A Foundation for Trauma-Informed Understanding

Neuroplasticity is the ability of the brain’s neuronal circuits structurally and functionally to adapt. Epigenetics, neurogenesis, synaptic plasticity, and white matter plasticity are four neuroplastic mechanisms that facilitate learning and adaptation. An epigenetic influence enhances adaptation to current or future environments by regulating gene expression; neurogenesis involves the integration of new neurons to integrate novel information and adapt affective behaviors, while synaptic and white matter plasticity work together to strengthen synapses and myelination, resulting in efficient and automatic neural pathways (Peckham, 2023).

Cognitive Implications and Dysfunctional Pathways of Trauma on Neuroplasticity

Considering the negative cognitive implications of trauma, it is essential to investigate how it affects neuroplasticity. Thomason and Marusk (2017) investigated the effects of trauma on the neural stress pathway, emotional processing, and emotional regulation pathway. A reduction in hippocampal volume was evident in combat-related post-traumatic stress disorder (PTSD). Psychopathology, including anxiety, depression, and PTSD, has also been associated with a dysregulated hypothalamic-pituitary-adrenal (HPA) axis. A maladaptive experience triggers different stress responses depending on its severity and nature. Moreover, individuals with PTSD often exhibit dysfunction in three important Intrinsic Connectivity Networks (ICNs): default mode network (DMN), central executive network (CEN), and salience network (SN) (Nicholson et al., 2020). During idle thoughts, it is typical for one’s attention to focus on oneself, activating the DMN and focusing attention inward. However, trauma patients display reduced activation in this region responsible for self-awareness. (Van der Kolk, 2014). CEN abnormality is associated with cognitive dysfunction, while an overactive SN leads to irregular hypervigilance (Nicholson et al., 2020). Furthermore, diminished medial prefrontal cortical (mPFC) activation, a region regulating emotions, may contribute to the signature overactivity of the amygdala in PTSD (Reiter, 2016).

Neuroplasticity permits adaptation to different environments that ensure the survival of an organism. Although stress can induce necessary neuroplastic alterations in the brain, maladaptive stress-induced changes may have adverse effects on the brain. The process of neurogenesis appears to be triggered by a variety of environmental factors, including environmental enrichment, learning, and exercise, and is hindered by chronic stress, depression, and other psychological disorders (Depperman et al., 2014). Similarly, negative and positive stress have been found to result in increased HPA axis activity, thereby altering neuroplasticity in opposing ways. Accordingly, optimal stress facilitates long-term memory and cognitive functioning, whereas traumatic stress can lead to cognitive impairment and psychological disorders. Traumatic and stressful events can lead to maladjusted mechanisms of consolidation and reconsolidation, or memory preservation, that promote neuroplasticity. Psychophysiological hyperarousal is associated with PTSD, which reinforces stress-induced reconsolidation and reinforces dysfunctional behavior. In essence, it reinforces negative neuroplastic changes.

Traumatic Stress and PTSD: Psychological and Physiological Implications

Psychological disorders, including PTSD, are becoming increasingly prevalent among refugees who flee war-related events. Arntez et al. (2020) stress that trauma-induced neuroplastic reorganization of the limbic brain circuitry of the amygdala and hippocampus plays a critical role in the pathophysiology of PTSD. The researchers investigated how pre-displacement trauma affects brain-derived neurotrophic growth factor (BDNF) and nerve growth factor (NGF) levels, which are involved in neuroplasticity and mental health. BDNF and NGF levels were associated with worse scores on validated scales for PTSD, anxiety, and depression. These neurotrophins mediate neuroplastic changes in synaptic connections, supporting memory and learning.

Despite the brain’s inherent neuroplasticity, including synaptic connectivity, why does this not simply occur after a traumatic incident? It is likely due to the chronic stress induced by PTSD symptoms, resulting from dysregulation of the HPA axis (Krystal et al., 2017). This, and reduced plasma BDNF levels, a hormone crucial for neural growth, are reported in individuals with PTSD and may hinder neuroplasticity. Therefore the chronic nature of PTSD may be attributed to HPA dysfunction impeding synaptic connectivity restoration.

