Gall’s disciple Johann Spurzheim later introduced the term phrenology, more familiar to us than Gall’s original name for the theory. The phrenological map shown in Figure 9 displays regions corresponding to functions with names like “acquisitiveness,” “firmness,” and “ideality.” These particular correspondences are now considered fanciful imaginings based on flimsy evidence, but the phrenologists eventually turned out to be more right than wrong. Their emphasis on the cortex is widely accepted today, and their approach of localizing mental functions to particular cortical regions is still taken seriously. It now goes by the name of cortical or cerebral localizationism.
Figure 9. Phrenological map
The first real evidence for localization came later in the nineteenth century from observations of patients with brain damage. At that time, many French neurologists worked at two Parisian hospitals. Salpêtrière, on the Left Bank of the Seine River, housed female patients; male patients were placed farther from the city center, in Bicêtre. Both hospitals were founded in the seventeenth century and had functioned as prisons and mental asylums too. (The distinction was blurred by Bicêtre’s most famous inmate, the Marquis de Sade.) Both hospitals had pioneered humane methods for the treatment of the insane, such as not confining them in chains. I imagine that they remained depressing places all the same.
In 1861 the French physician Paul Broca was called to examine a fifty-one-year-old patient suffering from an infection in his surgical ward at Bicêtre. According to the records, the patient had been incarcerated since the age of thirty. At the time of admission he had already lost the ability to speak any word except the monosyllable “tan,” which became his nickname. Since Tan could communicate with hand gestures, it seemed that he could comprehend language, although he could not speak it.
A few days after the examination, Tan succumbed to his infection, and Broca performed an autopsy. He sawed open the skull, removed the brain, and placed it in alcohol for preservation. The most prominent damage to Tan’s brain—see Figure 10 —was a large cavity in the left frontal lobe.
Figure 10. Tan’s brain, with damage to Broca’s region
Broca announced his discovery to the Anthropological Society the next day. He claimed that the damaged region in Tan’s brain was the source of speech, which was distinct from comprehension. Today, loss of language ability is known as aphasia. Loss of speech, in particular, is called Broca’s aphasia, and the damaged location in Tan’s cerebral cortex is known as Broca’s region. With his discovery, Broca managed to settle a debate that had raged for decades. The phrenologist Gall had asserted at the beginning of the nineteenth century that linguistic functions were located in the frontal lobe of the brain, but had been met with skepticism. Broca finally provided some convincing evidence, as well as a specific location in the frontal lobe.
As time went on, Broca encountered more cases similar to Tan’s and found that they all involved damage to the left hemisphere of the brain. Given that the two hemispheres looked so similar to each other, it was hard to believe that they could be different in their functions. But the evidence mounted, and Broca concluded in an 1865 paper that the left hemisphere was specialized or dominant for language. Subsequent researchers have confirmed that this is the case for almost all people. Thus Broca’s findings supported not only cortical localization but also cerebral lateralization, the idea that mental functions are located in either the left or the right hemisphere.
In 1874 the German neurologist Carl Wernicke described a different kind of aphasia. Unlike Tan, his patient could speak words fluently, but the sentences didn’t make sense. Furthermore, the patient could not comprehend questions asked of him. Autopsy showed damage to part of the temporal lobe of the left hemisphere. Wernicke concluded that loss of comprehension was the primary effect of damage to this region. Production of nonsensical sentences was a secondary effect, which could have arisen because a person may need to comprehend what he or she is saying in order to say something that makes sense. The symptoms caused by damage to Wernicke’s region are known today as Wernicke’s aphasia.
Together, Broca and Wernicke provided a double dissociation of speech production and comprehension. Damage to Broca’s region halted production of words but left comprehension intact; damage to Wernicke’s region destroyed comprehension but spared production. This was important evidence that the mind is “modular.” It might seem obvious that language is distinct from other mental abilities, since it is possessed by humans but not other animals, but it’s less obvious—or was less obvious, before Broca and Wernicke—that language can be further subdivided into separate modules for production and comprehension.
