of Infancy
The mind emanates from the interface between neurophysiological processes and interpersonal relationships. Experience selectively shapes genetic neuronal potential and thus directly influences the structure and function of the brain.
—DANIEL J. SIEGEL, M.D.
BEHIND THE FOREHEAD in the vicinity of the right eye is where one of the most important regulatory centers in the brain is located: the orbitofrontal cortex.1 It is part of the prefrontal cortex, that area of the gray matter most involved in social intelligence, impulse control and attention. It is also important in short-term working memory. The orbitofrontal cortex—so named because of its proximity to the eye socket, known as the orbit—is more developed on the right side and appears to dominate its counterpart in the left hemisphere.
A complex condition like ADD cannot be traced to just one part of the brain. Many circuits and systems must be involved. According to a lot of recent evidence, however, disturbances of the orbitofrontal cortex are, indeed, implicated in disorders of impulse inhibition and emotional self-regulation, including ADD. It is probably here that the neurophysiological effects of stressed attunement and attachment are most pronounced.
Nature’s goal for human growth is for the eventual maturation of a self-motivated, self-regulated and self-reliant adult. The infant lacks these attributes. We may say that the natural agenda is really the transformation of regulation from dependence on another individual to independence, from external regulation to internal regulation. This shift from external to internal regulation requires the development of the prefrontal cortex, the cortex in the very anterior portion of the brain, including and especially the orbitofrontal cortex.
The right orbitofrontal cortex, which for the sake of brevity we will call the OFC, has connections with virtually every other part of the cortex. It also has rich connections with the lower brain structures, where the body’s internal physiological states are controlled and monitored, and where the most primitive and powerful emotions such as fear and rage are generated. It is at the center of the brain’s reward and motivation apparatus and contains more of the reward chemicals associated with pleasure and joy—dopamine and endorphins—than almost any other area of the cortex.
Via its connections with the vision centers of the cortex, the OFC plays a role in visual-spatial orientation, the locating of objects in space. When visual-spatial orientation is impaired, a person tends to bump his head a lot or run into people unseeingly and have difficulty following physical directions—all features of ADD I am intimately familiar with.
The OFC has a major role in the control of attention. From all the information about the external environment and internal body states entering our brain, the OFC helps to pick out what to focus on. While the explicit meaning of words spoken is analyzed in the left hemisphere, the right OFC interprets the emotional content of communications—the other person’s body language, eye movements and tone of voice. It carries out a constant and instantaneous computation of the emotional significance of situations. It is deeply concerned with the assessment of relationships between the self and others. According to a number of studies, it is “dominant for the processing, expression, and regulation of emotional information.”2
The OFC also functions in impulse control, helping to inhibit the lower centres in the brain where urgent emotional drives originate. When it is working smoothly, it can delay emotional reactions long enough to allow mature, more sophisticated responses to emerge. When its connections are disrupted, it lacks this capacity. At such times primitive, unprocessed emotions will flood our minds, overwhelm our thinking processes and control our behavior.
Finally, the OFC records and stores the emotional effects of experiences, first and foremost the infant’s interactions with his or her primary caregivers during the early months and years. Its imprinting of the earliest interactions with the primary caregivers is the unconscious model from which all later emotional reactions and interactions will be formed. Groups of neurons in the OFC encode the emotional footprints of these important experiences—footprints in which, willy-nilly, we tend to follow later in life, again and again and again.
The great Canadian researcher Donald Hebb showed that groups of neurons that have fired together once are more likely to fire simultaneously in the future. This Hebbian principle has been expressed as “neurons that fire together wire together.” The early emotional imprinting is encoded in the form of potential neuronal patterns: groups of nerve cells primed to fire together. We experience them later in life when we find to our surprise that some relatively minor stimulus, being cut off in traffic, for example, triggers in us an irrational rage, leaving us scratching our head and wondering, What was that about? It was about the early imprinting of the OFC with the rage and frustration of the infant and toddler, and about the Hebbian principle. Each time we scream at someone in traffic, we are telling a story from the earliest part of our life.
A vast body of research supports this understanding of the functions of the right prefrontal cortex. Most dramatic to observe are the deficiencies and impairments suffered by people who have been injured in this area of the brain.3 Their behavior and emotional reactions are like a textbook description of ADD. Among other ADD-like features, these so-called prefrontal patients often digress and have to be frequently reminded to finish a line of thought; are easily distracted; when listening, will often shift attention to whatever snippet of speech catches their interest; during tasks will often seem to lose track of what the instructions were; will be given to childish emotional outbursts; will have difficulty inhibiting their physical impulses; will find it nearly impossible to learn from experience.
Sustaining physical damage, such as an injury to the brain, is not the only way that the chemical and electrical functions of the prefrontal cortex may become disrupted. In ADD there is no brain damage, but there is impaired brain development. As I wrote in an earlier chapter, it is not that a disorder develops, but that certain important brain circuits do not develop. Interference with the conditions required for the healthy development of the prefrontal cortex, I believe, accounts for virtually all cases of ADD.
