top of page

The Lasting Neurological Effects of Childhood Trauma

What happens during childhood can have consequences throughout the human lifespan. Children growing up under extremely stressful conditions have a significantly increased risk of smoking, illegal drug use, alcoholism and suicide. Early Life Stress (ELS) includes trauma, abuse, neglect and serious family dysfunction. Significant stress or trauma in the early years of life can also impact the neurological development of children and has been linked to emotional, social and cognitive impairment. Furthermore, it is suggested that ELS may be a leading cause of adult neurological disorders, disability and earlier death (Anda et al., 2009; Targum & Nemeroff, 2019). Prenatal and postnatal stress can both have serious consequences throughout life. Stress on the mother can cause stress to the child in utero and affect the prenatal development of the nervous system (Provencal & Binder, 2015). Early life experiences, both positive and negative, shape the brain’s development and impact mental and physical health (Smith & Pollak, 2020).

Figure 1: Stress and Health Across Lifespan (Taylor, 2010).

What is an Early Life Stressor?

There are many causes of ELS. Any traumatic events that occur during childhood can result in ELS, including sexual and physical abuse, neglect and loss of a parent. These crises can have a detrimental effect on the brain’s development and can have lasting consequences. ELS is recognised as one of the causes of neurological disorders in adults (Targum & Nemeroff, 2019). When an ELS event occurs below the age of seven, the knock-on effects may be even more drastic. During the early years of life, the brain undergoes rapid development and neural connections are made. The brain changes a lot during this time. The changing state of the nervous system makes the brain vulnerable. Trauma and ELS that occurs when the brain is most at risk can have the most severe consequences (Gilmore et al., 2018). There is a critical age (four to seven years) where ELS can cause the most harm. If an ELS event occurs during this time, there is a higher chance this will lead to a neurological or developmental disorder in adulthood than if ELS occurred at a more stable time (Williams et al., 2016).

How ELS Affects the Nervous System:

A key function of the central nervous system is its ability to adapt and modify itself through a process called ‘neural plasticity’, or 'neuroplasticity', where the structure and function of neural connections strengthen or weaken in response to experience or injury. This is the system by which learning, skills and memory can occur. In neuroplasticity, dendritic spines and neuronal networks physically change and are strengthened, weakened and reorganised in response to environmental stimuli. As plasticity is driven by experience, the effect of the nervous system is specific to every individual (Galván, 2010; Johnston, 2009; Von Bernhardi et al., 2017).

Figure 2: Effect of Early Life Stress on the Brain and Behaviour (Brunton, 2015).

Mechanisms of neural plasticity include neurogenesis, programmed cell death and activity-dependent synaptic plasticity. Activity-dependent synaptic plasticity affects neuronal synapses depending on how little or often those synapses are used over time through Long-Term Potentiation (LTP) and Long-Term Depression (LTD). LTP is the strengthening of synaptic connections between neurons through repeated stimulation. Conversely, in LTD, synaptic connections are reduced and synaptic transmission weakens when these networks are not used. LTP and LTD cause lasting changes in synaptic strength and consequently determine neuronal signalling (Bliss & Cooke, 2011). Most neuroplasticity occurs during postal development, as an abundance of neuronal synapses is produced. These synapses are then pruned in an activity-dependent manner throughout childhood and into adolescence (Johnston, 2009). As a result, the experiences of early life can drastically shape a person's cognitive, behavioural and psychological development, with long-lasting effects (Smith & Pollak, 2020).

The Role of Genetics:

Although childhood trauma and ELS have been shown to play a significant role in the onset of neurological disorders in adulthood, a combination of ELS and genetic factors shows the greatest risk of adult disorders. The greatest impact of genetics on neurological and psychological make-up occurs during neurodevelopment and can affect the response to new stressful events throughout life (Williams et al., 2016). Genetics play a role in the extent to which stressors can impact the brain. Epigenetic mechanisms that regulate gene expression can negatively impact stress response regulation in those who experience ELS. Changes to the epigenetic mechanisms in genes involved in the hypothalamic–pituitary–adrenal (HPA) axis can cause an increase in the HPA stress response (Provencal & Binder, 2015).

Figure 3: Impact of Stress on Epigenetics (Park et al., 2019).

