro, or bang his head against the wall. More disconcerting, he may not be able to conduct anything remotely resembling a normal conversation. Even though he can experience emotions such as fear, rage and pleasure, he may lack genuine empathy for other people and be oblivious to subtle social cues that most children would pick up effortlessly.
Here, we have the stereotypical depiction of an autistic person as being odd, otherworldly, and perhaps most disturbingly, deceptive in his initial appearance of being “normal”. This, perhaps, gets right to the root of some of the most significant prejudices that exist toward autistics—the “normal” appearance (at least in terms of basic physical features) is almost seen as an amplifier of the “wrongness” of being autistic, since people tend to associate a standard human appearance with typical behavior and mannerisms. When it is discovered that the person in question does not demonstrate typical behaviors and mannerisms, the nonautistic person might somehow feel “cheated” out of a normal interpersonal experience. At least in the paragraph above the authors concede that autistics “experience emotions”, however, they go on to suggest a lack of “genuine empathy” (as opposed to artificial empathy?). The narrative continues:
Although the chief diagnostic signs of autism are social isolation, lack of eye contact, poor language capacity and absence of empathy, other less well known symptoms are commonly evident. Many people with autism have problems understanding metaphors, sometimes interpreting them literally. They also have difficulty miming other people’s actions. Often they display an eccentric preoccupation with trifles yet ignore important aspects of their environment, especially their social surroundings. Equally puzzling is the fact that they frequently show an extreme aversion to certain sounds that, for no obvious reason, set off alarm bells in their minds.
Inappropriately biased language appears in spades here. The description of autistics as having an “eccentric preoccupation with trifles”, for instance, is extremely presumptuous, as it assumes that an autistic person’s interests have no actual merit but are merely the side effect of a dysfunctional cognition. But who, really, gets to decide which things are worth paying attention to? Why is it “not okay” for a child to fixate on railway schedules or food ingredients labels, but perfectly okay to fixate on fashion fads, sports, or celebrities? Do the scientists studying autism with “cure” in mind really dream of a world in which everyone pays attention to the same things all the time? One person’s “trifle” is another person’s hobby is another person’s career, after all, even exclusive of any discussion of autism.
Additionally in the Scientific American article, the common autistic sensitivity to certain sounds is described as “puzzling”. That descriptor itself is puzzling—is it really so strange an idea that perhaps some people simply have more sensitive hearing than other people? Would these same researchers describe the communicative behavior of bats as “puzzling”? What about the scenario in which dogs react to the high pitch of a dog whistle?
The supposedly missing “obvious reason” for the “setting of alarm bells” in response to sensory overload is, in fact, quite obvious: different brains are attuned to different sorts of stimuli. If your auditory processing system can hear sounds and frequencies that others cannot, then it makes more sense for you to react to these sounds than not react to them—and there’s nothing remotely puzzling about it. The quoted passages from the Scientific American article are even more bizarre in the context of attempting to relate autistic reactions to sound and autistic interest patterns to “mirror neurons”; it isn’t clear how either of these things relates at all to that theory, nor what any of it has to do with empathy or emotions.
The question also still remains as to whether (and how) autistic “imitation” abilities are impaired in the first place, and if this has anything to do with mirror neurons. In the paper, Imitation and action understanding in autistic spectrum disorders: How valid is the hypothesis of a deficit in the mirror neuron system?, Antonia F. de C. Hamilton, Rachel M. Brindley, and Uta Frith state in their abstract:
Recently, it has been proposed that a deficit in this mirror neuron system might contribute to poor imitation performance in children with autistic spectrum disorders (ASD) and might be a cause of poor social abilities in these children. We aimed to test this hypothesis by examining the performance of 25 children with ASD and 31 typical children of the same verbal mental age on four action representation tasks and a theory of mind battery. Both typical and autistic children had the same tendency to imitate an adult’s goals, to imitate in a mirror fashion and to imitate grasps in a motor planning task. Children with ASD showed superior performance on a gesture recognition task. These imitation and gesture recognition tasks all rely on the mirror neuron system in typical adults, but performance was not impaired in children with ASD. In contrast, the ASD group were impaired on the theory of mind tasks. These results provide clear evidence against a general imitation impairment and a global mirror neuron system deficit in children with autism.We suggest this data can best be understood in terms of multiple brain systems for different types of imitation and action understanding, and that the ability to understand and imitate the goals of hand actions is intact in children with ASD.
