Child sexual abuse versus adult sexual assault: A review of psychological and neurobiological sequelae

Abstract

Sexual trauma (ST) occurs with alarming frequency in the United States (U.S.) in the form of both childhood sexual abuse (CSA) and adulthood sexual assault (ASA). It is well-established that the effects of ST are pervasive, and that ST can be a risk factor for the development of several psychiatric disorders. However, the potential for distinct psychological consequences or neural correlates between CSA and ASA has received little attention. Furthermore, despite the high prevalence of sexual revictimization, the combinatorial effects of CSA and ASA are understudied in comparison to each form of ST on its own. In the current review, we present results from both clinical psychology and neuroscience research on the impacts of CSA and ASA, describing major psychological, biopsychosocial, and neuroimaging findings for each form of ST. We further highlight limitations in the current state of the research and needed areas of future research to better understand the distinct, overlapping, and cumulative effects of ST in both childhood and adulthood. The present study summarizes the state of the literature on this critical form of trauma and provides recommendations for future clinical research practices to mitigate the deleterious outcomes of ST.

1. Introduction

Sexual trauma (ST) occurs pervasively across the world with emotionally and socially devastating consequences that disproportionately impact women and girls (Finkelhor et al., 2014; Kessler et al., 1995). In the United States (U.S.) alone, research suggests that 15-32% of girls will experience childhood sexual abuse (CSA) in their lifetimes (Briere & Elliott, 2003; Finkelhor et al., 2014; Vogeltanz et al., 1999), and 13-25% of women will be sexually assaulted in adulthood (ASA) (Dworkin et al., 2017; Elliott et al., 2004; Gillespie et al., 2009). Further, 5-14% of boys will experience CSA (Briere & Elliott, 2003; Finkelhor et al., 2014) and 1-4% of men will experience ASA (Breiding, 2014; Elliott et al., 2004), with higher prevalence among gay men (Peterson et al., 2011). From a psychiatric perspective, ST conveys higher risk for posttraumatic stress disorder (PTSD) than other types of traumatic events (Kelley et al., 2009; Kessler et al., 1995; Norris, 1992). Further, ST elevates risk for other types of psychopathology including depression, anxiety, bipolar disorders, disordered eating, problematic substance use, and suicidality (Dworkin et al., 2017; Molnar et al., 2001; Paolucci et al., 2001; Thompson et al., 2003).

Despite the documented effects of ST, whether CSA and ASA have distinct psychological outcomes remains poorly understood. Prior work suggests certain types of psychological effects and their severity due to CSA may depend on the timing of exposure during specific developmental windows (e.g., Dunn et al., 2018; Ogle et al., 2013). However, other research suggests ASA may be more likely to result in PTSD than CSA because an adult’s cognitive abilities contribute to heightened processing of trauma-specific information (Xu et al., 2013). There is also evidence suggesting revictimization may be the strongest predictor for adverse outcomes (Arata, 2002; Rowland et al., 2022). Disentangling the differential impacts of CSA and ASA on psychological domains has the potential to significantly impact approaches to precision psychiatry. For example, doing so may enhance prediction of individual susceptibility to, and variation within, psychological outcomes. Better understanding of outcomes of different types of ST may also inform future selection of evidence-based treatments that have the greatest likelihood of success.

Sexual trauma may also have unique neurobiological effects compared to other trauma types. Sexual assault-related variability in the brain may be both structural and functional; for example, repeated CSA especially between the ages of 3 and 5 is associated with reduced hippocampal volume (Andersen et al., 2008). Evidence also suggests that in the first month post-sexual assault there are alterations in resting-state intrinsic connectivity in adult women (Quidé et al., 2021). A more fine-tuned understanding of the neural circuits affected by CSA and ASA may contribute to more targeted neuromodulatory interventions. For example, there is compelling evidence that transcranial magnetic stimulation (TMS) may be an effective treatment for disorders resulting from trauma including PTSD and generalized anxiety disorder (Cirillo et al., 2019; Karsen et al., 2014). Knowledge of ideal target regions for TMS interventions based on trauma type may be influential in improving outcomes. Furthermore, treatment outcomes for PTSD may be predicted by varying patterns of brain activation, and increased activation in certain brain areas (e.g., amygdala) may be implicated in trauma-focused therapy (Van Rooij et al., 2016). Thus, identification of neural alterations related to ST type could inform prediction of recovery trajectories and needed interventions for those most at risk for more persistent forms of PTSD. However, there is currently limited knowledge about the potentially distinctive impacts of CSA versus ASA on both psychological and neurobiological outcomes.

In addition, it is clear that childhood maltreatment in general, and CSA in particular, has significant potential to disrupt neurodevelopment in ways that transpose risk for psychiatric conditions (Cassiers et al., 2018; Teicher et al., 2002). More precise knowledge of the specific neurodevelopmental effects of CSA could allow for earlier, more targeted neurobiological-based interventions and pharmacological treatments to mitigate or even prevent downstream effects from manifesting in the form of severe psychopathology.

In the current review, we discuss findings from clinical psychology and neuroscience research on the impacts of CSA and ASA. We describe the major psychological and broader biopsychosocial impacts of ST throughout the lifespan, as well as findings from neuroimaging studies, to highlight differential effects of CSA and ASA. Finally, we highlight needed areas of investigation to understand the unique, overlapping, and combinatorial effects of ST at different life stages. The present review provides an overview of the psychological and neurobiological impacts of sexual trauma during different developmental periods and provides a framework for further investigations of this topic.

