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Cognitive Behavioral Therapy for Chronic Depression - Case Study Example

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 In the paper “Cognitive Behavioral Therapy for Chronic Depression,” the author provides the case study of 42-year-old Ruth, who is a known patient with chronic depression, referred for treatment. She has a history of depressive episodes for the preceding 20 years…
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Cognitive Behavioral Therapy for Chronic Depression
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Cognitive Behavioral Therapy for Chronic Depression Case Scenario 42 year old Ruth is a known patient of chronic depression, referred for treatment. She has history of depressive episodes for the preceding 20 years, almost every year. Most of the times the depressive episodes are precipitated by identifiable and significantly stressful events. In the past, she had incomplete remission of symptoms between episodes. She suffered from postnatal depression after each of the four child births. She has a strong family history of depression both maternal and paternal side. All these years, Ruth's depressive symptoms were controlled with tricyclic antidepressants and monoamine oxidase inhibitors. However, currently, she has failed to respond to these drugs and options for electroconvulsive therapy were refuted for concerns of side effects. Ruth had found cognitive behavioural therapy to be useful in controlling her symptoms, although complete remission was not possible because Ruth stopped practicing those techniques after she stopped attending the psychotherapy sessions. In this essay, the role of cognitive behavioural therapy with reference to major-depressive disorder in Ruth with be discussed as a treatment option. Major Depressive Disorder or MDD Ruth suffers from MDD. Major depression disorder or MDD is a common mental illness that falls into the category of mood disorders. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, 2000, diagnosis of MDD is made as in table-1. The symptoms indicative of MDD in Ruth are low mood, diurnal variation of mood, inability to experience pleasure in previously pleasurable activities, pessimistic thoughts about herself, the world and the future, excessive guilt, occasional suicidal ideation, loss of concentration and poor memory, loss of energy, loss of libido, hyperphagia and restricted physical and social activity. Table-1: Diagnosis of MDD (Nestler et al, 2002) When a certain number of depression symptoms (as below) are reported for longer than 2 week period of time, and when the symptoms disrupt normal social and occupational functioning. Symptoms of Depression Depressed mood, irritability, low self esteem, feelings of hopelessness, worthlessness, and guilt, decreased ability to concentrate and think, decreased or increased appetite, weight loss or weight gain, insomnia or hypersomnia, low energy, fatigue, or increased agitation, decreased interest in pleasurable stimuli (e.g., sex, food, social interactions) and recurrent thoughts of death and suicide The importance of MDD lies in the fact that it causes considerable impairment in social functioning, role functioning, employment and physical health of the afflicted person (Wells et al, 1989). MDD is a debilitating and complex psychiatric disorder that involves multiple neural circuits and genetic and non-genetic risk factors (Sahay et al, 2007). Whether environmental factors or genetic factors play a major role in the pathogenesis of MDD is still debated. Exaggerated early error-detection processes have been incriminated in the etiology and maintenance of major depressive disorder and thus such processes may then recruit excessive neural and cognitive resources that manifest as symptoms of depression (Chiu and Deldin, 2007). Studies have shown that 40-50% of the risk for depression is genetic (Nestler et al, 2002). However, no single gene has been attributed to this so far probably because of the possibility of many genes involved in a complex manner (Nestler et al, 2002). The environmental factors which are implicated in the etiology of depression are viral infections, reduced omega-2 fatty acids in diet, stress, reduced sleep, emotions and insults during brain development (Nestle et al, 2002) and sometimes even trivial brain injury (Rapoport et al, 2003). In prolonged conditions of stress, the levels of glucocorticoids are elevated for a long time and may damage hippocampal neurons especially the CA3 pyramidal neurons (Nestler et al, 2002). This reduces the inhibitory control of hippocampus on the Hypothalamic-Pituitary-Adrenal axis leading to further increase in glucocorticoid levels and further hippocampus damage. There may also be a component of glucocorticoid resistance related in part to impaired functioning of the glucocorticoid receptor, which, in turn, may contribute to excessive inflammation as well as hyperactivity of corticotropin releasing hormone and sympathetic nervous system pathways, which