Broca and Wernicke showed how to map the cortex by relating the symptoms of patients to the locations of brain lesions. By using this method, their successors were able to identify the functions of many other regions of the cortex. They created maps resembling those of the phrenologists, but based on solid data. Could their findings on cortical localization be used to understand mental differences?
When Albert Einstein died in 1955, his body was cremated. His brain was not, because it had been removed by the pathologist Thomas Harvey during an autopsy. Fired from Princeton Hospital a few months later, Harvey kept Einstein’s brain. Over the following decades he carried 240 pieces with him in a jar as he moved from city to city. In the 1980s and 1990s, Harvey sent specimens to several researchers who shared his goal of finding out what was special about the brain of a genius.
Harvey had already determined that the weight of Einstein’s brain was average, or even slightly below average; thus brain size couldn’t explain why Einstein was extraordinary. Sandra Witelson and her collaborators proposed another explanation in 1999. They argued, based on the photographs Harvey had taken during the autopsy, that a cortical region called the inferior parietal lobule was enlarged. (This region is part of the parietal lobe of the brain.) Perhaps Einstein was a genius because part of his brain was enlarged. Einstein himself reported that he often thought in images rather than words, and the parietal lobe of the brain is known to be involved in visual and spatial thinking.
Anatole France and Albert Einstein belong to a long tradition of public fascination with geniuses’ brains. Nineteenth-century enthusiasts preserved the brains of luminaries like the poets Lord Byron and Walt Whitman, which still sit today in dusty jars relegated to the back rooms of museums. I find it strangely heartening that Tan and Paul Broca, the wordless patient and the neurologist who studied him, are now companions for eternity, as the same Parisian museum preserves both of their brains. Neuroanatomists also preserved the brain of Carl Gauss, one of the greatest mathematicians of all time. They pointed to an enlarged parietal lobe to explain his genius, anticipating Witelson’s explanation of Einstein’s.
So the strategy of studying the sizes of specific brain regions rather than overall brain size is not new at all. In fact, it was originally invented by the phrenologists. Their founding father, Franz Joseph Gall, titled his 1819 treatise The Anatomy and Physiology of the Nervous System in General, and of the Brain in Particular, with Observations upon the possibility of ascertaining the several Intellectual and Moral Dispositions of Man and Animal, by the configuration of their Heads. Gall held that each mental “disposition” is correlated with the size of the corresponding cortical region. More dubiously, Gall argued that the shape of the skull reflected the shape of the underlying cortex and could be used to divine a person’s dispositions. Phrenologists roamed the world offering to predict the fortunes of children, assess prospective marriage partners, and screen job applicants by feeling bumps on heads.
Gall and his disciple Spurzheim proposed functions for cortical regions based on anecdotes about extreme dispositions. If a genius had a large forehead, intelligence must be in the front of the brain. If a criminal’s head bulged on the sides, the temporal lobe must be important for telling lies. Their anecdotal methods led to localizations that were mostly preposterous. By the second half of the ninetee
nth century, phrenology had become an object of ridicule.
Today we have technologies that the phrenologists could only fantasize about. MRI gives us precise measurements of the sizes of cortical regions, eliminating the silly method of feeling head bumps. And by scanning the brains of many humans, researchers can collect enough data to go beyond anecdotes like Witelson’s study of Einstein’s brain. What have the neo-phrenologists found?
They have demonstrated that IQ is correlated with the sizes of the frontal and parietal lobes. The correlation has turned out to be slightly stronger than that between IQ and overall brain size, in keeping with the idea that these lobes are more critical to intelligence. (The occipital and temporal lobes are mainly devoted to sensory abilities like vision and hearing.) Still, the correlation is disappointingly weak.