2. Psychological and behavioral sequalae of sexual trauma

Several hypotheses attempt to explain the especially deleterious psychological effects of ST as compared to other trauma types. The greater conditional risk of psychopathology after ST may be because interpersonal traumas have the capacity to alter an individual’s perceptions about the safety, predictability, trustworthiness, and fundamental goodness of others in a way that accidents and natural disasters do not (Forbes et al., 2011; Kelley et al., 2009). It follows that ST may be a particularly salient form of interpersonal trauma in terms of adverse outcomes. Rose (1986) posited that ST is especially traumatic because of the threat of loss of life, both literally and in the sense that important aspects of the self are destroyed; in this way “[r]ape disrupts the sense of autonomy, control, and mastery over one’s body” (p. 820), as does CSA. Other proposed reasons for the distinctiveness of ST draw on the role of rape myth acceptance and cognitive theories. One such prominent theory is the just-world belief, which holds that individuals’ actions determine what happens to them, providing a sense of agency and predictability in the world (Hayes et al., 2013; Lerner, 1965). When a just-world belief is held by those who have experienced or learned of ST, it may lead to self-blame and/or victim-blaming, which have implications for psychopathology and treatment outcomes (Foa et al., 1989; Moor, 2007; van der Bruggen & Grubb, 2014). In sum, cognitive processes underlying effects of ST are distinct from other trauma types. Below, we discuss evidence on the behavioral and psychological outcomes of CSA and ASA.

2.1. Childhood sexual abuse (CSA)

2.1.1. Psychological outcomes

CSA has negative impacts on mental health through the lifespan. PTSD is the most commonly diagnosed psychopathology following CSA victimization (Maniglio, 2013; Paolucci et al., 2001; Trask et al., 2011; Weinstein et al., 2000). PTSD symptoms include unwanted and intrusive memories of the abuse, avoidance of internal and external reminders of the abuse, negative changes in mood and cognition, and alterations in arousal and reactivity related to the trauma (American Psychiatric Association, 2013). A dissociative subtype of PTSD includes symptoms of depersonalization and derealization and is associated with markedly different neurobiological responses from typical PTSD (Lanius et al., 2012). Of note, pediatric presentations of PTSD can differ slightly in form from presentations of PTSD in adulthood, with recollections of the trauma more likely to manifest in daydreams and be reenacted in play, rather than as visual flashbacks (Carrion et al., 2002; Scheeringa et al., 1995). When evaluated in both clinical and nonclinical samples, prevalence estimates of PTSD in CSA survivors (both child and adult populations) range from 38%–64% (Carey et al., 2008; McLeer et al., 1988; Widom, 1999).

Anxiety disorders and major depressive disorder (MDD) are also observed following CSA, with prevalence between 24-31% (anxiety disorders) and 20-28% (MDD) (Adams et al., 2018; Amado et al., 2015; Kisiel et al., 2014; Maniglio, 2013). In a large general population study, Briere and Elliott (2003) found that CSA was associated with higher anxiety and depression symptoms, irritability, and intrusive experiences after controlling for sociodemographic variables and other co-occurring or subsequent trauma. CSA survivors also show higher prevalence of other disorders including attention-deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), substance use disorders (SUDs), conduct disorders, and dissociative disorders (Caspi et al., 2008; Fergusson et al., 1996; Maniglio, 2013; Trickett et al., 2011; Weinstein et al., 2000). Dissociative disorders in particular are very likely to be preceded by CSA, and in a psychiatric population, 74% of those with dissociative disorders reported CSA (Foote et al., 2006). The link between CSA and dissociation is likely related to the child’s inability to fight or flee from the abuser, as CSA often involves significant violence such as choking (Kate et al., 2021).

However, despite the clear link between CSA and psychiatric disorder development, there remains significant heterogeneity in mental health outcomes, and the reasons for the variability are not well understood. For example, the use of more adaptive or maladaptive coping strategies in the aftermath of abuse may predict PTSD symptoms (Filipas & Ullman, 2006), and reactions to disclosure of CSA play a significant role in survivors’ well-being (Brenner & Ben-Amitay, 2015; Ullman, 2003). Mental health outcome variability may also be due to the significant heterogeneity in abuse characteristics that can constitute CSA severity, such as perpetrator type, the use of threat or violence, and duration and frequency of abuse (Yancey & Hansen, 2010). A relatively more recent concern has been whether CSA is commodified online as child sexual abuse material, and how this may further contribute to the severity of abuse and its psychological outcomes (Salter & Whitten, 2022). Aggregate measures of CSA “severity” may overly reduce these important variables leading to inconsistent prediction of mental health outcomes. Standardization of assessments for abuse characteristics and environmental factors will contribute to more conclusive understanding of individual susceptibility to adverse psychopathology.

