Chapter Two: Literature Review
Introduction
Anxiety is perhaps an emotion that predates man’s evolution. As Trivedi and Gupta (2010) point out, its ubiquity in in humans, as well as prevalence in various types of anxiety disorders, makes it a critical clinical issue that is worth focusing on. The word “anxiety” is derived from a Latin word “anxietas,” meaning to choke, upset, or throttle (Trivedi & Gupta, 2010). It encompasses behavioural, cognitive, and affective responses to the perception of danger. In moderation, Trivedi and Gupta (2010) contend that anxiety stimulates an anticipatory and adaptive response to perceived danger or any challenging or stressful situations. Nosological, epidemiological, as well as psychobiological developments have influenced significant advancements in the human understanding of a range of anxiety disorders in recent decades (Trivedi & Gupta, 2010). Anxiety disorders are most prevalent mental health conditions, which despite being less visible than other mental disorder such as schizophrenia, bipolar disorder, and depression, Bystritsky et al. (2013) contend can be disabling.
According to Shelton (2004), the prevalence of anxiety disorders among women is higher than among men (i.e. approximately two times higher in women than in men). Although the tendency towards anxiety disorders seems hereditary or familial, Wittchen et al. (1994) and Breslau et al. (1998) cited in Shelton (2004, p.2) contends other factors, including environomental factors may play a significant role in the development or acquisition of anxiety disorders. For instance, the homeostatic balance in the human body, and which Shelton (2004) defines as a stressor can be disrupted by certain changes in the human environment. Such disruption causes the reestablishment of the homeostatic balance by physiologic adaptations that take place in response to the stress response (Sapolsky, 2003). Such stress response is characterised by cascade of hormonal activities, including the release of corticotropin-releasing factor (CRF), which then triggers the release of corticotropin, and the subsequent release of glucocorticoids and epinephrine (i.e. stress hormones) from the adrenal cortex (Heim & Nemeroff, 2001). The release of CRF is decreased by the negative feedback sent to the hypothalamus by the glucocorticoids. Besides physical challenges, the tress response mechanism in primates can also be triggered by a perceived or anticipated homeostatic challenge (Shelton, 2004). This explains why an individual is more likely to develop paranoia, neurosis, or anxiety whenever he or she chronically or erroneously anticipates the occurrence of a homeostatic challenge (Sapolsky, 2003).
The Diagnostic and Statistical Manual of Mental Disorder, 4th edition (DSM-IV) (APA, 1994) recognises nine major categories of anxiety disorders namely: panic disorder (PD) (with or without agoraphobia); agoraphobia without panic; social phobia (social anxiety disorder); specific phobia; generalised anxiety disorder (GAD); acute stress disorder; posttraumatic stress disorder (PSD); obsessive compulsive disorder (OCD); as well as anxiety disorder not otherwise specified (cited in Trivedi & Gupta, 2010, p.211). Agoraphobia (AG) and panic disorder (PD) are some of the common types of anxiety disorders whose nosology have fluxed the DSM iterations. AG can be described as a person’s persistent and irrational fear of certain activities or situations, which occasion the development of a compelling desire to avoid the stimulus. Typically, people suffering from AG refrain from traveling away from their homes or rely on being in the company of others while travelling away from home. Individuals suffering from mild AG would leave their homes, but avoid specific situations such as strange areas, crowded places such as supermarkets or lifts, public transport areas or driving their cars. However, patients suffering from severe AG may develop inability to leave their homes or certain rooms within the house. AG is regarded as the most common and disabling phobia among clinically significant phobia. Both patients and physicians perceive panic attacks (PAs) as life threatening, given their severity and sudden onset, especially when the attacks are characterised by symptoms like chest pain and tachycardia. It is estimated that about 65% of individuals who experience PAs are more likely to develop AG. Both AG and PD are characterised by common main physical and emotional symptoms such as increased heart rate, sweating, muscle tension, and difficulty of concentration, all which make the two disorders form part of anxiety. However, AG and PD vary in certain ways. For instance, unlike the case in AG, the physical symptoms in PD start gradually to attain the highest level in 10 minutes, hence making a panic victim to exaggerate the explanation of his/her body symptoms and develop the fear of a repeat attack. Nevertheless, research shows that the relationship between the two types of anxiety disorder (i.e. AG and PD) remain a controversial topic in the contemporary nosology. This chapter therefore reviews existing relevant theoretical and empirical literature AG, PD, GAD, and depression. In particular, it explores the relationship between AG/PD and depression, common symptoms of AG and PD as part of anxiety, the co-morbidity of AG and PD, the role of using psychometrics in diagnosing AG and PD, as well as the role of Mobility Inventory (MI) in measuring AG in different cultures.
