The Autistic Brain: Thinking Across the Spectrum (14 page)

5

I
HAD MY EYE
on Jack. He was ten years old, and he had taken only three skiing lessons in his life. I was in high school, and I’d been taking skiing lessons for three years. Yet I would watch Jack pass me on the slope, and I would see him execute these gorgeous stem christie turns, and, man, he could handle the four-foot ski jump with no problem. Meanwhile, I was still working my way up to
one
good christie, and every single time I tried the ski jump, I fell, until I was scared to use it.

What was so special about Jack?

Nothing, it turns out. What was so special, instead, was me—me and my autism. The connection between my autism and my poor athletic performance is pretty obvious in retrospect. At the time, though, I didn’t see it. Not until I was in my forties and I had the brain scan showing that my cerebellum—the part of the brain that helps control motor coordination—is 20 percent smaller than normal did I put two and two together. Now it all made sense! I couldn’t keep my skis together without falling because—

Because what? Because I’m autistic? Or because I have a small cerebellum?

Both answers are correct. Which, however, is more useful? That depends on what you want to know. If you’re looking for a label, something that will help you understand who I am in a general sense, then “because I’m autistic” is probably good enough. But if you’re looking for how I got that way specifically—if you’re looking for the biological source of the symptom—then the better answer is definitely “because I have a small cerebellum.”

The difference is important. It’s the difference between a diagnosis and a cause.

My research on subtypes of sensory problems for the previous chapter got me thinking about the limitations of labels. I realized that two different labels—underresponsive to sensory input and overresponsive to sensory input—can describe the same experience:
too much information!
The labels might be useful, but, as in the skiing example, their usefulness depends on what you want to know. Do you want to know what the behavior looks like from the outside? Or do you want to know what the experience feels like from the inside? Do you want a description for a set of symptoms—a diagnosis? Or do you want a source for a particular symptom—a cause?

Parents come up to me all the time and say things like, “First my kid was diagnosed with high-end autism.
Then
he was diagnosed with ADHD.
Then
he was diagnosed with Asperger’s. What is he?” I understand their frustration. They’re at the mercy of a medical system that’s full of label-locked thinkers. But the parents are part of that system too. They’ll ask me, “What’s the single most important thing to do for an autistic kid?” Or “What do I do about a kid who misbehaves?” What does that even
mean?

I call this kind of thinking label-locked because people get so invested in what the word for the thing is that they no longer see the thing itself. I’ve encountered the same kind of label-locked thinking elsewhere as well. A livestock handler might say to me, “My horse is wild. What should I do?” Or someone who has read my books on animal behavior will say to me, “My dog’s crazy. What should I do?” Well, first you have to tell me what
wild
or
crazy
even means in each case. I don’t have a clue unless you give me one. Does the dog try to bite the hands of strangers? Or does he jump on people because he’s really happy?

What I say in all these cases is the same: Don’t worry about the label. Tell me what the problem is. Let’s talk about the specific symptoms.

First question I ask parents who want me to advise them is “How old is the kid?” What I might recommend for a three-year-old is going to be completely different from what I might recommend for a sixteen-year-old.

Next question is “Does the kid talk?” If he’s nonverbal, that’s one thing. Let’s start trying to teach him and see what happens. If he’s verbal, I’ll say, “How good is his speech?” If the description is too vague, I’ll say, “Give me an example.” I want to know if the child is speaking in complete and grammatically correct sentences. Does he speak only in single words? Does he pronounce words accurately or does he say, as I did,
buh
for
ball
?

Can the kid hold a conversation? Can he place an order at a fast-food counter? If not, then the first thing you want to do is teach the kid social skills, starting with taking turns and saying “Please” and “Thank you.”

Does she have trouble making friends? Is she in school? Does she have a favorite subject?