The results of the experiments described in the Hamilton, et. al, paper seemed not only to suggest that autistics can imitate in certain contexts but that the ability to imitate in particular ways does not necessarily correlate to anything about the ability to infer mental or emotional states. The experiments did not, in fact, test for “automatic mimicry or emotional imitation abilities” (9)—they tested instead for directed imitation of mechanical movements. Note that the Hamilton, et. al. paper does not take on issues of empathy or go into great detail regarding the possible explanations for poor autistic performance on Theory of Mind tasks; it has been referenced here because its findings do at least seem to suggest that theories attempting to attribute all manifestations of the autistic difference to mirror neuron “dysfunction” represent oversimplifications.
With regard to empathy in autism—something that has not been thoroughly addressed in any of the studies or articles quoted thus far—it is perhaps most appropriate to look to actual autistic people (or parents of autistic children, in some cases) to get an idea of how such individuals perceive themselves and their empathic abilities. Autistic activist Jim Sinclair writes on the subject:
“Empathy” is a nebulous term that is often used to mean projection of one’s own feelings onto others; it is therefore much easier to “empathize” with (i.e., to understand the feelings of) someone whose ways of experiencing the world are similar to one’s own than to understand someone whose perceptions are very different. But if empathy means being able to understand a perspective that is different from one’s own, then it is not possible to determine how much empathy is present between persons without first having an adequate understanding of each person’s perspective and of how different those perspectives are from each other. (This would require an observer with perfect empathy for all parties!)
When I am interacting with someone, that person’s perspective is as foreign to me as mine is to the other person. But while I am aware of this difference and can make deliberate efforts to figure out how someone else is experiencing a situation, I generally find that other people do not notice the difference in perspectives and simply assume that they understand my experience.
Jim Sinclair’s assessment of the empathic communication paradigm seems indeed to reflect the assertion made earlier in this writing—that people tend to assume that others’ minds work similarly to their own, which is very, very different from having an ability to simulate and understand another person’s state of mind without explicit information about it. Similarly, Joel Smith writes in Autism Myth of the Week - Empathy:
Perhaps the tests and experiments measuring empathy don’t actually measure empathy? It is hard for us to understand many of the things neurotypicals do (just as it is hard for them to understand us). We also have different responses when confronted with, for instance, someone who is sad. For me, it is overwhelming, threatening to wash my being away, when someone I care about is upset. The only thing I can do is to freeze and look into myself. This isn’t because I don’t realize someone is suffering, it is instead because they are suffering. I feel the pain very deeply. A differing response to that pain doesn’t mean that pain isn’t felt!
Clearly, Joel’s writing quoted above does not represent the thoughts of someone incapable of feeling deep emotions in response to the emotions of others. And yet, Joel was diagnosed autistic at the age of four. The passage here suggests that perhaps the experiments looking for “evidence of empathy” simply were not looking in the right places.
From the parental angle, Kristina Chew, who has an autistic son, notes the following observation:
Due to his limited language ability, I cannot provide certain evidence of this but I can listen to Charlie’s own way of telling me without words. Time and again, Charlie has signalled his deep awareness and understanding when one of us is worried or elated via the tensing of his boy, or his rapid running back and forth; via his tensed shoulders and drawn face, or his peaceful easy-feelingness.
The common thread joining the accounts noted above is the idea that while autistics may not provide typical responses to the emotional expressions of others, autistics are by no means incapable of responding to (and by extension, detecting) emotions in the first place. Just because someone does not respond in the way that you think they ought to in a given situation does not mean that a response is not happening, internally or otherwise.
Mirror neuron articles which attempt to explain autistic empathy away without even looking to see if perhaps empathy simply manifests differently in autistics seem downright irresponsible in light of all this. Regardless of what the experiments designed to test “mirror neuron” response show, it seems quite likely that none of these experiments so far (at least not the ones that have prompted articles to be written about them) have actually put forth a robust test of autistic empathy. If empathy is not dependent upon typical mirror neuron activity (presuming again that mirror neurons even exist in humans), then good, unbiased science ought to reveal this. And there is ample evidence that the science is very frequently biased.
All things considered, many of the mirror neuron studies (along with other autism studies) all seem to suffer from the same fundamental flaw: that of presuming the autistic brain to be a “broken” version of a typical brain, as opposed to an entity unto itself. There is nothing ethically wrong with researching autism or researching autistic brains (so long as the research itself is conducted ethically, with full acknowledgement of the personhood of all involved), but it is of great concern that so few studies are being conducted from the standpoint of trying to figure out how autistic brains actually work—as opposed to how they supposedly don’t work, or how they represent deviations from some imagined ideal.
Evolution, after all, has no specific goal in mind; the future of sentient life on the planet (and what the range of this sentient life will look like) depends greatly on how closely humanity is willing to scrutinize the basic assumptions many people make with regard to what comprises humanity in the first place. And it seems a great shame to risk losing a rich, deep segment of cognitive and perceptual diversity on the basis of poor experimental design and unexamined bias.