But these studies don’t fully follow the spirit of phrenology, which not only divided the brain into regions but also divided the mind into separate abilities. We all know people who are superb at mathematics but less skilled verbally, and vice versa. Today many researchers reject the notion of IQ and general intelligence as simplistic. They prefer to speak of “multiple intelligences,” and these turn out to be correlated with the sizes of specific brain regions. London taxi drivers have an enlarged right posterior hippocampus, which is a region of the cortex thought to be involved in navigation. In musicians, the cerebellum is larger and certain cortical regions are thicker. (The enlargement of the cerebellum makes sense, as it is thought to be important for fine motor skills.) Bilinguals have a thicker cortex in the lower part of the left parietal lobe.
While these findings are fascinating, they are only statistical. If you read the fine print, you’ll see that the brain regions are only larger on average. It remains the case that the sizes of brain regions are almost useless for predicting the abilities of an individual.
Differences in intellectual ability can cause difficulties, but they’re usually not catastrophic. Other kinds of mental variation, however, exact terrible suffering and are hugely costly to our society. In industrialized countries, an estimated six of every hundred people have a severe mental disorder, and almost half suffer a milder disorder at some point in their lives. Most disorders respond only partially to behavioral and drug therapies, and many have no known treatment at all. Why is it so difficult to fight mental disorders?
The discoverer of a disease is usually the first to describe its symptoms. In 1530 the Italian physician Girolamo Fracastoro utilized the unusual medium of an epic poem, Syphilis sive morbus Gallicus (“Syphilis or the French Disease”). He named the disease in honor of the first man to contract it, the mythical shepherd Syphilus, who was punished with sickness by the god Apollo. In three books of Latin hexameter, Fracastoro described the symptoms of syphilis, recognized that it was sexually transmitted, and prescribed some remedies.
Syphilis causes ugly skin lesions and awful physical deformities. Later on, another horrible symptom can emerge: insanity. In his 1887 horror story “Le Horla,” the French writer Guy de Maupassant imagined a supernatural being who torments the narrator, first by physical sickness and then by madness: “I am lost! Somebody possesses my soul and governs it! Somebody orders all my acts, all my movements, all my thoughts. I am no longer anything in myself, nothing except an enslaved and terrified spectator of all the things which I do.” The narrator finally resolves to end his suffering by killing himself. The story seems semi-autobiographical, as Maupassant suffered from syphilis contracted in his twenties. In 1892 he attempted suicide by cutting his throat. Committed to an asylum, Maupassant died the next year at the age of forty-two.
The painter Paul Gauguin and the poet Charles Baudelaire may also have suffered from syphilis. We have no proof, however, because a disease cannot be reliably diagnosed based on symptoms alone. Two people with the same disease may have different symptoms, and two people with different diseases may have similar symptoms. To diagnose and treat a disease, we’d like to know its cause rather than its symptoms. The bacterial cause of syphilis was discovered in 1905, and the first drugs that killed the bacteria soon followed. These drugs were effective in the early stages of syphilis, but they could not eradicate the disease after it invaded the nervous system. In 1927 the German physician Julius Wagner-Jauregg won the Nobel Prize for his bizarre cure for neurosyphilis. In addition to administering drugs, he deliberately infected patients with malaria. The resulting fever somehow killed off the syphilis bacteria, at which point he introduced drugs that cured the malaria. After World War II, Wagner-Jauregg’s cure was replaced by penicillin and the other antibacterial drugs known as antibiotics. Syphilis is no longer a major cause of brain disease.
Diseases caused by infection are relatively easy to cure, because we know the cause. But what about other kinds? Alzheimer’s disease (AD), which commonly strikes the elderly, starts with memory loss and progresses to dementia, a generalized deterioration of mental abilities. In the late stages, the brain shrinks, leaving empty space inside the skull. Were they alive today, the phrenologists would explain AD as being caused by a decrease in brain size, but this explanation would be unsatisfactory. Shrinkage of the brain occurs long after memory loss and other symptoms first appear, and furthermore, shrinkage is itself more a symptom than a cause. It happens because brain tissue dies, but what causes that?
