Welcome to Your Child's Brain: How the Mind Grows From Conception to College (41 page)

Under good rearing conditions, the outcomes for these children may be better than for dandelion children in many ways. For example, in one prospective study of high-stress families, high-reactive children were sick much more often than low-reactive children in the same families. In low-stress conditions, the advantage was reversed: high-reactive children were sick less often than low-reactive children. In short, outcomes for orchids were more variable, for good and for bad.

Similar results were found in an experimental study with rhesus monkeys. Highly reactive infants raised by especially nurturing mothers showed the most resilience in response to stress and ended up high in the colony’s dominance hierarchy. High-reactive infants raised by average mothers had the worst outcomes. For infants born to average mothers, in contrast, being raised by nurturing or average mothers had little effect on adult behavior.

The orchid idea is consistent with several other findings. For example, inborn difficulties with reading could be associated with greater artistic capacity (
chapter 25
), and an interest in science might be associated with susceptibility to autism (
chapter 27
). Parents can take heart from the idea that the special care that’s necessary in handling their difficult children may lead to good outcomes later on.

In general, gene-environment interactions are complex and thus difficult to demonstrate, so all these findings remain somewhat controversial. The interaction between the 5-HTT gene and early life stressors is the strongest result. It has been replicated in sixteen studies, though some others drew different conclusions. The marijuana-schizophrenia link is the weakest, resting on a single study so far.

The study of resilience in the face of adversity has contributed a great deal to our understanding of how experience affects child development. It’s become increasingly clear that some environmental influences are individually variable, having different effects on different children. We know that life events can lead to different outcomes depending on which genes a child carries. There are likely to be even more complicated interactions that researchers cannot identify with current techniques, such as those involving multiple environmental conditions and multiple genes. Scientists may never unravel all these influences, but we can say for certain that neither genetic inheritance nor environmental conditions alone are destiny for any child.

Chapter 27
MIND-BLINDNESS: AUTISM

AGES: ONE YEAR TO FOUR YEARS

Most babies are interested in socializing from birth, but for children with autism, the social aspects of brain function are severely impaired. As we described in
chapter 2
, the first steps in development are programmed by genetic mechanisms and go awry only in cases of severe environmental flaws such as high doses of toxins. Sometimes, though, flaws in the genetic program can have a profound effect. Development is a complex business, depending on thousands of genes. When by chance children inherit unlucky combinations of alleles from one or both parents, neurodevelop-mental problems such as autism can result.

At autism’s core is a distinctive and profound disorder. One way to describe the problem is a deficit in
theory of mind
, the ability to imagine what other people know and what they are thinking or feeling (see
chapter 19
). Autistic people have difficulty recognizing when others are lying, being sarcastic, mocking them, or taking advantage of them. They have particular trouble in reading facial expressions, especially of emotion. In analogy to traits such as color-blindness, autistic children seem to have “mind-blindness.”

Autism as originally defined in 1943 by its discoverer, Leo Kanner, is relatively rare, affecting one or two children per thousand born in the U.S. It is diagnosed based on three major problems: impaired social interactions, defective or absent communication, and repetitive or restricted behavior. Since then, other researchers have found that autism is not the same in all cases. Many children with autism also have other types of disrupted brain function such as mental retardation or epilepsy. Related to autism are less severe disorders such as Asperger’s syndrome, in which language and cognitive ability are largely intact. Collectively, these so-called autism spectrum disorders affect about one in 150 children, 75–80 percent of whom are boys. Siblings of these children are also at risk: they are almost ten times more likely to have an autism spectrum disorder than the general population (though the risk is still only one in twenty).

The recorded rate of autism spectrum disorders has increased dramatically in the last few decades. Much of this increase is due to changes in diagnosis. Autism was not recognized as a formal diagnostic category of the American Psychiatric Association until 1980, and a 1994 revision of the criteria made a larger fraction of children eligible for the diagnosis. In addition, more children are being screened, as many pediatricians now routinely administer questionnaires to identify autism. Some researchers believe that these factors can account for most of the apparent rise in the rate of autism.

Other possible contributors are increases in birth before full gestation, for instance, due to early induction of labor, and decreases in infant mortality due to improved care for premature and at-risk babies (see
chapter 2
). Unlike changes in diagnosis, such birth-related causes can lead to genuine increases in the number of children with neurodevelopmental problems. Another possible cause is increasing parental age over the last few decades, which may lead to more spontaneously occurring genetic changes in sperm and egg. The overall result is a boom in reported cases—and in public awareness.

SPECULATION: ARE FERAL CHILDREN AUTISTIC?

