Defining the Generalized Anxiety Disorder - Lab Report Example

Running Head: GENERALIZED ANXIETY DISORDER Generalized anxiety disorder Name Instructor Course Date Generalized Anxiety Disorder (GAD) Introduction Definition Generalized anxiety disorder has been termed as the basic anxiety disorder as it is a component of other disorders related to anxiety by definition. Inception of GAD as a diagnostic illness occurred in 1980 and since then its definition has been revised over and over by medical experts and agencies such as the Diagnostic and Statistical Manual of Mental Disorders (DSM) (Hazlett-Stevens, 2008). GAD is basically a common anxiety disorder which involves chronic nervousness, tension and worrying. The condition is rather diffuse and unique among other anxiety conditions since it involves a generalized feeling of worry and dread that is not specific to any situation. Goldberg (2010), state that the individual suffering from the conditions becomes uncertain about all aspects of his life including education, family, health, friends among others. Although GAD is less intense in comparison to other anxiety disorders, it effects are much long lasting hence curtailing the normal life activities and relaxation. In a more elaborate and specific definition, GAD is an anxiety disorder characterized by uncontrollable and excessive worry about a number of life activities or events and it is accompanied by at least three out of the six symptoms associated with negative symptoms or affects. However, the condition is only diagnosed a GAD if it runs for six months consecutively. According to this definition, worry is defined as any situation that the patient find hard to control or totally impossible. Controllability of the worry is measured using different parameters such as the percentage during the day, number of worry spheres, frequency of worry and self perceptions of controlling the worry (Nutt, 2003). Onset and causes Patients with GAD often demonstrate a life-long history of generalized anxiety. For, instance, several studies have revealed that patients of GAD cannot exactly report a clear age of its onset since it dates back in their childhood. Unlike other anxiety disorders such as panic disorder, characterized by remissions, exacerbations, later and more acute onset, GAD is shown to have more characterological presentation (Behar et al, 2009). However, initial studies have indicated that GAD is not exclusively associated with early age onset. The disorder may also occur in individuals at the age group ranging between 15 to 24 years. Nevertheless, some cases of adulthood onset of GAD have been reported in several survey studies. Individuals who present the disorder late in life are specifically those who have undergone serious and stressful life event. Keady and Watts, (2011) noted that an individual exposed to at least three negative life situations is by threefold more likely to develop GAD. GAD does not occur in isolation. Several community surveys have revealed about 90% of GAD patients have experienced other mental disorders at one point in their lives. At the time of diagnosis of GAD, 65% of the patients were diagnosed with one other disorder. Some of these side disorders detected include mood disorders (such as dysthymia), panic attacks, social phobia and substance use disorder. In actual fact, many of the patients are diagnosed with GAD while seeking treatment with other mental disorders. Among other mental disorders associated with stress, GAD is the most common in such patients (Nutt et al, 2001). Causes of GAD are yet been exploited fully although there are several explanations to that line. The first suggested cause is genetics. Initial research indicated that patients with GAD emanate from families with a long history of the disorder which in turn exposes other individuals in the family to the risk of developing the disorder. Another factor that might cause GAD is brain biochemistry. GAD, like other mental disorders is closely related to low levels of neurotransmitters in the brain. Neurotransmitters are special kinds of chemical messengers that are used to convey information from one cell to another and more so the nerve cells. Therefore, imbalances in the level of neurotransmitters imply improper functioning of the brain which ultimately leads to impairment of the brain reaction towards certain situations hence anxiety. Yehuda (1999) explains that environmental factors may also contribute to development of GAD. This includes trauma caused by stressful events such as the demise of a loved one, abrupt change of environments like school or workplace and physical abuse. Anxiety is also quite prevalent among individuals addicted to alcohol and hard drugs as well as those under rehabilitation from such behavior. Symptoms of GAD The symptoms of GAD are not consistent and do fluctuate from time to time. Similarly, symptoms of GAD differ from one individual to another depending on the environment. However, most people experience a set of combined physical, emotional and behavioral symptoms. The patient experiences constant worries and anxiety. He is finds the anxiety uncontrollable and in the process avoids anything that might get him in such a situation (Beck et al, 1996). In addition, the patient cannot tolerate uncertainty which puts him into the task of finding out what might unfold in the future. He is therefore, unable to enjoy life since he is always in a state of unease, dread