• No results found

Trauma, executive function and posttraumatic stress in children : how are they associated?

N/A
N/A
Protected

Academic year: 2021

Share "Trauma, executive function and posttraumatic stress in children : how are they associated?"

Copied!
25
0
0

Bezig met laden.... (Bekijk nu de volledige tekst)

Hele tekst

(1)

Faculty of Social and Behavioral Sciences Graduate School of Child Development and Education

Trauma, executive function

and posttraumatic stress in

children: How are they

associated?

Rosanne op den Kelder

Research Master Child Development and Education Research Project II

Supervisors:

Prof. dr. G.J (Geertjan) Overbeek Drs. J.B. (Judith) Ensink

Reviewers:

Dr. B.J.H. (Bonne) Zijlstra

Dr. R.J.L. (Ramón) Lindauer (subject matter expert)  

(2)

Abstract

Background This study examined whether there is a mediating or moderating role of

executive function (EF) in the relationship between traumatization and posttraumatic stress in children. We investigated the link between traumatization, EF and posttraumatic stress in relation to exposure to single or chronic trauma in children. Additionally, we compared the results of a screening questionnaire for EF and neuropsychological tasks in a subsample. Methods Children were recruited at an academic center for child psychiatry in Amsterdam. The total sample consisted of 119 children from 9 to 17 years old (M = 13.65, SD = 2.445). The sample was further divided in three groups based on retrospective life event information; a control group (n = 40), single trauma group (n = 39), and chronic trauma group (n = 40). Results The study revealed that chronically traumatized children had lower levels of EF. Results also demonstrated that EF was found to partly mediate posttraumatic stress for chronically traumatized children, but not for children exposed to single trauma. There was no moderating mechanism for EF found. Additionally, slightly moderate associations were found between different EF measurement instruments in non-traumatized children.

Conclusions We found strong indications that EF partially mediates posttraumatic stress. This means that chronically traumatized children showed more deficits in EF, which was

associated with higher levels of posttraumatic stress. Future research should replicate these findings longitudinally, which may yield improvements for clinical practice.

(3)

Introduction

What happens to children’s executive functions (EF) when they have been under chronic stress or have been exposed to a severely stressful moment? Many children encounter traumatic events before entering adulthood, with prevalence rates varying from 14% (Alisic, Van der Schoot, Van Ginkel, & Kleber, 2008) to 82% (Breslau, Wilcox, Storr, Lucia, & Anthony, 2004). Several studies suggest that exposure to these events can affect cognitive processing, for example EF (DePrince, Weinzierl, & Combs, 2009). However, very little is known about these mechanisms, especially about the association between traumatization and posttraumatic stress in relation to exposure to single and chronic trauma. Increasing

knowledge about these mechanisms will optimize therapies and/or reduce risk for posttraumatic stress.

We defined a traumatic event as one in which somebody experiences or witnesses a threat or violation of a person’s physical or psychological integrity. The traumatic event is thereby accompanied by extreme feelings of helplessness, horror, disgust, or extreme fear either during or after the event (American Psychiatric Association, 2000; Lindauer & Boer, 2013). Single trauma is defined as exposure to one single traumatic event such as a traffic accident or rape. Likewise, we defined chronic trauma as exposure to multiple or recurrent traumatic events for example, child maltreatment or neglect and domestic violence. Chronic trauma often consists of an interpersonal component (Alisic, Van der Schoot, Van Ginkel, & Kleber, 2008).

Almost all traumatized children show stress reactions such as difficulty sleeping, anxiety and irritability. However, in some children, stress reactions persist over time and cause severe impairment in daily life. These children might qualify for a Posttraumatic Stress Disorder (PTSD) diagnosis. Results of a meta-analysis suggested that approximately 16% of traumatized children developed PTSD (Alisic et al., 2014). Using the current criteria for

(4)

PTSD according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.: DSM-IV-TR; American Psychiatric Association, 2000), PTSD symptoms are intrusive re-experiences (e.g. intrusive thoughts about the traumatic event and nightmares), persistent avoidance (e.g. emotional numbing and avoidance of feelings, thoughts, and conversations in relation to the traumatic events), and increased arousal (e.g. sleep problems, hypervigilance, irritability). The prevalence of PTSD in children differs across single and chronic trauma. Of those exposed to single trauma, 10% develop PTSD. Increasingly, 25% of children develop PTSD after experiencing chronic trauma such as repeated child sexual abuse and

psychological maltreatment (Alisic et al., 2014). Furthermore, posttraumatic stress can negatively affect children’s development in various areas such as academically, socially, emotionally, and physically (Alisic, Jongmans, Wessel, & Kleber, 2011).

Comparing single to chronic trauma, it is shown that the latter has a stronger and, more negative impact on levels of posttraumatic stress and depression in children (English, Graham, Litrownik, Everson, & Bandiwala, 2005). In addition, it is suggested that exposure to chronic trauma across multiple developmental phases results in more complex symptoms and additional problems, such as attachment and behavioral problems, when compared to

exposure to single trauma (Jonkman, Verlinden, Bolle, Boer, & Lindauer, 2013).

