Limbic scars

Background: Childhood maltreatment represents a strong risk factor for the development of depression and posttraumatic stress disorder (PTSD) in later life. In the present study, we investigated the neurobiological underpinnings of this association. Since both depression and PTSD have been associated with increased amygdala responsiveness to negative stimuli as well as reduced hippocampal gray matter volume, we speculated that childhood maltreatment results in similar functional and structural alterations in previously maltreated but healthy adults.

Methods: One hundred forty-eight healthy subjects were enrolled via public notices and newspaper announcements and were carefully screened for psychiatric disorders. Amygdala responsiveness was measured by means of functional magnetic resonance imaging and an emotional face-matching paradigm particularly designed to activate the amygdala in response to threat-related faces. Voxel-based morphometry was used to study morphological alterations. Childhood maltreatment was assessed by the 25-item Childhood Trauma Questionnaire (CTQ).

Results: We observed a strong association of CTQ scores with amygdala responsiveness to threat-related facial expressions. The morphometric analysis yielded reduced gray matter volumes in the hippocampus, insula, orbitofrontal cortex, anterior cingulate gyrus, and caudate in subjects with high CTQ scores. Both of these associations were not influenced by trait anxiety, depression level, age, intelligence, education, or more recent stressful life events.

Conclusions: Childhood maltreatment is associated with remarkable functional and structural changes even decades later in adulthood. These changes strongly resemble findings described in depression and PTSD. Therefore, the present results might suggest that limbic hyperresponsiveness and reduced hippocampal volumes could be mediators between the experiences of adversities during childhood and the development of emotional disorders.

https://pubmed.ncbi.nlm.nih.gov/22112927/

Effects of early life trauma

The number of children who experience neglect or abuse is high—about ten out of every thousand children in the United States in 2008.29 Identifying and helping these children is especially difficult unless there are bruises or physical injuries. The effects of early life attachment can lie dormant in the brain until later life. The impact of these hidden effects is that, by adolescence, eighty percent of abused children will be diagnosed with a major psychiatric disorder. Imaging studies of abuse survivors often show that brain areas controlling emotion and cognition are abnormal and underlie these psychiatric disorders and difficulties functioning as a productive citizen. Animal research has provided great insight into how early life caregiving can impact these brain areas and has highlighted unexpected functioning of the brain in early life and the enormous role of the caregiver in controlling the brain’s response to trauma. The comparison of normal attachment formation and pain-related attachment suggests similar behaviors in early life are expressed as attachment to the caregiver, and the activation of different neural substrates may lay the foundation for the enduring effects of early life trauma.

https://www.ncbi.nlm.nih.gov/p<a href="http://&lt;!– wp:paragraph –> <p>The number of children who experience neglect or abuse is high—about ten out of every thousand children in the United States in 2008.<sup><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774302/#R29">29</a></sup> Identifying and helping these children is especially difficult unless there are bruises or physical injuries. The effects of early life attachment can lie dormant in the brain until later life. The impact of these hidden effects is that, by adolescence, eighty percent of abused children will be diagnosed with a major psychiatric disorder. Imaging studies of abuse survivors often show that brain areas controlling emotion and cognition are abnormal and underlie these psychiatric disorders and difficulties functioning as a productive citizen. Animal research has provided great insight into how early life caregiving can impact these brain areas and has highlighted unexpected functioning of the brain in early life and the enormous role of the caregiver in controlling the brain’s response to trauma. The comparison of normal attachment formation and pain-related attachment suggests similar behaviors in early life are expressed as attachment to the caregiver, and the activation of different neural substrates may lay the foundation for the enduring effects of early life trauma.</p> <!– /wp:paragraph –> <!– wp:paragraph –> <p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774302/&quot; target="_blank" rel="noreferrer noopener">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774302/</a></p&gt; mc/articles/PMC3774302/

Brain Development

Much of this experience-dependent control of brain development relies upon the experiences either increasing or decreasing the neural activity of a cell. For example, unused neurons (neurons with little neural activity) will die, while used neurons will survive. This is a normal process that occurs in the developing brain—too many cells are born and are then pruned. While new neurons are born in the brain throughout life, the enormity of early life growth is never replicated in later life. The implications of this process for custodial decisions in very early life are enormous—early life deprivation fails to activate neurons, which means that a greater number of neurons will die. Equally important, neurons that would typically die under “normal” conditions could be retained under deprivation or conditions of abuse. In either situation, brain function for the typical social environment in our Western culture might be compromised. For example, Romanian orphans reared in extreme physical and social isolation have smaller brains, and adopted orphans from Romania and China have a larger amygdala than their non-adopted counterparts.5 The amygdala is a brain area concerned with emotion and fear, and a larger amygdala would suggest altered emotion and fear processing.

Next, more refined control of brain development is accomplished by changing the activity of specific connections between neurons. Activity patterns between neurons can cause some neurons to grow more dendritic branches and synapses but prune others, and so particular types of information processing are enhanced. Importantly, a specific level of neural activity is needed because both too much and too little activity has been shown to be suboptimal. Equally important, the optimal types and intensities of experiences will vary at each stage of development. For example, while rough and tumble play or watching a video might be appropriate sensory stimulation for a four-year-old child, they are likely inappropriate for an infant or a toddler. A more appropriate pattern and intensity of sensory stimulation for a one-year-old would be socially interacting with a nurturing and interesting caregiver. The implications of experience instructing fine-tuning of brain development are critical for custodial issues. If early life experience does not activate the attachment system, it is likely that the development of future attachment formation will be compromised. This seems to have occurred in some orphans adopted from China and Romania. Or, if early life attachment coexists with fear, then the activity of these systems could be overly coordinated.6 Of course, exploring these issues in the human brain is extremely difficult, but animal research in both rodents and primates certainly supports this view, as discussed below.

Importantly, we also know that no brain area functions in isolation and that brain changes induced by early life experiences are ubiquitous throughout the brain. Thus, information about brain development for a given brain area needs to be interpreted within the context of other neural changes because brain activity is a coordinated process of functional connectivity between areas. Moreover, the contribution of learning and interventions, which can dramatically alter brain activity, needs to be considered as we relate neuroscience to behavior and policy.7

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774302/

How does trauma bonding affect the brain?

One of many ways victims can help their brain break a trauma bond is by facilitating the release of calming oxytocin (from the amygdala). Igniting oxytocin receptors of this type can reduce cravings, ease withdrawal, and lessen pain.

What causes someone to violate a person they claimed to love? There are many reasons, for example, substance or alcohol abuse, a neurological condition impacting behavior, or a disorder of character such as antisocial personalitypsychopathy, borderline personality disorder, or narcissistic personality disorder.

https://www.psychologytoday.com/us/blog/neurosagacity/201701/the-brain-can-work-against-abuse-victims