The questions can go on and on, of course, just as they can for anybody—autistic or not. We’re all individuals. We all have a range of skills, habits, preferences, limitations. What would a totally normal brain even be like? A brain that is average in every way, that has the average number of neural connections, the average size of amygdalae and cerebellum, the average length of corpus callosum?

It would probably be pretty boring.

The differences are what makes us individuals—the departures from the norm, the variations in the brain. Take the corpus callosum, which is the collection of neural cables that stretch the length of the brain and connect the left and right hemispheres. I have more of those cables than normal, but obviously someone can have even more than I do, or fewer than I do, or the normal amount, or fewer than normal. And my brain’s language circuit branches more than a normal brain’s, but, again, the extent to which language circuits branch exists on a continuum. The cerebellum size that probably affects my skiing—another continuum. The number of de novo copy number variations in someone’s DNA? The particular position of those CNVs on the chromosome? Continuum and continuum. I have often thought that eventually we’re going to be asking ourselves at what point this or that autism-related genetic variation is just a normal variation. Everything in the brain, everything in genetics—they’re all one big continuum.

The addition of Asperger’s to the
DSM-IV
in 1994 validated the idea of an autistic spectrum, but the meaning of “on the spectrum” itself has changed over the years. “In scientific circles,” a 2011 article
in
Nature
reported, “many accept that certain autistic traits—social difficulties, narrow interests, problems with communication—form a continuum across the general population with autism at one extreme.”

In other words, you don’t have to have an autism spectrum disorder diagnosis to be “on the spectrum.”

This notion was popularized by the psychologist Simon Baron-Cohen. In 2001, he and his colleagues at the Autism Research Centre in Cambridge, England, introduced the autism-spectrum quotient questionnaire.
People often take the AQ test online just to see whether they fall on the autistic spectrum. They might be wondering if they have Asperger’s or high-functioning autism. Or they might want to see what traits they have that, if amplified, would qualify them for one of those labels.

If nothing else, the AQ test got a lot of people thinking about behavior in a new way—the behavior of autistics, certainly, but the behavior of nonautistics too. Their own behavior. The behavior of a neighbor, or a coworker, or oddball Uncle Ned with his disturbingly thorough stamp collection. Behavior that previously had seemed peculiar or perhaps aggressively strange now made a kind of sense.

The test consists of fifty statements. (See appendix.) For each statement, you choose from four responses, ranging from “definitely agree” to “definitely disagree.” Definitely agreeing with the statement “I would rather go to a library than a party” might indicate that a person has an autistic bent. Definitely agreeing with the statement “I find myself drawn more strongly to people than to things” would suggest a more neurotypical person. When Baron-Cohen and his colleagues administered the test in a clinical setting, the average score in the control group was 16.4 out of 50, while 80 percent of those diagnosed with autism or a related disorder scored 32 or higher. But if you scored 33, would you be autistic? Not necessarily. What about 36? Or 39? What is the cutoff point?

Label-locked thinkers want answers.

This kind of thinking can do a lot of damage. For some people, a label can become the thing that defines them. It can easily lead to what I call a handicapped mentality. When a person gets a diagnosis of Asperger’s, for instance, he might start to think,
What’s the point?
or
I’ll never hold down a job.
His whole life starts to revolve around what he
can’t
do instead of what he
can
do, or at least what he can try to improve.

Label-locked thinking goes the other way too.
You
might be comfortable with your diagnosis but worry that it will define you in the eyes of others. What will your boss think? Your coworkers? Your loved ones? Half the employees at Silicon Valley tech companies would be diagnosed with Asperger’s if they allowed themselves to be diagnosed, which they avoid like the proverbial plague. I’ve been to their offices; I’ve seen the work force up close. Many of the hits on my home page come from Silicon Valley and other areas with a high concentration of tech industries. A generation ago, a lot of these people would have been seen simply as gifted. Now that there’s a diagnosis, however, they’ll do anything to avoid being ghettoized.

