A core feature of GAD, excessive and uncontrollable worry, may be indicative of poor attentional control and difficulty disengaging attention from threatening or emotional information (e.g., Fox, 2004; Mathews, Fox, Yiend, & Calder, 2003; Yiend & Mathews 2001). The current study examined the performance of college students with and without self-reported GAD (N = 63) on measures of attentional control and a spatial cueing task designed to assess engagement-disengagement processes from emotionally valenced (aversive, pleasant) and neutral picture stimuli. Attentional control abilities were examined using the Stroop Color-Word Association Test (SCW Test) and Trail-Making Test (TMT). Separate analyses of variance (ANOVAs) demonstrated that GAD participants performed more poorly on the Stroop Color subtest and the TMT: Part B than non-GAD participants. Mixed ANOVAs of response times measured during the spatial cueing task revealed significant main effects for Cue Valence and Cue Validity, as well as several significant interactions of these variables with GAD status. The significant Cue Valence x Cue Validity x GAD status interaction indicated that GAD participants were slower to disengage their attention from aversive stimuli, relative to pleasant or neutral stimuli, than non-GAD participants who did not exhibit this bias. This interaction effect, however, did not remain significant upon covarying for depression. Together, these findings suggest that individuals with GAD evidence poorer attentional control and demonstrate difficulties disengaging from threatening stimuli compared to persons without the disorder. Impairment in these attentional processes may, therefore, contribute to the etiology and maintenance of GAD. / Psychology

Social anxiety disorder (SAD) is one of the most prevalent psychological disorders and one that is particularly disruptive of social relationships. Socially anxious individuals often have trouble forming and maintaining intimate relationships, as evidenced by a high divorce rate and low relationship satisfaction within existing relationships. However, little is known about the specific reasons why relationships involving socially anxious individuals suffer. Initial research suggests that such relationships may be characterized by lower levels of emotional intimacy and difficulties managing and resolving conflict. The current study aimed to detect specific problems socially anxious individuals have communicating with their partners during conflict and support-seeking conversations. Male (n = 50) and female (n = 57) undergraduates ("actors") and their intimate partners ("partners") completed two videotaped conversations in our laboratory. One conversation featured a topic of conflict within the relationship, whereas the other focused on a personal problem experienced by the actor. Outcomes of interest included level of engagement and expressiveness of the actor, presence of positive (e.g., humor) and negative (e.g., withdrawal) communication behavior by the actor, feelings of satisfaction and closeness of both partners, and emotions experienced by both partners. We hypothesized that social anxiety would be associated with lower levels of engagement and expressiveness overall, but especially during conflict. Further, we hypothesized that those higher on social anxiety would demonstrate more negative communication behavior (such as expressing hostility toward their partners) during conflict. Results provided some evidence that socially anxious individuals were less engaged and expressive when speaking with their partners. However, there was no evidence that they used more negative communication behaviors. Our hypothesis that social anxiety would be associated with greater difficulty during conflict had minimal support; rather, conversations in which the actor elicited support appeared to be the most difficult for socially anxious individuals, particularly when emotional experience was considered. Clinical implications and ideas for further research are explored. / Psychology

Little to no research has evaluated factors that explain the manifestation and maintenance of bipolar disorder-anxiety disorder (BD-AD) comorbidity. The literature has shown that disruption of social and circadian rhythms is associated with mood episode onset. This association is especially pronounced among individuals who have a sensitive behavioral approach system (BAS). Inasmuch as anxiety sensitivity and trait anxiety have been associated both with BD and social rhythm disruption, it is worth examining whether anxiety sensitivity and trait anxiety confer risk for mood episode onset. The aims of this project were to: 1) evaluate trait anxiety and anxiety sensitivity as predictors of social rhythm disruption and BD-AD comorbidity, 2) examine social rhythm disruption (SRD) as a mediator of the association between trait anxiety and anxiety sensitivity and