The Relationship between Agoraphobia, Panic Disorder, GAD, and Depression
The term “agoraphobia’ is derived from a Greek word “agora,” which refers to a public place or where people gathers publicly such as a market place. In this regard, AG is deemed as the fear of public places. Brown, Gaudiano, and Miller (2010) and Hara et al. (2012) described AG as the fear of places where a person thinks escape is hard or consider help in the event of an unexpected attack or situationally predisposed panic attack (PA) is unavailable. Places that make an individual to feel embarrassed, trapped, or helpless, such as public transport areas can induce AG on a person (En-Young et al., 2015). People who have had a previous experience of panic attack or a series of panic attacks are more likely to develop AG, which is likely to become fearful of further, future attacks, and thus avoiding perceived situations in which such attacks occurred or are likely to occur. People diagnosed with AG are characterised by reduced everyday functioning well-being and are likely to suffer from other serious forms of psychopathology, such as depression, substance misuse, and social isolation.
PD on the other hand is defined by its central feature – panic attack (PA), which the DSM-IV defined as a discrete period of intense fear or discomfort in the absence of actual danger that arises suddenly and reaches its peak within 10 minutes (APA, 2000). de Ruiter and Van Ijzendoorn (1992) described PD as a condition that is characterised by spontaneous Panic attacks without phobic avoidance. According to the DSM-IV, PA is characterised by a number of symptoms, and at least four of such attacks have to be present in a patient to qualify as a victim of panic attack. The characteristics symptoms of PA as outlined by the DSM-IV are fear of dying; palpitations; parenthesis; accelerated hear rate; feeling of chocking; fear of losing control; sweating; chest pain; depersonalization; chills; abnormal distress or nausea; feeling dizzy; sensation of shortness of breath or smothering; unsteadiness, and trembling (APA, 2000). According to Goodwin (2003) possessing panic symptoms per se does not indicate that a person has PD. However, a person is considered to be having PD is he/she exhibits the PA characteristic symptoms and subsequently experiences other attacks within a period of one month, a phenomenon that leaves the victim to worry about the implications of the attacks that are likely to emerge, and hence developing an avoidance behaviour of the situation in which the attack took place, as a way of self-protection (Goodwin, 2003). A number of previous researches have recognised PD as a chronic illness that causes patients to exhibit little spontaneous improvement with a highly non-uniform disease progression (Breier, Charney, & Heninger, 1986; Keller & Hanks, 1993; Katschnig et al., 1995; Fava & Mangelli, 1999; Fava et al., 2001; Andersch & Hetta, 2003; Hara et al., 2012).
The generalized anxiety disorder (GAD) on the other hand is a type of anxiety disorder, which is characterised by extreme anxiety and worry about a range of events experienced or anticipated by an individual for a number of days within a period of six months (Shelton, 2004). A person diagnosed with GAD manifests both physical and psychological symptoms, which degenerate into significant impairment and/or distress associated with social functions (Shelton, 2004). Most patients with GAD experience muscle tension, dry mouth, diarrhoea, sweating, cold hands, nausea, as well as urinary frequency (Shelton, 2004). GAD can lead to the development of other anxiety disorders, depression, as well as substance abuse disorders (Rickels & Schweizer, 1997; Yonkers et al., 2000).
Under the DSM-III and DSM-IV, agoraphobia was not considered as an independent capable disorder, but rather a variant or sequel of the PD spectrum. This implies that a person was diagnosed with either PD with AG (PDA) or without AG (PDWA). For instance, in the 1980, the DSM-III identified three main classifications: (1) panic disorder; (2) agoraphobia with panic disorder; and (3) agoraphobia without panic disorder (Andrews et al., 2009). According to DSM-III (1980) and Gelder and Johnston (1981), AG is a separate syndrome from other phobic disorders as well as depression disorders. Available evidence suggest that the relationship between AG and PD is a controversial and hotly contested topic. Majority of psychiatrists in North America perceive PA as a central feature of the disorder and regards AG as a consequence of PD, which arises after a first panic attack (FPA) (Andrews et al., 2009). The DSM-III’s diagnostic system therefore did not therefore diagnose AG as a discrete disorder, but only in relation to PD, a phenomenon that is inconsistent with the current classification under the DSM-V as well as recent research in AG, which suggest that AG is a separate and discrete disorder (APA, 2015; Bienvenu, et al ., 2006; Wittchen, et al ., 2008). Research on AG also suggest that AG is a depilating disorder just like PD.