The HPA Axis:

Responding to stress is a crucial part of maintaining homeostasis in the body. When a stressful event occurs, the HPA axis mediates the stress response through hormonal signalling. The HPA axis is the main stress system in the body. In healthy humans, hormonal interactions between the hypothalamus, pituitary gland and adrenal glands aid an appropriate stress response and regulate when and for how long the body is in a stressful state. When a stressor activates the hypothalamus, corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are secreted. These hormones act on the posterior pituitary, which secretes the adrenocorticotropin hormone (ACTH), which, in turn, prompts the adrenal cortex to produce cortisol. The HPA axis is regulated by a negative feedback loop: high cortisol levels in the blood inhibit the production of CRH in the hypothalamus, ending the stress response. By appropriately responding to stress, the ‘fight or flight’ response is activated and it is possible to escape a stressful or dangerous situation. The activation of the pituitary also activates noradrenergic neurons in the brain, which release adrenaline and noradrenaline. These neurotransmitters drive the immediate ‘fight or flight’ response (Guilliams & Edwards, 2010).

Figure 4: The Hypothalamic–Pituitary–Adrenal (HPA) Axis (Provencal & Binder, 2015).

Cortisol is known as the ‘stress hormone’. Cortisol’s role in the HPA axis stress response is to redirect the body’s energy and cellular processes to prioritise immediate survival. However, the body cells cannot withstand exposure to this stress response for too long (Dedovic et al., 2009; Guilliams & Edwards, 2010). ELS can cause epigenetic changes, such as DNA demethylation, in regulators of the HPA axis, impairing the negative feedback loop. Cortisol binding to the glucocorticoid receptor is integral to stopping continued cortisol production in the negative feedback loop. However, demethylation of the DNA of genes of the glucocorticoid receptor caused by ELS results in reduced sensitivity of this receptor. As a result, cortisol secretion and the stress response continue (Provencal & Binder, 2015). Most cells in the body have cortisol receptors, so the effect of this stress hormone is wide and can impact other systems, such as the immune, cardiovascular and metabolic systems. Dysfunction of the negative feedback loop impacts cell function and can affect proper organ function (Dedovic et al., 2009; Guilliams & Edwards, 2010).

Other areas of the brain associated with emotion and stress regulation, such as the anterior cingulate cortex and the amygdala, are modulated by the prefrontal cortex (Wang & Saudino, 2011). While these brain regions are developing in utero, stressors upon the mother may impact the development of these regions. Defects in this early programming caused by stress can cause dysfunction in emotion and stress regulation systems (Provencal & Binder, 2015).

Figure 5: The Brain Under Stress (Arnsten, 2015).

Dying Young:

Some of the leading causes of death in adults in Western countries, such as heart disease, cancer, unintentional injury, suicide and HIV/AIDS have been traced to ELS (Anda et al., 2009; Ahmad & Anderson, 2021). ELS significantly increases the risk of succumbing to these conditions. Adults with depression are significantly more likely to have experienced ELS (Williams et al., 2016).

The aftermath of ELS does not end there. Studies have shown that adults who experienced ELS are less responsive to neurological treatments (e.g. psychotherapy and pharmacotherapy than adults who did not suffer ELS. ELS may have the potential as an indicator of which antidepressants a particular patient may respond to (Targum & Nemeroff, 2019; Williams et al., 2016). It was found by Shamseddeen et al. (2011) that combination treatments (use of multiple medications to treat one issue) for depression had a significantly lower effect on patients with a history of abuse. Furthermore, the nature of the abuse strongly correlated with which treatment combinations the patients responded to best. Patients who had been sexually abused had a similar response to combination treatment and the use of one drug, while those who suffered physical abuse had a lower response to combination treatment than to just one drug. This suggested that the type of abuse patients experienced could be used to determine their best course of treatment (Michel & Staskin, 2022; Williams et al., 2016).

Figure 6: Impact of ELS on body systems (Fogelman and Canli, 2019).


There are clear associations between significant stress in early life and neurological disorders in adults. The long-reaching effects of ELS can affect humans at a biological level. ELS can be a double-edged sword: a person that suffers from ELS is more likely to develop depression and ELS may also make some treatments for depression ineffective (Targum & Nemeroff, 2019). As neuroplasticity is most active in the developing brain, ELS can have a significant effect on the structure and function of the brain. As part of normal human development, neuroplasticity is beneficial and important for learning and memory. However, ELS can negatively affect plasticity and cause many health issues and can be responsible for many neurological disorders (Johnston, 2009). Some of the leading causes of death in humans are also strongly related to childhood experiences (Anda et al., 2009). By furthering the understanding of the multilayered impact of ELS, it may be possible to predict neurological conditions in adults and determine treatments.

