Behavioral biology is also revealing the workings of our normal inhibitions. Over the course of an average day there must be a dozen times in which you have a thought—lustful or angry or petulant or self-pitying—that you would never ever say. Damage a certain part of your brain’s frontal cortex and you now say those things; the frontal cortex is the closest thing we have, neuroanatomically, to a superego. Phineas Gage, a nineteenth-century railroad worker, wound up a celebrated neurological patient and fairground exhibit after his left frontal cortex was destroyed in a freak accident. He was transformed from a taciturn man to a pugnacious loudmouth who told everyone just what he thought. “Frontal disinhibition,” involving aggressiveness, inappropriate frankness, and hypersexuality, is also often seen in individuals who have sustained stroke damage to that part of the brain. Remarkably, the same appears to happen in Huntington’s disease, a rare congenital neurological disorder. Scientists have long thought of the disease as a movement disorder—around age forty to forty-five, patients begin to demonstrate uncontrolled swinging of limbs as an inhibitory motor pathway in the brain degenerates. With time, the movement becomes all-encompassing, constant whole body writhing that incapacitates the person. A lesser-known feature of the disease is a social disinhibition, one that often even precedes the motoric aspects, and in recent years it has been shown that Huntington’s individuals also have damage to their frontal cortex.
Some neuroscientists even use the word “frontal” in a sardonic sense: A terrified student gives a quavering lecture to his elders, and some insensitive big shot rises and savages the kid over some minor point, taking the opportunity to toot his own horn while he’s at it. “Christ,” someone will mutter in the back of the lecture hall, “he’s getting more frontal all the time.”
Blow away that part of the brain and you can still remember the name of your kindergarten teacher, still do a polka, still feel what all of us feel. You just let other people know about it far more often than do most of us. Is it absurd to hypothesize that there is something a little bit wrong with the frontal cortex of the insensitive big shot in the lecture hall?
Another version of neuropsychiatric disinhibition is seen in Tourette’s syndrome, once a diagnostic backwater but fast threatening to become a fad. Tourette’s patients are famed for their scatology, their uncontrolled cursing. But this doesn’t even begin to scratch the surface. Tourette’s patients do indeed curse, but they also emit a stream of animal sounds—yips and barks and growls—along with facial tics, and violent or lewd body gestures. These are the first genetic and neurochemical hints as to what the disease is about, but it remains, for the most part, a mystery. What is striking, though, is how it differs from the disinhibition of a frontal patient. A frontal individual does or says what the rest of us think about but would never let out of our well-restrained minds. Tourette’s patients do not wish to bark like a dog or grab repeatedly at their crotch—these are simply emotive twitches, uncontrolled outbursts that are randomly tossed on top of the person struggling to maintain continuity. Like hiccups of the id.
Thus, a variety of these neuropsychiatric disorders result in marked and puzzling disinhibition. Some epileptics undergo a personality shift in the opposite direction. Roughly defined, an epileptic seizure is an abnormal electrical discharge in the brain. Neurologists have known for a long time that just before the onset of a seizure there will often be a strange sensation, or “aura,” and the location of the seizure in the brain can influence the type of aura—for example, epileptics will typically have a sensory aura, perhaps imagining a particular smell. The existence of auras demonstrates the not very surprising fact that sudden bursts of electrical activity in different parts of the brain will influence thought and sensation. Now neurologists are coming to recognize that different types of epilepsy also shape personalities, influencing the person all the time, not merely seconds before a seizure.
People with a type of temporal lobe epilepsy, for example, tend to be extraordinarily serious, humorless, and rigid in their ways. They tend to be phobic about doing new things, and instead perseverate on old behaviors and tastes, tending to walk to work the same way each day, usually wearing the same types of clothes, ordering the same meal in restaurants. Similarly, they rely upon a very small circle of friends, showing what neuropsychologists pungently call a “viscous” or “sticky” personality. Such people also tend to have an intense interest in religion or philosophy. And, most oddly, they not only think obsessively about their problems, they write about them—endlessly. Temporal lobe epileptics are renowned among neurologists for this “hypergraphia.” In a typical scenario, someone first seeing a new neurologist will present the doctor with a carefully handwritten eighty-page diary, insisting that reading it will give the doctor vital insight into the patient. At the next visit the epileptic will return with a new, fifty-page addendum. One might speculate that having a serious neurological illness like epilepsy would make anyone serious and cause people to focus on the philosophical things in life, narrow their horizons, and rely on comfortable, familiar patterns. But this personality change does not arise from other types of epilepsy of an equally serious nature, is not a function of the frequency or severity of seizures or the magnitude with which it disrupts a person’s life. Instead, have an uncontrolled and rhythmic outburst of electrical activity in the temporal lobe every now and then and, the rest of the time, you get very interested in philosophy and always order the same meal in a restaurant.