However, Buller et al. (1986); Garvey & Tuason (1984); and Klein (1981) contended that agoraphobia is not a separate and independent entity, but instead is a secondary response to panic disorder. According to Buller et al. (1986); Garvey & Tuason (1984); and Klein (1981), prior to panic attacks, agoraphobia remain uncommon and both panic disorder and agoraphobia were characterised by clinical similarities, in terms of presentation. A study on familial transmission of agoraphobia and panic disorder conducted by Noyes et al., (1986) corroborated the notion that agoraphobia is not a separate entity, but a severe variant of panic. In this regard, the revised DSM-III (DSM-III-R) reclassified agoraphobia as a sequel of panic disorder, which can exhibit itself with or without agoraphobia (Andrews et al., 2009). The DSM-III-R’s classification of agoraphobia was upheld by the DSM-IV. Therefore, in light of the classifications by DSM-III-R and DSM-IV, emphasis is given to panic as the key feature, while agoraphobia is considered as a complication of the panic disorder. This notion is expounded by Andrews et al. (2009) in their seminal work dubbed; Stress-Induced and Fear Circuitry Disorders: Refining the Research Agenda for DSM-5. According to the classification of the relationship between panic and agoraphobia as advanced by ICD-10, the phobic attitude is the main aspect of AG.
However, under the DSM-V, agoraphobia became distiquished from the PD, given that there are some instances where a patient may suffer AG without showing any history of having panic. Nevertheless, APA (2013) observes that both AG and PD are types of anxiety disorders. No significant variations exist between patients with AG with panic and those with AG without panic. The same argument for the relationship between AG with panic and those with AG without panic could be used in to support the relationship between AG and depression. In their study, Buller, Maler, and Benkert (1986) found that a clear relationship existed between PD and depression.
Research also indicates that AG/PD and depression are correlates of self-reported behavioural inhibition in children and adolescents (Muris et al., 2001). In their study, Muris et al. (2001) examined the relationship between self-reported behavioural inhibition and AG/PD and depression systems among a sample of 968 adolescents aged between 12 and 18 years. The study findings indicated that highly behaviourally inhibited adolescents recorded higher scores of AG/PD and depression symptoms than their counterparts with low or middle behavioural inhibitions (Muris et al., 2001). Using structural equations modelling to test hypothetical models on the contribution of behavioural inhibition to the development of PD and depression, the study found that behavioural inhibition occasioned the development of PD, which in turn led to depression (Muris et al., 2001). The study by Muris et al. (2001) reflects the findings of a number of previous studies. For instance, in a study that examined the correlation between behavioural inhibition and PD among pre-school children, Biederman et al. (1993) found that behaviourally inhibited children were more likely to develop AG and/or PD than their non-behaviourally inhibited counterparts. Besides, Biederman et al. (1993) also observed that from baseline to follow-up, the rates of PD and AG increased significantly among the behaviourally inhibited children. In another similar study, Biederman et al. (1995) like Muris et al. (1999) and Muris et al. (2001) found that behavioural inhibition among pre-school children not only influenced the development of AG and PD, but also had a direct role in the development of depression among such children. Another theory is that panic serves as an antecedent in the connection between behavioural inhibition and depression among children. This theory was confirmed in a study conducted by Cole et al. (1998), which found that higher levels of panic among behaviourally inhibited children at one point in time served as predictors of higher levels of depression at a subsequent point in time among such children, especially when controlling for prior levels of depression among the subjects. In view of the foregoing, it can be argued that depression among behaviourally inhibited children is a function of higher levels of panic among such children, a hypothesis that supports the notion advanced by Biederman et al. (1995); Muris et al. (1999); and Muris et al. (2001) that behavioural inhibition occasions AG and/or PD, which in turn leads to depression.
Some empirical studies have also attempted to examine the relationship between various subtypes of agoraphobia (i.e. agoraphobia with panic and agoraphobia without panic attack) and depression. For instance, using a sample of high school students who had experienced a first panic attack (FPA), Wilson and Hayward (2005) examined the relationships between depression symptoms and pre-panic vulnerabilities, panic severity, as well as post-panic agoraphobia. In doing so, Wilson and Hayward (2005) hypothesised that: (1) pre-panic anxiety severity, childhood behavioural inhibitions, and negative affect serve as predictors for agoraphobia and depressive symptoms following a panic attack; (2) pre-panic anxiety severity, childhood behavioural inhibitions, and negative affect lead to severe panic attacks; (3) severe and spontaneous panic attacks serve as predictors for subsequent agoraphobia and depressive symptoms; and (4) the interaction between panic severity and pre-panic anxiety severity, childhood behavioural inhibitions, as well as negative affect is associated with severe outcomes following a panic attack. While the study findings confirmed the first three hypotheses, Wilson and Hayward (2005) reported no evidence to support the fourth hypothesis. According to Buller et al. (1986), patients who are diagnosed with agoraphobia are more likely to develop secondary depression. A number of previous studies have also reported that panic patients with longer history of panic with agoraphobia are more likely to exhibit more depressive symptoms (Klerman, 1990; Strodl & Noller, 2003).