De Bellis’ (2001) proposed a developmental traumatology theory that suggests that traumatization leads to the development of PTSD through its effects on the brain, cognitive development, and the biological stress systems. For example through its influence on EF, in this study referred to as: “the efficiency with which individuals go about acquiring knowledge as well as how well problems can be solved across nine areas (attention, emotion regulation, flexibility, inhibitory control, initiation, organization, planning, self-monitoring, and working memory)” (Goldstein & Naglieri, 2013, p. 4). Following this developmental traumatology

(5)

theory, EF could be a mediating factor in the association between trauma and posttraumatic stress symptoms in children.

The potential mediating role of EF can be viewed in relation to specific areas of brain functioning: the cingulate, dorsolateral prefrontal cortex, basal ganglia, and cerebellum (Carrion, Wong, & Kletter, 2013; De Bellis, Hooper, Woolley, & Shenk, 2009; De Bellis, Hooper, Spratt, & Woolley, 2009; Neigh, Gillespie, & Nemeroff, 2009;Williams, Suchy, & Rau, 2009). More specifically, during exposure to stress, the hypothalamus-pituitary-adrenal (HPA) axis is activated, which leads to a higher level of glucocorticoid production (Lupien, McEwen, Gunnar, & Heim, 2009). This might lead to dysfunction of the prefrontal cortex through cell death and a decrease in branching of dendrites (De Bellis, Hooper, Spratt, & Woolley, 2009; MacDonald, Ellis, Pulsifer, & Lyons, 2015). The amygdala, prefrontal cortex, and hippocampus are the most vulnerable brain regions for stress exposure. The vulnerability of these different regions changes over time; the hippocampus is most vulnerable during childhood while the prefrontal cortex is most vulnerable during adolescence (Lupien, McEwen, Gunnar, & Heim, 2009). Furthermore, chronic stress leads to higher levels of secretion of neurotransmitters resulting in more persistent functional brain changes (De Bellis, 1999a,b;  Rinne-Albers, Van der Wee, Lamers-Winkelman, & Vermeiren, 2013).

Thus, EF is related to functioning of the prefrontal cortex (Goldstein & Naglieri, 2013). The prefrontal cortex is also strongly connected with the limbic system (amygdala, hippocampus, thalamus and hypothalamus) and the brain stem. These areas are responsible for emotion regulation and anxious arousal(Williams, Suchy, & Rau, 2009). Importantly, decreased prefrontal cortex activation, and thus lower EF, might suppress inhibition of the amygdala, hippocampus and brain stem, which increases fear response, intrusive thoughts, and hypervigilance (Arnsten, Raskind, Taylor, & Connor, 2015; Leskin & White, 2007).

(6)

While lacking the ability of inhibiting fear responses to triggers of the trauma, children might develop an avoidant coping strategy (Aupperle, Melrose, Stein, & Paulus, 2012).

EF could also be a moderating factor in the development of posttraumatic stress symptoms in children (Williams, Suchy, & Rau, 2009)and thus change the relationship between traumatization and posttraumatic stress. In this line of reasoning, children with higher levels of EF might have more tools to cope with traumatization. Their prefrontal cortex might be able to inhibit fear responses and hypervigiliance when they are exposed to arousing stimuli (Arnsten, Raskind, Taylor, & Connor, 2015). Higher levels of EF could be a

moderator for a resilient trajectory after traumatization. On the other hand, deficits in EF could make children more vulnerable to develop posttraumatic stress symptoms following traumatization, as they are unable to inhibit the limbic system(Williams, Suchy, & Rau, 2009).

The Present Study

We investigated what happens to children’s EF when they have been exposed to severe stress and have experienced extreme emotions of insecurity. More specifically, we examined the potential mediating or moderating role of EF in the development of

posttraumatic stress after single and chronic trauma exposure. Additionally, there are various behavioral and cognitive instruments to assess EF (Anderson, Anderson, Northam, Jacobs, & Mikiewicz, 2002). To gain more insight into the association between these different

measurement instruments of EF, we investigated the association between outcomes on a screening questionnaire and neuropsychological tasks in a subsample. Our study adds to the current scientific knowledge by investigating the differences in EF between three main groups of children; those that have been exposed to single or chronic trauma compared to a control group of children who have not been exposed to trauma. Reducing this knowledge gap would

(7)

have many scientific and practical implications. For example, trauma therapy could benefit from more insight in the role of EF in PTSD development.

Drawing from the literature review and theoretical framework, the following research question was devised: To what extent is EF a mediator or moderator in the relationship between traumatization and posttraumatic stress in children? First, we hypothesized that there is a negative association between traumatization and EF in children. Second, we expected that children who experienced chronic trauma show more deficits in EF compared to children that experienced a single traumatic event. Third, we hypothesized that EF plays a mediating role in the relationship between chronic trauma and posttraumatic stress in children. Our fourth hypothesis was that EF plays a moderating role in this relationship. Finally, we hypothesized that there is a high association between performance on neuropsychological tasks and a screening instrument of EF.

