published_or_final_version / Clinical Psychology / Master / Master of Social Sciences

There is now considerable evidence that phobic responding is associated with a bias towards expecting aversive or traumatic outcomes following encounters with the phobic stimulus (e.g. Davey, 1995). In terms of conditioning contingencies, this can be described as a bias towards expecting an aversive or traumatic outcome (the unconditioned stimulus - UCS) following a phobic stimulus (the conditioned stimulus - CS). Research into the role of UCS expectancy biases in the development and maintenance of specific phobias has three basic requirements. First, it is not clear whether the ues expectancy biases evidenced in specific phobias represent a stimulus specific response or a more generalised associative phenomenon. Second, it is not clear what dispositional or state factors might contribute to the development and maintenance of such ues expectancy biases. Third, it is not clear what type of cognitive mechanisms might underlie UCS expectancy biases. This thesis uses a thought experiment version of a threat conditioning procedure to explore these requirements. The key findings indicate that spider phobics tend to overestimate the likelihood of aversive outcomes following phobic, but not other fear relevant stimuli, and tend to underestimate the likelihood of aversive outcomes following fear irrelevant stimuli in comparison to non-phobic controls. This dichotomous ues expectancy bias is mirrored both in the evaluation of stimuli in terms of dangerousness and valance, and in the generation of harm and safety cues with regards to these stimuli. Both positive and negative mood states, but not arousal states contributed to ues expectancy inflation, and in the case of revulsive animals induced state disgust also increased reported ues expectancies. The thesis concludes with an evaluation of the role of UCS'S expectancies in the development and maintenance of specific phobias, and a discussion of the implications of these findings for our understanding of the information processing mechanisms underlying the specific phobias.

No description available.

This paper examined the links between selective attention, memory bias, interpretive bias, and anxiety problems in a community sample of 81 children (38 females) aged 9-17 years. Cognitive biases were assessed using a word and picture Dot Probe Discrimination task to assess selective attention, a memory task to assess a memory bias, and the CNCEQ to assess interpretive bias. Childhood anxiety was assessed using the parent and child versions of the RCMAS and RCADS. Significant associations were found between the three cognitive biases and childhood anxiety problems. In addition, selective attention was found to be associated with the selective abstraction subscale of the CNCEQ. The results did not support the mediation of selective attention and interpretive bias by memory bias. Finally, the results supported a cognitive model that posited that interpretive bias may be predictive of childhood anxiety problems beyond what is predicted by selective attention and memory bias.

Thesis (M.A.)--Kent State University, 2008. / Title from PDF t.p. (viewed Oct. 29, 2009). Advisor: David Fresco. Includes bibliographical references (p. 34-43).

Thesis (M. Soc. Sc.)--University of Hong Kong, 2008. / Includes bibliographical references (p.33-37).

This study evaluated a treatment program for anxiety disordered children, ages five to twelve years, utilizing both qualitative and quantitative methodologies. The treatment program integrated Imipramine pharmacotherapy and brief psychotherapy. The participants' nuclear and extended family histories were examined in terms of the occurrence of psychopathology and endemic transactional patterns. The examination of family patterns utilized Murray Bowen's Generational Model, as well as the T-F-A model of Hutchins and Cole, as a means of explaining the transmission of anxiety in the family. Ten children suspected of experiencing anxiety disorders were referred by pediatric physicians for treatment. Following an initial diagnostic assessment, children were placed on 25 milligrams of Imipramine per day for four to six weeks, while participating in weekly conjoint psychotherapy with their mothers for a six to eight-week period. A post-treatment evaluation was conducted by selecting ten prototypic participants. Selection was based upon age, diagnosis of overanxious disorder or separation anxiety disorder in childhood, and a time interval of no more than one year or less than one week following treatment. Semi-structured interviews were conducted with mother-child pairs separately to evaluate participants' perceptions of pre- and post-treatment symptom levels and family dynamics. DSM-III diagnostic criteria, Bowenian and T-F-A models served as the frameworks for organizing and evaluating qualitative data. All child participants experienced a dramatic and lasting resolution of both OAD and SAD symptomology. A quantitative analysis was performed utilizing the Wilcoxon sign rank to compare pre- and post-treatment symptom levels, with a significant effect by treatment occurring at the .005 level of significance. Cross-validation of treatment outcome was achieved through review of medical records, original psychotherapy notes, and videotapes of the interviews. Qualitative data regarding transgenerational medical and psychological disorders and family dynamics was generated. The data supported the Unitary model of generational family pathology. Six of seven Bowenian constructs were confirmed in this sample. The T-F-A model was used to demonstrate a cyclical pattern of reassurance, anxiety reduction, and child dependency between anxious children and their mothers. These results were discussed to provide a better understanding of the etiology and treatment of childhood anxiety disorders (OAD and SAD). The term "anxogenic family" was suggested to convey the interaction of genetics and generational learning in the families of anxiety disordered children. Implications for future research and modification of the DSM-IV regarding childhood anxiety disorders were discussed. / Ph. D.

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

[Truncated abstract] Over the past several decades substantial research has been conducted investigating the association between attentional bias to emotionally threatening material and anxiety. Tasks such as the emotional Stroop, the dichotic listening task and the visual probe task have been used to document this association, with the visual probe task providing the most direct means of assessing this bias. That this association exists stands beyond contention, however relatively little research has been conducted directly examining the causal nature of this relationship. By using predictive and recovery approaches it is possible to determine how attentional bias and anxiety co vary but not the exact causal nature of this relationship. However, when the visual probe methodology is used attentional bias to threat can be directly manipulated and as such it is possible to determine if attentional bias to threat causally underpins the development and maintenance of anxiety. The purpose of the current research was to deliver an extended attentional training task to anxious individuals by capitalising upon the ability to directly manipulate attentional bias using the visual probe task methodology and assessing the possible therapeutic benefits of such an approach. ...Nevertheless these results provided support for the validity of the causal hypothesis and the technological difficulties associated with administering the task online were ameliorated. Due to the fact that characteristics of both situational and dispositional anxiety are present in a clinical population a revised version of the attentional training task was administered to two groups of non-clinically anxious individuals to determine the impact that avoid threat attentional training has on each of these types of anxiety. High trait anxious students and pregnant women were chosen for this purpose but due to substantial attrition these two experiments failed to provide sufficient evidence to evaluate the causal hypothesis. Two main reasons for this attrition were identified, the motivation of participants and the procedures that were in place to monitor their progress. To ensure that attrition would not compromise future experiments a series of modifications were made and the attentional training program was then readministered to a sample of individuals characterised by dispositional or situational anxiety. A group of self labelled worriers and a sample of Immigrating Singaporean students respectively, were chosen for this purpose. There was no significant influence of avoid threat training on attentional bias for the self labelled worriers, nor any evidence of an attenuation of emotional vulnerability. For the Immigrating Singaporean students, however; there was evidence of a significant reversal of attentional bias to threat post attentional training compared to the control group and a corresponding attenuation of emotional vulnerability and a trend towards a significant attenuation of emotional reactivity. The implications for the causal hypothesis and the therapeutic applicability are discussed as well as several avenues for future research.

published_or_final_version / Clinical Psychology / Master / Master of Social Sciences