I HAVE ARGUED, so far, that the bouba-kiki effect may have fueled the emergence of protowords and a rudimentary lexicon. This was an important step, but language isn’t just words. There are two other important aspects to consider: syntax and semantics. How are these represented in the brain and how did they evolve? The fact that these two functions are at least partially autonomous is well illustrated by Broca’s and Wernicke’s aphasias. As we have seen, a patient with the latter syndrome produces elaborate, smoothly articulated, grammatically flawless sentences that convey no meaning whatsoever. The Chomskian “syntax box” in the intact Broca’s area goes “open loop” and produces well-formed sentences, but without Wernicke’s area to inform it with cultivated content, the sentences are gibberish. It’s as though Broca’s area on its own can juggle the words with the correct rules of grammar—just like a computer program might—without any awareness of meaning. (Whether it is capable of more complex rules such as recursion remains to be seen; it’s something we are currently studying.)
We’ll come back to syntax, but first let’s look at semantics (again, roughly speaking, the meaning of a sentence). What exactly is meaning? It’s a word that conceals vast depths of ignorance. Although we know that Wernicke’s area and parts of the temporo-parieto-occipital (TPO) junction, including the angular gyrus (Figure 6.2), are critically involved, we have no idea how neurons in these areas actually do their job. Indeed, the manner in which neural circuitry embodies meaning is one of the great unsolved mysteries of neuroscience. But if you allow that abstraction is an important step in the genesis of meaning, then our bouba-kiki example might once again provide the clue. As already noted, the sound kiki and the jagged drawing would seem to have nothing in common. One is a one-dimensional, time-varying pattern on the sound receptors in your ear, whereas the other is a two-dimensional pattern of light arriving on your retina all in one instant. Yet your brain has no difficulty in abstracting the property of jaggedness from both signals. As we have seen, there are strong hints that the angular gyrus is involved in this remarkable ability we call cross-modal abstraction.
FIGURE 6.2 A schematic depiction of resonance between brain areas that may have accelerated the evolution of protolanguage. Abbreviations: B, Broca’s area (for speech and syntactic structure). A, auditory cortex (hearing). W, Wernicke’s area for language comprehension (semantics). AG, angular gyrus for cross-modal abstraction. H, hand area of the motor cortex, which sends motor commands to the hand (compare with Penfield’s sensory cortical map in Figure 1.2). F, face area of the motor cortex (which sends command messages to the facial muscles, including lips and tongue). IT, the inferotemporal cortex/fusiform area, which represents visual shapes. Arrows depict two-way interactions that may have emerged in human evolution: 1, connections between the fusiform area (visual processing) and auditory cortex mediate the bouba-kiki effect. The cross-modal abstraction required for this probably requires initial passage through the angular gyrus. 2, interactions between the posterior language areas (including Wernicke’s area) and motor areas in or near Broca’s area. These connections (the arcuate fasciculus) are involved in cross-domain mapping between sound contours and motor maps (mediated partly by neurons with mirror-neuron-like properties) in Broca’s area. 3, cortical motor-to-motor mappings (synkinesia) caused by links between hand gestures and tongue, lip, and mouth movements in Penfield’s motor map. For example, the oral gestures for “diminutive,” “little,” “teeny-weeny,” and the French phrase “en peau” synkinetically mimic the small pincer gesture made by opposing thumb and index finger (as opposed to “large” or “enormous”). Similarly, pouting your lips outward to say “you” or (in French) “vous” mimic pointing outward.
There was an accelerated development of the left IPL in primate evolution culminating in humans. In addition, the front part of the lobule in humans (and humans alone), split into two gyri called the supramarginal gyrus and the angular gyrus. It doesn’t require deep insight to suggest therefore that the IPL and its subsequent splitting must have played a pivotal role in the emergence of functions unique to humans. Those functions, I suggest, include high-level types of abstraction.
The IPL (including the angular gyrus)—strategically located between the touch, vision, and hearing parts of the brain—evolved originally for cross-modal abstraction. But once this happened, cross-modal abstraction served as an exaptation for more high-level abstraction of the kind we humans take great pride in. And since we have two angular gyri (one in each hemisphere), they may have evolved different styles of abstraction: the right for visuospatial and body-based metaphors and abstraction, and the left for more language-based metaphors, including puns. This evolutionary framework may give neuroscience a distinct advantage over classical cognitive psychology and linguistics because it allows us to embark on a whole new program of research on the representation of language and thought in the brain.
The upper part of the IPL, the supramarginal gyrus, is also unique to humans, and is directly involved in the production, comprehension, and imitation of complex skills. Once again, these abilities are especially well developed in us compared with the great apes. When the left supramarginal gyrus is damaged, the result is apraxia, which is a fascinating disorder. A patient with apraxia is mentally normal in most respects, including his ability to understand and produce language. Yet when you ask him to mime a simple action—“pretend you are hammering a nail”—he will make a fist and bang it on the table instead of holding a “pretend” handle as you or I might. If asked to pretend he is combing his hair, he might stroke his hair with his palm or wiggle his fingers in his hair instead of “holding” and moving an imaginary comb through his hair. If requested to pretend waving goodbye, he may stare at his hand intently trying to figure out what to do or flail it around near his face. But if questioned, “What does ‘waving goodbye’ mean?” he might say, “Well, it’s what you do when you are parting company,” so obviously he clearly understands at a conceptual level what’s expected. Furthermore, his hands are not paralyzed or clumsy: He can move individual fingers as gracefully and independently as any of us. What’s missing is the ability to conjure up a vibrant, dynamic internal picture of the required action which can be used to guide the orchestration of muscle twitches to mime the action. Not surprisingly, putting the actual hammer in his hand may (as it does in some patients) lead to accurate performance since it doesn’t require him to rely on an internal image of the hammer.
Three additional points about these patients. First, they cannot judge whether someone else is performing the requested action correctly or not, reminding us that their problem lies in neither motor ability nor perception but in linking the two. Second, some patients with apraxia have difficulty imitating novel gestures produced by the examining physician. Third and most surprisingly, they are completely unaware that they themselves are miming incorrectly; there is no sign of frustration. All of these missing abilities sound compellingly reminiscent of the abilities traditionally attributed to mirror neurons. Surely it can’t be a coincidence that the IPL in monkeys is rich in mirror neurons. Based on this reasoning my postdoctoral colleague Paul McGeoch and I suggested in 2007 that apraxia is fundamentally a disorder of mirror-neuron function. Intriguingly, many autistic children also have apraxia, an unexpected link that lends support to our idea that a mirror-neuron deficit might underlie both disorders. Paul and I opened a bottle to celebrate having clinched the diagnosis.