Neuroplasticity Enhancement and Therapeutic Interventions

Through brain scans, it has been shown that interventions such as Trauma-focused Cognitive Behavioral Therapy (tfCBT), mindfulness-based interventions, and Eye Movement Desensitization and Reprocessing therapy (EMDR) facilitate neuroplastic changes in areas crucial for emotional regulation, mood, and memory processes (Guendelman et al., 2017; Santarnecchi et al., 2019). EMDR focuses on inadequately processed traumatic memories and employs bilateral stimulation to reduce their emotional vividness. For example, one might recount details of a traumatic memory and their emotions at the time, while following the movement of a therapist’s finger from left to right (APA, 2017). This process, potentiality facilitated by neuroplasticity, has been shown to increase and restore gray matter density in prefrontal areas originally lost due to PTSD, contributing to improved emotional regulation (Boukezzi et al., 2017). However, these structural changes take several months to appear.

Furthermore, certain medications in current use may contribute to synaptic activity, thereby alleviating symptoms. Antidepressants, which are commonly prescribed, raise BDNF levels, enhancing synaptic connectivity and promoting neurogenesis (Krystal et al., 2017). Non-trauma-focused activities, such as exercise, can counteract the harmful effects of stress and demonstrate enhanced neuroplasticity. It is essential to note, however, that much of this research has been conducted on animal models.

Given the evolving understanding of PTSD, interventions directly targeting neuroplastic deficits have emerged as a promising pathway for recovery. Studies are investigating pharmacotherapies that directly target synaptic connectivity with the aim of improvement. A potential agent in enhancing fear extinction in patients unresponsive to exposure-based treatments is ketamine (Krystal et al., 2017). As opposed to long-term antidepressants, rapid-acting alternatives directly focusing on restoring synaptic deficits characteristic of PTSD may allow room for CBT to be more effective (Krystal et al., 2017).

Neurofeedback: Harnessing Neuroplasticity for PTSD

Among therapeutic approaches, neurofeedback stands out for its direct utilization of neuroplasticity in treating PTSD. This noninvasive therapeutic method relies on electroencephalogram (EEG) scans to identify abnormal brain wave patterns (Reiter, 2016). Traumatized individuals often exhibit asynchronous brainwave patterns, contrasting with the coherent patterns observed in normal participants. For example, in a study where participants were asked to filter out irrelevant information, participants with PTSD generated irregular brainwave patterns, which is a possible explanation for the attentional and focus problems found In individuals with PTSD (Van der Kolk, 2014). Other characteristic brain patterns in PTSD include increased activations in the right temporal lobe, housing the amygdala, and slow-wave activity in the frontal cortex, where faster frequencies such as alpha waves are expected. Neurofeedback aims to correct these dysfunctional patterns through real-time EEG feedback, acting as a “mirror” for the brain. Reinforcing desired brainwave patterns and discouraging dysfunctional ones through stimuli like auditory or visual cues, can change habitual dysfunctional brain patterns resulting from PTSD (Askovic et al., 2023). According to Van der Kolk (2014), this frees up “innate but stuck oscillatory properties” in the brain. Neurofeedback capitalizes on the brain’s extraordinary neuroplasticity to essentially rewire dysfunctional brain patterns. It has demonstrated changes in the connectivity of problematic networks in PTSD, such as the DMN and SNM as well as in the amygdala connectivity to the PFC, which regulates emotions (Askovic et al., 2023; Nicholson et al., 2020). This approach may be particularly beneficial at the beginning of treatment, stabilizing the nervous system and enabling patients to fully engage in subsequent therapies, especially those with more complex PTSD that are often not as receptive (Reither, 2016; Van der Kolk).

In summary, neuroplasticity plays a vital role in trauma recovery. Interventions can positively impact problematic cognitive dysfunction characteristic of PTSD, such as disrupted connectivity networks, and HPA axis dysregulation. Various therapeutic interventions, from tf-CBT to mindfulness-based strategies, have displayed neuroplastic changes. A recent focus of research is to facilitate neuroplasticity directly, as seen in recent, innovative pharmacotherapies. While still nascent, research regarding neurofeedback and PTSD has great clinical implications for the future.

References

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