Mythology and modern history contain many accounts of feral children. Typically these children are reported to lack the power of speech, usually grunting or howling instead. They reject clothing, reminiscent of perceptual difficulties in autistic persons, and are unable to socialize normally with others. Could it be that these children are not feral but autistic?

Such children are often said to be raised by animals, most often wolves but sometimes dogs, apes, bears, and even the occasional gazelle. Just as developmentally disabled children are mostly male, “wolf-reared children” are nearly always boys, whatever the country of the tale’s origin. Romulus and Remus were said to be suckled by a she-wolf. Other such children in ancient Greek and Roman lore are usually male, though some cases are highly fanciful, such as a god being nursed by bees. A more modern example is Victor the Wolf Boy of Aveyron, who appeared to be about eleven years old when he was found naked and wandering in the French countryside in 1800.

Of course these children are never found in the actual custody of animals; their improbable rearing is reflected in their behavior. In the few cases where children can speak, they often describe running away from home and joining a group of animals. It seems more plausible that an abandoned, high-functioning autistic child could manage to survive long enough to be found.

Signs of the social and communication deficits in autism can be seen at one year of age or even earlier. At this age, infants with autism are less likely than nonautistic mentally retarded infants to respond to their own names, to look at people, or to use gestures to communicate. There are striking deficits in joint attention
(shared attention with another person) to objects that people are holding, an early precursor to social behavior (see
chapter 20
), along with an inability to understand simple games such as peekaboo and sometimes tickling. These differences are relatively subtle, though, and few babies are diagnosed this young unless they have an autistic older sibling, a situation in which parents may be on the alert for unusual behavior. Autistic infants do form attachments to their parents (though these feelings may be expressed in unusual behaviors) and respond differently to strangers than to familiar people. In the second year of life, many autistic babies begin to have obvious developmental problems, such as language delay or repetitive behaviors.

Autism can be detected in a visit to the pediatrician or a developmental specialist, typically at twenty-four months. At that age, pediatricians often screen using a checklist for autism in toddlers. The Autism Diagnostic Observation Schedule survey can be given as early as twelve months, but there is some risk of making a premature interpretation. Some children simply take a little longer to develop but end up fine. By the third birthday, diagnosis is reliable.

It has been a challenge to researchers to understand how this strange combination of symptoms can arise. From a number of studies of brain structure at the levels of whole structures and individual cells, a few clues have emerged. There is still some ambiguity of interpreting results since typically brain abnormalities are observed after death, decades after the initial recognition of autism. It is unclear whether the abnormalities are present in early childhood, or whether they arise after years of the disorder’s progress. Still, in combination with brain scans, the following patterns are found.

In scans of the brains of living autistic people, a common feature is a malformed or small amygdala. The number of neurons in this region is also decreased compared with nonautistic persons. The amygdala is necessary for the generation of emotional reactions (see
chapter 18
) and is activated when people are asked to evaluate emotion in other people’s facial expressions, something autistic children have difficulty doing.

The structures most consistently affected in autistic brains are the cerebellum and other regions that are connected to it. In terms of numbers of neurons, reductions in cerebellar structures are seen in three fourths of autistic brains. Abnormalities are seen in whole-brain scans as well. When pediatric neurologists examined premature babies to look for a relationship between neurodevelopmental
problems and the location of any brain injuries, they found that autism was specifically associated with damage to the cerebellum, more than to other brain regions.

These findings provide potentially useful clues to what makes autistic brains different—but also present a puzzle to researchers. Traditionally, the cerebellum was thought to be principally involved in processing sensory information to guide movement, a function that is disrupted when the cerebellum is damaged in adults. Autistic children are sometimes clumsy, but not in a debilitating way. So what’s going on?

One possibility is that the cerebellum is essential for translating sensory events, such as the sight of a mother’s smiling face, into a message with social import. Recall that your child’s brain goes through phases of experience-expectant development (see
chapter 10
), in which the brain is ready to wire itself up, as long as it receives normal input. The brains of autistic children may have trouble translating everyday social experiences into a meaningful signal—thereby depriving themselves of a necessary experience early in life. If an abnormal cerebellum is involved in this derailed developmental process, it might do so through its connections to other brain regions, which include the anterior cingulate cortex, which is involved in face processing, and the prefrontal cortex, which is involved in complex planning and executive function. These brain regions also often show abnormalities in autistic people.

Abnormalities in the cerebellum may also cause deficits in perception. The cerebellum is important for distinguishing between touch from oneself and the touch of others. A prominent example is the phenomenon of tickling: you cannot tickle yourself because your brain generates signals large enough to feel the sensation only when it comes from another person. Activity is increased in the cerebellum during touch from others.