Neurological Consequences of Sexual Assault-Induced PTSD
How it works
This subject is important to me because I am a survivor of sexual assault. Going through this trauma made me feel very alone, and it took years of therapy to cope with what happened to me. My goal is to one day be a clinical therapist specializing in helping survivors of sexual assault. I hope to help them feel less alone, and to work with them so that this traumatic event does not define the rest of their lives and inhibit them from achieving their dreams.
According to Rape Abuse & Incest National Network (RAINN), one in six women in America has been the victim of an attempted or completed rape (“Scope of the Problem: Statistics” 1998). The prevalence of this crime demonstrates how imperative it is that we understand the effects it has on the victim. The psychological effects of this crime can, and often do, last a lifetime, with many victims suffering from post-traumatic stress disorder (PTSD) (should I cite 80% statistic?). Indeed, most of the discussion surrounding this issue focuses on its psychological effects on victims, but what are the neurological consequences of sexual assault-induced PTSD? Research in this area is important because the persistent traumatic memories that those suffering from sexual assault-induced PTSD experience has cascading effects on all aspects of their life. Re-living such a traumatic experience causes insomnia, hypervigilance, and increased anxiety (Brunet, Akerib, & Birmes, 2007). These negative affects further stress survivors, putting them at risk of becoming depressed, engaging in self-harming behavior, and committing suicide (“Effects of Sexual Violence” 2018). The more we understand the physical changes that happen in the brain after such a traumatic event, the more we can help survivors recover and protect them from these risks by developing more effective treatment options. Throughout this paper I will discuss some of the studies that have been done examining the effects that sexual assault-induced PTSD has on the brain, what those studies concluded, and what those conclusions mean for the future of treating this condition.
How it works
The amygdala is the primary focus of many studies on PTSD because it has been shown to be hyperactive in those suffering from this disorder. A hyperactive amygdala can impair memory function, automimic response, and the regulation of negative emotions such as fear (as cited in Protopopescu, Pan, Tuescher, Cloitre, Goldstein, Engelien Stern, 2005). In a study performed by Protopopescu et al., (2005) entitled “Differential Time Courses and Specificity of Amygdala Activity in Posttraumatic Stress Disorder Subjects and Normal Control Subjects” the authors found that when those suffering from PTSD were exposed to words associated with PTSD, the amygdala immediately became hyperactive, but the hyperactivity slowed as time progressed and the participants became habituated to those words.
These results are not surprising, as multiple studies have produced these same results. However, when the participants with PTSD in this study were exposed to words associated with panic (a neutral negative stimuli), their amygdala showed delayed hyperactivity when compared to participants in the control group. This research suggests that while the amygdala in those with PTSD reacts as expected to trauma-relevant stimuli, it responds differently to negative stimuli that is not related to the trauma. Instead of immediately becoming hyperactive, the amygdala of individuals with PTSD becomes sensitized to neutral negative stimuli later than those without PTSD.
The reason these results are significant is because the most common form of treatment for those suffering from PTSD is exposure therapy. Exposure therapy involves repeated exposure to memories associated with the traumatic event that caused the PTSD. The theory behind this treatment is that repeated exposure will create habituation to these memories and therefore reduce anxiety associated with the event. However, the results of this study suggest that when treating patients with exposure therapy, treaters need to carefully consider both the length of time a patient is exposed and the specific type of exposure (i.e. the words and memories used).
While exposure therapy is currently the most common used form of therapy to treat PTSD, it has limited success, as only 60% of those who complete treatment go into remission, according to a study cited by Cisler, Steele, Lenow, Smitherman, Everett, Messias, & Kilts, (2013, p. 47). In their own study, seeking to improve the efficacy of prolonged exposure therapy, Cisler et al. (2013) used functional magnetic resonance imaging (fMRI) to examine the effects of repeated exposure to the traumatic memory (RETM) on neural networks in those with sexual assault-induced PTSD. The results of this study indicate that repeated exposure therapy strengthens the connectivity of the anterior insular cortices with the amygdala, and the striatum with the hippocampus. The amygdala and hippocampus are significant because they are both involved in fear extinction (as cited in Cisler et al., 2013, p. 48). The amygdala detects and evaluates the conditioned stimulus (the memory of the event) and encourages the fear induced behavioral response. The hippocampus influences the amygdala to learn that it does not need to overreact to the conditioned stimulus in a safe environment. The striatum and anterior insular cortices, however, are involved in reward-based learning, and more importantly predicting the errors made through that form of learning (Cisler et al., 2013).