are known to contribute to a variety of diseases as well as behavioral alterations. The glucocorticoid receptor function impairment may be secondary to chronic exposure to inflammatory cytokines as may occur during chronic medical illness or chronic stress (Pace et al, 2007). It has been proposed that certain chemical imbalances in the brain cause clinical symptoms in MDD. These imbalances are said to occur in certain neurotransmitters like serotonin and noradrenaline. Even imbalances in dopamine have been noted in MDD (Bourin et al, 2002). Studies have shown that there are significant changes in the brains of those animal models afflicted with psychiatric illness The specific brain regions which have been implicated in the pathogenesis of MDD are hippocampus which is the center for mood and memory; and prefrontal cortex/ anterior cingulated region (Schatzberg, 2002) which are centers for cognition. In Ruth, both genetic factors and environmental precipitating factors have contributed to the development of the disease. The drugs which are used in the treatment of MDD are called anti-depressants. All anti-depressants act via monoamine neurotransmitters serotonin or noradrenaline. They down-regulate (decrease or desensitize) some receptors in a delayed time course, which is reflected by the time to onset of therapeutic effects (Stahl et al, 1996). Ruth was on tricyclic antidepressants and monoamine oxidase inhibitors, but later in life she failed to respond to these drugs. There are both pharmacotherapies and psychotherapies available to treat MDD. The efficacy of depression-targeted, time-limited psychotherapies as acute phase treatments for mild-to-moderately depressed outpatients with MDD is clear and is preferred in milder, uncomplicated, non-chronic cases. The most effective approach would be to convert medication responders into remitters with psychotherapy (Rush and Thase, 2001). Electroconvulsive therapy is one of the therapeutic approaches to severe depression, especially when the patient is not responding to medications, like in case of Ruth. In this therapy, electric current is passed through the brain of the patient to cause convulsions. Ruth refused this treatment because of concerns over potential side effects. There are many side effects for this treatment. Short-term side effects include head ache, muscle ache, feeling of muzzy headedness, feeling sick, distress and feeling fearful. In older patients, confusion can occur. There is small risk of death of 1 in 50,000 cases. The main impact of ECT is long term. The most important long term side effects are cognitive deficits, mainly memory problems. Memories return in most of the cases when the course has finished and a few weeks have passed by (RCP, 2008). Ruth is more comfortable with cognitive-behavioral therapy because of decrease in depressive symptoms. Cognitive-behavioural therapy or CBT Cognitive Behavioral Therapy or CBT is a form of psychotherapy that mainly influences dysfunctional and problematic cognitions, emotions and behaviors through a 'goal- oriented' systematic approach. CBT is known to be effective in many psychological conditions like mood disorders, anxiety-related disorders, eating disorders, substance abuse, personality disorders and also various psychotic disorders. In Ruth, CBT is recommended for MDD, a mood disorder. CBT can be of two types: Cognitive- oriented therapies and Behavior- oriented therapies. In cognitive- oriented therapies, the main objective of the treatment is to identify thoughts, beliefs, assumptions and behaviors that are related to debilitating, dysfunctional, inaccurate and unhelpful negative emotions and monitor them. The result expected out of such forms of therapy is to replace or transcend these emotions with more realistic and useful emotions. It is important to know that emotional dysfunction is maintained by metacognitive beliefs, inflexible self-focused attention, and perseverative thinking. CBT should be delivered only by those who are trained suitably. The therapists should adhere to empirically grounded treatment protocols (NICE guidelines, 2007). In depression, cognitive-oriented therapy, also known as cognitive therapy is more useful. Cognitive therapy is scientifically tested in over four hundred clinical trials which have proved its efficacy (Beck, 2008). The therapy is time- limited and problem-solving in nature. It is primarily focused on the 'present' and hence, solution to current problems is aimed at (Beck, 2008). Patients acquire certain skills which they are able to use through out their lives. The skills which are taught to the patients are modification of beliefs, identification of distorted thinking, changing behaviors and relating to others in different ways (Beck, 2008). According to cognitive therapy, it is not situation that decides the emotional well being of an individual (Wedding and Corsini, 2008). Rather, it is the way the individual perceives situation. How an individual feels is based on his thoughts. In times of distress, thoughts of