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Authors: Temple Grandin,Richard Panek

Tags: #Non-Fiction

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How did the two lateral ventricles become so different? One hypothesis is that when damage occurs early in the brain’s development, other areas of the brain try to compensate. In my case, the damage would have occurred in the white matter in the left hemisphere, and the left ventricle would have enlarged to fill the damaged area. At the same time, the white matter in the right hemisphere would have tried to compensate for the lost brain function in the left hemisphere, and that expansion in the right hemisphere would have squeezed the right ventricle’s growth.

 

These scans from 2006 highlight (the areas in black from top to bottom) my inferior longitudinal fasiculus (ILF) and my inferior fronto-occipital fasciculus (IFOF). The ILF is much thicker than what a normal brain would show, and you can easily see how wildly my IFOF branches out. In both cases, these white-matter tracts stretch all the way back to the primary visual cortex, perhaps helping to explain my superb visual memory.

© Dr. Marlene Behrmann, Brain Imaging Research Center, Carnegie Mellon University, Pittsburgh

 

This scan from the University of Utah in 2010 dramatically shows that my left ventricle is much longer than my right—57 percent longer. It’s so long that it extends into the parietal cortex, an area associated with short-term memory, perhaps accounting for my poor ability at recalling several pieces of information in short order.

© Cooperrider, J.R. et al. presentation at the 2012 Society for Neuroscience meeting in New Orleans

 

The other significant findings from the Utah MRI study included:

 

  • Both my intracranial volume—the amount of space inside the skull—and my brain size were 15 percent larger than the control subjects’. This too is likely the result of some sort of developmental abnormality. The neurons may have grown at an accelerated pace in order to compensate for the damaged area.
  • The white matter in my left cerebral hemisphere was nearly 15 percent greater than the controls’. Again, this anomaly could be the result of an early developmental abnormality in my left hemisphere and my brain’s attempt to compensate by generating new connections. This data reinforces for me the earlier University of Pittsburgh finding that my brain is overconnected.
  • My amygdalae are larger than normal. The mean size of the three control subjects’ amygdalae was 1,498 cubic millimeters. My left amygdala is 1,719 cubic millimeters, and my right is larger still—1,829 cubic millimeters, or 22 percent greater than the norm. And since the amygdala is important for processing fear and other emotions, this large size might explain my lifelong anxiety. I think of all the panic attacks that plagued me through much of the 1970s, and they begin to make sense in a new way. My amygdalae are telling me I have everything to fear, including fear itself.
           Since I started taking antidepressants, in the early 1980s, the anxiety has been under control, probably because the pounding sympathetic nervous system reaction is blocked. But the vigilance is still present, percolating under the surface. My fear system is always on the alert for danger. If the students who live near me are talking in the parking lot under my window at night, I can’t sleep. I actually turn on New Age music to block out the sound, even if the students are talking softly. (Though the music can’t have vocals.) Volume has nothing to do with the fear factor; the association with a possible threat does. Human voices are associated with a possible threat. New Age music isn’t associated with a possible threat. For that matter, neither is the sound of an airplane, so that sound doesn’t bother me, even when I’m in a hotel by an airport. A plane could land on the hotel and I wouldn’t wake up. But people talking in the next room? Forget it. I might as well turn on the light and read, because I know I’m not going to go to sleep until
    they
    go to sleep.
  • The cortical thickness in both my left and right entorhinal cortices was significantly greater than the controls’—12 percent in the left, and 23 percent in the right. “The entorhinal cortex is the golden gate to the brain’s memory mainframe,” says
    Itzhak Fried, a professor of neurosurgery at the David Geffen School of Medicine at UCLA. “Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells must send signals through this hub in order to form memories that we can later consciously recall.” Maybe this peculiarity in my brain anatomy helps explain my exceptional memory abilities.

 

Naturally, I find these results fascinating because they highlight some of the odd things going on in my brain that help make me who I am. But what I find
really
fascinating is that they match the results of studies of some other people with autism.

 

  • Preferring objects to faces? “These results are typical of individuals with autism,” the researchers who conducted the MRI study at Pittsburgh in 2006 later wrote me in a summary of their findings. “One thing that seems to be coming up repeatedly in these scanning studies with individuals with autism is the marked reduction in the cortical activation to faces.”
  • Enlarged amygdalae are also often seen in people with autism. Because the amygdala houses so many emotional functions, an autistic can feel as if he or she is one big exposed nerve.
  • And then there’s this, in an e-mail from Jason Cooperrider, a graduate student who led the 2010 imaging study at Utah: “Dr. Grandin’s head size is large by any standard, consistent with larger than average head/brain size/growth in autism.” An enlarged brain can be caused by a number of genetic misfires, any one of which can result in an early spurt of neuronal development. The growth rate eventually normalizes, but the macrocephaly remains. The latest estimate
    is that about 20 percent of autistics have enlarged brains; the vast majority of those seem to be male, for reasons that aren’t at all clear.