Emotional interactions stimulate or inhibit the growth of nerve cells and circuits by complicated processes that involve the release of natural chemicals. To give a somewhat simplified example, when “happy” events are experienced by the infant, endorphins—“reward chemicals,” the brain’s natural opioids—are released. Endorphins encourage the growth of nerve cells and of connections between them. Conversely, in animal studies, chronically high levels of stress hormones such as cortisol have been shown to cause important brain centers to shrink.
Emotions affect not only the release of brain chemicals in the short term but also the long-term balance of neurotransmitters, the molecular messengers telegraphing electrical impulses from one nerve cell to another. Just as the infant’s early interactions with the nurturing caregivers help to shape the structure of brain centers and circuits, so, too, do they play a role in determining the chemistry of the brain. Throughout the human life span there remains a constant two-way interaction between psychological states and the neurochemistry of the frontal lobes, a fact that many doctors do not pay enough attention to. One result is the overreliance on medications in the treatment of mental disorders. Modern psychiatry is doing too much listening to Prozac and not enough listening to human beings; people’s life histories should be given at least as much importance as the chemistry of their brains.
The dominant tendency is to explain mental conditions by deficiencies of the brain’s chemical messengers, the neurotransmitters. As Daniel J. Siegel has sharply remarked, “We hear it said everywhere these days that the experience of human beings comes from their chemicals.” Depression, according to the simple biochemical model, is due to a lack of serotonin—and, it is said, so is excessive aggression. The answer is Prozac, which increases serotonin levels in the brain. Attention deficit is thought to be due in part to an undersupply of dopamine, one of the brain’s most important neurotransmitters, crucial to attention and to experiencing reward states. The answer is Ritalin. Just as Prozac elevates serotonin levels, Ritalin or other psychostimulants are thought to increase the availability of dopamine in the brain’s prefrontal areas. This is believed to increase motivation and attention by improving the functioning of areas in the prefrontal cortex. Although they carry some truth, such biochemical explanations of complex mental states are dangerous oversimplifications—as the neurologist Antonio Damasio cautions:
When it comes to explaining behavior and mind, it is not enough to mention neurochemistry … The problem is that it is not the absence or low amount of serotonin per se that “causes” certain manifestations. Serotonin is part of an exceedingly complicated mechanism which operates at the level of molecules, synapses, local circuits, and systems, and in which sociocultural factors, past and present, also intervene powerfully.4
The deficiencies and imbalances of brain chemicals are as much effect as cause. They are greatly influenced by emotional experiences. Some experiences deplete the supply of neurotransmitters; other experiences enhance them. In turn, the availability—or lack of availability—of brain chemicals can promote certain behaviors and emotional responses and inhibit others. Once more we see that the relationship between behavior and biology is not a one-way street. As an example, in troops of monkeys the dominant, most successfully aggressive males have been found to have less serotonin than the others. This would seem to prove that low serotonin levels cause aggression. However, the serotonin levels drop only after these males achieve dominant status. So while the relative lack of serotonin may help to maintain the dominant male’s aggressive capacities, it could not have caused them. Emotional stress can similarly affect serotonin levels, contributing to symptoms of depression. When we prescribe Prozac, we are not so much treating the biology of inheritance as the biology of living and having experiences in the world.
Environmental influences also affect dopamine. From animal studies, we know that social stimulation is necessary for the growth of the nerve endings that release dopamine and for the growth of receptors that dopamine needs to bind to in order to do its work. In four-month-old monkeys, major alterations of dopamine and other neurotransmitter systems were found after only six days of separation from their mothers. “In these experiments,” writes Steven Dubovsky, Professor of Psychiatry and Medicine at the University of Colorado, “loss of an important attachment appears to lead to less of an important neurotransmitter in the brain. Once these circuits stop functioning normally, it becomes more and more difficult to activate the mind.”5
A neuroscientific study published in 1998 showed that adult rats whose mothers had given them more licking, grooming and other physical-emotional contact during infancy had more efficient brain circuitry for reducing anxiety, as well as more receptors on nerve cells for the brain’s own natural tranquilizing chemicals.6 In other words, early interactions with the mother shaped the adult rat’s neurophysiological capacity to respond to stress. In another study, newborn animals reared in isolation had reduced dopamine activity in their prefrontal cortex—but not in other areas of the brain. That is, emotional stress particularly affects the chemistry of the prefrontal cortex, the center for selective attention, motivation and self-regulation. Given the relative complexity of human emotional interactions, the influence of the infant-parent relationship on human neurochemistry is bound to be even stronger.
In the human infant, the growth of dopamine-rich nerve terminals and the development of dopamine receptors is stimulated by chemicals released in the brain during the experience of joy, the ecstatic joy that comes from the perfectly attuned mother-child mutual gaze interaction. Happy interactions between mother and infant generate motivation and arousal by activating cells in the midbrain that release endorphins, thereby inducing in the infant a joyful, exhilarated state. They also trigger the release of dopamine. Both endorphins and dopamine promote the development of new connections in the prefrontal cortex. Dopamine released from the midbrain also triggers the growth of nerve cells and blood vessels in the right prefrontal cortex and promotes the growth of dopamine receptors. A relative scarcity of such receptors and blood supply is thought to be one of the major physiological dimensions of ADD.
The letters ADD may equally well stand for Attunement Deficit Disorder.