2.1.2. Behavioral outcomes

CSA is further associated with deleterious alterations in behavior. CSA survivors are more likely than their peers to display disturbances in sleep, develop disordered eating, and experience disruptions in academic performance (e.g., lower GPA) (Browne & Finkelhor, 1986; Chandy et al., 1996; Mitchell et al., 2021; Noll et al., 2006). In a large cohort of adults, history of CSA was associated with a significantly increased risk of problematic substance use and interpersonal difficulties (i.e., marital and family conflicts) (Dube et al., 2005). CSA survivors further appear to engage in behaviors that carry a high risk of harm such as risky sexual behavior (e.g., greater number of partners, unprotected sex), sex work, and both suicidal and non-suicidal self-injury (Browne & Finkelhor, 1986; Fergusson et al., 1996; Kisiel et al., 2014; Kisiel & Lyons, 2001; Lacelle et al., 2012). Of note, these behaviors can also be associated with increased risk of revictimization (Lalor & McElvaney, 2010; Messman-Moore & Long, 2003).

The effects of CSA on behavior go above and beyond the effects of often co-occurring childhood maltreatment or polytrauma (Arata et al., 2007; Fergusson et al., 2008; Hébert et al., 2018; Lacelle et al., 2012; Lewis et al., 2016; Senn & Carey, 2010). Evidence suggests that behavioral outcomes of CSA may also differ by sex, such that male adolescents display more externalizing problems and female adolescents display more internalizing problems. Specifically, male teenagers may be more likely to display poor school performance and engage in delinquent behaviors (e.g., vandalism, fighting, stealing, cheating) and sexually risky activities (e.g., younger age at onset of sexual activity, less frequent use of protection), while female teenagers are at higher risk for suicidal ideation and behavior and disordered eating behaviors (Chandy et al., 1996). However, as with psychological outcomes, accurate predictive models for behavioral outcomes remain elusive. In summary, adverse behavioral sequalae often coincide with psychopathology following CSA.

2.1.3. Developmental timing

There is mixed evidence regarding whether the timing of CSA relative to early developmental stages may confer differential risk for psychological outcomes. Some studies suggest that later age of abuse in childhood was associated with greater psychological symptomatology overall (Briere & Elliott, 2003) and a greater relative risk for more severe PTSD specifically (Schoedl et al., 2010). This may be because when CSA occurs later in childhood, older children’s more mature brains can ruminate about the abuse when it is not occurring and thus experience more depression and anxiety symptomology (Adams et al., 2018). However, there is also evidence that earlier age of abuse is associated with a greater relative risk of having severe depressive symptoms in adulthood (Schoedl et al., 2010). Furthermore, one study found that CSA before age 5 was a stronger predictor of adult depression and PTSD than later CSA (Jaye Capretto, 2020). Earlier age of CSA onset was also associated with a greater likelihood of anxiety and arousal symptoms at time of disclosure (Kaplow et al., 2005).

Differing methodology may explain these discrepancies, given that some studies assessed symptoms in childhood (as in Kaplow et al., 2005), and some retrospectively in adulthood (as in Briere & Elliott, 2003; Schoedl et al., 2010), introducing large variability in years since exposure and thus potential differences in the dampening of effects over time. Another challenge within the childhood maltreatment literature is the lack of a standard for classifying developmental timing groups, making it difficult to compare across samples (e.g., ages 13-18 may be considered late childhood, as in Jaye Capretto (2020), or adolescence, as in Dunn et al. (2017)). Identification of vulnerability windows for specific symptoms may further contribute to more specialized, targeted treatment interventions for CSA survivors.

2.1.4. Section summary

In summary, CSA confers an increased risk for psychopathological and behavioral sequalae, and this risk is increased beyond other types of childhood maltreatment and independent of polyvictimization. Consideration of age of abuse as well as certain abuse characteristics are predictive of later outcomes, but identifying a consistent pattern to inform diagnosis and treatment remains difficult within the current literature.

2.2. Adult sexual assault

2.2.1. Psychological outcomes

As seen in CSA, ASA is a risk factor for nearly every psychiatric condition (Dworkin et al., 2017), with comorbid PTSD and depression most common following victimization (Basile et al., 2016; Ullman et al., 2007). Therefore, ASA may contribute to a more general posttraumatic response rather than the formation of distinct disorders (Au et al., 2013; Zinzow et al., 2012). Other prevalent psychiatric outcomes that often co-occur with PTSD after ASA include anxiety disorders, SUDs, disordered eating, dissociation, and suicidality (Dancu et al., 1996; Dworkin et al., 2017; Iverson et al., 2013; Nöthling et al., 2015; Ullman et al., 2006; Xu et al., 2013; Zinzow et al., 2012). The comorbidity between problematic alcohol use and PTSD may be explained by the self-medication effect, by which drinking to cope with distress due to ASA results in more PTSD symptoms rather than less (Ullman et al., 2013). Across diverse samples, binge drinking and nicotine use are each more common in those with prior ASA than those without (Basile et al., 2016; Xu et al., 2013).

However, understanding of how ASA characteristics may contribute to risk for specific sequalae is limited. There is evidence to suggest that rape involving both substance facilitation and forcible tactics (i.e., using force or threatening to harm) is associated with the highest prevalence of PTSD, major depressive episodes, and problematic alcohol use (Zinzow et al., 2012). However, other aspects of ASA including pre-traumatic risk factors, peri-traumatic responses and post-traumatic reactions may confer differential outcomes, and their individual contributions to psychopathology have not yet been elucidated (Elliott et al., 2004; Ullman et al., 2007; Xu et al., 2013).