Method Procedure

Participants were recruited from the department of Trauma and Family at De Bascule, an Academic Center for Child and Adolescent Psychiatry in Amsterdam. Recruitment differed between traumatized children and the control group. First, traumatized children aged 8 to 18 years were recruited during the intake phase of trauma treatment. Researchers provided information about the study, its aims and the research procedure. While informing them about the research, we highlighted that participation is voluntarily and would not affect their current treatment program. The traumatized group was then subdivided into a single trauma and chronic trauma group based on retrospective information about exposure to traumatic events. Children that were exposed to prolonged or recurrent traumatic events were divided into the chronic trauma group. Age was the only inclusion criteria for the traumatized groups; children

(8)

had to be aged 8 – 18 years. Children older than 12 years-old and parents with custody had to sign informed consent forms. Similarly, children in the control group had to be 8 to 18 years-old and have a non-clinical PTSD score on the CRIES-13 (a posttraumatic stress screening questionnaire; see under Measures). As the control group was recruited through convenience sampling, the control group was compared to both single and chronic trauma group on age and gender composition.

Sample

This study is part of an ongoing research on genetic vulnerability, including EFing, in the development of PTSD in children. In accordance, the current study compared EF between non-traumatized, single traumatized and chronically traumatized children in a cross-sectional research design. Twelve participants were excluded from analyses because of missing

screening questionnaires due to language barriers of parents, excessive loads on the parental burden, and unstable home environment with changing caregivers. The total sample consisted of 119 participants (66 girls) aged 9 to 17 years old (M = 13.65, SD = 2.445). The control group existed of 40 children (17 girls) aged 9 to 17 years-old (M = 13.88, SD = 2.493), the single trauma group existed of 39 children (23 girls) aged 10 to 17 years-old (M = 14.08, SD = 2.057), and the chronic trauma group existed of 40 children (26 girls) aged 9 to 17 years (M = 13.00, SD = 2.660).

Variables

Executive function. The parent version of the Behavior Ratings Inventory Executive Function (BRIEF) was used to measure EF in children (Huizinga & Smidts, 2009). This version consists of 75 items, divided into eight subscales, covered by two indices, which results in a single overall total score. Statements such as: “he/she struggles with starting homework or chores” and “he/she gets upset very quickly” are scored on a three-point scale (1= never, 2 = sometimes, 3 = often). Research findings have shown that the BRIEF is a

(9)

highly reliable and valid instrument to evaluate EF (Huizinga & Smidts, 2009). This was validated in our sample with a Chronbach’s alpha of .976.

In addition to the BRIEF, a subsample of participants (n = 24) performed additional neuropsychological tasks. First, the Test of Everyday Attention for Children (TEA-Ch) was used. TEA-Ch is a standardized test battery that measures task switching, response inhibition, and selective or sustained attention. It consists of nine different subscales from which two were selected for this study: Score! and Creature Counting. Score! is a 10-item subtest that measures sustained attention. Each item is comprised of 9 to 15 identical tones separated by a silent interval. Children were asked to count these tones without using any external resources. They did not receive feedback or reward based on their responses. The second subtest

Creature Counting was used to measure task switching and cognitive flexibility. In this

subtest children were asked to start counting creatures. They were told to use the arrows to either add a creature or subtract one. The accuracy in which they counted and the speed at which they reacted was measured. Each participant was given two sample exercises in which they received feedback. During the task no feedback was provided to the child. Secondly, the

Behavior Assessment Dysexecutive Syndrome for Children (BADS-C) was used to measure EF

in daily life by using several tests. We used three subtests of the BADS-C: Zoo Map Test,

Playing Cards Test, and the Six Parts Test. Planning ability was measured using the Zoo Map Test; participants were instructed to plan a route in a zoo. Cognitive flexibility and response

inhibition was measured using Playing Cards Test, a card-sorting task whereby children need to adapt to changing cards while measuring accuracy and speed. Lastly, the Six Parts Test was used to measure planning and behavior monitoring. In this task, children were asked to

perform six tasks within a time limit using a rule regarding the order of tasks.

Posttraumatic stress. The Dutch version of the Children’s Revised Impact of Events Scale-13 (CRIES-13), a 13-item-questionnaire, was used to measure posttraumatic stress in

(10)

children after experiencing a traumatic event (Verlinden et al., 2014). The CRIES-13 is a screening questionnaire that assesses the risk for PTSD in children. The questionnaire has a good construct validity and factor structure (Perrin, Meiser-Stedman, & Smith, 2005). A score above the cut-off (>30) is associated with an increased risk of PTSD. For example, items as “Do pictures about it pop into your mind?” and “Do you stay away from reminders of it?” were scored on a four-point scale (0 = not at all, 1= rarely, 3 = sometimes, 5 = often). Three subscales that correspond to the DSM-IV TR criteria of PTSD can be distinguished in this questionnaire: intrusion, avoidance and arousal. Internal consistency and test-retest reliability of the CRIES-13 is high (Verlinden et al., 2014). This was also the case in our sample with a Chronbach’s alpha of .899.

Results

Prior to analysis, background variables were checked to assess whether or not the three groups differed with regard to age and gender composition. Results of the one-way ANOVA and Chi-square test showed that the three groups did not differ significantly on age (F (2,116) = 2.223, p = .113) nor gender (Χ2 (2) = 4.398, p = .111). In other words, age and gender composition of the control, single trauma, and chronic trauma groups were similar, and could be excluded as possible confounder variables in further analyses.