BD-AD comorbidity status, and 3) explore behavioral approach system sensitivity in these processes as contributing to the vulnerability to BD-AD comorbidity. A sample of 156 young adults participated in a multi-wave study in which they completed diagnostic interviews, symptom measures, and life event interviews which assessed the occurrence of positive and negative life events and the degree of SRD following these events every six months. Partial support for the hypotheses was found. Initial anxiety sensitivity, but not trait anxiety, positively predicted SRD for rewarding life events and follow-up bipolar symptoms. Additionally, SRD following positive life events predicted increases in depressive symptoms, but not hypomanic symptoms. SRD mediated the relationship between anxiety sensitivity and depressive symptoms. Furthermore, this relationship was stronger for healthy controls than for those with a bipolar disorder (BD) diagnosis or at-risk for developing BD. Moreover, individuals with a comorbid BD-AD diagnosis tended to have greater social rhythm disruption following negative life events than BD only or healthy individuals. Unexpectedly, individuals with comorbid BD-AD did not exhibit greater anxiety sensitivity or trait anxiety. Overall, the results suggest that anxiety sensitivity is a factor that may help to identify individuals who are vulnerable to bipolar symptoms. Furthermore, SRD is a mechanism that may partially explain this relationship. / Psychology

Ethnic minority youth use mental health services less frequently than Caucasian youth, despite similar rates of psychopathology. Research has documented ethnic differences in (1) parents' beliefs about the seriousness, prognosis, and etiology of child symptoms and (2) preferences for help-seeking, which may partially explain disparities in treatment utilization; however, few studies have examined underlying cultural factors that may account for ethnic differences or parent's beliefs and preferences with regard to youth anxiety. This study examined parents' beliefs about separation anxiety disorder (SAD) and preferences for help-seeking among 117 Indian-American (IA; n = 39), Puerto Rican (PR; n = 39), and European-American (EA; n = 39) mothers. After reading four vignettes describing SAD symptoms, parents rated the seriousness, prognosis, and etiology of symptoms and the likelihood of help-seeking. Parents also completed measures of acculturation, independent/interdependent self-construal, and strength of religious faith. RM-MANCOVA (controlling for SES) revealed that PR mothers were more likely than EA mothers to endorse medical etiology and were more likely than IA mothers to seek help from a physician. Hierarchical multiple regression revealed that acculturation and strength of religious faith predicted parents' etiological beliefs and preferences for help-seeking, after accounting for variance associated with SES and child gender. Results highlight the importance of examining cultural constructs that may contribute to ethnic differences. Implications for future research and clinical practice are discussed. / Psychology

Although several efficacious treatments exist for social anxiety disorder (SAD), less research has been devoted to identifying specific mechanisms involved in the etiology of SAD using high-risk, longitudinal designs. Given the high prevalence and personal and societal burden associated with a diagnosis of SAD, research is needed to elucidate causal factors at play in the development of SAD to inform innovative prevention programs for at-risk individuals. Theoretical models and empirical research suggest that biased attention toward threat-relevant information is an important factor in the maintenance of SAD. However, relatively little is known about the role of attention bias to threat in the development of SAD, and evidence is inconclusive with regard to whether attention biases lead to increases in anxiety over time. Also, only one study has examined attentional control as a potential factor moderating this relationship despite long-held assertions that "control over cognitive processes" may be an important individual difference factor determining the strength of the relationship between attention bias and development of excessive anxiety. Finally, a few studies have shown that attention bias to threat predicts stress reactivity, but these studies have only been conducted in unselected samples rather than with individuals at risk for developing SAD. Thus, the aims of this study were to examine the moderating effects of risk for SAD and attentional control on the relationships between attention bias to threat and (1) psychological and biological social stress reactivity and (2) development of SAD. The primary aim of the study was to examine the aforementioned relationships using attention bias to threat as assessed using the modified probe detection task (MPDT). In