Further, individuals who have experienced ASA are more likely to have a history of CSA than those who have not experienced ASA, making it difficult to disentangle psychiatric consequences of one experience from the other (Elliott et al., 2004). In a large nationally representative sample, it was rare for individuals without a history of CSA to report ASA (only 2.5%) (Xu et al., 2013). Other national prevalence estimates suggest that just 30-39% of individuals first experience sexual victimization after the age of 18, again supporting that the majority of ST begins in childhood (Basile et al., 2007). Future work is needed to understand the interplay and differential effects of ASA and CSA (e.g., Elliott et al., 2004; Rowland et al., 2022; Ullman et al., 2013) to better understand potentially unique outcomes of ASA in adults.

2.2.2. Behavioral and psychosocial outcomes

ASA is further associated with adverse behavioral and psychosocial outcomes. Psychosocial sequalae are more broad than just mental health outcomes, encompassing physical and social health as well as aspects like coping strategies, social support, and social reactions from others (Holder et al., 2023; Ullman et al., 2007). In a sample that distinguished between ASA, CSA, and military sexual assault, ASA was associated with poorer physical health functioning, health satisfaction, social functioning, and social satisfaction than CSA or military sexual assault alone (Holder et al., 2023). Emotional distancing, social withdrawal, and decreased involvement in social activities were also apparent after ASA (Peterson et al., 2011; Walker et al., 2005).

Importantly, reactions from others to disclosures of ASA also play a role in subsequent psychosocial functioning (Dworkin et al., 2019; Ullman, 1999; Ullman et al., 2007; Ullman & Peter-Hagene, 2014). Positive reactions (e.g., emotional support, being believed, not being blamed) from others to ASA disclosure may contribute to better emotional health, physical health, and posttraumatic growth and adjustment (Borja et al., 2006; Orchowski et al., 2013; Ullman, 2014). Negative reactions (e.g., victim-blaming, disbelief) are associated with PTSD symptoms, hindered recovery and poorer adjustment (Campbell et al., 2001; Orchowski et al., 2013; Ullman, 1996; Ullman & Peter-Hagene, 2014), even after controlling for demographics, trauma history and assault-related factors (Ullman et al., 2007). Timing of disclosure also appears to be important, with delayed disclosure associated with more severe PTSD symptoms (Ullman et al., 2007). However, the interplay between reactions from others and social withdrawal, engagement, and support is complex and highly inter-related, and this dynamic is necessary to disentangle in future investigations of the psychosocial outcomes of ASA.

ASA is also linked to poorer psychological functioning in education and career domains which are especially relevant given the high prevalence of ASA on college campuses (Krebs, 2005; Mellins et al., 2017). Among college students, ASA is associated with poorer academic achievement, including lower GPA and scholastic conscientiousness as well as increased class absences, likelihood of taking time off, dropout rates, and taking longer to complete degrees (Banyard et al., 2020; Mengo & Black, 2016; Molstad et al., 2023; Potter et al., 2018). These academic effects often persist long-term, resulting in negative professional outcomes and significantly disrupted occupational functioning as well. Survivors of ASA may take time off, experience difficulties in performance, or leave their jobs due to increased psychopathology, vulnerability following assault, or time-consuming involvement in the legal system (Potter et al., 2021; Resick et al., 1981). Adverse career outcomes in the form of lost work productivity may partially account for the substantial per-victim cost of rape ($122,461) and on a larger scale, the lifetime economic burden of rape ($3.1 trillion) (Peterson et al., 2017). However, whether it is the direct effect of ASA itself or its many downstream consequences (e.g., time spent in Title IX or legal investigations) that are responsible for the negative impacts detailed above is a question that merits further investigation. Regardless, the devastating educational, occupational, and financial outcomes of ASA for individuals are an added burden to the psychological, behavioral, and psychosocial challenges.

2.2.3. Section summary

In summary, ASA is associated with negative outcomes including risk for multiple psychiatric diagnoses and/or increased severity of symptoms, psychosocial impairment, and disrupted academic and career performance. However, given the high rate of CSA among those with ASA and varying methods across investigations, the precise contributions of ASA alone toward these domains remain opaque. Controlling for CSA and other lifetime trauma should be employed more consistently in psychological research to better elucidate these effects.

3. Neurobiological outcomes of sexual trauma

Extant literature suggests ST both in childhood and adulthood is associated with alterations in brain function and structure. Specifically, prior research suggests that ST is associated with changes in neurocircuitry that supports threat processing such as the amygdala, hippocampus, and prefrontal cortex (PFC) (Andersen et al., 2008; Cassiers et al., 2018; Stein et al., 1997). However, the neurobiological impacts of ST may be related to its timing and may also affect other brain regions and circuits. For example, CSA may disrupt typical development of sensory regions given the significant maturation that happens in childhood and adolescence (Sydnor et al., 2023; Teicher et al., 2016). A complication in the literature is the relative sparsity of research investigating the effects of CSA or ASA specifically on the brain. Below, we highlight literature on neural circuitry associated with adverse effects of ST with a focus on research that has specifically investigated ST differentiated from other forms of trauma, as well as relevant gaps in our collective knowledge.