There is another version of a constrained life that is being defined biologically. At some time each of us has, to our irritation, left on a trip and felt such nagging doubt as to whether we locked the door that we returned home to check. Or after dropping a letter into a mailbox, we have peeked in a second or third time just to make sure it went down. Or, during a tough, anxious period in our lives, we find ourselves unable to concentrate because some ridiculous television jingle keeps running through our heads. This is normal and common. But among people with obsessive-compulsive disorder, these thoughts dominate and ruin their lives. They miss vacations because they return home repeatedly to check if the oven was turned off. They lose their jobs because they are late each day, spending hours each morning washing their hands. They torture themselves by obsessively counting numbers in their heads. For most of us, little rituals of thought or behavior can calm us and provide structure at an anxious time. For someone with obsessive-compulsive disorder—now thought to be caused by an imbalance of brain chemicals, possibly serotonin and dopamine—there are no limits, and the person becomes a creature of these rituals.
What does this tour of neuropsychiatric oddities mean? We are learning to draw that line in new places. Most of these disorders did not exist a few decades ago; we did not even have names for how biology could occasionally destroy the life of an individual. Now we have those names. We are beginning to learn what certain parts of the brain, what specific genes, or what our early development has to do with these tragedies. In the process we are extending our definition of illness. For some time we have generally accepted that people who rave and gibber are ill, that they cannot control these things, are made miserable by them, and deserve care, protection, and forgiveness. Slowly we are coming to recognize that you can also be made miserable by a ceaseless march of number counting in your head, or by paralyzing fears of anything new, and that these too can be uncontrollable illnesses that demand understanding and treatment.
This field continues to move forward, and we might even be able to cure some of these maladies. Another form of progress will be the recognition of increasing numbers of these disorders, the coining of more names to describe our behavioral oddities. What will happen when, eventually, we have a few of these labels?
I recognize facets of myself in these pages. At times when I am overworked and anxious, I develop a facial tic and I count stairs as I climb them. I usually wear flannel shirts. In Chinese restaurants I always order broccoli with garlic sauce. Invariably I think, “I’ll get b
roccoli and garlic sauce,” then I think, “Nah, order something different,” then I think, “Well, I enjoyed broccoli last time, why get something different?” and then I think, “Careful, I’m becoming a perseverating drudge,” and then the waiter is standing there and I become flustered and order broccoli with garlic sauce.
I do not have temporal lobe epilepsy, obsessive-compulsive disorder, or any of the other problems I have discussed. Yet it is reasonable to assume that there is some sort of continuum of underlying biology here—whatever it is about the temporal lobe of some epileptics that makes them perseverate may share some similarity with my own temporal lobe, at least when it is menaced with options like Buddha’s Delight or General Po’s Szechwan Chicken. Perhaps whatever neurochemical abnormality causes a schizophrenic to believe that voices are proclaiming her the empress of California is the same abnormality that, in a milder form, leads a schizotypal person to believe in mental telepathy. In an even milder form it may allow the rest of us to pass a few minutes daydreaming that we are close friends with some appealing movie character.
What if eventually we come to understand the genetics, the neurochemistry, and the hormonal bases of clothing preference, of who votes Democratic, of religiosity, or of why some worry too much about money and others too little? Some of these irritating traits that are, at worst, character weaknesses, but nothing more pathological. Slowly we will be leaving the realm of them and their disorders. We will be defining instead a biology of us and our strengths and weaknesses, of our potentials and constraints.
In 1992, the newspapers were teeming with stories about one such advance. For years scientists have searched for differences between heterosexual and homosexual men, and nothing very consistent had ever emerged. But in August 1992, the prestigious journal Science published a paper by neurobiologist Simon Levay demonstrating just such a difference. And it’s a whopper of an interesting one. It concerns the hypothalamus, a part of the brain central to sexual behavior. The size of one subregion at the front of the hypothalamus, known by the not terribly titillating title of the third interstitial nucleus, differs by sex; males have a larger one than do females. Levay reported that homosexual men have smaller nuclei than do heterosexual men—as small, in fact, as those found in women.1
For some homophobes this is a bellwether observation: “You see, there is something wrong with their brains.” For some gays it is an affirmation: “You see, I’ve always told you I just felt gay. This is what I was meant to be.” And for those concerned with social policy, fearing that a gay teacher will make children gay is as preposterous as a blue-eyed teacher influencing children’s eye color. Predictably, the scientific jury is still out: while Levay is a superb neuroscientist, his sample size was small, and the brain tissue he examined came from AIDS patients, so the disease might have altered it. Also, Levay doesn’t know if the small size is the cause or the result of sexual orientation.
