The Tell-Tale Brain

dysfunction will still stand. More important, such observations highlight the fact that the MNS is composed of many far-flung subsystems in the brain that are interconnected for a common function: action and observation. (As an analogy, consider the lymphatic system of the body, which is distributed throughout the body but is functionally a distinct system.)

     It is also possible that this part of the MNS itself is normal but its projections or recipient zones in the brain are abnormal. The net result would be the same kind of dysfunction that I originally suggested. In another analogy, consider the fact that diabetes is fundamentally a disturbance of carbohydrate metabolism; no one disputes that. While it is sometimes caused by damage to the pancreatic islet cells, causing a reduction of insulin and an elevation of blood glucose, it can also be caused by a reduction of insulin receptors on cell surfaces throughout the body. This would produce the same syndrome as diabetes without damage to the islets (for islets in the pancreas, think “mirror neurons in the brain’s premotor area called F5”), but the logic of the original argument is unaffected.

     Having said all this, let me emphasize that the evidence for MNS dysfunction in autism is, at this point, compelling but not conclusive.

3. The treatments I have proposed for autism in this chapter were inspired in part by the mirror-neuron hypothesis. But their plausibility does not in itself depend on the hypothesis; they would be interesting to try anyway.

4. To further test the mirror-neuron hypothesis of autism, it would be interesting to monitor the activity of the mylohyoid muscle and vocal cords to determine whether autistic children do not show unconscious subvocalization when listening to others talking (unlike normal children, who do). This might provide an early diagnostic tool.

CHAPTER 6 THE POWER OF BABBLE: THE EVOLUTION OF LANGUAGE

1. This approach was pioneered by Brent Berlin. For cross-cultural studies similar to Berlin’s, see Nuckolls (1999).

2. The gestural theory of language origins is also supported by several other ingenious arguments. See Corballis (2009).

3. Even though Wernicke’s area was discovered more than a century ago, we know very little about how it works. One of our main questions in this chapter has been, What aspects of thought require Wernicke’s language area? In collaboration with Laura Case, Shai Azoulai, and Elizabeth Seckel, I examined two patients (LC and KC) on whom I did several experiments (in addition to the ones described in the chapter); here is a brief description of these and other casual observations that are revealing:

     (a) LC was shown two boxes: one with a cookie, one without. A student volunteer entered the room and looked at each box expectantly, hoping to open the one with the cookie. I had previously winked to the patient, gesturing him to “lie.” Without hesitation LC pointed out the empty box to the student. (KC responded to this situation the same way.) This experiment shows you don’t need language for a theory-of-mind task.

     (b) KC had a sense of humor, laughing at nonverbal Gary Larson cartoons and playing a practical joke on me.

     (c) Both KC and LC could play a reasonable game of chess and tic-tac-toe, implying that they have at least a tacit knowledge of if-then conditionals.

     (d) Both could understand visual analogy (for example, airplane is to bird as submarine is to fish) when probed nonverbally using pictorial multiple choice.

     (e) Both could be trained to use symbols designating the abstract idea “similar but not identical” (wolf and dog, for example).

     (f) Both were blissfully unaware of their profound language problem, even though they were producing gibberish. When I spoke to them in Tamil (a south Indian language), one of them said, “Spanish,” while the other nodded as if in understanding and replied in gibberish. When we played a DVD recording of LC’s own utterances back to him, LC nodded and said, “It’s okay.”

     (g) LC had profound dyscalculia (for example, reporting 14 minus 5 as 3). Yet he could do nonverbal subtraction. We showed him two opaque cups A and B, and dropped three cookies in A and four in B while he watched. When we removed two cookies from B (as he watched), LC subsequently went straight for A. (KC was not tested.)

     (h) LC had a profound inability to understand even simple gestures such as “okay,” “hitchhike,” or “salute,” Nor could he comprehend iconic signs like the restroom sign. He couldn’t match a dollar with four quarters. And preliminary tests showed he was poor at transitivity.

     A paradox arises: Given that LC was okay at learning paired associations (for example, pig = nagi) after extensive training, why can’t he relearn his own language? Perhaps the very attempt to engage his preexisting language introduces a software “bug” that forces the malfunctioning language system to go on autopilot. If so, then teaching the patient a completely new language may, paradoxically, be easier than retraining the patient to the original.

     Could he learn pidgin, which requires only that words be strung together in the right order (given that his concept formation is unimpaired)? And if he could be taught something as complex as “similar but not same,” why can’t he be taught to attach arbitrary Sassurian symbols (that is, words) to other concepts such as “big,” small,” “on,” “if,” “and,” and “give”? Would this not enable him to understand a new language (such as French or American Sign Language), which would allow him to at least converse with French people or signers? Or if the problem is in linking heard sounds with objects and ideas, why not use a language based on visual tokens (as was done with Kanzi, the bonobo)?

     The oddest aspects of Wernicke’s aphasia are the patients’ complete lack of insight into their own profound inability to comprehend or produce language, whether written or spoken, and their total lack of any frustration. We once gave LC a book to read and walked out of the room. Even though he couldn’t understand a single word, he kept scanning the print and turning the pages for fifteen minutes. He even bookmarked some pages! (He was unaware of the fact that the video camera filming him had been left on during our absence.)

CHAPTER 7 BEAUTY AND THE BRAIN: THE EMERGENCE OF AESTHETICS

1. One has to be careful to not overdo this type of reductionist thinking about art and the brain. I recently heard an evolutionary psychologist give a lecture about why we like kinetic art, which includes pieces like Calder mobiles made up of moving cutout shapes dangling from the ceiling. With a perfectly straight face he proclaimed that we like such art because an area in our brain called the MT (middle temporal) area possesses cells that are specialized for detecting the direction of motion. This claim is nonsense. Kinetic art obviously excites such cells, but so would a snowstorm. So would a copy of the Mona Lisa set spinning on a peg. Neural circuitry for motion detection is certainly necessary for kinetic art but it’s not sufficient: It doesn’t explain the appeal of kinetic art by any stretch of logic. This chap’s explanation is like saying that the existence of face-sensitive cells in the fusiform gyrus of your brain explains why you like Rembrandt. Surely to explain Rembrandt you need to show how he enhanced his images and why such embellishments elicit responses from the neural circuits in your brain more powerfully than a realistic photograph does. Until you do that, you have explained nothing.

2. Note that peak shift should also be applicable in animation. For example, you can create a striking perceptual illusion by mounting tiny LEDs (light-emitting diodes) on a person’s joints and having her walk around in a dark room. You might expect to see just a bunch of LEDs moving around randomly, but instead you get a vivid sense of seeing a whole person walking, even though all her other features—face, skin, hair, outline, and so forth—are invisible. If she stops moving, you suddenly cease to see the person. This implies that the information about her body is conveyed entirely by the motion trajectories of the light spots. It’s as though your visual areas are exquisitely sensitive to the parameters that distinguish this type of biological motion from random motion. It’s even