and anxiety. It is also impossible for them to focus on specific things and their concentration levels are quite low. According to Reevy et al (2010), the symptoms sometimes manifest physically whereby the patient experiences body aches and muscle tightness as a result of continued tension. The patients find it hard to fall asleep as their minds are always engaged in thought. Such individuals are quite jumpy and restless in a bid to find a position that will make them relaxed. They may also constant stomach problems such as diarrhea and nausea. Epidemiology and Aetiology of GAD Lifetime studies on the prevalence of GAD in the general population have provided estimated figures ranging from 1.9% to 5.4%. The National Comorbidity Survey conducted structured interviews on 8,000 persons aged 15 to 54 years. The study which utilized the DSM-IV-TR criteria indicated prevalence estimates of 1.6% and 5.1% for current and lifelong GAD respectively. Becker and Altamura (2005) point out that research of GAD prevalence on older populations is yet to be exploited. However, evidence suggests that GAD is one of the most common disorders found among the elderly. For instance, the researchers Himmelfarb and Murrell (1984) noted that about 21.5% of elderly women and 17% of elderly men suffer from anxiety disorder although this has not been fully proven to meet the GAD criteria. Many elderly persons use tranquilizers which are directly linked to GAD development and this further explains why GAD could be more prevalent among this population. GAD is more predominant in women than in men with statistics with a ratio of 2:1 for female to men. The disorder is less prevalent among young people and increases with age. Research has also found that GAD is more common among individuals who are not mindfully active. Such individuals include house wives, retirees and unemployed persons who spend most of their time at home and have much time to think over things. Completely disabled persons also have a tendency of developing the disorder due to the fact that they are quite uncertain about what the future holds for them (Kessler et al, 2001). Social factors such as marital status, urbanicity and education also play a major role in the prevalence of GAD. Single persons over the age of 30 are at a higher risk of developing the disorder since they become uncertain of acquiring life partners. Individuals who have acquired considerable levels of education are less likely to develop GAD as they have undergone rigorous training on matters pertaining stress management. GAD is also more prevalent among the marginalized societies especially those discriminated due to race and tribe. In communities where women are disregarded, there is a high prevalence of the disorder among their females as their roles are highly undermined (Portman, 2009). Treatment Options There is a vast variety of available interventions for the treatment of GAD. They are as numerous as the number of conceptualizations is. As such, selecting a most appropriate treatment is challenging and demands an in-depth analysis of the individual presentation of the condition, interventions efficacy, tolerability, and long-term management (Koponen et at, 2007). This is in addition to the relative cost of the intervention. Literature appreciates that there are two main options for psychological care-givers in dispensing GAD treatment. A care giver will either take a pharmacological approach or a psychological one. The pharmacological approach entails the use of psychotropic medications (Behar et al, 2009). These include selective serotonin reuptake inhibitors (SSRIs) or the selective nor-epinephrine reuptake inhibitors (SNRs). The APA has reported efficacy of both interventions in childhood and adolescent anxiety (APA, 2006). However, much as these two stand-out an intervention’s rating of efficacy will determine whether or not it is used alone or alongside other interventions. There is current evidence showing that psychotropic medications have high efficacy at reducing anxiety symptoms but score poorly on eliminating worry, the defining characteristic of GAD (Behar et al, 2009). A major psychological approach is the cognitive behavior therapy (CBT). This therapy is built on the primacy of cognition in mediating psychological disorder (Longmore & Worrell, 2007). Behar et al, (2009) analyse five models pursuing the description of GAD. These models also propose intervention components based on the theoretical concepts of the model. They include the avoidance model of worry and GAD, intorelance of uncertainty model, metacognitive therapy, emotion dysregulation model and the acceptance-based model of GAD. Under the umbrella of CBT there are therapies such as cognitive therapy, problem-solving, cognitive-processing, meta-cognitive therapy, rational-emotive therapy, schema-focused therapy and mindfulness-based cognitive therapy (Guadiano, 2008). Over the recent years, CBT has gained popularity amongst practioners, the public and researchers. It is in deed becoming the majority orientation of practicing psychologists (Guadiano, 2008). This is because of amongst other reasons, its short-term structured nature. Due to this, it is relatively easy to use and more amenable to empirical investigation attracting a large research base. This research base makes is applicable as more an evidence-based treatment than psychotropic medicine. Currently, there are numerous clinical trials for