Neural Development’s Impact on Emotional and Social Regulation

By Emily Beard Johnson, BA, CD, Asst. Assoc. of ECE, Neurological Reorganization Practitioner
Permission to copy this article with appropriate attribution is granted (503) 981-0635. Babies are not innately born with the ability to regulate emotions and social behavior. Healthy brain development facilitates infants’ ability to acquire emotional and social skills. Ground-breaking studies in the 1990’s confirmed that activity in the premotor cortex called the mirror neuron system allows individuals to observe and mimic emotional and social behavior. Infants must complete the developmental sequence, an exact sequence of movement, reflex, and sensory experience, to stimulate the neural growth through which they gain access to all parts of their brain, including the mirror neuron system. If the developmental sequence is not completed and babies do not gain access to these parts of their brain, lifelong functional deficits will result[1] unless rectified through a program of neurological reorganization.

Chronological age does not automatically translate into increased function. Just because a child reaches a year of age, she does not inevitably gain the ability to walk. To walk well with a smooth gait, the child must first complete the developmental skills of crawling on her abdomen and creeping on hands and knees. These trigger the postural and structural reflexes which allow the child to walk well. This process applies to social, emotional, and cognitive skills as well: each of these rely on the developmental sequence to insure appropriate function and, lacking completion of the developmental sequence, deficits manifest. A March, 2005 study summarized the critical importance of the foundational layers of the central nervous system to facilitate more advanced function: “New learning isn’t simply the smarter bits of our brain such as the cortex ‘figuring things out.’ Instead, we should think of learning as interaction between our primitive brain structures and our more advanced cortex. In other words, primitive brain structures might be the engine driving even our most advanced high-level, intelligent learning abilities.”[2]

When a baby is born, the myelin (a white, fatty substance that facilitates neural movement in the brain) is present to the medulla. At this stage of development, all activity is reflexive. As stated by an infant cognition scientist, “Babies have to learn everything….They start with a few primitive reflexes to get things going.”[3] Initiating the developmental sequence through unrestricted movement, reflex, and sensory experience facilitates myelin growth and, hence, increased function. As described in a February, 2007 study, newborn brains grow movement and vision regions first (compromised mainly of gray matter), which facilitates the growth of the white matter (myelin) and corresponding increased function.[4] As stated by the research author, “This study gives us the first glimpse that there are regional differences in how quickly the brain is growing, and these regional differences are probably related to functional development.” A December, 1997 study demonstrated that sensory experience influences the development of brain areas that control movement:[5] “The research suggests that sensory feedback to the brain’s motor cortex system is one of the major driving forces that shapes motor function during development,” critical for the development of the mirror neuron system. When this visual and sensory-motor development begins, mirror neuron function in the form of social mimicking is observed in infants as young as two to three weeks old.[6] This is the foundation of later, complex emotional and social behavior.

Once the developmental sequence is initiated, myelin reaches the pons at approximately one to five months of age. The pons is responsible for all vital, life-preserving function as well as extreme emotional content, including attachment, bonding, sense of safety and security, fear, and anxiety. One visual milestone of a pons-level baby is her ability to recognize basic face structure, which she uses as a primary perceptual mechanism. This ability is so critical that babies develop the ability to recognize face structure long before they recognize body structure.[7] This face recognition also plays a critical role in the development of new object recognition,[8] a key cognitive skill. A pons-level baby uses her new visual skills to maintain eye-contact and promote bonding and attachment with caregivers, especially her biological mother while breast-feeding. Breast-feeding offers an array of important sensory experiences to support healthy neurological function nutritionally, emotionally, behaviorally, and cognitively. According to an August, 2006 study, “The quality of physical contact [during breastfeeding] between mother and baby may influence the development of the offspring’s neural and hormonal pathways.”[9] Abnormal face processing and an unwillingness to maintain or avoidance of eye contact is a predictor for neuropsychiatric disorders, especially autism spectrum disorders[10],[11] and bipolar disorder. “The more [children] misinterpreted the faces as hostile, the more their amygdala flared. Such a face-processing deficit could help account for the poor social skills, aggression, and irritability that characterizes the disorder in children.”[12]