To investigate the bivariate links between traumatization and EF, we calculated Pearson correlations (see Table 1). Positive significant correlations (p < .05) between traumatization and EF measures were found. This shows that traumatized children reported lower levels of EF, compared to children in the control group. In order to investigate bivariate links between EF and posttraumatic stress, again Pearson correlations were calculated (see Table 1). Fairly high, positive correlations were significant between the subscales of EF and posttraumatic stress. This shows that increased problems in EF are associated with higher levels of posttraumatic stress in children.

(11)

Table 1

Correlations between traumatization, executive function and posttraumatic stress

Executive function Posttraumatic stress

Traumatization T B M In Av Ar Executive function Total (T) .339* Behavior evaluation (B) .294* .905* Metacognition (M) .316* .949* .765* Posttraumatic stress Intrusion (In) .252* .382* .379* .319* Avoidance (Av) .410* .415* .421* .361* .782* Arousal (Ar) .452* .491* .505* .421* .710* .760* Total .397* .470* .472* .400* .871* .900* .883*

Note. Dutch norm scores of the BRIEF were used. * p < .05.

Although the results from the correlational analyses indicated a general association between type of trauma and EF, this did not indicate whether there would be a linear decrease in EF between the control, single trauma, and chronic trauma group. Thus, to investigate group differences in EF between control group, single trauma group and chronic trauma group an one-way ANOVA was conducted. Results indicated that the groups differed significantly on EF (F (2,116) =18.716, p = .000, η2 = .244, power = .672). Table 2 displays the mean scores and standard deviations. Post hoc Bonferonni comparisons showed that while the control group did not differ significantly (p = .526) from the single trauma group in terms of EF, it did differ significantly from the chronic trauma group (p= .000). There was also a significant difference between the single trauma group and chronic trauma group (p= .000). This indicates that children in the chronic group showed more deficits in EF compared to both control group and single trauma group.

(12)

Table 2

Means and standard deviations in control, single trauma and chronic trauma groups

Control Group Single trauma Group Chronic trauma group

Mean SD Mean SD Mean SD

Executive function Total 47.10 9.075 50.08 9.418 59.80 10.547 Behavior evaluation 48.20 9.796 50.44 10.840 60.13 10.425 Meta cognition 47.15 8.319 49.46 8.140 58.10 10.137 Posttraumatic stress Intrusion 4.45 4.038 5.62 6.536 9.55 5.857 Avoidance 3.10 3.350 5.51 6.407 11.68 5.731 Arousal 4.20 3.421 7.87 6.165 13.35 6.815 Total 11.75 8.494 19.00 17.887 33.48 16.864

To investigate the mediating effect of EF in the relationship between traumatization and posttraumatic stress, a mediation analyses with a multi-categorical independent variable was conducted based on the Process Macro by Hayes (2008) and the tutorial by Hayes and Preacher (2014). The estimated model coefficients are displayed in Table 3 and the analyzed mediation model is presented in Figure 1. The association between single trauma and EF compared to the control group was not significant. On the other hand, the association between chronic trauma and EF was significant compared to the control group. In other words,

children in the chronic trauma group scored 12.7 points higher on EF (which corresponds with more deficits) compared to the control group. Furthermore, when including EF in the model, the association of chronic trauma with posttraumatic stress remained significant. EF had a small, but significant, negative association with posttraumatic stress. The total indirect effect of chronic trauma on posttraumatic stress through EF was also significant with a coefficient (B = 5.643, boot SE = 1.921, 95% CI = 2.277 - 9.911). This means that there is a genuine, but partial-mediating role for EF in the relationship between chronic trauma and posttraumatic stress.

(13)

Table 3

Coefficients of PROCESS mediation model

Outcome Executive function Posttraumatic stress

Coefficient (SE) Coefficient (SE) Coefficient (SE) Constant I1 47.100(1.534)* I3 11.750(2.370)* I2 -9.180(6.887) Single trauma A1 2.977 (2.184) C1 7.250(3.373)* C’1 5.9272 (3.271) Chronic trauma A2 12.700 (2.170)* C2 21.725(3.352)* C’2 16.082 (2.670)* Executive Function B .444 (.138)* Note. * p <.05.

Figure 1. Conceptual mediation model

To investigate the moderating role of EF in the relationship between traumatization and posttraumatic stress, a moderation analysis with a multi-categorical independent variable was conducted based on the same macro and tutorial as the mediation analysis (see Hayes, 2008; Hayes & Preacher, 2014). Results showed that, by using mean centering, the interaction between single trauma and EF (p = .1347) nor the interaction between chronic trauma and EF (p = 0.8047) were significant (see Table 4). This indicates that there is no moderation effect of EF for both the single and chronic trauma group compared to the control group. This means that children who experienced chronic trauma were at higher risk for developing

(14)

Table 4

Coefficients of PROCESS moderation model

Coefficient SE t p

Constant 15.743 1.477 10.6624 .000

Executive function .454 .150 3.032 .003

Single trauma 7.4780 3.381 2.212 .029

Chronic trauma 17.989 3.589 5.0122 .000

Executive function * single trauma .487 .323 1.506 .1347

Executive function * chronic trauma .082 .332 .248 .805

Finally, to investigate the bivariate links between a screening questionnaire for EF and neuropsychological tasks, we calculated Pearson’s correlations (see Table 5 and Table 6). No significant correlations were found in the traumatized group, indicating that performance on the neuropsychological tasks was not associated with scores on the screening questionnaire. However, some significant negative correlations were found in the control group between performance on the Zoo Map Test and the subscales plan/organize (r = -609, p = .047) and

monitoring (r = -.741, p = .009). This means that non-traumatized children who performed

worse on the neuropsychological task had more deficits in EF, especially in planning, organizing and monitoring of behavior.