CBT in areas such as anxiety disorders, mood disorders, post-traumatic disorder and anger amongst others with meta-analyses indicating better efficacy for the disordes. In addition to this, the use of CBT is cited as having commonsense and clear principles. It is one of the psychotherapies taught in academic psychiatry programs. This comes with well developed evidence-based and specified manualised protocols creating more ease of dissemination and implementation. There are indications from clinical trials that CBT is efficacious compared to non-directive supportive therapy, pill placebo, no treatment and being on the wait-list (Behar et al, 2009). In addition to this they have shown that improvements resulting from the therapy are maintained for long. The CBT model proposes that psychopathology results from faulty information processing which is demonstrated by dysfunctional thinking leading to maladaptive behaviors and negative emotions (Guadiano, 2008). As such, it is possible for a therapist to walk a patient through cognitive processes helping the patient evaluate and modify distortions and be self-treated. This approach treats the core source of GAD, unlike psychtrophic medicines which treat symptoms. The involvement of the patient through the therapy makes the improvements be sustainable for a longer time. Pharmacological interventios have been linked with relapses. Although there is high efficacy rating CBTs, they fall short since a majority of individuals who are treated do not meet the criteria for high-end state functioning. As such, further treatment may be needed. There are numerous factors that contribute to this scenario. They include interpersonal difficulties, personality disorders, and severity of disorder symptoms, emotions avoidance, Axis 1 comorbidity and low motivation for treatment. Similar to DSM-IV-TR, CBT is criticized for being developed majorly from clinical observations and opinions of experts leading to codification. Compared to psychotropic intervention, CBT is not laboratory related hence lacks the scientific back-up and validation. There is literature indicating that there is virtue absence of multiple baseline studies comparing behavioral and cognitive approaches effectiveness (Longmore & Worrell, 2007). Longmore and Worrell add that it would be better to remain with pharmacological interventions until the value of CBT is empirically verified. This is in addition to the fact that GAD has connections with other areas other than cognitive and behavioral facets: there is need to treat related physiological problems. Psychotropic interventions Major psychiatric drugs being used today include anxiety drugs, antidepressants and antipsychotics. There others used to treat specific disorders such as Ritalin and lithium. Anti-anxiety medications calm down and decrease the severity of symptoms. There are medications such as benxodiazepines, beta-blockers, inderal, antihistamines, and BuSpar which works through serotonin. There is general consensus today recommending the use of SSRIs or SNRIs for treatment of GAD as first line drugs (Koponen et at, 2007; (Starcevic, 2005)). A study done in Germany delineated that evidence-based guidelines recommend SSRIs, tricyclic antidepressants (TCAs), benzodiazepines (BDZ), and venlafaxine (Berger & et al, 2009). This is due to tolerability and efficacy. A key component is duloxetine. There are various studies demonstrating long-term efficacy in GAD treatment (Koponen et at, 2007; Davidson, et al, 2008). Davidson et al demonstrated in a 6-month study that patients who initially responded to duloxetine had a reduced risk of relapse. A placebo administered in the same study yielded in worsened symptoms severity, outcomes and increased relapse risk. This demonstrates the efficacy of such an intervention. However, withdrawal of the drug leads to relapse indicating that patients may develop dependency. This has been related to the abuse of psychotropic drugs. The major disadvantages linked with the use of pharmacological treatments of GAD include a myriad of side effects, and risk of dependence and related relapse. For the SSRIs, there are adverse side-effects such as nausea, diarrhea, insomnia, appetite loss, dis-inhibition, tremor, sedation and sexual dysfunction. In children and adolescents, there has been an association between anti-depressant use and increasing risk of suicide (APA, 2006). Imipramine has been linked to cardiac arrhythmia and death. Compared to non-anxious controls, GAD patients have demonstrated decreased platelet benzodiazepine receptor binding. It is also indicated that patients do show decreased chemotaxic response after pharmacological treatment (Heimberg, Turk, & Mennin, 2004). Such side effects have propelled the APA to recommend the use of combined interventions. This has been corroborated by Lieshout & Lalonde, (2011) who indicated that trials of adjunctive atypical antipsychotics not located by Medline search failed to demonstrate efficacy. In their study, half of GAD patients did not respond to SSRIs and BDZ. This indicates the need for more efficacious evidence-based treatments. There other drugs which have been linked to side-effects such as cardiotoxicity, anticholinergic effects, hypertensive crisis. This is despite their strength is treating co-morbidity (Western Australian Psychotropic Drugs Committee, 2008). There is insufficient literature on the bilogical basis of GAD. This is key critique that challenges