Label-locked thinking can affect treatment. For instance, I heard a doctor say about a kid with gastrointestinal issues, “Oh, he has autism. That’s the problem”—and then he didn’t treat the GI problem. That’s absurd. Just because gastrointestinal problems are common in people with autism
doesn’t mean that the GI problems are untreatable on their own. If you want to help the kid with GI issues, talk about his diet, not his autism.

And label-locked thinking can affect research. “One of the curses in this field,” a study
on vision in autism concluded, “is the size of the error bars, which always seem to be at least twice as large in the ASD data compared to the controls.” Error bars twice as large as the controls’ error bars? Right there, that should tell you that you have a huge variation in the sample—that you have subgroups in the population that need to be identified and separated out. You throw people with Irlen syndrome and people who look out of the sides of their eyes into the same sample and you’ll end up comparing apples and oranges. The error bars aren’t a
curse.
They’re an obstacle that the researchers have created for themselves and then placed in their own path.

The same is true for studies that conclude that some solutions to sensory problems, like weighted vests or Irlen glasses, don’t work for people with autism. I used to read these studies, and I would tell myself,
But
I’ve
seen
weighted vests work, again and again!
The problem with the research, I’ve realized, is that autistic people don’t all have the same sensory problems. If you have twenty people with autism, shaded glasses or weighted vests will help maybe three or four. So researchers say, “Well, look—these devices work on only 15 or 20 percent of the autistic population!” So what? That result doesn’t mean that colored glasses don’t work for autism; it means that colored glasses
do
work for autistics with certain specific visual problems. They work on a
subgroup
of the autistic population.

I’m not saying that we shouldn’t use labels. Of course we should. Without the label that Leo Kanner gave it, autism might have gone undiagnosed, untreated, and just plain ignored. Labels have been incredibly important, and they will continue to be incredibly important. For the purposes of medicine, educational benefits, insurance reimbursements, social programs, and so on, they’re necessary. And if you’re a researcher looking into autism, sometimes it makes sense to test only autistic subjects against controls.

But sometimes it doesn’t, because autism is not a one-size-fits-all diagnosis.

However the APA defines autism, the diagnosis is going to be imprecise. That’s the nature of a spectrum. The lack of a diagnosis was what the first formal set of standards in the
DSM-III
tried to correct, and the lack of precision in the diagnoses for autism and autism-related disorders was what subsequent editions tried to correct. Unfortunately, I don’t think the latest effort—the
DSM-5
—is going to be much help in clearing up the confusion, and in some ways, it’s only going to complicate the situation.

In the
DSM-IV,
a diagnosis of autism depended on three criteria, called the triad model. Those criteria were:

• Impairment in social interaction.
  
• Impairment in social communication.
  
• Restricted, repetitive, and stereotyped patterns of behavior, interests, and activities.
  

The first two might sound similar to each other in that they both involve issues of socializing. In fact, that’s the official justification for collapsing them into one criterion for the
DSM-5.
In a 2010 presentation
before the federal Interagency Autism Coordinating Committee, the chair of the
DSM-5
Neurodevelopmental Workgroup said, “Deficits in communication are intimately related to social deficits. The two are ‘manifestations’ of a single set of symptoms that are often present in differing contexts.” As a result, the
DSM-5
uses a two-criteria, or dyad, model:

• Persistent deficits in social communication and social interaction.
  
• Restricted, repetitive patterns of behavior, interests, or activities.
  

I understand why the APA might consider changing from a triad to a dyad model. The idea of separating the social from the behavioral does have a basis in science; the two domains are in fact biologically different. In lab tests on mice, researchers have shown
that risperidone, an antipsychotic drug, does not affect social behaviors but does affect fixated behaviors—possibly because it sedates the mice. Conversely, researchers have shown that the social behavior of mice was improved by training, but the fixated behavior was not. Those results alone tell us that repetitive behaviors and social problems operate in separate systems in the brain. So a dyad system that recognizes the distinction between those two systems does make sense.