While conceding that more research needs to be done, Cisler et al. (2013) hypothesize that these findings may show the physical process of habituation in the brain. When the conditioned stimulus (traumatic memory) is presented without the traumatic event being present, (a prediction error is generated?) prediction errors are generated. Over time, the response to those prediction errors teach the brain that it does not have to overreact to these memories, thus creating habituation/fear extinction. The theory proffered by Cisler et al. (2013) is that the strengthened connectivity with the striatum and anterior insular cortices integrates the tracking of prediction errors with the areas of the brain responsible for fear extinction (the amygdala and hippocampus). This process teaches the brain that thinking about the traumatic event does not predict the traumatic event and thus there is no need to become hyperactive. The study concludes that more research in this specific area may help improve the efficacy of prolonged exposure therapy, which is welcome news because it does not call for a completely new approach to treating sexual assault-induced PTSD.
Although improving the efficacy of exposure therapy is important, determining the specific changes in the brain that this trauma causes is critical to improved treatment for survivors as well. In a research paper by Quidé, Cléry, Andersson, Descriaud, Saint-Martin, Barantin, El-Hage (2017) titled “Neurocognitive, Emotional and Neuroendocrine Correlates of Exposure to Sexual Assault in Women” the researchers looked at the early effects of being sexually assaulted behaviorally, cognitively, and biologically. The authors note that to the best of their knowledge, this is the first study that compares the neurobiological and neurophysiological effects that happen quickly after a woman experiences a sexual assault. By looking into these initial changes, we can perhaps identify which structures are affected early on, which may be able to help prevent the emotional symptoms from progressing and become chronic.
The experiment took twenty-seven female survivors who had all been assaulted within the previous four weeks and compared the results of multiple tests with those of an age-matched control group. One of the tests performed included measuring the participants diurnal salivary cortisol level. Cortisol, which is produced by the adrenal glands, is the main stress hormone in the body and contributes to our “flight or fight response (“What is Cortisol” 2018). Both high and low levels of cortisol can cause anxiety and depression. The results of this study showed that the cortisol levels of sexual assault survivors were significantly lower in the morning than those in the control group. Surprisingly, despite the low morning cortisol levels, they performed better on executive functioning tasks (Quidé et al., 2017). While more studies are needed to confirm these results, these findings suggest that survivors of sexual assault do not demonstrate the same cognitive deficits as those who experience chronic PTSD, which can dictate how to treat survivors after they are sexually assaulted. In other words, differences between sexual assault-induced PTSD and PTSD caused by other traumas suggests that the type of early interventions or personalized therapy could be tailored to the specific trauma, and sexual assault-induced PTSD could possibly prevent the disorder from developing into chronic PTSD.
In another study of brain activity by S. Kim, Chung, B. Kim, Lee, Yoon, and An (2011), the researchers used multiple functional neuroimaging techniques to look at how neural pathways are affected in a person diagnosed with sexual assault induced PTSD, and how the disruption of these pathways leads to the neurophysiologic symptoms experienced by those with PTSD. The reason this study is noteworthy is because while multiple studies have shown that PTSD modifies neural activity, when it comes to the specific neural patterns that are created as a result of PTSD, the previous results have been inconsistent. This study, however, confirmed that PTSD causes a pattern of decreased blood flow and glucose metabolism in the hippocampus. These changes may be connected with the memory problems and difficulties extinguishing learned fear responses that those suffering from PTSD experience. This study also showed that PTSD patients had considerably higher glucose metabolic activity in both the right and left hemispheres of the cerebellum, which may explain other symptoms that PTSD patients experience, such as hyperarousal, exaggerated startle response, abnormal sleep patterns, and an increased heart rate.
Thus, the altered neural activity patterns seen in this study, shown through the use of neuroimaging techniques, are strongly associated with the neurobiological signs of PTSD. By locating which neural areas are modified because of trauma, future research can be focused on these areas in order to develop new treatments for symptoms such as repeated memories, hyperarousal, and insomnia that consume those suffering from PTSD.