the use of evidence-based interverntions. As such, the interventions have been said to treat sypmtoms thus having a short-term efficacy. This makes the long-term efficacy controversial adding more to the growing popularity of pschological and behavioral approaches. Conclusions There are many models seeking to elaborate on GAD. Prior to the publication of DSM-III-R, GAD was often used as a residual diagnosis for patients whose symptoms did not meet the diagnostic threshold for a different disorder. DSM-IV-TR published in 2000 further delineated the condition by describing a threshold for its diagnosis. Despite this established standard of the APA there is no one specific model for the description of the etiology, epidemiology and diagnostic. There are models and vast research-based literature with conflicting opinions concerning GAD. These models and research have yielded into similarly vast options of treatment. There has been advancement of studies to identify a most efficacious treatment. Currently, there are two approaches with significant efficacies: psychotropic medicine and cognitive behavior therapy. Despite the progress in creating the efficacies, it is important that more a comprehensive understanding of the disorder be developed so that the treatment efficacies are enhanced. This is because GAD patients’ recovery is rare (Baldwin et al, 2005). It is also important that the psychological and pharmacological approaches be enhanced and combinative efficacy pursued. References APA. (2006). Report of the Working Group on Psychotropic Medications for Children and Adolescents: Psychopharmacological, Psychosocial, and Combined Interventions for Childhood Disorders: Evidence Base, Contextual Factors, and Future Directions. Washington, DC: American Psychological Association. Baldwin, D. et al. (2005). Evidence-based guidelines for the pharmacological treatment of anxiety disorders: recommendations from the British Association for Psychopharmacology. Journal of Psychopharmacology, 19(6) , 1-30. Beck, J. G., Stanley, M. A., & Zebb, B. J. (1996). Characteristics of generalized anxiety disorder in older adults: A descriptive study. Behaviour Research and Therapy, volume 34, p.225–234. Becker, L., and Altamura, c. (2005). The epidemiology of generalized anxiety disorder in Europe. Eur Neuropsychopharmacol., volume 15, issue 4. P. 445-452. Behar, V., iMarco, I.,Hekler,L., Mohlman and Staples, A. (2009). Current theoretical models of generalized anxiety disorder (GAD): Conceptual review and treatment implications. Journal of Anxiety Disorders. Volume 23, p. 1011-1023. Berger, A. et al. (2009). Patterns of healthcare utilization in patients with generalized anxiety disorder in general practice in Germany. The European Journal of Psychiatry . Blaney, P., Davis, R and Millon, T. (1999). Oxford textbook of psychopathology. New York: Oxfrod University Press. Davidson, J. et al. (2008). Duloxetine treatment for relapse prevention in adults with generalized anxiety disorder: A double-blind placebo-controlled trial. European Neuropsychopharmacology, 18 , 673-681. Goldberg, D. (2010). Diagnostic issues in depression and generalized anxiety disorder. Arlington: American Psychiatric Association. Guadiano, B. (2008). Cognitive-behavioural therapies: achievements and challenges. Evidence Based Mental Health, 11 , 5-7. Hazlett-Stevens, H. (2008). Psychological approaches to generalized anxiety disorder : a clinician's guide to assessment and treatment. New York: Springer. Heimberg, R., Turk, C., & Mennin, D. (2004). Generalized anxiety disorder : advances in research and practice. New York: Guilford Press. Himmelfarb, S., & Murrell, S. A. (1984). The prevalence and correlation of anxiety symptoms in older adults. Journal of Psychiatry, volume 116, p.159–167. Keady, J.and Watts, S. (2011). Mental health and later life: delivering an holistic model for practice. New York : Routledge. Kessler, R., Keller, M. and Wittchen H. (2001). The epidemiology of general anxiety disorder. Psychiatrist Clinic North America Journal, Volume 24, Issue 1, p. 19-39. Koponen et al. (2007). Efficacy of Duloxetine for the Treatment of Generalized Anxiety Disorder: Implications for Primary Care Physicians. Clinical Psychiatry, 9(2) , 100-107. Lieshout, R., & Lalonde, C. (2011). Trials of Adjunctive Atypical Antipsychotics for Treatment Resistant Generalized Anxiety Disorder Not Located by a Medline Search. Pharmacotherapy, 31(2) , 56-57. Longmore, R., & Worrell, M. (2007). Do we need to challenge thoughts in cognitive behavior therapy? Clinical Psychology Review, 27 , 173-187. Nutt, D. (2003). Anxiety disorders. Malden: Blackwell. Nutt, D., Argyropoulos, S. and Forshall, S. (2001). Generalized anxiety disorder: diagnosis, treatment and its relationship to other anxiety disorders. London: Martin Dunitz. Portman, M.(2009). Generalized anxiety disorder across the lifespan : an integrative approach.new York: Springer. Reevy, G., Ozer, Y., and Ito, Y. (2010). Encyclopedia of emotion. Santa Barbara: Greenwood. Starcevic, V. (2005). Anxiety disorders in adults : a clinical guide. Toronto: Oxford University Press. Western Australian Psychotropic Drugs Committee. (2008). Anxiety disordes drug treatment guidelines. Sydney : Western Australian Psychotropic Drugs Committee. Yehuda R. (1999). Biological factors associated with suscep­tibility to posttraumatic stress disorder. Canadian Journal of Psychiatry. Volume 44, Issue1, p. 34–39. Read More