The cycle of response is a pons-level function and crucial component in the development of safety, security, attachment, and bonding. Pons-level infants have a vital cry that communicates, “Help me! Help me! Come save me; I’m dying!” Pons-level infants perceive the world in terms of black and white as the part of the brain responsible for abstract reasoning is not yet myelinated. This communication reflects the pons-level infant’s perception that her life is at stake if she is hungry, cold, hot, in pain, or separated from her mother. To establish safety, security, attachment, and bonding, it is necessary that the infant’s needs are adequately met when she vitally cries. Releasing the vital cry and then having her needs adequately met establishes a cycle of response, builds a healthy mirror neuron system, and allows the baby to feel safe, secure, attached, and bonded. Conversely, if the baby uses her vital cry and her needs are not met, the pons initiates the fight or flight response. At that time, the brain releases stress hormones (such as cortisol, epinephrine, and adrenaline) to facilitate escape from what the infant perceives as a life-threatening situation. For an infant with limited capacity to move and minimal control over her environment, these hormones are released to the point that they become detrimental and cause an injury to the pons. Consequently, even when the infant is in a nurturing and responsive environment, the stress-response is hard-wired into her brain and she continues to act as if her life is threatened.

The correlation between an adequate reaction to the cycle of response and lifelong emotional and behavioral competence is well-documented. An April, 2001 study demonstrated that children with depressed mothers have difficulty regulating their emotions and getting along with others because their mothers are unable to show adequate warmth and sensitivity. In other words, the cycle of response was not sufficiently completed and the children have poorly functioning mirror neuron systems. As stated by the study author, “Our study showed that one possible reason these children may have trouble getting along might be the inability of depressed mothers to cultivate emotion regulation skills in their children. Emotion regulation skills have been found to be an important component of social competence.”[13] An additional study demonstrated the lifelong impacts of poor infant attachment. “Expressions of emotions in adult romantic relationships can be related back to a person’s attachment experiences during early social development. Those participants who were secure and attached as infants were rated with higher social competence as children” and this social competence was tracked through to expressive and emotional attachment in romantic relationships in adulthood. As stated by the lead author, “The current findings highlight one developmental pathway through which significant relationship experiences during the early years of life are tied to the daily experiences in romantic relationships in early adulthood.”[14] A May, 2003 study found that in utero and infant environments shape the development of stress behaviors and learning abilities. The study author stated that “the findings of [the] study demonstrate the significant role of the [pre- and post-natal] environment in regulating certain behaviors,” such as stress-associated behaviors and cognitive performance in adulthood.[15] Successful completion of the pons-level developmental sequence facilitates lifelong attachment, emotional regulation, and appropriate responses to stress.

Another emotional skill developed in the pons is compassion and empathy. Pons-level infants perceive extreme sensations, including pain. As regulated by the mirror neuron system, feeling pain appropriately facilitates compassion and empathy: if it doesn’t hurt me if I am pushed down, then there is nothing to prevent me from pushing you. Conversely, if it does hurt me to be pushed, I am much less likely to deliberately push you. Several studies confirm the correlation between pain perception and the development of compassion and empathy. A February, 2004 study demonstrated that the same brain region engaged when one feels pain physically as when one empathizes for a loved one in pain. As stated by the study author, “For the first time, brain imagers were able to study empathetic processes…and show that emotional and not cognitive processes are triggered by the mere perception that your loved-one is in pain…The results suggest that we use emotional representations reflecting our own subjective feeling states to understand the feelings of others. Probably, our ability to empathize has evolved from a system for representing our own internal bodily states.”[16] Individuals who have issues with pons function (such as those with post-traumatic stress disorder) experience less pain sensitivity, with decreased ability to empathize and express compassion.[17] For those with neuropsychiatric disorders, the mirror neuron system isn’t firing appropriately and, consequently, the individual struggles to empathize. As stated by the lead author of a May, 2007 study, “These results support the notion that a dysfunctional mirror neuron system may underlie the impairments in imitation and in
empathizing with other people’s emotions…This may lead to a cascade of negative consequences for the development of key aspects of social cognition and behavior.”[18]