Table 5

Correlations between neuropsychological tasks and screening questionnaire of executive function in the non-traumatized group (n = 11)

Inhibit Shift Emotional control Initiate Working memory Plan/ organize Organization of materials Monitor Score! .180 .294 .226 .472 .513 .381 .297 -.294 Creature counting .364 -.063 -.059 -0.83 .027 .087 -.166 -.144 Zoo 1 -.247 -.112 -.413 .083 -.123 -609* -.581 -.741* Zoo 2 .307 .158 -.488 -.090 .559 -.147 -.069 -.313 Playing Cards -.480 -.019 .188 -.190 -.699* -.266 -.021 .032 Six Parts .282 .178 .126 .482 .515 .109 -.146 -.469 Note. * p < .05.

(15)

Table 6

Correlations between neuropsychological tasks and screening questionnaire of executive function in the chronically traumatized group (n = 23)

Inhibit Shift Emotional control Initiate Working memory Plan/organize Organization of materials Monitor Score! .269 -.080 .357 .103 .039 .292 .162 .428 Creature counting -.118 -.178 -.050 -.346 .052 -.222 -.185 -.176 Zoo 1 -.047 -.278 -.010 -.304 -.168 -.052 .226 .076 Zoo 2 -.279 -.420 -.231 -.258 -.245 -.123 .236 -.079 Playing Cards .067 -.023 .159 -.271 -.175 -.221 -.102 -.126 Six Parts -.281 -.611 -.146 -.294 -.400 -.248 -.087 -.207 Note. * p < .05.   Discussion

The main purpose of this study was to investigate the mediating or moderating role of EF in the relationship between traumatization and posttraumatic stress in children. Our research findings confirm previous research (DePrince, Weinzierl, & Combs, 2009), which showed that there is a strong relationship between traumatization and posttraumatic stress. Results revealed that EF partially mediates the relationship between chronic traumatization and posttraumatic stress. That is, after experiencing chronic trauma, children decrease in their EF, and this in turn was associated with more posttraumatic stress symptoms. No evidence was found for moderation, which showed that higher EF does not function as a buffer in the relationship between traumatization and posttraumatic stress.

In line with our hypothesis and previous research, traumatization was associated with lower levels of EF (Aupperle, Melrose, Stein, & Paulus, 2012; DePrince, Weinzierl, & Cobs, 2009; Kremen et al., 2007; Parslow & Jorm, 2007). Chronically traumatized children in our sample showed more deficits in EF compared to children exposed to single trauma or non-traumatized children. We also found that chronically non-traumatized children had a subclinical mean score on the EF measure.Additionally, children exposed to single trauma did not have

(16)

psychopathology (Flouri & Kallis, 2007) and the cumulative stressors model (Jaffee, Caspi, Moffit, Polo-Tomás, & Taylor, 2007) help explain these findings: children’s developing brains might be more resilient against exposure to one severe traumatic event in terms of EF compared to exposure to chronic stress or trauma. Exposure to chronic stress results in a constantly activated biological stress system, which influences the brain regions involved in EF (Arnsten, Raskind, Taylor, & Connor, 2015; Wilson, Hansen, & Li, 2011). Besides the model of cumulative stressors, another plausible explanation could be the nature of

traumatization. Generally, chronic traumatization has an interpersonal character while single traumatization mostly includes events such as traffic accidents or earthquakes (Alisic, Van der Schoot, Van Ginkel, & Kleber, 2008). Previous research has shown that an emotionally charged trauma such as child sexual abuse has more severe effects on EF and the developing brain than non-interpersonal trauma such as earthquakes or traffic accidents (Wamser-Nanney & Vanderberg, 2013). The emotional valence of a trauma might have a large impact on the limbic system in terms of perceiving (non-)threatening stimuli, which is also tightly linked to the prefrontal cortex and thus EF (Wilson, Hansen, & Li, 2011). In this case, it is not the accumulation of traumatic events that cause executive dysfunction, and in turn posttraumatic stress, but rather the emotional character of the traumatic events.

The mediation analysis showed that EF is as a partial mediator in the relationship between chronic trauma and posttraumatic stress. However, traumatization plays the most important role in levels of posttraumatic stress. In line with the developmental traumatology framework (De Bellis, 2001; De Bellis & Zisk, 2014), this suggests that chronically

traumatized children show more severe posttraumatic stress symptoms through lower capacities in EF. Due to problems inhibiting the limbic system, problems in fear responses and hypervigiliance arise. Subsequently, because these children cannot inhibit the fear

(17)

response on triggering stimuli, they develop an avoidant coping strategy (Aupperle, Melrose, Stein, & Paulus, 2012), one of the fundamental symptoms of PTSD.