Hara et al. (2012) identified the fear of being alone outside one’s home, being in a crowded place or queuing in a public place, travelling using a public transport system, or being on a bridge as some of the common situations that induce agoraphobic fears. Existing biological and psychological models of AG and PD uphold that a relationship exists between PA and the development or inducement of AG (Margraf, Ehlers, & Roth, 1986; Telch et al., 1989 cited in Hara et al., 2012, p.2). According to Amering et al. (1997), identification of early predictors for the development of AG is essential for effective clinical practice. Features of the first panic attack (FPA) are considered as the early predictors of the development of AG (Amering et al., 1997). Hara et al. (2012) contend that the situation in which a patient experienced his/her FPA constitutes the key features of the patient’s FPA. While a number of previous studies have attempted to explore the relationship between the situation in which patients experienced their FPAs and the subsequent development of AG, available evidence suggest that the findings of such studies indicate a somewhat controversial relationship between FPA and the subsequent development of AG. For instance, in their study of the onset PD with AG, Lelliott et al. (1989) found that patients who had experienced their FPAs in public spaces were more likely to be diagnosed with AG with PD. Similarly, in their examination of the onset of PD, Faravelli et al. (1992) found that patients who had had their FPAs in phobogenic circumstances were more likely to be diagnosed with AG with PD. Besides, in a study that explored precipitating events, locations, and reactions associated with FPAs, Shulman et al. (1994) found that patients diagnosed with extreme AG were more likely to have experienced their FPAs in classic agoraphobic situations such as while using public transportation.
The findings by Shulman et al. (1994) were corroborated by a study conducted by Hara et al. (2012). Hara et al. (2012) sought to investigate the probability of a patient’s FPA and the subsequent development of agoraphobia. In doing so, the study classified a sample of 830 panic disorder patients into five groups based on the places where the FPA was experienced (i.e. home, outside home, school/office, driving a car, and while using public transportation). The clinical characteristics of each group were investigated and recorded. The clinical features of the panic disorder patients with agoraphobia who had experienced their FPAs in the home environment were them compared with those of their counterparts who had experienced their FPAs in the rest of the places (i.e. outside home, school/office, driving a car, and while using public transportation). The study reported significant variations among sex ratio, severity of the FPA, patients’ drinking status, smoking status, ratio of agoraphobia, the degree of patients’ avoidance behaviour, as well as patients’ depression score. Variations were also reported among the participants, in terms of rate of sweating, severity of chest pain, feeling of dizziness, as well as fear of dying (Hara et al., 2012). Higher incidences of comorbid agoraphobia were recorded among patients who had experienced their FPAs while driving a car or while using public transportation compared to their counterparts who had experienced their FPA at home, outside home, or in school/office (Hara et al., 2012). In addition, the findings of the study indicated that the panic disorder patients with agoraphobia who indicated to have experienced their FPAs at home exhibited higher frequencies of the fear of dying and a feeling of severe distress occasioned by the FPA compared to their counterparts who had had their FPAs outside the home environment. The findings of the study by Hara et al. (2012) thus corroborate the argument that panic disorder patients with agoraphobia exhibit varying clinical features based on where the patient under examination experienced his/her FPA. For instance, the at-home patients more frequently expressed the ‘fear of dying’ and felt more distressed compared to their counterparts who indicated that they had experienced their FPAs outside the home environment. The implications for practitioners therefore is that treatment of at-home panic disorder patients with agoraphobic symptoms needs to focus more on the fear and distress occasioned by the FPA.