While it may seem counter-intuitive, pons-level emotional development has lifelong cognitive consequences as well. According to a February, 2003 study, the vision development typical of a pons-level infant allows her to fill in perceptual gaps by four months of age. As stated by the study author, “These results suggest that visual completion of a simple object trajectory is not functional at birth, but emerges across the first several months after the onset of visual experience.”[19] Because this perceptual ability is not innate and completion of the developmental sequence is required to lay the foundation for this capacity, early life stress interferes with the normal process, thus causing memory loss and cognitive decline later in life. “Psychological stress during infancy has been found to cause early impaired memory and a decline in related cognitive abilities. The study suggests that emotional stress may contribute to the type of memory loss during middle-age years that is normally seen in the elderly.”[20]

After the pons is developed, myelin reaches the midbrain-level. This occurs at approximately seven to fourteen months of age. (For our purposes, the midbrain is a region of the brain that encompasses many parts, one of which is called the midbrain). The midbrain is responsible for regulating, filtering, and balancing almost all internal and external stimuli. Important emotional growth occurs at this level as well. Visual development continues, with infants developing vertical eye tracking, the beginnings of convergence, and appreciation of detail within detail. Infants use these skills to further refine the mirror neuron system. A November, 2002 study demonstrated the importance of these increasing skills to infants’ expanding emotional and cognitive capacities. “This work is important because following another person’s line of sight is crucial for learning about language and understanding the emotions of other people.”[21] Another study reinforced the point that infants use visual cues to shape appropriate emotional responses through the mirror neuron system. Using infants’ visual skills as a measurement, researchers found that twelve-month old infants “begin to interpret the behavior of other individuals based on inferences about other persons’ emotions, desires, and beliefs.”[22] Completion of the developmental sequence allows infants to reinforce and build on emotional and cognitive skills.

The midbrain-level is responsible for filtering distracting stimuli, as demonstrated by a March, 2007 study. The ability to filter out distractions is not automatic, but requires myelination of this part of the brain. “Our brains fend off distractions. If we are busy with something, we suppress disrupting external influences…suppression is not automatic.”[23] Filtering distractions is critical for emotional and academic success. When this is not in place, learning disabilities such as attention deficit disorder and attention deficit hyperactivity disorder can result. Because of the pons-level cycle of response’s interplay with the mirror neuron system, the quality of parenting also predicts whether or not an ADHD child also exhibits conduct problems, such as lying, fighting, bullying, and stealing. As the lead author of an April, 2007 study stated, “Research has suggested that children with both ADHD and conduct problems are at the greatest risk of becoming chronic criminal offenders.”[24] Additionally, these self-regulation skills, beyond intelligence, are a greater indicator of children’s early academic success, laying the roadmap for either lifelong academic success or struggle.[25]

When midbrain-level myelinazation does not occur appropriately, neuropsychiatric disorders, such as depression, bipolar disorder, schizophrenia, and autism spectrum disorders, can result. A February, 2007 study reinforced this point: “This study suggests that in autistic children, something may go awry during gray matter growth in the first year of life.”[26] An April, 2007 study found that a growth factor involved in brain development causes pathological changes in brain’s white matter (myelin). “These changes lead to alterations in biochemical signaling and behaviors suggestive of mental illness,” especially with schizophrenia and bipolar disorder.[27] These issues negatively impair an individual’s ability to process both emotion and cognition, according to an October, 2005 study. As stated by the study’s author, “We found that the amygdala, the part of the brain that is supposed to react to emotional stimuli, is over-reactive to negative stimuli in children with bipolar disorder and the part of the brain that controls cognitive behavior is under-reactive.”[28] Successful myelinization triggers the mirror neuron system, critical for minimizing issues related to neuropsychiatric disorders and for maximizing emotional and cognitive function.

At approximately a year of age, the myelin reaches the cortex, or the rational, verbal, intelligent part of the brain. However, if the developmental sequence was not completed in the pons and midbrain, issues will be evident in the cortex, because toddlers use their rudimentary mirror neuron system to further refine appropriate emotional and social behavior. At this point, the foundation of the mirror neuron system must be in place so that healthy emotional and social development can continue. Research demonstrates that toddlers’ imitation predicts a well-developed conscience[29], toddlers engage in emotional eavesdropping to guide their behavior[30], and fears learned by observing others are neurologically identical to those directly experienced.[31] Basically, according to a March, 2007 study, the apex of cortical function, moral judgment, fails without healthy emotional processing.[32] This processing is reliant on the successful completion of the developmental sequence within the first year of life.