3.1. Childhood sexual abuse

3.1.1. Sensory cortices

Research suggests that CSA exerts significant adverse influence on sensory cortices, which are among the earliest parts of the brain to develop (Sydnor et al., 2023; Teicher et al., 2016), with the visual cortex as particularly sensitive (Kim et al., 2023; Tomoda et al., 2012). In adults with a history of CSA and an MDD diagnosis, gray matter volume (GMV) in the right middle occipital gyrus was significantly decreased in comparison to those without CSA or a psychiatric diagnosis (Kim et al., 2023). Greater duration of CSA (i.e., years between age of first abuse and age of last abuse) was associated with reduced GMV if CSA began prior to age 12, but there was no association in individuals with CSA that began after 12, suggesting that there may be a sensitive period for the maturation of the visual cortex related to the onset of puberty (Tomoda et al., 2009). Prior work found that women with CSA-related PTSD showed decreased blood flow in a visual association cortex in response to autobiographical scripts of CSA (Bremner et al., 1999). Further, CSA has been associated with cortical thinning in areas of the primary somatosensory cortex associated with genital representation, and this effect was specific to CSA among other types of childhood maltreatment (Heim et al., 2013). Together, these data suggest that sensory cortices, likely due to developmental trajectories and neuroplasticity early in life, are especially vulnerable to the effects of CSA. Thus, during sensitive developmental windows in childhood, these sensory cortices may adapt themselves to provide protection from the observed deleterious effects of CSA on typical cortical development of sensory processing regions.

3.1.2. Hippocampus

CSA is also associated with alterations in the hippocampus. Individuals with CSA show lower hippocampal volume relative to those without CSA (Andersen et al., 2008; Bremner et al., 1997, 2003; Stein et al., 1997); however, this finding is not replicated in all of the literature (e.g., (Rinne-Albers et al., 2017; Teicher et al., 2003). It may be that there are specific windows of developmental sensitivity, such as ages 3-5 and 11-13, where CSA may have a more pronounced effect on the hippocampus (Andersen et al., 2008). CSA is also related to decreased stress-elicited hippocampal activity, blood flow, and stress-elicited activation in the hippocampus in functional neuroimaging studies (Bremner et al., 1999, 2003; Purcell et al., 2021). Given the importance of the hippocampus to emotion and memory, and consistent findings of atrophy in adulthood PTSD (Logue et al., 2018), effects of CSA on the hippocampus may contribute to increased risk of developing psychopathology in adulthood.

3.1.3. Prefrontal cortex

There is also evidence that suggests CSA may affect subdivisions of the PFC. Young adults who reported high levels of CSA showed lower stress-elicited activity in ventromedial PFC (vmPFC) and dorsolateral PFC (dlPFC) during a psychosocial stress task (Purcell et al., 2021). Furthermore, in response to CSA memories during script-driven imagery, Bremner and colleagues (1999) observed decreased blood flow in medial PFC in adults. Functional activity in medial PFC during fear extinction was also decreased in a group with CSA-related PTSD compared to healthy controls (HCs) (Bremner et al., 2005). Reports of structural alterations in the PFC are much more limited, though Andersen and colleagues (2008) reported decreased GMV in the PFC associated with CSA between the ages of 14 and 16. In adolescents, significantly reduced GMV in dorsal anterior cingulate cortex (dACC) was observed in those with CSA-related PTSD compared with healthy controls (Rinne-Albers et al., 2017). Together, these data suggest that CSA disrupts function and potentially structure of the PFC in ways that persist into adulthood.

3.1.4. Amygdala

Though often implicated in the broader trauma literature, findings linked to amygdala structure and function are far less conclusive in relation to CSA. Several studies have observed no effect of CSA on amygdala volume (Andersen et al., 2008; Bremner et al., 1997; De Bellis et al., 2001). However, there is some evidence for functional alterations in the amygdala related to CSA. An early PET neuroimaging study found that women with a history of CSA and PTSD had increased amygdala activation to fear acquisition during a fear conditioning task (Bremner et al., 2005). Furthermore, CSA was related to increased right amygdala activity during a negative mood induction task (Yamamoto et al., 2017). A group of adolescents with CSA-related PTSD also had increased amygdala activation, as well as relatively fast habituation, during an emotional face-processing task compared to a group with internalizing disorders but not CSA (van den Bulk et al., 2016).

3.1.5. Corpus callosum

CSA has also been linked to volume loss in the corpus callosum (CC), the white matter structure that connects the left and right hemispheres (Hart & Rubia, 2012). Findings of CC alterations are well-established in relation to childhood maltreatment in general and are thought to be related to adverse effects of stress hormones on myelination of white matter tracts (Jackowski et al., 2008; Teicher et al., 2004, 2010). In a sample of adolescents with PTSD secondary to CSA, fractional anisotropy (FA; a measure of white matter microstructure) was decreased in the CC relative to HCs, and this reduced white matter integrity was related to anger symptoms (Rinne-Albers et al., 2016). CSA was more strongly associated with reduced CC volume in girls than neglect, physical abuse, or PTSD, though this relationship was not present in boys (Teicher et al., 2004). CC volume may be particularly vulnerable to CSA occurring in middle childhood (ages 9-10; Andersen et al., 2008). Thus, the effects of CSA on white matter structure in the CC are therefore likely dependent on sex and age at which the abuse occurred.

3.1.8. Section summary

The current state of the literature suggests that CSA disrupts normal development of sensory cortices and brain regions critical for threat processing (Andersen et al., 2008; Bremner et al., 1999, 2005; Heim et al., 2013; Tomoda et al., 2009), potentially conferring greater vulnerability to the development of later psychopathology such as PTSD and MDD. More recent work suggests that other regions may be playing a role as well, including the ITG. Specifically, CSA-related MDD was associated with abnormal brain activity measured by amplitude of low-frequency fluctuations in the right inferior temporal gyrus (Liu et al., 2023). This is consistent with new work showing that ITG connectivity is related to future PTSD symptoms (Harnett et al., 2021). More broadly, results suggest that total GMV was significantly reduced in correlation with severity of CSA in patients with psychotic disorder (Sheffield et al., 2013).