people are distorted and clear thinking is not possible. Cognitive therapy helps individuals identify these thoughts and change the way they view situations (Beck, 2008). Cognition means thought process. It reflects what we think, believe and perceive. Cognition therapy focuses on perception of thoughts (Kaplan, et al, 1998). This is because distorted and unrealistic thoughts result in misinterpretations which lead to symptomatology in anxiety and depression. Stressful states like depression, anxiety and anger are exacerbated by biased or exaggerated ways of thinking (Leahy, 2006). The main objective of the treatment in Ruth is to identify thoughts, beliefs, assumptions and behaviors that are related to debilitating, dysfunctional, inaccurate and unhelpful negative emotions and then monitor them. The result expected out of such forms of therapy is to replace or transcend these emotions with more realistic and useful emotions. It is important to know that emotional dysfunction is maintained by metacognitive beliefs, inflexible self-focused attention, and perseverative thinking (Beck, 2008). Cognitive therapy will help Ruth to understand and step out of automatic thoughts (Herkov, 2006). The role of a cognitive therapist is to help Ruth in understanding and recognizing the idiosyncratic thinking and help modification of this thought process through application of logic and evidence (Leahy, 2006). The therapist helps Ruth with her thinking errors (Wedding and Corsini, 2008). Some of the errors which are targeted are (Herkov, 2006): 1. Magnification- Minimization: These thoughts distract the importance of particular events or situations. 2. Dichotomous thinking: This type of thinking arises when a person is able to generate only two choices in any given situation or event. The individual sees things as black or white or both. 3. Selective Abstraction: The individual mainly focuses on the negative aspects of a situation, and becomes sad. 4. Personalization: This thought process makes an individual relate all negative things to himself with no basis for such an assumption. There are two ancillary assumptions which guide the cognitive therapist while treating Ruth. They are: 1. Ruth is capable of identifying his or her own thoughts and change them. 2. Thoughts which have been elicited by stimuli may not reflect reality accurately. The aim of cognitive therapy is to correct only those distortions that are root causes of distress. While examining Ruth, the therapist must try and understand Ruth's point of view. Both Ruth and therapist must work collaboratively exploring the thoughts, interferences and assumptions of Ruth. Once these thoughts and assumptions are identified, the therapist must teach Ruth to test these against reality and other assumptions. The process of checking will need to continue even outside the therapeutic session (Mulhauser, 2008). Various studies have demonstrated the efficacy of cognitive therapy in treating depression. The effectiveness of this form of treatment is comparable to anti-depressants. Cognitive therapy should be considered as a first line treatment for mild to moderate depression. In severe or chronic depression a combination of cognitive therapy and antidepressants has been shown to be effective. Cognitive therapy is also effective in treating depression that is only partially responsive to anti-depressants (Rupke, Blecke and Renfrow, 2006). It is useful in treating depression in adolescents. Cognitive therapy helps correct false self-beliefs. It is not yet clear as to what type of patients benefit the most in cognitive therapy. It is presumed that those who are motivated, who have the capacity to introspect and have an internal locus of control are benefited the most (Rupke, Blecke and Renfrow, 2006). In many cases of depression, behavior therapy is also incorporated into the treatment program. Cognitive therapy also reduces the chances of relapse in depression. It is effective in those who have residual symptoms after adequate antidepressants. Some studies have shown that those treated with cognitive therapy have fewer residual symptoms (Rupke, Blecke and Renfrow, 2006). During cognitive therapy, Ruth is guided through a number of structured learning experiences (Rupke, Blecke and Renfrow, 2006). The first step is making Ruth understand that some of her or his beliefs or thoughts or perceptions may be false and these self- beliefs are the ones which lead to certain behaviors and moods and not situations or events. The next step is to help her recognize 'negative' or 'automatic' thoughts. Ruth is asked to maintain a diary and write down negative thoughts and mental images and then associate these with behavior, feelings and physiology. After these are identified, alternative thoughts that are more close to reality must be discovered and mentioned to the patient. Ruth must be encouraged to pip in alternate thoughts. She must then be asked to decide internally whether automatic thoughts or alternate thoughts are realistic. In the beginning sessions, she