an exploratory analysis, the relationships were examined using an index of attention disengagement bias assessed with the Posner spatial cueing task (PSCT). Attentional control was represented by four indices, analyzed in separate regression analyses given their weak bivariate associations (i.e., Antisaccade task reaction time and accuracy rate, Attention Network Test executive control score, and total score on the Attentional Control Scale). First-year college students at low or high risk for developing SAD completed assessments of attention bias, attentional control, and anxiety during their first month of college. Approximately four months later, they completed a social stressor task and the same self-report measures of social anxiety. At the end of their first year in college, they completed the self-report measures of social anxiety once more, as well as a diagnostic interview for SAD. Correlational analyses indicated that attention bias to threat on the MPDT was associated with concurrent self-reported social anxiety but did not prospectively predict psychological or biological social stress reactivity, self-reported social anxiety, or SAD diagnostic status at the end of the first year in college. Hierarchical regression analyses supported the hypothesized double moderation for concurrent social anxiety, such that high levels of attentional control weakened the association between attention bias toward threat and social anxiety, only among the individuals at high risk for SAD. However, analyses did not support this relationship in predicting prospective outcomes, and several unexpected patterns emerged in which interactions between attention bias and attentional control were observed to predict prospective outcomes, but only among individuals at low risk for developing SAD. Likewise, exploratory analyses using the PSCT index of attention bias revealed unexpected interactions between risk group, attention bias, and attentional control. Considered together, results of the current study highlight the importance of considering individual differences in attention bias and attentional control in the maintenance and development of SAD. / Psychology

The degree to which patients and their therapists align over time on their perceptions of therapeutic processes and intermediary outcomes has generally been regarded as an important element of effective psychotherapy; however, few studies have examined empirically the influence of such dyadic convergences on ultimate treatment outcomes. This study examined (a) whether early treatment convergences in patient-therapist alliance and session progress ratings were associated with subsequent worry and distress reduction (and final posttreatment level) in psychotherapy for generalized anxiety disorder (GAD), and (b) whether treatment type and the initial (session 1) levels of perceived alliance and session progress moderated these associations. Data derived from a clinical trial in which patients with severe GAD were randomly assigned to receive either 15 sessions of cognitive-behavioral therapy (CBT; n = 43) or 4 sessions of motivational interviewing (MI) followed by 11 integrative CBT-MI sessions (n = 42). Patients and therapists rated the alliance and session progress after each session. Patients rated their worry and distress multiple times throughout treatment. Dyadic multilevel modeling revealed, as predicted, that alliance convergence over the first half of therapy was associated with greater subsequent worry (p = .03) and distress (p = .01) reduction. Additionally, the combination of low initial patient-rated alliance and early divergence was associated with the worst trajectory for the distress outcome (p = .04). Unexpectedly, session progress divergence had a near significant association with lower posttreatment worry (p = .05) and was significantly associated with more accelerated subsequent distress reduction (p = .03). Additionally, for patients who perceived their initial progress more positively, whether dyads converged or diverged in early session progress ratings affected the trajectories (though not the ultimate amount) of distress change (p = .02). These findings suggest that divergence of early patient-therapist alliance perspectives, especially when coupled with lower initial patient-rated alliance quality, may be an important marker for patient nonresponse and therapist responsiveness (e.g., use of alliance repair strategies). The findings on patient-therapist session progress convergence are less straightforward, though several possible implications are discussed.