However, several limitations are present in the neuroimaging literature that should be considered. First, in samples that do not account for psychiatric diagnoses, it is difficult to determine whether alterations in brain structure and function are the result of CSA itself or of CSA-related psychopathology (e.g., Bremner et al., 1997; Kim et al., 2023; Rinne-Albers et al., 2017; Rinne-Albers et al., 2016; Sheffield et al., 2013). Another limitation is that many studies do not specifically investigate neurobiology of CSA survivors but rather those with childhood maltreatment in general. Especially in childhood trauma research, it is common for studies to conduct analyses with general questionnaires to measure childhood trauma and may then investigate specific subtypes of endorsed maltreatment (e.g., Kim et al., 2023; Liu et al., 2023). While general questionnaires can increase sample size, it is more difficult to determine the unique neurobiology of CSA compared to other childhood trauma experiences. Further work is needed to better understand if neural alterations are consequences of childhood trauma in general or specific to CSA. Another common limitation is that sample sizes for many studies are small and may result in findings that are not replicable. Further, several studies did not include non-trauma-exposed control groups for comparison to determine if effects are trauma-specific (e.g., Bremner et al., 1999; Shin et al., 1999). Ongoing work should seek to include multiple control groups as feasible, such as including a non-trauma-exposed control group and a trauma-exposed group without a psychiatric diagnosis (e.g., Bremner et al., 2003). Doing so would isolate the effects of CSA alone from CSA with a resulting psychiatric diagnosis or co-occurring trauma and allow for more nuanced discussion of how CSA affects brain structures. Finally, cross-sectional studies cannot determine causal relationships and prospective, longitudinal investigation would provide valuable insight into the neurobiological effects of CSA.

3.2. Adult sexual assault

3.2.1. Sensory cortices

ASA is also associated with alterations in both brain structure and function. ASA may be associated with alterations in sensory cortices, though evidence is more preliminary. Adults with ASA and PTSD show reduced gray matter density (GMD) in fusiform gyrus compared to HCs (Sui et al., 2010b), but also showed increased GMD within the inferior parietal lobule (Sui et al., 2010a).

3.2.2. Subcortical regions

As was observed in CSA literature, the reductions in GMD are not specific to sensory regions, and adults with ASA also show decreased GMD in threat-related brain regions such as the amygdala and hippocampus (Sui et al., 2010b). Decreased hippocampal volume, however, may not uniquely be a consequence of ASA, as prior work found that lower hippocampal volume in the early aftermath of ASA was associated with future PTSD symptoms (Quidé et al., 2018a). Finally, ASA was more strongly linked to overall white matter hyperintensity (WMH) volume, an early marker of brain disease, than any other type of trauma, although this was most pronounced for parietal lobe WMHs (Thurston et al., 2022). Taken together, these data suggest that both sensory cortices and regions involved in threat processing may be affected by ASA, but it is unclear if the effects are due to trauma itself or are outcomes of development of psychopathology.

3.2.3. Prefrontal regions

Furthermore, several functional neuroimaging studies of individuals with ASA suggest that the experience impacts multiple regions involved in emotion regulation. New and colleagues (2009) found in a sample of women that regardless of PTSD status, ASA was related to impeded ability to downregulate emotional responses in regions of the PFC in response to negative stimuli. Similarly, when processing emotional material, ASA was associated with a lack of deactivation in the right dorsal anterior cingulate cortex (dACC) and superior frontal gyrus (Quidé et al., 2018b). As in New et al. (2009), this finding was specific to ASA rather than PTSD status. Though the amygdala has been hypothesized to be related to ASA, as with CSA, there is not clear evidence that amygdala function is impacted by this trauma type. New and colleagues (2009) did not observe group differences in amygdala responsiveness during emotional processing between those with ASA and HCs. Furthermore, there was no association between amygdala reactivity or habituation to fearful faces and ST in trauma-exposed samples (Rowland et al., 2022, 2023). Therefore, ASA may not exert a uniform influence on all regions typically involved in emotion regulation.

3.2.4. Section summary

In summary, there is little conclusive evidence on the neurobiological alterations associated with ASA. Notably, neuroimaging studies of ASA are often limited by the lack of control for or assessment of CSA, introducing a potential revictimization variable that may not be accounted for (e.g., Quidé et al., 2018b). Furthermore, as in the CSA literature, many investigations reveal differences in ASA with PTSD versus ASA without PTSD, making it difficult to isolate effects of the trauma itself, rather than of the development of resulting psychopathology (e.g., Sui et al., 2010a, 2010b). Finally, it is possible that mixed directionality in associations is related to significant heterogeneity in coping responses and psychological outcomes. For example, the use of dissociation as a coping mechanism corresponds with differential neural signatures in numerous brain structures (Lotfinia et al., 2020). Overall, further research is needed to parse the effects of ASA as a unique trauma type on neurobiological consequences.