But suppose his finding turns out to be accurate. And suppose a small interstitial nucleus in a male turns out to be more a cause than a consequence of homosexuality. What will happen when brain imaging techniques improve to the point, as they inevitably will, where we can measure the size of this brain structure in a person? Being gay is not a disease. (If you don’t believe me, just ask the American Psychiatric Association. Being gay used to be a mental illness until the APA, in a spasm of political correctness and enlightenment, changed its mind and struck homosexuality from its bible, the Diagnostic and Statistical Manual of Mental Disorders. Overnight, millions of people had one less disease, which is a pretty impressive outcome of a committee meeting.) Do we inform adolescents of their nucleus size when they have not yet become sexually active and haven’t expressed a sexual preference? What do we do with an openly and happily gay or straight adult whose nucleus is the “wrong” kind? What will we make of nuclei of intermediate sizes? And will the Food and Drug Administration move to squelch the predictable festering of quacks flogging their methods of changing nucleus size?
This world of understanding will be rife with old dangers. In some sectors, this sort of knowledge, this ever-increasing number of diagnostic labels, will probably guarantee more reasons why the poor or poorly connected will be denied jobs or fair housing or health insurance. Even more menacingly, with scientific understanding comes the potential for manipulation, and the temptation to judge and fix things that aren’t broken is never far behind. In every generation, there will be brownshirts whose biological ideal comes with an Aryan profile, and in every generation there will be some scientists and physicians who will be happy to march into hell with them.
But this new knowledge will be rife with promise as well. Recognizing the continuity between the workings of our benign little personality quirks and the versions that might qualify as disease would benefit those with the latter. When science teaches us repeatedly that there but for the grace of God go I, when we learn to recognize kinship in neurochemistry, we will have to become compassionate and tolerant, whether looking at an illness, a quirk, or a mere difference. And when this recognition spreads, we will have learned that drawing a boundary between “the essence of a person” and “the biological distortion of that essence” is artificial. It is simply a convenient way to classify the biological limitations common to most of us and other, rarer limitations. Being healthy, it has been said, really consists of having the same disease as everyone else.
FURTHER READING
At the end of each piece, I will be including some annotated references. This is both to document claims or findings mentioned and to point readers in the right direction should they want to learn more about specific topics. Unfortunately, in most cases, the references cited are pretty technical. I will try to note the ones that are more accessible, and to warn about the ones that are anything but.
For an overview of schizotypalism, see M. Vollema and R. van den Bosch, “The Multidimensionality of Schizotypy,” Schizophrenia Bulletin 21 (1995): 19. For discussions of how schizotypalism and schizophrenia are on a genetic continuum (i.e., often occur in the same families), see K. Kendler, A. Gruenberg, and D. Kinney, “Independent Diagnoses of Adoptees and Relatives as Defined by DSM-III in the Provincial and National Samples of the Danish Adoption Study of Schizophrenia,” Archives of General Psychiatry 51 (1994): 456. Also see C. Webb and D. Levinson, “Schizotypal and Paranoid Personality Disorder in the Relatives of Patients with Schizophrenia and Affective Disorders: A Review,” Schizophrenia Research 11 (1993): 81.
For a review of the behavioral features of Huntington’s disease, see J. Cummings, “Behavioral and Psychiatric Symptoms Associated with Huntington’s Disease,” Advances in Neurology 65 (1995): 179. Also see M. Mendez, “Huntington’s Disease: Update and Review of Neuropsychiatric Aspects,” International Journal of Psychiatry in Medicine 24 (1994): 189.
Frontal disinhibition syndromes are reviewed in J. Cummings, “Frontal-Subcortical Circuits and Human Behavior,” Archives of Neurology 50 (1993): 873.
Tourette’s syndrome is covered in O. Sacks, The Man Who Mistook His Wife for a Hat and Other Clinical Tales (New York: Summit Books, 1985). This is a highly readable collection of case studies of patients of Sacks’s, an acclaimed neurologist.
Temporal lobe personality features are covered in S. Waxman and N. Geschwind, “Hypergraphia in Temporal Lobe Epilepsy,” Neurology 24 (1974): 629. The late Geschwind, one of the giants of neurology, formalized much of the thinking about temporal lobe personality.
A wonderful introduction to obsessive-compulsive disorder can be found in J. Rapoport, The Boy Who Couldn’t Stop Washing (New York: Signet, 1989). The author, probably the leading authority on the subject, has assembled some fascinating case histories.
Simon Levay’s work on the biological bases of sexual orientation is covered in a number of publications. His key paper concerning structural differences in the brain is S. Levay, “A Difference in Hypothalamic Structure between Heterosexual and Homosexual Men,” Science 253 (1991): 1034. He reviews t
he subject in a popular book, S. Levay, The Sexual Brain (Cambridge, Mass.: MIT Press, 1993). Levay’s findings and, to an even greater extent, work by Dean Hamer concerning the possible genetic bases of sexual orientation remain controversial. The features of that controversy are summarized in a very accessible debate: S. Levay and D. Hamer, “Evidence for a Biological Influence in Male Homosexuality,” Scientific American 270 (May 1994): 44; and W. Byne, “The Biological Evidence Challenged,” Scientific American 270 (May 1994): 50.
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