Searching for clues, scientists examined autopsy tissue from AD patients and discovered microscopic “junk” called plaques and tangles littering the brains. In general, an abnormality in the cells of the brain associated with a disease is known as a neuropathology. Plaques and tangles appear in the brain well before the death of cells, and closer to the onset of AD symptoms. These neuropathologies are currently regarded as the defining characteristic of AD, as the symptoms of memory loss and dementia can also occur in other diseases. Scientists have not yet figured out what causes plaques and tangles to accumulate, but they hope that reducing these neuropathologies might cure AD.
The most puzzling mental disorders come with no clear and consistent neuropathology. Here we are really stumped. These disorders, still defined only by their psychological symptoms, are the furthest from being cured. They may involve anxiety, as in panic and obsessive-compulsive disorders, or mood, as in depression and bipolar disorder. Two of the most debilitating are schizophrenia and autism.
The symptoms of autism are most memorably conveyed by clinical description:
David was 3 when he was diagnosed as autistic. At that time he hardly looked at people, was not talking, and seemed lost in his own world. He loved to bounce on a trampoline for hours and was extremely adept at doing jigsaw puzzles. At 10 years of age David had developed well physically, but emotionally remained very immature. He had a beautiful face with delicate features. . . . He was and still is extremely stubborn in his likes and dislikes. . . . More often than not his mother has to give in to his urgent and repeated demands, which easily escalate into tantrums.
David learned to talk when he was 5. He now goes to a special school for autistic children, where he is happy. He has a daily routine, which he never varies. . . . Some things he learns with great skill and speed. For example, he learned to read all by himself. He now reads fluently, but he doesn’t understand what he reads. He also loves to do sums. However, he has been extremely slow to learn other skills, for example, eating at the family table, or getting dressed. . . .
David is now 12 years old. He still does not spontaneously play with other children. He has obvious difficulties in communicating with other people who don’t know him well. . . . He makes no concessions to their wishes or interests and cannot take onboard another person’s point of view. In this way David is indifferent to the social world and continues to live in a world of his own.
This case study includes all three of the symptoms that define autism: social impairment, difficulties with language, and repetitive or rigid behaviors. The symptoms appear before three years of age and often lessen later on, but most autistic adults are unable t
o function without some sort of supervision. No known treatment is very effective, and there is certainly no cure.
Speaking more poetically, Uta Frith has described autism as a “beautiful child imprisoned in a glass shell.” Many other types of disabled children may have heart-wrenchingly obvious physical deformities. That’s not the case for the autistic, who look superficially fine or even beautiful. Their appearance deceives parents, who have difficulty believing that something is fundamentally wrong. They hope in vain to break through the “glass shell”—the social isolation of autism—and liberate a normal child. But the healthy guise of the autistic child hides a brain that is not normal.
The best-documented abnormality is one of size. When the American psychiatrist Leo Kanner originally defined the syndrome in a landmark 1943 paper, he noted in passing that five children out of his eleven case studies had large heads. Over the years, researchers have studied many more autistic children and found that their heads and brains are indeed enlarged on average—especially the frontal lobe, which contains many areas involved in social and linguistic behaviors.
Does that mean brain size is a good predictor of autism? If it were, we could be confident that the phrenological approach is on the right track toward explaining autism. But we should be careful not to commit a common statistical fallacy concerning rare categories. Consider a very special type of person, professional football players. They are markedly larger than the average person. Can we turn this around and predict that anyone much larger than average is likely to be a professional football player? This prediction rule would work well with what’s called a balanced population—one containing equal numbers of football players and regular people. If you sorted them by size, you’d be pretty accurate. But if you looked instead at the general population and predicted that any large person drawn from it was a football player, you’d be wrong most of the time. These people would just be tall, muscular, or obese for other reasons. Similarly, predicting that all children with big brains are autistic would be highly unreliable. There is much more to playing in the NFL than being large, and much more to being autistic than having a big brain.
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