While there have been numerous studies done on how PTSD alters neural function, there is less literature on how these changes can lead to revictimization because of the social deficits these alterations create. In another study by Cisler, Bush, Steele, Lenow, Smitherman and Kilts (2015), the researchers cite several studies that lead them to theorize that survivors of physical (not just sexual) assault have a harder time determining the amount of risk in social situations. They also theorize that the more exposure that survivors have to assault and the more severe their symptoms of PTSD are, the more they are likely to be revictimized.
Cisler et al. (2015) note that these theories cannot be explained by the known neural modifications caused by PTSD. For example, the increased activity in the amygdala that is seen in those suffering from PTSD would ordinarily lead to the conclusion that the survivor would be better able to predict the level of risk in social situations since this hyperactivity facilitates an attention bias towards threats, but the research suggests the opposite happens. Therefore, Cisler et al. (2015) hypothesized that not only does assault-induced PTSD alter neural connections, it also alters social learning behavior.
In order to test their hypothesis in this study, Cisler et al. (2015) had participants with assault-related PTSD and a control group of participants who had no history of assault exposure complete a multi-trail trust game, and then had a subset of those participants complete both a social and non-social reinforcement learning task while undergoing an fMRI. The results of this study showed that after the trust game, those with PTSD had a harder time returning to baseline levels of trust compared to those in the control group. The results of the reinforcement task suggest that prediction errors have less of an impact on future behavior for those with PTSD compared to those without PTSD. The results further suggest that those with PTSD have a more difficult time revising their expectations in social settings that is to say as the social environment around them changes, it is harder for them to alter expectations of that situation. These results also suggest that those with PTSD do not rely on social experiences to guide their decisions in social settings as much as those without PTSD do.
The results of the fMRI showed that the women with PTSD related to sexual assault experienced a negative relationship between social expectations and activity in the following areas of the brain: the perigenual anterior cingulate cortex (pgACC) which is involved in emotional regulation, the left temporoparietal junction (TPJ) which is associated with the ability to develop ideas about the mental states of others, the middle frontal gyri (bilateral MFG) which is involved in semantic processing, and the dorsomedial prefrontal cortex (dmPFC) which is involved in various complex cognitive processes (Cisler, et al., 2015). This suggests that PTSD alters these areas of the brain, causing the brain to encode a negative expectation of social situations, which creates a constant state of hypervigilance. What Cisler et al. (2015) believe is a plausible conclusion to be drawn from these results is that after a person with PTSD experiences a constant heighted state in which one is expecting a negative outcome, but then that outcome does not happen, the brain learns to ignore the danger signals it is sending out, which can then unfortunately increase the risk of danger to the person.
Interestingly, the researchers note that the negative relationship with the TPJ also suggests that it is harder for those with PTSD to understand the intentions of others when experiencing prediction errors in a social setting. However, because the TPJ is associated with various other cognitive processes, more research is needed before definitively saying that it is responsible for this specific deficit in understanding (Cisler et al., 2015).
The results of this study show how the neurological changes that occur due to sexual assault-related PTSD may impact social behavior in a way that puts survivors at risk for revictimization. By not relying on past experiences to guide decisions, ignoring danger signals, and having increased difficulty reading others’ intentions, along with difficulty in changing expectations as the environment changes, it is easy to see how these social deficits can lead to revictimization. Therefore, future treatment can be modified to address specific behavioral factors as well as neurological factors.
All of these studies all lead to a greater understanding of the greatly-underreported condition of sexual assault-induced PTSD. According to a Detroit Area Survey of Trauma, 80% of survivors of sexual assault suffer from PTSD (Breslau, Davis, Andreski, & Peterson, 1991), and unfortunately, it is a problem with no outward symptoms. Therefore, is so important to continue to research the neurological effects sexual assault-induced PTSD has on the brain so that there is a better understanding of the condition for both treaters and victims so that more victims will recognize the condition. Additionally, further research will lead to improved and expanded treatment options so those who are treated achieve better results.
As we can see from these studies, multiple areas of the brain are affected by sexual assault, and the effects occur in many different ways. These studies make clear that a better understanding of which areas of the brain are affected by sexual assault-induced PTSD and how these effects alter brain activity will directly lead to more effective treatments of the condition by targeting the specific processes at issue. Because of the wide-ranging impact of the condition on nearly all aspects of a survivor’s life, these treatments will unquestionably improve the lives of survivors immensely. However, as the studies cited herein explicitly concede, more research is needed in these areas, and the work is far from done. Nevertheless, they do provide hope for the future.