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Psychiatric Times. Vol. 15 No. 5
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Brain Development, Attachment and Impact on Psychic Vulnerability

By Deborah A. Lott | May 1, 1998

The orbitofrontal cortex sits at the apex of the limbic system, and controls the sympathetic and parasympathetic branches of the autonomic nervous system. Schore conceptualizes psychobiological attunement as "direct right brain to right brain communication" in which the mother's right brain, "involved in the unconscious expression and processing of emotional information," serves as a template for the infant's developing neural circuitry (Schore, 1997).

These attachment experiences occur at the same time that the neonatal brain is undergoing a growth spurt. Brain researchers Greenough and Black (1992) first described a model of the brain's "experience-dependent synaptogenesis" in which there is a surge of metabolic activity--an overpro-liferation of synapses. Regardless of genetic encoding, synapses that fail to form connections die off in a process of pruning. Schore contends that abuse, neglect and chronic states of misattunement lead to an overpruning of synapses in the right orbitofrontal cortex, leaving individuals with impaired ability to modulate and regulate emotion in response to stress.

By regulating affect, the caregiver is also regulating the release of neurohormones in the infant's brain. High levels of cortisol, a stress hormone that may well be released in the brain during states of distress, has been shown in some animal studies to destroy synapses.

In the inevitable event of distress states in the infant, the caregiver's moving in to repair the connection and comfort the infant reduces the levels of cortisol and related stress hormones. As a result, the frontal cortex develops a greater concentration of glucocorticoid receptors that can modulate stress responses (Schore, 1996).

When there is no interactive repair; when the caregiver is abusive, neglectful or continually misattuned, infants may remain in chronically negative states, their corticosteroid levels chronically elevated. This results in a reduction in the number of synapses, even the death of neurons, according to Schore's hypothesis.

Cortisol Rises

Attachment researchers have recently begun to document the endocrinological correlates to insecure attachment (Main, 1996). In the classic strange-situation test developed by attachment researchers, a mother first takes the baby into a room where they encounter a stranger. The mother leaves the infant alone with the stranger briefly and then returns. The infant's response to these stressful separation and reunion events provides a measure of the security of attachment. Securely attached infants may be moderately upset at the disappearance of the mother, but welcome her return fairly unequivocally and are quickly soothed by her ministrations. These children exhibit a rise in cortisol at separation followed by a diminution at reunion.

In the most pathological attachment category, the insecure-disorganized attachment, infants react to the mother's return with disorganized, conflicted, sometimes self-harming behavior. Siegel described their behavior: "Children may go toward the parent, then go away, spin around, bang their heads on the wall, kick the floor." Instead of comfort, the return of the parent leads to a "state of disorganization in the child." Disorganized attachments appear to occur in the presence of abuse or frightening and disorienting parental behavior. Children with these disorganized attachments exhibit a greater rise in cortisol and prolonged cortisol elevations across the course of the strange-situation test. When children with disorganized attachments were followed for 17 years, they also showed the greatest vulnerability to mental disorders later in life.

Animal research, which allows for the direct examination of brain tissue following particular social experiences, has long suggested that social relationships alter the very structure of the brain. Monkeys raised in social isolation not only manifest symptoms of emotional dysregulation, but also a lack of fundamental neurons in portions of the hippocampal formation, a region of the brain involved in regulating emotion (Nelson and Bloom, 1997).

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