Establishing the neural foundations that support healthy emotional and behavioral processing begins at birth when infants initiate the developmental sequence through unimpeded movement, reflex, and sensory experience. If an infant’s movement is constricted, she will be unable to complete the developmental sequence and, consequently, trigger appropriate neural growth in the mirror neuron system. As a result, functional deficits will result in the form of abnormal emotional and social behavior. Most severely, these present as neuropsychiatric disorders. Numerous studies confirm that the presence of abnormal function within the first years of life predict life-long emotional, social, or behavioral issues just as healthy function in the first years sustain healthy function throughout one’s life.[33],[34],[35] Neurological reorganization is currently the only discipline that replicates the developmental sequence to stimulate neural growth and eliminate the underlying cause of emotional, social, and behavioral dysfunction. Completion of the developmental sequence is critical for lifelong emotional, social, and, ultimately, cognitive competence.

1 Association for Psychological Science, May 4, 2007.
2 Earl K. Miller et al., Nature, February 24, 2005.
3 Michael Brunton, “What Do Babies Know?,” Time, January 29, 2007.
4 Dr. John Gilmore et al., Journal of Neuroscience, February 7, 2007.
5 George Huntley, Journal of Neuroscience, December 1, 1997.
6 Association for Psychological Science, May 4, 2007.
7 Virginia Slaughter et al., Current Directions in Psychological Science, December, 2004.
8 Isabel Gauthier, PhD, Michael J. Tarr, et al., Nature Neuroscience, June, 1999.
9 British Cohort Study, Archives of Disease in Childhood, August, 2006.
10 Katarzyna Chawarska et al., Presented at the International Meeting for Autism Research, May 4, 2007.
11 Kim Dalton et al., Nature Neuroscience, March 6, 2005.
12 Dr. Ellen Leibenluft et al., Proceedings of the National Academy of Sciences, May 29, 2006.
13 Dr. Chi-Ming Kam, Presented at Society for Research in Child Development, April 21, 2001.
14 W. Andrew Collins, Journal of Personality and Social Psychology, February, 2007.
15 Darlene Francis, PhD, et al., Nature Neuroscience, May, 2003.
16 Dr. Tania Singer, Science, February 20, 2004.
17 Elbert Geuze, PhD, et al., Archives of General Psychiatry, January, 2007.
18 Mirella Dapretto and Stephany Cox, Presented at the International Meeting for Autism Research, May 4, 2007.
19 Scott P. Johnson et al., Child Development, February, 2003.
20 Dr. Tallie Z. Baram et al., Journal of Neuroscience, October 12, 2005.
21 Rechele Brooks and Andrew Meltzoff, Developmental Psychology, November 5, 2002.
22 Valerie Kuhlmeier et al., Psychological Science, September, 2003.
23 Harm Veling, Released by Netherlands Organization for Scientific Research, March 26, 2007.
24 Andrea Chronis et al., Developmental Psychology, January, 2007.
25 Clancy Blair et al., Child Development, March 26, 2007.
26 Dr. John Gilmore et al., Journal of Neuroscience, February 7, 2007.
27 Gabriel Corfas, PhD, et al., Proceedings of the National Academy of Sciences, April 23, 2007.
28 Dr. Mani Pavuluri et al., Presented at the American Academy of Child and Adolescent Psychiatry and the Canadian Academy of Child and Adolescent Psychiatry, October 20, 2005.
29 David Forman, Psychological Science, October, 2004.
30 Betty Repacholi and Andrew Meltzoff, Child Development, March/April, 2007.
31 Elizabeth Phelps et al., Released by Oxford University Press, March 16, 2007.
32 Antonio Damasio, Ralph Adolphs, et al., Nature, March 22, 2007.
33 The Unit of Child and Adolescent Psycopathology, Universitat Autonoma de Barcelona, December 20, 2006
34 Michael Lewis, PhD, Child Development, March/April, 2006.
35 Eero Kajantie, Annals of the New York Academy of Sciences, March 1, 2007.