The default mode network (DMN) is active in the absence of task demands and during self-referential thought. Considerable evidence suggests that the DMN is involved in normative aspects of social cognition, and as such, disruptions in the function of DMN would be expected in disorders characterized by alterations in social function. Consistent with this notion, work in autism spectrum disorder (ASD) and social anxiety disorder (SAD) has demonstrated altered activation of several core regions of the DMN relative to neurotypical controls. Despite emergent evidence for alterations within the same brain systems in SAD and ASD, as well as a behavioral continuum of social impairments, no study to date has examined what is unique and what is common to the brain systems within these disorders. Therefore, the primary aim of the current study is to precisely characterize the topology of neural connectivity within the DMN in SAD and ASD and neurotypical controls in order to test the following hypotheses through functional and structural connectivity analyses of the DMN. Our analyses demonstrate increased coavtivation of the dorsomedial prefrontal cortex in ASD and SAD compared to controls, as well as over and under connectivity in structural brain connectivity in ASD. These results may reflect general deficits in social function at rest, and disorder specific alterations in structural connectivity in ASD. / Master of Science

Thesis (PhD)--Stellenbosch University, 2014. / ENGLISH ABSTRACT: The etiology of anxiety disorders remains incompletely understood. Clear evidence for a genetic component has been proposed; however, there is also an increasing focus on environmental factors and the interaction between these and the genetic components that may mediate (anxiety) disorder pathogenesis. No single gene or genetic component has been explicitly identified as being involved in the development of anxiety disorders. This is most likely due to a number of reasons, which include, for example, the heterogeneity of anxiety disorders, the contribution of environmental factors and methodological limitations (e.g. small sample size) of research studies. Until now, genetic association studies usually focused on one particular psychiatric disorder at a time. However, with the difficulty in identifying susceptibility genes and/or loci in heterogeneous disorders like obsessive-compulsive disorder and other conditions in the anxiety spectrum, it is perhaps timely to consider multivariate genetics and epidemiological studies in a number of disorders sharing a core characteristic – such as anxiety. In addition to genetic underpinnings, a number of environmental variables have also been identified as risk factors for pathological anxiety, including adverse life events like childhood physical and sexual abuse. The hypothesis for this project is that a pre-existing genetic vulnerability (or genetic risk) interacts with the impact of adverse life events to result in the development of one or more anxiety disorder(s). Considering phenotypic overlap amongst the anxiety disorders, it is likely that diverse networks of genes and/ or interacting pathways are responsible for the phenotypic manifestations observed. Sprague Dawley rats exhibiting behaviours indicative of anxiety in the context of environmental stressors (maternal separation and restraint stress) were used as model for the identification of novel susceptibility genes for anxiety disorders in humans. The striatum has previously been implicated as a candidate in the brain architecture of anxiety pathogenicity, and is also a site exhibiting a high degree of synaptic plasticity. The synaptic plasticity pathway was investigated using the dorsal striatum of the rat brain and several genes were identified to be aberrantly expressed in “anxious” rats relative to controls (Mmp9, Bdnf, Ntf4, Egr2, Egr4, Grm2 and Arc). In humans, it was found that the severity of early adversity was significantly and positively associated with the presence of an anxiety disorder in adulthood. When the human homologues of the susceptibility candidate genes that were identified using the animal model were screened in a human cohort of patients with obsessive-compulsive disorder (OCD), panic disorder (PD) or social anxiety disorder (SAD) (relative to controls), five single nucleotide polymorphisms (SNPs) were found to be significantly associated with these conditions. Four of these SNPs were also found to significantly interact with the severity of childhood trauma. Haplotype analysis of variants within the identified susceptibility candidates revealed novel haplotype associations, four of which are located in the MMP9 gene. Notably, this the first study to link these particular mutations in the MMP9 gene with anxiety disorders and this finding is consistent with previous work suggesting that MMP9 is involved in conditions like cardiovascular disease and cancer which have been associated with increased prevalence of anxiety disorders. In conclusion, this project yielded important findings pertaining to the etiology of anxiety disorders. The use of a combined anxiety disorders cohort (OCD, PD and SAD) may suggest that the associations found here may hold true for anxiety