 

For the first time, thanks to hundreds if not thousands of neuroimaging studies of autistic subjects, we’re seeing a solid match between autistic behaviors and brain functions. That’s a huge deal. As one review article
summarized the era, “This body of research clearly established autism and its signs and symptoms as being of neurologic origin.” The long-held working hypothesis has now become the consensus of the evidence and the community: Autism really is in your brain.

 

The problem is, what’s in
my
autistic brain is not necessarily what’s in
someone else’s
autistic brain. As the neuroanatomy pioneer Margaret Bauman once told me, “Just because your amygdala is larger than normal doesn’t mean that every autistic person’s amygdala is larger than normal.” While some similarities among autistic brains have emerged, we have to be careful not to overgeneralize. In fact, neuroimaging researchers face three challenges to finding common ground among autistic brains.

Homogeneity of brain structures.
While the 2010 Utah study revealed several striking anatomical anomalies in my brain, it also showed, as Cooperrider e-mailed me, that “for about 95% of the comparisons” with the control subjects, “the differences were negligible.” This overwhelming normalcy in the autistic brain is the rule, not the exception.

“Anatomically, these kids are normal,” Joy Hirsch,
an autism researcher then at Columbia University Medical Center in New York, said regarding the subjects in a study of hers. “Structurally, the brain is normal on any scale that we can look at.”

Which is not to say that the structures of the brains in her study, or autistic brains in general, don’t vary from one brain to the next. They do. But that’s true of normal brains too. It’s just that the variations among the autistic brains predominantly fall within the range of what’s normal. Thomas Insel, director of the National Institute of Mental Health, told
USA Today
in 2012,
shortly after the Centers for Disease Control raised the estimated prevalence of autism from 1 in 110 to 1 in 88, “Even when you look at a child who has no language, who is self-injuring, who’s had multiple seizures, you would be amazed at how normal their brains look. It’s the most inconvenient truth about this condition.”

Nonetheless, some patterns are emerging. In addition to the variations in my own brain that seem consistent with those of many other autistics—enlarged amygdalae, macrocephaly, lack of cortical engagement when looking at faces—these widespread patterns include:

 

  • Avoiding eye contact. Different than a preference for objects over faces, this is the active avoidance of faces. A 2011 fMRI study
    in the
    Journal of Autism and Developmental Disorders
    found that the brains in a sample of high-functioning autistics and typically developing individuals seemed to respond to eye contact in opposite fashions. In the neurotypical brain, the right temporoparietal junction (TPJ) was active to direct gaze, while in the autistic subject, the TPJ was active to averted gaze. Researchers think that the TPJ is associated with social tasks that include judgments of others’ mental states. The study found the opposite pattern in the left dorsolateral prefrontal cortex: in neurotypicals, activation to averted gaze; in autistics, activation to direct gaze. So it’s not that autistics don’t respond to eye contact, it’s that their response is the opposite of neurotypicals’.
           “Sensitivity to gaze in dlPFC demonstrates that direct gaze does elicit a specific neural response in participants with autism,” the study said. The problem, however, is “that this response may be similar to processing of averted gaze in typically developing participants.” What a neurotypical person feels when someone won’t make eye contact might be what a person with autism feels when someone
    does
    make eye contact. And vice versa: What a neurotypical feels when someone does make eye contact might be what an autistic feels when someone
    doesn’t
    make eye contact. For a person with autism who is trying to navigate a social situation, welcoming cues from a neurotypical might be interpreted as aversive cues. Up is down, and down is up.
  • Overconnectivity and underconnectivity. A highly influential paper
    published in
    Brain
    in 2004 introduced an underconnectivity theory—the idea that underconnectivity between cortical regions might be a common finding in autism. On a global scale, the major sections of the brain can’t coordinate their messages. Since then, numerous other studies have made the same argument, finding a relationship between underconnectivity between cortical areas and deficits in a variety of tasks related to social cognition, language, and executive function.
           In contrast to this long-distance underconnectivity, other studies have found overconnectivity on a local scale. Presumably, this overgrowth occurs in ways I’ve already described, an attempt of one part of the brain to compensate for a deficit in another. The result can be positive. As I’ve mentioned, I exhibit overconnectivity in an area corresponding to visual memory. Fortunately I can manage the visuals. I can sit at a consulting session and run the movie in my mind of how a piece of equipment will work, and then I can turn it off when I’m done. Some people with autism, however, don’t have an Off switch that works, and for them, overconnectivity leads to a barrage of information, much of it jumbled.
           Which is not to say that the underconnectivity theory describes all autistic brains. Like many initial attempts to describe a solution to a problem, it probably oversimplifies the situation. As a 2012 study
    from the University of 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 study
in 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.

BOOK: The Autistic Brain: Thinking Across the Spectrum
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