Post-traumatic stress disorder (PTSD) can result from highly stressful events or situations that leave an individual feeling fearful, anxious, angry, and unable to process memories and other sensory cues properly. The physical and emotional trauma of the experience of victims of sexual assault, for example, can lead to structural changes in their brains in a variety of ways.
The brain activity of an individual suffering from post-traumatic stress disorder reflects on aberrant connectivity in the prefrontal cortex and the amygdala (Sadeh et al, 2014; Ito et al, 2015; Jorge, 2015), as well as poor synaptic branching in the hippocampus (Kasai et al, 2010) and poor electrical conductance between neurons (Bennett & Lagopoulos, 2014; Kassem et al, 2013).
Structural changes in the brains of PTSD patients include impaired dendritic spines in the hippocampus (Winston et al, 2013) and significantly reduced hippocampal volume (Bremner et al, 1995; Woon et al, 2010). Alongside these neurobiological differences between typical (non-PTSD affected) brains and those of individuals suffering from PTSD, multiple behavioral, perceptual, cognitive and socio-emotional changes can also be observed as manifestations of the aberrant structural pathology in PTSD patients.
Such changes include an impaired ability to process social situations (Abrahams et al, 2013), affected social judgment (Adolphs et al, 1998), attachment anxiety (Brenner & Ben-Amitay, 2015), impaired memory storage and processing (Mechanic et al, 1998; Bremner et al, 1999; Ehlers, 2010; Garfinkel et al, 2014), intrusive thoughts and impaired understanding and processing of trauma triggers (Ehlers et al, 2004), guilt and self-blame (Miller et al, 2010; Ullman et al, 2014), states of denial and dissociation (Foa et al, 1996), heightened physiological sensitivity to auditory, olfactory or visual cues (Cortese et al, 2015), attentional issues (Olatunji et al, 2013), sleeping difficulties (Nishith et al, 2001) and substance abuse as a coping mechanism for emotion dysregulation (Weiss et al., 2013).
DSM-5 Criteria for PTSD
To formulate a DSM-5 diagnosis of PTSD, at least two of the following four symptoms need to be present: re-experiencing (intrusion; flashbacks and nightmares), arousal (irritability and hyper vigilance), negative emotion (guilt and estrangement), and effortful avoidance of trauma-related stimuli.
The neurobiological processing behind these behavioral, cognitive and socio-emotional dysfunctions includes 1) impaired limbic-temporal structures and 2) neuroplastic thinning of the cortex (Heim et al, 2013).
Furthermore, emotionally excited memories in the hippocampus are not processed as healthy memories are processed, resulting in prolonged effects such as intrusive thoughts and flashbacks. These phenomenon is associated with increased cortisol levels in rape victims suffering from PTSD (Gola et al, 2012), and the chronic exposure to cortisol has an adverse impact on excessive production of myelin in hippocampal and amygdala neurons (Chetty et al, 2014; Lupien et al, 2009, Bremner’s 1999).
Three of the most salient neural structures involved in PTSD are the amygdala, the hippocampus and the medial prefrontal cortex (Shin et al, 2006). The amygdala’s function in the assessment of threat-based stimuli relates to the processing of fear conditioning. Because of the hyper-activity of the amygdala in PTSD cases, people tend to be hyper vigilant and negatively appraise events or potential threats in their environment (Höistad et al, 2008).
The relationship of the medial prefrontal cortex (mPFC) to the amygdala is also significant in this regard, since the mPFC regulates the extinction of fear conditioning. When the mPFC becomes hypo responsive or traumatized or damaged, individuals suffering from trauma inaptly express their fear responses to daily life stimuli (Hanson et al, 2015).
The hippocampus is involved in explicit memory processing (Tsien et al, 2013) and contextual retrieval of fear-related memories (Corcoran & Maren, 2001; Corcoran et al, 2005). If individual is not facilitated to reprocess these memories in a controlled therapeutic setting then inappropriate processing of emotionally-laden memories in hippocampal dendrites in victims keeps the excited memories in place for years.
Psychiatric medications address the physiological, biological and neurological symptoms of a disorder such as PTSD, while counseling and psychotherapy tend to address the psychological, behavioral and social aspects of dysfunction in traumatized individuals.
Research indicates that interventions such as counseling, psychotherapy and behavioral techniques can facilitate the long-term emotional ventilation of individuals suffering from PTSD. Most of these therapies (supportive, interpersonal, critical incident stress debriefing, cognitive behavioral therapy, exposure, eye movement desensitization and reprocessing therapy) facilitate recovery, and help rehearse these memories in the hippocampus – a process that helps PTSD individuals to deal with consequential thoughts, behaviors and fears after the traumatic event.
Hypothesis – Process of memory channelization
If interventions such as psychotherapy can release the trapped emotions properly (van her Kolk et al, 1996; Straube et al, 2014) then we advocate the idea that psychotherapy is not only addressing these memories at psycho-social level, but also impacting 1) dendritic reformation, 2) cell body growth and 3) synaptic branches in the hippocampus with continued reinforcement and rehearsal (the process of memory channelization).
A question arises here, can dendritic connections be reformed and changes occur at a molecular level? If the dynamic nature of dendritic spine structures is necessary for plasticity at excitatory synapses (Kasai et al, 2010), and if emotionally-loaded memories are being stored and carried in the dendrites instead of being typically processed in the neuronal cell bodies then can reprocessing emotions in psychotherapy for trauma help to restore the healthy structural/anatomical and functional aspects of neuronal cell bodies in the hippocampus?
Would any neuroimaging study on cell body growth and dendritic structure indicate any physiological changes as a result of emotional processing through therapy? The proposed neuroimaging method most suitable for studying the proposed structural and temporal changes in hippocampal dendrites would be a molecular MRI.
Previous researches indicate that different psychotherapies do influence cognitive and emotional memory processing (Lane et al, 2015; Jaycox et al, 2002), but the new information of a neuroimaging (mMRI) technique on PTSD-related cases could add to the arena considerably.
The goal of future discourse in this regard would not be to diminish the importance and efficacy of medication, but to further enhance the understanding of the effects of psychotherapy at a molecular level.
Early exposure to therapy (for memory channelization and emotional processing) could improve a patient’s chance of early recovery from the trauma. Knowledge of neuroanatomical functions, particularly those of the dendrites in hippocampal neurons, would also be enhanced by such studies wherein progress and efficacy of psychotherapeutic interventions are measured by dendritic reformation and synaptic activity.
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