disorders in general and not only for a particular clinically delineated condition. Childhood trauma was confirmed as an increased susceptibility risk for anxiety disorders. Also, this research contributed several novel susceptibility genes (MMP9, EGR2, EGR4, NTF4, and ARC), five significant SNP associations, four significant SNP-environment interactions and five haplotype associations (within MMP9 and BDNF) as candidates for anxiety pathogenicity. The identified polymorphisms and haplotypes were demonstrated to be associated with susceptibility to anxiety disorders in a gene-environment correlation and gene-environment interaction. / AFRIKAANSE OPSOMMING: Die oorsake van angssteurings word steeds nie volledig verstaan nie. Daar is duidelike bewyse vir 'n genetiese komponent, maar daar is ook toenemende fokus op omgewingsfaktore en die interaksie tussen hierdie omgewingsfaktore en genetiese komponente by angssteurings. Geen enkele geen of genetiese komponent is al geïdentifiseer as diè wat betrokke is by die ontwikkeling van angssteurings nie. Dit is waarskynlik weens 'n aantal redes, wat byvoorbeeld, die heterogeneïteit van angssteurings, die bydrae van omgewingsfaktore en metodologiese beperkings (bv. klein steekproef) van die navorsingstudies, insluit. Verder het genetiese assosiasiestudies tot nou toe gewoonlik net op een spesifieke psigiatriese versteuring op 'n slag gefokus. Maar, gegewe die uitdaging om vatbaarheidsgene en / of loci in heterogene steurings soos obsessief – kompulsiewe steuring (OKV) en ander toestande op die angsspektrum te identifiseer, is dit tyd om genetiese en kliniese studies in ‘n aantal steurings - met ‘n oorvleuende kern-element soos angs -, gesamentlik te oorweeg. Bykomend tot die genetiese boustene, is ‘n aantal omgewingsveranderlikes soos traumatiese lewenservarings tydens die kinderjare as risikofaktore vir patologiese angs geidentifiseer. Die hipotese vir hierdie projek is dat daar 'n interaksie tussen genetiese kwesbaarheid (of genetiese risiko) en traumatiese lewensevarings is en dat dit tot die ontwikkeling van 'n / veelvoudige angssteuring(s) kan lei. Inaggenome die fenotipiese oorvleueling tussen die angssteurings, is dit waarskynlik dat diverse netwerke van gene en / of interaktiewe geen-paaie vir die manifestasie van hierdie toestande verantwoordelik is. Sprague Dawley-rotte met gedragswyses aanduidend van angs, in die konteks van omgewingstressore (d.i. skeiding van die ma-rot en bedwang-stres [restraint stress]), is as model gebruik vir die identifisering van nuwe vatbaarheidsgene vir angssteurings in mense. Die striatum is voorheen as ‘n kandidaat in die brein-argitektuur van patologiese angs voorgehou, en is ook ‘n plek met ‘n hoë mate van sinaptiese plastisiteit. Die sinaptiese plastisiteit is ondersoek deur te fokus op die dorsale striatum van die rotbrein en daar is verskeie gene gevind wat anders is in “angstige” rotte in vergelyking met kontroles (Mmp9, Bdnf, Ntf4, Egr2, Egr4, Grm2 en Arc). In mense is daar gevind dat die ernstigheidsgraad van vroeë trauma beduidend en positief met die teenwoordigheid van ‘n angssteuring tydens volwassenheid verband hou. Toe die menslike ekwivalente van die vatbaarheidsgene wat met die dieremodel geïdentifiseer is in ‘n mens-kohort met obsessief-kompulsiewe steuring (OKS), panieksteuring (PS) en sosiale angssteuring (SAS) ondersoek is, is gevind dat daar 5 enkele nukleotied polimorfismes (ENPs) is wat met die toestande verband hou. Daar is ook gevind dat vier van hierdie ENPs beduidend verband hou met die ernstigheidsgraad van trauma tydens die kinderjare. Haplotipe analise van variante binne die geïdentifiseerde vatbaarheidsgene het op nuwe haplotipe assosiasies – waarvan 4 op die MMP9-geen geleë is – gedui. Hierdie is dus die eerste studie wat gevind het dat dié spesifieke mutasies van die MMP9-geen met angssteurings verband hou. Hierdie bevinding strook met vorige werk wat daarop dui dat die MMP9-geen by toestande soos kardiovaskulêre siekte en kanker wat ook met verhoogde voorkoms van angssteurings verband hou, betrokke is. Ter afsluiting kan ons sê dat hierdie projek belangrike bevindinge oor die oorsake van angssteurings gemaak het. Die gebruik van ‘n gekombineerde angssteurings-kohort (OKS. PS en SAS) kan moontlik suggereer dat die assosiasies wat ons hier gevind het, waar is vir alle angssteurings en nie net vir ‘n spesifieke afgebakende toestand nie. Traumatiese ervarings tydens die kinderjare is ook bevestig as ‘n risiko vir die ontwikkeling van angssteurings. Hierdie navorsing het ook verskeie nuwe vatbaarheidsgene (MMP9, EGR2, EGR4, NTF4, en ARC), 5 beduidende ENP assosiasies, 4 beduidende ENP-omgewings-interaksies en 5 haplotipe assosiasies (by MMP9 en BDNF) geïdentifiseer as moontlike kandidate wat ‘n rol speel by die ontstaan van patologiese angs. Daar is ook gevind dat die geïdentifiseerde polimorfismes en haplotipes met vatbaarheid vir angssteurings in ‘n geen-omgewing- korrelasie en geen-omgewing- interaksie verband hou. Stellenbosch University http://scholar.sun.ac.za

