The Autistic Brain: Thinking Across the Spectrum by Temple Grandin, Richard Panek Read Free Book Online

Amsterdam noted, “some patterns of abnormal functional connectivity in ASD are not captured by current theoretical models. Taken together, empirical findings measuring different forms of connectivity demonstrate complex patterns of abnormal connectivity in people with ASD.” The theory, the paper concluded, “is in need of refinement.”
     
    Heterogeneity of causes.
Even when researchers do think they’ve found a match between an autistic person’s behavior and an anomaly in the brain, they can’t be sure that someone else manifesting the same behavior would have the same anomaly. Part of the title of a 2009 autism studyin the
Journal of Neurodevelopmental Disorders
captured the situation succinctly: “Same Behavior, Different Brains.” In other words, just because you’re prone to extreme anxiety doesn’t mean your autistic brain has an enlarged amygdala.
    Heterogeneity of behaviors.
Conversely, when researchers find an anomaly in the brain, they can’t be sure that that anomaly will have the same behavioral effect in a different brain. Or any effect, for that matter. Just because you have an enlarged amygdala doesn’t mean that you’re autistic.
    But what if it did?
    Not necessarily an enlarged amygdala. But what if some neuroanatomical finding or combination of them could serve as a reliable diagnostic tool? A diagnosis based not on behaviors alone but on biology as well would make a big difference in predicting deficits and targeting treatments. Doctors and researchers could:
     
Apply early intervention, even in infancy, when the brain is still highly susceptible to being rewired.
Target areas in the brain more locally, rehabilitating parts of the brain that they think they can help and not wasting time on parts that are unrecoverable.
Test new therapies and monitor existing therapies more narrowly.
Tailor a prognosis to an individual patient on a case-by-case basis.
     
    For the patient, such a diagnosis would have a tremendous psychological benefit as well, by allowing him or her to know what’s actually unusual. Personally, I
like
knowing that my high level of anxiety might be related to having an enlarged amygdala. That knowledge is important to me. It helps me keep the anxiety in perspective. I can remind myself that the problem isn’t
out there
—the students in the parking lot under my bedroom window. The problem is
in here
—the way I’m wired. I can medicate for the anxiety somewhat, but I can’t make it go away. So as long as I have to live with it, I can at least do so secure in the knowledge that the threat isn’t real. The
feeling
of the threat is real—and that’s a huge difference.
    Given the obstacles to investigating autism from a neurological perspective—the homogeneity of brains, the heterogeneity of behaviors and causes—you might ask whether finding a biomarker is a realistic goal. Yet in recent years, researchers have made tremendous progress toward reaching that goal, and now many speak of
when,
not
if.
    “We still don’t have a litmus test for autism,” the neuroscientist Joy Hirsch said. “But we have a basis for it.”
    As the director of the Functional MRI Research Center at the Columbia University Medical Center in New York City, Hirsch has tried to build that foundation in the search for a litmus test. In a studyher group conducted between 2008 and 2010, fifteen autistic subjects ranging in age from seven to twenty-two and twelve control children ranging from four to seventeen underwent fMRI scans of the superior temporal gyrus—the part of the auditory system that processes the sounds of speech into meaningful language. “The most obvious disability in autism is the disability of speech,” she said, regarding the rationale behind the experiment. “Our hypothesis was that at the first stage we could begin to see differences.” And they felt they did: Their measures of activity in that region could identify fourteen out of fifteen of the autistic subjects, a