Furthermore, our findings suggest that EF does not play a moderating role in the relationship between traumatization and posttraumatic stress. EF does not work as a buffer in the development of posttraumatic stress in children and the relationship is not stronger for children with lower EF. A plausible explanation for this finding lies in the association between traumatization and EF. There might not be many children that are chronically traumatized and still have high levels of EF, because chronically traumatized children often grow up in a physically, cognitively or emotionally deprived environment (De Bellis, 2001).

The examination of associations between the screenings questionnaire and

neuropsychological tasks showed that there were little significant associations between them. This could be explained by previous research findings that demonstrated a discrepancy between behavioral and cognitive measures of EF (Anderson, Anderson, Northam, Jacobs, & Mikiewicz, 2002). In our study, parents assessed the screening questionnaire while children themselves performed the neuropsychological tasks. Informant discrepancies are a well-known phenomenon in the assessment of psychopathology (De Los Reyes & Kazdin, 2005). Future research should take both children and parents as informants to gain a comprehensive view of children’s EF.

There are several limitations to our study. The most prominent limitation is our cross-sectional research design. It prohibits us from drawing causal conclusions based on the analyses. Although it is logical that posttraumatic stress follows traumatization as it is within the definition, it could be possible that impaired EF leads to a higher risk of exposure to traumatic events due to parental conflicts or interpersonal problems (Williams, Suchy, & Rau). To the best of our knowledge, there are no prospective studies that measured the possible predictive relationship from EF to the exposure to traumatic events. As an

(18)

experimental design is not feasible within this research context, the next step in this scientific area should be to employ research with a longitudinal design. This would enable researchers to investigate the developmental trajectory of posttraumatic stress in relation to EF in

children. In addition, prior to analysis, group composition was only tested for the variables age and gender. More demographic variables such as socio-economic status, ethnicity, and IQ should be included to exclude possible confounding variables. Third, the use of screenings instruments for assessing posttraumatic stress and EF is limited. However, the screening questionnaires have shown to be reliable and valid instruments, which enable us to draw conclusions based on these measurement instruments.

Future research

Based on our findings, we suggest that the strong association between EF and posttraumatic stress demonstrates that chronic traumatization is associated with a broader range of problems in children. This is aligned with earlier research findings that chronically traumatized children, compared to children exposed to single trauma, show more

developmental problems besides posttraumatic stress symptoms such as intrusion, avoidance, and arousal (Copeland, Keller, Angold, & Costello, 2007; Jonkman, Verlinden, Bolle, Boer, & Lindauer, 2013). In accordance with our findings, many propositions have been made for the concept of developmental trauma disorder after exposure to chronic or complex trauma (Van der Kolk, 2005). Although we cannot draw conclusions about the etiology of

posttraumatic stress through EF, our findings may give scientists and clinicians guidelines to investigate a broader range of consequences following exposure to chronic traumatization. Therefore, we strongly recommend research at the neurological level – through MRI or fMRI analyses- to gain more insight in the possible mediating role of EF in posttraumatic stress. A superior research approach would be to conduct this brain imaging research in a longitudinal

(19)

design in order to investigate the developmental trajectory of posttraumatic stress in children possibly through EF.

Our findings can have important implications for clinical practice. When deficits in EF are acknowledged as additional consequences of chronic traumatization in children or as a mediator in the development of posttraumatic stress, trauma therapy and prevention can be adjusted or expanded. Several research findings indicated that a good-functioning prefrontal cortex improves patients’ regulation of thoughts, emotions and behavior, because the

prefrontal cortex regulates the limbic system and brain stem to inhibit hyperarousal

symptoms, flashbacks, and fear responses (Arnsten, Raskind, Taylor, & Connor, 2015).For example, cognitive training could focus on improving EF and thereby diminish its negative consequences on children’s academic and social development. In turn, it could prevent children from developing posttraumatic stress and thereby reduce or alleviate adverse consequences on their development. Additionally, combining cognitive training and trauma therapy might enable children to benefit more or faster from techniques learned in

psychotherapy.

In conclusion, we found strong associations between chronic trauma, EF and

posttraumatic stress in children with strong indications for a partial mediating role of EF on the development of posttraumatic stress. This means that chronically traumatized children show more deficits in EF, which is associated with higher levels of posttraumatic stress. Our research findings should be replicated longitudinally to give definitive answers to the question how traumatization, EF and posttraumatic stress are associated in children. This may yield more effective clinical practice that is able to tackle the negative consequences of

(20)

References

Alisic, E., Van der Schoot, T. A., Van Ginkel, J. R., & Kleber, R. J. (2008). Looking beyond posttraumatic stress disorder in children: Posttraumatic stress reactions, posttraumatic growth, and quality of life in a general population sample. Journal of Clinical

Psychiatry, 69, 1455-1461. Retrieved from:

http://www.psychiatrist.com/Pages/home.aspx

Alisic, E., Jongmans, M.J., Van Wesel, F., Kleber, R.J. (2011). Building child trauma theory from longitudinal studies: A meta-analysis. Clinical Psychology Review, 31, 736-747. doi:10.1016/j.cpr.2011.03.001

Alisic, E., Zalta, A. K., Van Wesel, F., Larsen, S. E., Hafstad, G. S., Hassanpour, K., & Smid, G. E. (2014). Rates of post-traumatic stress disorder in trauma-exposed children and adolescents: meta-analysis. The British Journal of Psychiatry, 204, 335-340.

doi:10.1192/bjp.bp.113.131227

American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR Fourth Edition, Text Revision). Washington, DC: American Psychiatric Association.