Thesis (MA)--Stellenbosch University, 2013. / ENGLISH ABSTRACT: Background: Both human and animal studies indicate that early trauma can influence brain development and can lead to dysregulation and dysfunction. This includes cognitive deficits. The risk of childhood trauma (CHT) and resulting cognitive deficits are well established in Posttraumatic Stress Disorder (PTSD). This is not the case for Social Anxiety Disorder (SAD). The experience of CHT does not inevitably lead to later psychopathology, suggesting that resiliency factors may be at play. Indeed, research shows that resilience is protective against the development of PTSD although this has not been well studied in SAD, particularly in the context of childhood trauma and neurocognition. Methods: This exploratory study assessed for the possible contribution of CHT on cognitive functioning in adults with SAD. We assessed 44 individuals who formed part of a larger study on neurocognitive and neuroimaging correlates in a sample drawn from the Western Cape, South Africa. Using a neuropsychological test battery, memory, attention and executive functioning (EF) (underpinned by hippocampal, cingulate cortex and pre frontal-cortex function respectively) were assessed. CHT was assessed with the Childhood Trauma Questionnaire (CTQ). We compared neurocognitive and resilience (CD-RISC) variables across four groups (SAD with trauma, SAD without trauma, PTSD and healthy controls) using analysis of variance (ANOVA) statistics. Results: None of the groups differed significantly on cognitive variables, however, on average all outcomes were in the predicted direction. Separate analyses for the traumatised groups only showed a significant effect for EF and attention, suggesting an association between EF, attention and CHT. On a measure of resilience, healthy controls had significantly higher resilience scores than the other 3 groups. Unexpectedly, SAD and PTSD groups with CHT had higher resilience scores than the SAD group without CHT, suggesting that resilience moderates CHT. Lastly individuals with SAD and PTSD with CHT reported more emotional abuse and neglect than any other type of childhood trauma. Conclusion: This exploratory study is unique in its comparative assessment of the effects of CHT and resilience on discussed. / AFRIKAANSE OPSOMMING: Agtergrond: Beide mens- en dierestudies dui daarop dat vroeë trauma brein ontwikkeling kan beïnvloed en kan lei tot disfunksie. Dit sluit kognitiewe tekortkominge in. Die risiko van vroeë kinderjare trauma (KJT) en die gevolglike kognitiewe tekortkominge is goed gevestig in Posttraumatiese stresversteuring (PTSV). Dit is egter nie die geval in Sosiale angsversteuring (SAV) nie. Die ervaring van KJT lei nie noodwendig tot latere psigopatologie nie, wat daarop dui dat veerkragtigheidsfaktore 'n rol kan speel. Trouens, navorsing toon dat veerkragtigheid beskermend is teen die ontwikkeling van PTSV, maar dit is egter nie behoorlik nagevors in SAV nie - veral nie in die konteks van vroeë kinderjare en neurokognisie nie. Metodologie: Hierdie verkennende studie het die invloed van KJT op kognitiewe funksionering in 44 individue geëvalueer. Hierdie studie het deel gevorm van 'n groter studie oor neurokognitiewe- en neurobeeldingskorrelate in 'n steekproef wat gewerf is uit die Wes-Kaap, Suid-Afrika. ‘n Neurosielkundige toetsbattery was gebruik om geheue, aandag en uitvoerende funksionering (UF) (wat onderskeidelik deur die hippokampus, cingulate korteks en prefrontale korteks ondersteun word) te assesseer. KJT is beoordeel met die "Childhood Trauma Questionnaire" (CTQ). 'n Analise van variansie (ANOVA) was gebruik om die neurokognitiewe en veerkragtigheid (CD-RISC) veranderlikes oor vier groepe (SAV met trauma, SAV sonder trauma, PTSV en gesonde kontrole) te vergelyk. Resultate: Nie een van die groepe het beduidend verskil van mekaar op grond van kognitiewe veranderlikes nie, maar oor die algemeen was alle uitkomste in die voorspelde rigting. Afsonderlike analises op die getraumatiseerde groepe het 'n beduidende effek gehad vir UF en aandag, wat dui op 'n assosiasie tussen UF, aandag en KJT. Die gesonde kontrole het beduidende hoër veerkragtigheid tellings as die ander 3 groepe gehad. SAV en PTSV groepe met KJT het teen verwagtinge hoër veerkragtigheidstellings gehad as die SAV sonder KJT, wat daarop dui dat veerkragtigheid KJT modereer. Laastens, individue met SAV en PTSV met KJT het meer emosionele mishandeling en verwaarlosing gerapporteer as enige ander tipe kinderjare trauma. Bespreking: Hierdie verkennende studie is uniek in sy vergelykende evaluering van die invloed van KJT en veerkragtigheid op die neurokognisie in deelnemers met SAV en PTSV. Beperkings en aanbevelings vir toekomstige navorsing word bespreek.

No description available.