The disorder may also occur in individuals at the age group ranging between 15 to 24 years. Nevertheless, some cases of adulthood onset of GAD have been reported in several survey studies. Individuals who present the disorder late in life are specifically those who have undergone serious and stressful life event. Keady and Watts, (2011) noted that an individual exposed to at least three negative life situations is by threefold more likely to develop GAD. GAD does not occur in isolation. Several community surveys have revealed about 90% of GAD patients have experienced other mental disorders at one point in their lives.

At the time of diagnosis of GAD, 65% of the patients were diagnosed with one other disorder. Some of these side disorders detected include mood disorders (such as dysthymia), panic attacks, social phobia and substance use disorder. In actual fact, many of the patients are diagnosed with GAD while seeking treatment with other mental disorders. Among other mental disorders associated with stress, GAD is the most common in such patients (Nutt et al, 2001). Causes of GAD are yet been exploited fully although there are several explanations to that line.

The first suggested cause is genetics. Initial research indicated that patients with GAD emanate from families with a long history of the disorder which in turn exposes other individuals in the family to the risk of developing the disorder. Another factor that might cause GAD is brain biochemistry. GAD, like other mental disorders is closely related to low levels of neurotransmitters in the brain. Neurotransmitters are special kinds of chemical messengers that are used to convey information from one cell to another and more so the nerve cells.

Therefore, imbalances in the level of neurotransmitters imply improper functioning of the brain which ultimately leads to impairment of the brain reaction towards certain situations hence anxiety. Yehuda (1999) explains that environmental factors may also contribute to development of GAD. This includes trauma caused by stressful events such as the demise of a loved one, abrupt change of environments like school or workplace and physical abuse. Anxiety is also quite prevalent among individuals addicted to alcohol and hard drugs as well as those under rehabilitation from such behavior.

Symptoms of GAD The symptoms of GAD are not consistent and do fluctuate from time to time. Similarly, symptoms of GAD differ from one individual to another depending on the environment. However, most people experience a set of combined physical, emotional and behavioral symptoms. The patient experiences constant worries and anxiety. He is finds the anxiety uncontrollable and in the process avoids anything that might get him in such a situation (Beck et al, 1996). In addition, the patient cannot tolerate uncertainty which puts him into the task of finding out what might unfold in the future.

He is therefore, unable to enjoy life since he is always in a state of unease, dread and anxiety. It is also impossible for them to focus on specific things and their concentration levels are quite low. According to Reevy et al (2010), the symptoms sometimes manifest physically whereby the patient experiences body aches and muscle tightness as a result of continued tension. The patients find it hard to fall asleep as their minds are always engaged in thought. Such individuals are quite jumpy and restless in a bid to find a position that will make them relaxed.

They may also constant stomach problems such as diarrhea and nausea. Epidemiology and Aetiology of GAD Lifetime studies on the prevalence of GAD in the general population have provided estimated figures ranging from 1.9% to 5.4%. The National Comorbidity Survey conducted structured interviews on 8,000 persons aged 15 to 54 years. The study which utilized the DSM-IV-TR criteria indicated prevalence estimates of 1.6% and 5.1% for current and lifelong GAD respectively. Becker and Altamura (2005) point out that research of GAD prevalence on older populations is yet to be exploited.

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