In addition, Amering et al. (1997) found that a significant relationship existed between FPA accompanied by feelings of embarrassment and the subsequent development of AG. Moreover, some studies have also reported an association between FPAs experienced in home environments and the subsequent development of AG. For instance, Craske et al. (1990) found that some of the patients who had experienced their FPAs at home also developed AG. In most studies, the percentages of PD patients being diagnosed with AG, who indicate to have experienced their FPAs in the home environment have ranged from 8-17%. For instance, in their study of the onset of PD with AG, Lelliott et al. (1989) found that 8% of the PD patients participating in the study had developed AG as a consequent of experiencing their FPAs at home. Similarly, Faravelli et al. (1992) reported that 10.3% of the PD patients participating in the study had developed AG after experiencing their FPAs at home. In another study by Amering et al. (1997), the percentage of PD patients diagnosed with AG after experiencing their FPAs at home was found to be 17%. Previous studies have also indicated that more PD patients who experienced their FPAs at home are more likely to become minimal avoiders. For instance, in two separate studies that sought to compare minimal and extensive avoiders, Shulman et al. (1994) and Craske et al. (1990) found that the percentage of extensive avoiders who had experienced their FPAs at home was 2.6% and 29.4% respectively.
Chapter Three: Methodology
Introduction
The current study sought to ration the agoraphobia (AG) scale (Mobility Inventory – MI) to the Arabic language in the Saudi (Riyadh) environment and explore the relationship between AG and depression. In doing so, the study hoped to achieve three specific goals, including, translate to translate the AG scale into Arabic for purposes of providing a suitable tool for psychotherapy sessions within the Saudi environments; to establish whether a relationship exists between AG and depression; and to determine if there is a difference in depression between AG with panic disorder (PD) and AG without PD. The study intended to answer four research questions namely: Are agoraphobia and panic the same?; Is agoraphobia accompanied by panic always?; Are there relationships between agoraphobia, panic disorder, and general anxiety disorder or mood disorder?; and Is the level of comorbidity higher in AG groups with PD or AG groups without PD? This chapter therefore outlines the methodology that was adopted by the study in achieving the outlined goals and answering the research questions.
Study Participants
The subjects for this study comprised 20 patients diagnosed with agoraphobia aged between 25 and 45 years (both males and females), and who are currently under psychiatric supervision following diagnosis, and as classified by psychiatric services at King Khaled University Hospital’s (KKUH) Psychiatry Department. The sample size will be determined using the following formula:
n = (Za/2)2 s2 / d2
Where:
n: is the sample size;
S: is standard deviation (1.02) derived from a previous study by Chambless et al. (1985);
d: is the accuracy of estimate, taken as 0.5 difference score in the mean score; and
Za/2: is a normal deviate that reflects the type I error taken as 1.96 at 95% confidence level.
Therefore applying the above formula;
The sample size (n) = (1.96)2 * (1.02)2 / (0.5)2
= 3.84 * 1.04 / 0.25
=15.97 ~ 16 participants.
Considering that cases of missing data were likely to be experienced, the study adopted a sample size of 20 participant.
Procedure
The agoraphobia test materials were translated into Arabic before being administered to the sampled participants. In order to ensure high validity and reliability of the translation process, the study adopted Sousa et al.’s (2011) 5-step translation procedure. The first step involved the translation of the original agoraphobia test instrument into the target language (Arabic) (forward translation or one-way translation). In the second step, the two translated versions of the agoraphobia scale or test instrument (i.e. agoraphobia scale in the English language – TL2 and agoraphobia scale in the Arabic language – TL1) were compared. The third step involved undertaking a blind translation exercise (i.e. blind backward translation or blind double translation) of the primary initial translated version of the agoraphobia test instrument. In the fourth step, the study undertook a comparison of the two back-translated versions of the instrument (B-TL1 and B-TL2). The final stage involved pilot testing of the pre-final agora test instrument translated in the Arabic language with a monolingual sample, cognitive debriefing. The validity and reliability of the agoraphobia test instrument or scale translated into the Arabic language will be assessed and compared with the PHQ-9 score to determine any existing relation between the two instruments.
It is worth noting that the Agora test instrument was translated from the English language to the Arabic language by two independent and experienced translators. The translated version of the Agoraphobia test instrument was revised by the research committee and a consensus reached on the most accurate and suitable translated version of the Agoraphobia scale. The translated Agoraphobia test instrument was then back-translated from the Arabic language to the English language by two independent experienced translators. The back-translated version of the Agoraphobia test instrument was sent to the scale author to decide on whether the translation was accurate enough or not.
At the outset of the study, the necessary ethical approval was sought from the KKUH, and the actual engagement with the sampled participants only commenced after the ethical approval was granted by the hospital. Patient interviews were conducted in the outpatient psychiatric clinic in KKUH for about 30-45 minutes for every individual participant. The interview took place under typical psychometric clinic conditions (i.e. relative light, noise, as well as conducive or comfortable environment). The purpose of and processes involved in the study were explained to the sampled participants, with a view of obtaining their informed consents. In addition, the participants were assured of their anonymity during the entire study and notified that the information their volunteer in the course of their participation in the study will treated as confidential as possible, and only be used for purposes of achieving the goal of the study. Furthermore, the participants were informed of their right to withdraw from the study at any given time without any physical, emotional, health, or social consequences. Moreover, the sampled Agoraphobic participants had received a ‘diagnosis’ via psychiatric services at KKUH’s Psychiatric Department. The patient who already diagnosed in referred to the psychologist – these participants were given three measures.