will obviously choose automatic thoughts as realistic. However, as the treatment sessions go by and evidence is provided against unreality of automatic thoughts, she improves. During the progression of therapy, the therapist will focus more on 'core' beliefs (Rupke, Blecke and Renfrow, 2006). For treating depression by cognitive therapy, the full course includes 14- 16 sessions. During the initial sessions, evaluation and modification of dysfunctional thoughts occurs. After that, the remaining sessions are used to modify these beliefs and enhance relapse prevention skills. In most patients remission occurs in 8- 12 sessions. Occasional booster sessions during the first year maintain treatment gains (Butler and Beck, 1995). The most important advantage of CBT is that it is brief and time oriented (Cooper, 2008). Also, it can be used both in individual cases and in group settings. Many techniques of CBT are adapted for self- help applications. CBT is a highly structured therapy. Hence it can be provided in a number of different formats such as computer interface, self- help books and training material. Conclusion Cognitive therapy is one of the most useful psychotherapeutic interventions. It is mainly used for the treatment of depression and anxiety. The concept behind this therapy is that distorted thoughts and beliefs are the main causes of emotional distress and behavior and not situations. Hence helping the patient identify these thoughts and convert them to alternate realistic thoughts relieves symptoms in patients. Most of the times, cognitive therapy is given along with behavioral therapy, the combination of which is known as cognitive- behavioral therapy. References Beck, J.S. (2008). Questions and Answers about Cognitive Therapy. The Beck Institute for Cognitive Therapy and Research. Retrieved on May 16th, 2010 from http://beckinstitute.org/Library/InfoManage/Zoom.asp?InfoID=220&RedirectPath=Add1&FolderID=237&SessionID={30B583AB-3266-48ED-BC20-09A7829F5FA0}&InfoGroup=Main&InfoType=Article&SP=2 Bourin, M., David, D.J., Jolliet, P., Gardier, A. (2002). Mechanism of action of antidepressants and therapeutic perspectives. Therapies, 57(4), 385-96. Butler, A. C. & Beck, A. T. (1995). Cognitive therapy for depression. The Clinical Psychologist, 48(3), 3-5. Cooper, M. (2008). Essential Research Findings in Counselling and Psychotherapy: The Facts are Friendly. London: SAGE Publications. Chiu, P.H., Deldin, P.J. (2007). Neural evidence for enhanced error detection in major depressive disorder. Am J Psychiatry, 164(4), 608-16. Herkov, M. (2006). About Cognitive Psychotherapy. PsychCentral. Retrieved on May 16th, 2010 from http://psychcentral.com/lib/2006/about-cognitive-psychotherapy/ Kaplan, M.D, Harold, I. and Sadock, M.D, Benjamin, J. (1998). Synopsis of Psychiatry (8th Edition). Baltimore: Williams & Wilkins. Leahy, R.L. (2006). Cognitive Therapy Techniques. London: Guilford Press: Mulhauser, G. (2008). An Introduction to Cognitive Therapy & Cognitive Behavioural Approaches. Counselling resource. Retrieved on May 16th, 2010 from http://counsellingresource.com/types/cognitive-therapy/index.html Nestler, E.J., Barrot, M., DiLeone, R.J., Eisch, A.J., Gold, S.J., Monteggia, L.M. (2002). Neurobiology of Depression. Neuron, 34, 12-25. NICE Guidelines. (2007). Anxiety. Retrieved on May 16th, 2010 from http://www.nice.org.uk/Guidance/CG22/NiceGuidance/pdf/English Pace, T.W., Hu, F., Miller, A.H. (2007). Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain Behav Immun., 21(1), 9-19. Rapoport, M.J., McCullagh, S., Streiner, D., Feinstein, A. (2003). The clinical significance of major depression following mild traumatic brain injury. Psychosomatics, 44, 31-37. Rupke, S.J., Blecke, D., and Renfrow, M. (2006). Cognitive Therapy for Depression. American Family Physician. Retrieved on May 16th, 2010 from http://www.aafp.org/afp/20060101/83.html Rush, A.J., and Thase, M.E. (1999). Psychotherapies for depressive disorders: a review. In: Maj M, Sartorius N, eds. Depressive Disorders. Chichester, England: John Wiley & Sons Ltd;161-206. WPA Series: Evidence and Experience in Psychiatry; vol 1 Schatzberg, A.F. (2002). Major depression: Causes or effects? American Journal of Psychiatry, 159(7), 1077-1079 Sahay, A., Drew, M.R., Hen, R. (2007). Dentate gyrus neurogenesis and depression. Prog Brain Res., 163, 697-822. Stahl, S.M. (1996). Essential Psychopharmacology. Cambridge, MA: Cambridge University Press. The Royal College of Psychiatrists (RCP). (2008). Electroconvulsive Therapy. Retrieved on May 16th, 2010 from http://www.rcpsych.ac.uk/mentalhealthinfoforall/treatments/ect.aspx Wedding, D and Corsini, R.J. (2008). Current Psychotherapies. London: Peacock publishers. Wells, K.B., Stewart, A., Hays, R.D., Burnam, M.A., Rogers, W., Daniels, M., Berry, S., Greenfield, S., Ware, J. (1989). The functioning and well being of depressed patients: results from the Medical Outcomes Study. The Journal of American Medical Association, 262, 914-919. Read More
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