Anderson, V.A., Anderson, P., Northam, E., Jacobs, R., & Mikiewicz, O. (2002).

Relationships between cognitive and behavioral measures of executive function in children with brain disease. Child Neuropsychology, 8, 231-240.

doi:10.1076/chin.8.4.231.13509

Arnsten, A.F.T., Raskind, M.A., Taylor, F.B., & Connor, D.F. (2015). The effects of stress exposure on prefrontal cortex: Translating basic research into successful treatment for post-traumatic stress disorder. Neurobiology of Stress, 1, 89-99.

(21)

Aupperle, R. L., Melrose, A. J., Stein, M. B., & Paulus, M. P. (2012). Executive function and PTSD: disengaging from trauma. Neuropharmacology, 62, 686-694.

doi:10.1016/j.neuropharm.2011.02.008  

Breslau, N., Wilcox, H. C., Storr, C. L., Lucia, V. C., & Anthony, J. C. (2004). Trauma exposure and posttraumatic stress disorder: a study of youths in urban

America. Journal of Urban Health, 81, 530-544.  doi:10.1093/jurban/jth138 Carrion, V. G., Wong, S. S., & Kletter, H. (2013). Update on neuroimaging and cognitive

function in maltreatment-related pediatric PTSD: Treatment implications. Journal of

Family Violence, 28, 53-61. doi:10.1007/s10896-012-9489-2

Copeland, W. E., Keeler, G., Angold, A., & Costello, E. J. (2007). Traumatic events and posttraumatic stress in childhood. Archives of General Psychiatry, 64, 577-584. doi:10.1001/archpsyc.64.5.577.

De Bellis, M. D. (2001). Developmental traumatology: The psychobiological development of maltreated children and its implications for research, treatment, and

policy. Development and psychopathology, 13, 539-56. doi:10.1017/S0954579401003078

De Bellis, M. D., Baum, A. S., Birmaher, B., Keshavan, M. S., Eccard, C. H., Boring, A. M., Jenkins, F.J. & Ryan, N. D. (1999a). Developmental traumatology part I: Biological stress systems. Biological Psychiatry, 45, 1259-1270. doi

:10.1016/S0006-3223(99)00044-X

De Bellis, M. D., Keshavan, M. S., Clark, D. B., Casey, B. J., Giedd, J. N., Boring, A. M., Frustaci, K., & Ryan, N. D. (1999b). Developmental traumatology part II: Brain development. Biological Psychiatry, 45, 1271-1284.

(22)

De Bellis, M.D., Hooper, S.R., Spratt, E.G., & Woolley, D.P. (2009). Neuropsychological findings in childhood neglect and their relationship to pediatric PTSD. Journal of the

International Neuropsychological Society, 15, 868-878.

doi:10.1017/S1355617709990464  

De Bellis, M. D., Hooper, S. R., Woolley, D. P., & Shenk, C. E. (2009). Demographic, maltreatment, and neurobiological correlates of PTSD symptoms in children and adolescents. Journal of Pediatric Psychology,35, 570–577. doi:10.1093/jpepsy/jsp116

De Bellis, M. D., & Zisk, A. (2014). The biological effects of childhood trauma. Child and

Adolescent Psychiatric Clinics of North America, 23, 185-222.

doi:10.1016/j.chc.2014.01.002

De Los Reyes, A., & Kazdin, A. E. (2005). Informant discrepancies in the assessment of childhood psychopathology: a critical review, theoretical framework, and

recommendations for further study. Psychological Bulletin,131(4), 483-509. doi:10.1037/0033-2909.131.4.483

DePrince, A. P., Weinzierl, K. M., & Combs, M. D. (2009). Executive function performance and trauma exposure in a community sample of children. Child Abuse & Neglect, 33, 353-361. doi:10.1016/j.chiabu.2008.08.002

English, D. J., Graham, J. C., Litrownik, A. J., Everson, M., & Bangdiwala, S. I. (2005). Defining maltreatment chronicity: Are there differences in child outcomes? Child

Abuse & Neglect, 29, 575-595. doi:10.1016/j.chiabu.2004.08.009

Goldstein, S., & Naglieri, J. A. (2013). Handbook of Executive Function. Springer. Flouri, E., & Kallis, C. (2007). Adverse life events and psychopathology and prosocial

behavior in late adolescence: testing the timing, specificity, accumulation, gradient, and moderation of contextual risk. Journal of the American Academy of Child &

(23)

Hayes, A.F. (2008). Introduction to mediation, moderation, and conditional process analysis:

A regression-based approach. Guilford Press.

Hayes, A.F. & Preacher, K.J. (2014). Statistical mediation analysis with a multicategorical independent variable. British Journal of Mathematical and Statistical Psychology, 67, 451-470. doi:10.1111/bmsp.12028

Huizinga, M., & Smidts, D. (2009). BRIEF: Vragenlijst executieve functies voor 5-18 jarigen. Amsterdam: Hogrefe Uitgevers.