The sampled participants were then asked to fill in the Agoraphobia Scale (the Mobility Inventory – MI scale), translated into Arabic. The filling in of the translated MI scale was intended to confirm the participants’ ‘diagnosis’ and evaluate their improvement during the psychotherapy sessions. Depression was measured using PHQ-9 while PD was measured using Patient Health Questionnaire – panic Scale (PHQ). In addition, panic attacks were documented using the MI scale.
The Mobility Inventory (MI) for Agoraphobia is a 27-item inventory that was developed by Chambless et al. (1985). The MI for Agoraphobia asks participants to rate, on a 5-point scale, their level of avoidance for 26 situations (e.g. supermarkets, restaurants, buses, standing in lines, e.t.c.), both when accompanied by a trusted companion and when alone. In this study, only alone scale was utilised for purposes of measuring the participants’ levels of avoidance of various situations outlined in the MI. The Patient Health Questionnaire (PHQ-9) on the other hand is a 3-page questionnaire which can entirely be self-administered by the patient. When using the PHQ-9, the clinician scans the completed questionnaire, verifies positive responses, and applies diagnostic algorithms that are abbreviated at the bottom of each page. The PHQ assesses eight (8) diagnoses, which are divided into threshold disorders (i.e. disorders that correspond to specific DSM-IV diagnoses such as major depressive disorder, panic disorder, other anxiety disorder, and bulimia nervosa) and subthreshold disorders (i.e. disorders whose criteria encompass fewer symptoms than are required for any specific DSM-IV diagnoses, including other depressive disorder, probable alcohol abuse/dependence, somatoform, and binge eating disorder).
Data Collection and Analysis
The necessary quantitative data for analysis in this study was collected from the sampled agoraphobic patients using a self-administered questionnaire (see appendix) based on three measures (i.e. diagnoses and patients’ improvement during the psychotherapy sessions; panic disorder, and depression).
The Statistical Package for Social Sciences (SPSS) version 21 was used to compute the necessary descriptive statistics, and perform the necessary analyses of variance. The structural equations modelling program (EQS) devised by Bentler (1989) was used to test the models on the role of panic on the development of agoraphobia and depressive symptoms among the participants. The EQS program integrates multiple regression and path analysis and generate a range of goodness-of-fit indices suggesting how significant the test model accounts for the established correlation structure for the analysed data (Muris et al., 2001).
Discussion
This chapter analyses and discusses the findings of the study.
References
Ainsworth, M. D., Blehar, M. C., Waters, E., & Wall, S. (1978). Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Erlbaum.
Al Aseri, Z. A., Suriya, M. O., Hassan, H. A., Hasan, M., Sheikh, S. A., Al Tamimi, A., Alshathri, M., & Khalid, N. (2015). Reliability and validity of the hospital anxiety and depression scale in an emergency department in Saudi Arabia: A cross-sectional observational study. BMC Emergency Medicine, 15(28), 1-6. Doi: 10.1186/s12873-015- 0051-4
American Psychiatric Association (APA). (1994). Diagnostic and statistical manual for the assessment of mental disorders (4th ed). Washington, DC: American Psychiatric Association.
Amering, M., Katschnig, H., Berger, P., Windhaber, J., Baischer, W., Dantendorfer, K. (1997). Embarrassment about the first panic attack predicts agoraphobia in panic disorder. Behav Res Ther, 35(1), 517-521.
Andersch, S. & Hetta, J. A. (2003). 15-year follow-up study of patients with panic disorder. Eur Psychiatry, 18(1), 401-408.
Andrews, G., Charney, D. S., Sirovatka, P. J., & Regier, D. A. (2009). Stress-Induced and Fear Circuitry Disorders: Refining the Research Agenda for DSM-5. Arlington VA: American Psychiatric Association.
Bentler, P. M. (1989). EQS: Structural equations program manual. Los Angeles, CA: BMDP Statistical Software Inc.
Biederman, J., Rosenbaum, J. F., Bolduc-Murphy, E. A., Faraone, S. V., Chaloff, J., Hirshfeld, D. R., & Kagan, J. (1993). A 3-year follow-up of children with and without behavioral inhibition. Journal of the American Academy of Child and Adolescent Psychiatry, 32(1), 814-821.