4. Conclusion & Future Directions

4.1. Comparative psychological and neurobiological outcomes

The extant literature demonstrates ST has severe adverse consequences. Further, CSA and ASA appear to have partially overlapped yet different psychobiological consequences. While CSA is associated with primarily PTSD (Maniglio, 2013; Paolucci et al., 2001; Trask et al., 2011; Weinstein et al., 2000), ASA is associated with a more general posttraumatic profile of comorbid PTSD and depression (Au et al., 2013; Basile et al., 2016; Ullman et al., 2007; Zinzow et al., 2012). Both CSA and ASA are related to the development of anxiety disorders, eating disorders, SUDs, and self-harm behavior (Adams et al., 2018; Amado et al., 2015; Maniglio, 2013), but CSA appears more likely to be linked with ADHD, OCD, conduct disorders, and dissociative disorders than ASA (Caspi et al., 2008; Fergusson et al., 1996; Weinstein et al., 2000). In turn, ASA may be more closely related to poorer physical health, health satisfaction, and social functioning and satisfaction (Holder et al., 2023). In addition, there is more extensive literature suggesting that ASA is related to poorer academic, professional, and occupational functioning than there is of CSA (Banyard et al., 2020; Mengo & Black, 2016; Molstad et al., 2023; Potter et al., 2018; Potter et al., 2021; Resick et al., 1981). However, some of these differences may be explained by methodological constraints; for example, studies investigating the effects of ASA must necessarily include adult participants who are more likely to be employed and thus experiencing potential occupational dysfunction than studies of CSA, which often include only children.

The neurobiological correlates of CSA and ASA are highly overlapping. It appears that sensory cortices and threat-related regions are impacted by both CSA (Andersen et al., 2008; Bremner et al., 1999, 2005; Heim et al., 2013; Tomoda et al., 2009) and ASA (Quidé et al., 2018a; Sui et al., 2010a; Sui et al., 2010b), though with potential differences in potency of these impacts. In particular, there appears to be more evidence to support claims of the impacts of CSA on hippocampus, amygdala, and PFC structure and function than ASA (Andersen et al., 2008; Bremner et al., 1997, 1999, 2003, 2005; Purcell et al., 2021; Stein et al., 1997; Yamamoto et al., 2017). Furthermore, CSA appears to be related to CC volume losses (Andersen et al., 2008; Rinne-Albers et al., 2016; Teicher et al., 2004), a finding which is not replicated in the ASA literature to our knowledge. On the other hand, there is evidence that ASA is related to WMHs and alterations in dACC function (Quidé et al., 2018b; Thurston et al., 2022).

4.2. Limitations and future directions

Although the current literature provides an important foundation for considering psychobiological effects of CSA and ASA, there are noted gaps in our current understanding of ST. For one, most samples in studies of ST are comprised of women; despite the previously established high prevalence of ST in certain populations of men such as the LGBTQ community, existing research does not yet reflect this recruitment need. Future research should focus on diversifying samples and specifically probing psychological and neurobiological effects of ST in marginalized, high-risk communities like those who are LGBTQ. Furthermore, only a small number of studies have attempted to compare CSA and ASA to determine how they may differentially impact survivors, and most focus on psychological rather than neurobiological effects. While a few studies have revealed differences, such as that those who experienced only ASA had modestly worse outcomes than those who experienced only CSA (Holder et al., 2023), it appears more likely that the severity of psychopathology does not differ significantly based on whether individuals experienced CSA alone versus ASA alone (Rowland et al., 2022; Thompson et al., 2003). However, there is not currently conclusive evidence, and future research should seek to elucidate potential differences in severity and types of diagnoses from differing forms of ST. Large-scale investigations should be leveraged to gather sample sizes large enough to separate those who have experienced only CSA, only ASA, both, and neither form of ST with sufficient power.

In addition, studies that focus specifically on individuals with ST would be a benefit to the literature. Researcher-clinicians who specialize in work in trauma and ST should be paired in collaborations with researchers experienced in neuroimaging work. Ideal study designs could include psychometric and neuroimaging assessment alongside psychoeducation and prevention interventions for those who have experienced CSA or ASA both with and without resulting psychopathology. Researchers could draw from settings like sexual assault recovery centers, though important considerations must be made in these sensitive populations to minimize burden and the potential for harm. Especially in recent ASA survivors, it is burdensome to undergo neuroimaging research, and the need for timely and effective psychiatric treatment (as well as the time-intensive involvement in the legal system when this occurs) should and does take priority over research involvement. There are also structural challenges to research participation including the need for reliable communication, transportation to the research facility, and the ability to take time away from work and other responsibilities. On the other hand, ASA survivors may find fulfillment in the opportunity to give back through participation in research studies, especially if these studies have an intervention or treatment component.

A significant aspect complicating the state of the existing literature are the high rates of revictimization, such that many survivors of CSA also experience subsequent ASA (Campbell et al., 2008). Rates of revictimization in the general population range from 10-69% (Campbell et al., 2008; Classen et al., 2005; Filipas & Ullman, 2006; Walsh et al., 2012). A recent meta-analytic review reported a mean prevalence of 47.9% (Walker et al., 2019). For women, the risk of experiencing ASA is as much as four to six times greater for survivors of CSA (Desai et al., 2002; Filipas & Ullman, 2006). Similarly, men who experienced CSA are between two and five times as likely to experience ASA as those who did not (Aosved et al., 2011; Elliott et al., 2004). Importantly, research suggests cumulative ST (or revictimization), rather than ST occurring in either developmental timeframe alone, is the best predictor of psychopathology like PTSD (Arata, 2002; Classen et al., 2005; Follette et al., 1996; Lau & Kristensen, 2010; Rowland et al., 2022; Walsh et al., 2012). Therefore, further study of the impact of revictimization on psychological and neurobiological outcomes is needed to best understand the deleterious effects of ST. Neuroimaging studies must therefore be sure to assess and consider previous CSA and ASA, given established high rates of revictimization, to elucidate specific effects of CSA, ASA, and revictimization. Additionally, a greater focus of neuroimaging work going forward should be to isolate the effects of the trauma (whether CSA, ASA, or both) from the effects of resulting psychopathology to avoid identifying neural correlates of the development of symptomology rather than of ST itself.