Jaffee, S.R., Caspi, A., Moffit, T.E., Polo-Tomás, M., & Taylor, A. (2007). Individual, family, and neighborhood factors distinguish resilient from non-resilient maltreated children: A cumulative stressors model. Child Abuse & Neglect, 31, 231-253.

doi:10.1016/j.chiabu.2006.03.011

Jonkman, C.S., Verlinden, E., Bolle, E.A., Boer, F., & Lindauer, R.J.L. (2013) Traumatic stress symptomatology after child maltreatment and single traumatic events: Different profiles. Journal of Traumatic Stress, 26, 225-232. doi:10.1002/jts.21792

Kremen, W. S., Koenen, K. C., Boake, C., Purcell, S., Eisen, S. A., Franz, C. E., Tsuang, M. T., & Lyons, M. J. (2007). Pretrauma cognitive ability and risk for posttraumatic stress disorder. Archives of General Psychiatry, 64, 361–368. doi:10.1001/archpsyc.64.3.361 Leskin, L.P., & White, P.M. (2007). Attentional networks reveal executive function deficits in

post traumatic stress disorder. Neuropsychology, 21, 275-284. doi:10.1037/0894-4105.21.3.275

Lindauer, R., & Boer, F. (2013). Trauma bij kinderen. Lannoo Meulenhoff-Belgium. Lupien, S.J., McEwen, B.S., Gunnar, M.R., & Heim, C. (2009). Effects of stress throughout

the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10, 434-445. doi:10.1038/nrn2639

(24)

MacDonald, H.Z., Ellis, B.H., Pulsifer, M.B., & Lyons, M. (2015). Executive functioning in children with posttraumatic stress disorder symptoms. Journal for Child and

Adolescent Trauma, 8, 1-11. doi:10.1007/s40653-015-0037-0

Neigh, G.N., Gillespie, C.F., & Nemeroff, C.B. (2009). The neurobiological toll of child abuse and neglect. Trauma, Violence & Abuse, 10, 389-410.

doi:10.1177/1524838009339758

Rinne-Albers, M. A., Van der Wee, N. J., Lamers-Winkelman, F., & Vermeiren, R. R. (2013). Neuroimaging in children, adolescents and young adults with psychological trauma.

European Child & Adolescent Psychiatry, 22(12), 745-755.

doi:10.1007/s00787-013-0410-1

Parslow, R., & Jorm, A. (2007). Pretrauma and posttrauma neurocognitive function and PTSD symptoms in a community sample of young adults. American Journal of

Psychiatry, 164, 509-515. doi:10.1176/ajp.2007.164.3.509

Perrin, S., Meiser-Stedman, R., & Smith, P. (2005). The Children's Revised Impact of Event Scale (CRIES): Validity as a screening instrument for PTSD. Behavioural and

Cognitive Psychotherapy, 33, 487-49. doi:10.1017/S1352465805002419

Verlinden, E., Meijel, E.P.M. , Opmeer, B.C., Beer, R., De Roos, C., Bicanic, I.A.E., Lamers-Winkelman, F., Olff, M., Boer, F., & Lindauer, R.J.L. (2014). Characteristics of the Children's Revised Impact of Event Scale in a Clinically Referred Dutch Sample.

Journal of Traumatic Stress, 27, 338-344. doi:10.1002/jts.21910

Wamser-Nanney, R. & Vandenberg, B.R. (2013). Empirical support for the definition of a complex trauma disorder in children and adolescents. Journal of Traumatic Stress, 26, 671-678. doi: 10.1002/jts.21857

(25)

Williams, P.G, Suchy, Y., & Rau, H.K. (2009). Individual differences in executive

functioning: Implications for stress regulation. Annals of Behavioral Medicine, 37, 126-140. doi: 10.1007/s1260-009-9100-0

Wilson, K.R., Hansen, D.J., & Li, M. (2011). The traumatic response in child maltreatment and resultant neuropsychological effects. Agression and Violent Behavior, 16, 87-97. doi:10.2016/j.avb.2010.12.007

Referenties

GERELATEERDE DOCUMENTEN

De ellos se desprende que la población holandesa tiene un nivel medio bastante alto de habilidades digitales tanto operacionales como formales, pero los niveles que alcanzan

In the process of arriving at the aforementioned model, activity counts were also explored as a possible input signal. Activity counts were used together with RR

Through micro-CT analysis of explanted lung cores from a lung transplant recipient with bronchiolitis obliterans syn- drome, an obstructive lung disease‚ and longitudinal CT

For the environmental condition munificence I find that underperforming firms who operate in munificent environments increase their risk taking when they rely on

We analysed the production, impact factor of, and scientific collaboration involved in viticulture and oenology articles associated with South African research

Wanneer bij gebruikmaking van stiermoeder- toetsbedrijven de pinken al gespoeld worden (TOETS+) dan is de opbrengst ongeveer f 1,50 hoger dan wanneer de vaarzen pas na de eerste

Medica- tions were grouped using the anatomical therapeutic chemical classification system (ATC) starting from the most specific scope of medications and moving up to the more

This indicated that deletion of two putative EPCONS components (i.e. Similarly, in pex25 vps13 cells lacking two putative VAPCONS proteins functional peroxisomes