Bowlby, N. (1973). Attachment and loss: Vol.2. Separation, anxiety, and anger. New York: Basic Books.
Bowlby, N. (1980). Attachment and loss: Vol.3. Loss. New York: Basic Books.
Bowlby, N. (1982). Attachment and loss: Vol.1. Attachment. New York: Basic Books.
Breier, A., Charney, D. S., & Heninger, G. R. (1986). Agoraphobia with panic attacks: Development, diagnostic stability, and course of illness. Arch Gen Psychiatry, 43(1), 1029-1036.
Breslau, N., Kessler, R. C., Chilcoat, H. D., Schultz, L. R., Davis, G. C., Andreski, P. (1998). Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma. Arch Gen Psychiatry, 55(1), 626-632.
Brown, L. A., Gaudiano, B. A., & Miller, I. W. (2010). The impact of panic-agoraphobia comorbidity on suicidality in hospitalized patients with major depression. Depress Anxiety, 27(3), 310-315. Doi: 10.1002/da.20609
Buller, R., Maler, W., & Benkert, O. (1986). Clinical subtypes in panic disorder. Their descriptive and prospective validity. Journal of Affective Disorders, 11(1), 105-114.
Bystritsky, A., Khalsa, S. S., Cameron, M. E., & Schiffman, J. (2013). Current Diagnosis and Treatment of Anxiety Disorders. Pharmacy and Therapeutics, 38(1), 30-57.
Chambless, D. L., Caputo, C. G., Jasin, S. E., Gracely, E. J., & Williams, C. (1985). The mobility inventory for agoraphobia. Behaviour and Research in Therapy, 23(1), 35-44.
Collins, N. L., & Read, S. J. 1990. Adult attachment, working models, and relationship quality in dating couples. Journal of Personality and Social Psychology, 58(4), 644-663.
Craske, M. G., Miller, P. P., Rotunda, R., & Barlow, D. H. (1990). A descriptive report of features of initial unexpected panic attacks in minimal and extensive avoiders. Behav Res Ther, 28(1), 395-400.
Culpepper, L. (2004). Effective Recognition and Treatment of Generalized Anxiety Disorder in Primary Care. Prim Care Companion J Clin Psychiatry, 6(1), 35-41.
de Ruiter, C. & Van Ijzendoorn, M. H. (1992). Agoraphobia and anxious-ambivalent attachment: An integrative review. Journal of Anxiety Disorders, 6(4), 365-381.
En-Young, N. W., Wagner, J. T., Glaus, J., Vandeleur, C. L., Castelao, E., Marie-Pierre, F. S., Vollenweider, P., Preisig, M., & von Känel, R. (2015). Evidence for Chronic Low-Grade Systemic Inflammation in Individuals with Agoraphobia from a Population-Based Prospective Study. PLoS ONE, 10(4), 1-19. Doi:10.1371/journal.pone.0123757
Faravelli, C., Pallanti, S., Biondi, F., Paterniti, S., Scarpato, M. A. (1992). Onset of Panic disorder. Am J Psychiatry, 149(1), 827-828.
Fava, G. A. & Mangelli, L. (1999). Subclinical symptoms of panic disorder: New insights into pathophysiology and treatment. Psychother Psychosom, 68(1), 281-289.
Fava, G. A., Rafanelli, C., Grandi, S., Conti, S., Ruini, C., Mangelli, L., & Belluardo, P. (2001). Long-term outcome of panic disorder with agoraphobia treated by exposure. Psychol Med, 31(1), 891-898.
Fava, M., Rankin, M. A., Wright, E. C., Alpert, J. E., Nierenberg, A. A., Pava, J., & Rosenbaum, J. F. (2000). Anxiety disorders in major depression. Comprehensive psychiatry, 41(2), 97-102.
Hara, N., Nishimura, Y., Yokoyama, C., Inoue, K., Nishida, A., Tanii, H., Okada, M., Kaiya, H., & Okazaki, Y. (2012). The development of agoraphobia is associated with the symptoms and location of a patient’s first panic attack. BioPsychoSocial Medicine, 6(12), 1-8.
Hazan, C. & Shawer, P. (1987). Romantic love conceptualized as an attachment process. Journal of Personality and Social Psychology, 52(1), 511-524.
Heim, C. & Nemeroff, C. B. (2001). The role of childhood trauma in the neurobiology of mood and anxiety disorders: Preclinical and clinical studies. Biol Psychiatry, 49(1), 1023-1039.