The study of sexual revictimization, however, is limited by methodological constraints. It is costly and often impractical to employ longitudinal designs to follow survivors of CSA through adulthood to assess potential occurrence and outcomes of ASA. Though frequently necessary, the reliance on cross-sectional studies limits the ability to understand the unique and combinatorial effects of CSA, ASA, and revictimization. For example, the adverse outcomes of CSA discussed here include PTSD, problematic substance use, risky sexual behavior, and depression, and these outcomes serve as risk factors for subsequent revictimization as well (Culatta et al., 2020; Lau & Kristensen, 2010; Messman-Moore et al., 2005, 2009; Walsh et al., 2013). Therefore, in a cross-sectional sample, it may be difficult to elucidate vulnerabilities to versus outcomes of sexual revictimization. Beyond this, existing psychological distress from previous CSA may also further compound adverse effects of revictimization itself. It is also important to note that those with more severe CSA (i.e., more frequent abuse and greater number of offenders) are more likely to be sexually revictimized as adults (Classen et al., 2005; Lau & Kristensen, 2010). Thus, it is possible that the increased likelihood of adverse posttraumatic outcomes in those who have been revictimized can be partially accounted for by the severity of CSA experiences, though there is not currently enough evidence to evaluate the accuracy of this hypothesis. To fully characterize the outcomes of revictimization, future work should utilize longitudinal models whenever possible and consider severity of CSA, symptomology resulting from CSA, and factors like substance use, self-dysfunction (e.g., disrupted sense of self, disturbances in intimate and sexual relations), and social support in relation to ASA.

In addition to above-mentioned study designs necessary for elucidating the distinct outcomes of ST types, additional investigations should continue to be conducted with resilience and strengths-based approaches. Such studies were not the focus of this review, but identifying neural correlates of resilience, recovery, and protective factors following CSA and ASA is crucial in informing treatment as well. A substantial portion of those who experience CSA will never go on to develop psychopathology and will instead develop resilience (Domhardt et al., 2015). One way to mitigate later risks of revictimization may be to identify such resilience factors, including internal, external, and neurobiological factors, and work to promote them earlier in life on small- and large-scale levels.

4.3. Conclusion

In conclusion, it is evident that ST, whether it occurs in childhood, adulthood, or both, is associated with deleterious outcomes across the lifespan. These adverse sequalae pervade psychological, behavioral, social, and neurobiological domains of those who experience ST. Future research should continue to attempt to disentangle the unique impacts of ST limited to isolated windows of development, to the extent that this does occur, through longitudinal study designs. Considering that as many as one in three individuals in the U.S. will experience ST, it is both imperative and urgent that its effects are well-understood and addressed with the most effective and individualized psychotherapeutic, pharmacological, and neurobiological treatments available.

However, individual treatment for the adverse psychological and neurobiological outcomes of ST is insufficient given the scale of this problem and the many aspects of life and society that it pervades. Recovery for survivors of ST is multifaceted and can include seeking justice in the criminal and civil systems as well as community and political organizing and advocacy. For some, seeking resolution through the legal system may be validating, but for others it may be harmful (Herman, 2005; Herman, 2023). There are multiple ways in which the broader community can respond to repair harm and offer accountability for those who have experienced sexual violence (e.g., Burns & Sinko, 2023). Overall, societal norms surrounding sexual violence must be changed such that survivors of CSA and ASA are no longer silenced but believed, taken seriously, and listened to in order to bring the widespread prevalence of this problem to light and enact long-term change.

Finally, the need for efforts toward prevention of ST is critical. The necessity of prevention is especially apparent given evidence for the intergenerational transmission of trauma, such that children of parents who were abused earlier in life are more likely to be sexually abused themselves (Widom et al., 2015). More broadly, CSA predicts greater likelihood of perpetrating sexual aggression in adolescence and young adulthood (Krahé et al., 2023). Some prevention programs work directly with children, often in school settings, aiming to increase children’s knowledge of and skills for preventing CSA, although it is unclear if these methods successfully lead to prevention of abuse (Fryda & Hulme, 2015; Topping & Barron, 2009; Walsh et al., 2018). Prevention programs could be designed more specifically to take into account the many ecological systems around a child that affect prevalence and prevention of CSA (e.g., Martinello, 2020). Resilience-based approaches can also be applied in preventative strategies at the primary (i.e., preventing a child from being abused), secondary (i.e., preventing adverse outcomes after a child is abused), and tertiary (i.e., overcoming symptomatic outcomes after abuse) levels (Borg et al., 2019). With knowledge of risk factors contributing to CSA, ASA, and revictimization, as well as resilience and protective factors, prevention strategies should be rigorously assessed and widely employed to reduce the prevalence of ST and its highly adverse sequalae.

Data Availability

Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.