Bibliographical References:

Ahmad, F. B., & Anderson, R. H. (2021). The Leading Causes of Death in the US for 2020. JAMA, 325(18), 1829.

Anda, R. F., Dong, M., Brown, D., Felitti, V. J., Giles, W. H., Perry, G. S., Valerie, E. J., & Dube, S. R. (2009). The relationship of adverse childhood experiences to a history of premature death of family members. BMC Public Health, 9(1).

Bliss, T. V. P., & Cooke, S. F. (2011). Long-term potentiation and long-term depression: a clinical perspective. Clinics, 66, 3–17.

Dedovic, K., Duchesne, A., Andrews, J., Engert, V., & Pruessner, J. C. (2009). The brain and the stress axis: The neural correlates of cortisol regulation in response to stress. NeuroImage, 47(3), 864–871.

Galván, A. (2010). Neural plasticity of development and learning. Human Brain Mapping, 31(6), 879–890.

Gilmore, J. H., Knickmeyer, R. C., & Gao, W. (2018). Imaging structural and functional brain development in early childhood. Nature Reviews Neuroscience, 19(3), 123–137.

Guilliams, T. G., & Edwards, L. (2010). Thomas, G. G., & LE, C. (2010). Stress and the HPA Axis: Clinical Assessment and Therapeutic Considerations. , 9(2). The Standard, 9(2).

Johnston, M. V. (2009). Plasticity in the developing brain: Implications for rehabilitation. Developmental Disabilities Research Reviews, 15(2), 94–101.

Michel, M. C., & Staskin, D. R. (2022). Study Designs for Evaluation of Combination Treatment: Focus on Individual Patient Benefit. Biomedicines, 10(2), 270.

Provencal, N., & Binder, E. B. (2015). The effects of early life stress on the epigenome: From the womb to adulthood and even before. Experimental Neurology, 268, 10–20.

Shamseddeen, W., Asarnow, J. R., Clarke, G. N., Vitiello, B., Wagner, K. D., Birmaher, B., Keller, M. B., Emslie, G. J., Iyengar, S., Goldstein, B. I., McCracken, J. T., Porta, G., Mayes, T. L., & Brent, D. A. (2011). Impact of Physical and Sexual Abuse on Treatment Response in the Treatment of Resistant Depression in Adolescent Study (TORDIA). Journal of the American Academy of Child and Adolescent Psychiatry, 50(3), 293–301.

Smith, K., & Pollak, S. D. (2020). Early life stress and development: potential mechanisms for adverse outcomes. Journal of Neurodevelopmental Disorders, 12(1).

Swayne, L. A., Sanchez-Arias, J. C., Agbay, A., & Willerth, S. M. (2016). What Are Neural Stem Cells, and Why Are They Important? Frontiers for Young Minds, 4.

Targum, S. D., & Nemeroff, C. B. (2019). The Effect of Early Life Stress on Adult Psychiatric Disorders. PubMed, 16(1–2), 35–37.

Von Bernhardi, R., Bernhardi, L. E., & Eugenín, J. (2017). What Is Neural Plasticity? In Advances in Experimental Medicine and Biology (pp. 1–15). Springer Nature.

Wang, M., & Saudino, K. J. (2011). Emotion Regulation and Stress. Journal of Adult Development, 18(2), 95–103.

Williams, L. M., DeBattista, C., Duchemin, A., Schatzberg, A. F., & Nemeroff, C. B. (2016). Childhood trauma predicts antidepressant response in adults with major depression: data from the randomized international study to predict optimized treatment for depression. Translational Psychiatry, 6(5), e799.

Visual Sources:

Author Photo

Maria McGovern

Arcadia _ Logo.png


Arcadia, has many categories starting from Literature to Science. If you liked this article and would like to read more, you can subscribe from below or click the bar and discover unique more experiences in our articles in many categories

Let the posts
come to you.

Thanks for submitting!

  • Instagram
  • Twitter
  • LinkedIn
bottom of page