Katschnig, H., Amering, M., Stolk, J. M., Klerman, G. L., Ballenger, J. C., Briggs, A., Buller, R., Cassano, G., Garvey, M., & Roth, M. (1995). Long term follow-up after a drug trial for panic disorder. Br J Psychiatry, 167(1), 487-494.
Keller, M. B. & Hanks, D. L. (1993). Course and outcome in panic disorder. ProgNeuropsychopharmacol Biol Psychiatry, 17(1), 551-570.
Klerman, G. L. (1990). Depression and panic anxiety: the effect of depressive co-morbidity on response to drug treatment of patients with panic disorder and agoraphobia. Journal of psychiatric research, 24(1), 27-41.
Lelliott, P., Marks, I., McNamee, G., Tobena, A. (1989). Onset of Panic disorder with agoraphobia. Arch Gen Psychiatry, 46(1), 1000-1004.
Levy, M. B. & Davis, K. E. (1988). Love styles and attachment styles compared: Their relations to each other and to various relationship characteristics. Journal of Social and Personal Relationships, 5(1), 439-471.
Mallinckrodt, B. (1992). Childhood emotional bonds with parents, development of adult social competencies, and availability of social support. Journal of Counselling Psychology, 39(4), 453-461.
Margraf, J., Ehlers, A., & Roth, W. T. (1986). Biological models of panic disorder and agoraphobia – A review. Behav Res Ther, 24(1), 553-567.
Mosing, M. A., Gordon, S. D., Medland, S. F., Statham, D. J., Nelson, E. C., Heath, A. C., Martin, N. G., & Wray, N. R. (2009). Genetic and environmental influences on the co- morbidity between depression, panic disorder, agoraphobia, and social phobia: A twin study. Depression and Anxiety, 26(11), 1004-1011. Doi: 10.1002/da.20611
Muris, P., Merckelbach, H., Schmidt, H., Gadet, B., & Bogie, N. (2001). Anxiety and depression as correlates of self-reported behavioural inhibition in normal adolescents. Behaviour Research and Therapy, 39(1), 1051-1061.
Muris, P., Merckelbach, H., Wessel, I., & Van De Ven, M. (1999). Psychopathological correlates of self-reported behavioural inhibition in normal children. Behaviour Research and Therapy, 37(1), 575-584.
Rickels, K. & Schweizer, E. (1997). The clinical presentation of generalized anxiety in primary- care settings: Practical concepts of classification and management. J Clin Psychiatry, 7;58(11):4-10.
Sapolsky, R. (2003). Taming stress. Sci Am., 289(1), 86-95.
Shelton, C. I. (2004). Diagnosis and management of anxiety disorders. The Journal of the American Osteopathic Association (JAOA), 104(3), s2-s5.
Shulman, I. D., Cox, B. J., Swinson, R. P., Kuch, K., & Reichman, J. T. (1994). Precipitating events, locations and reactions associated with initial unexpected panic attacks. Behav Res Ther, 32(1), 17-20.
Sousa, V. D., & Rojjanasrirat, W. (2011). Translation, adaptation and validation of instruments or scales for use in cross‐cultural health care research: a clear and user‐friendly guideline. Journal of evaluation in clinical practice, 17(2), 268-274.
Strodl, E. & Noller, P. (2003). The relationship of adult attachment dimensions to depression and agoraphobia. Personal Relationships, 10(2), 171-186.
Telch, M. J., Brouillard, M., Telch, C. F., Agras, W. S., & Taylor, C. B. (1989). Role of cognitive appraisal in panic-related avoidance. Behav Res Ther, 27(1), 373-383.
Torpy, J. M., Burke, A. E., & Golub, R. M. (2011). Generalized Anxiety Disorder. The Journal of the American Medical Association (JAMA), 305(5), 522. Doi:10.1001/jama.305.5.522
Trivedi, J. K. & Gupta, P. K. (2010). An overview of Indian research in anxiety disorders. Indian J Psychiatry, 52(1): S210-S218.
Wilson, K. A., & Hayward, C. (2005). A prospective evaluation of agoraphobia and depression symptoms following panic attacks in a community sample of adolescents. Journal of anxiety disorders, 19(1), 87-103.
Wittchen, H. U., Zhao, S., Kessler, R. C., & Eaton, W. W. (1994). DSM-III-R generalized anxiety disorder in the National Comorbidity Survey. Arch Gen Psychiatry, 51(1), 355- 364.
Yonkers, K. A., Dyck, I. R., Warshaw, M., & Keller, M. B. (2000). Factors predicting the clinical course of generalised anxiety disorder. Br J Psychiatry, 176(1), 544-549.
