Article: Behavioral Activation Treatment for Depression
Jacobson, N., Martell, C., & Dimidjian, S. (2001). Behavioral Activation Treatment for Depression: Returning to Contextual Roots.Clinical Psychology: Science And Practice, 8(3), 255-270.
In 1990, an experiment by Jackson et al. was done to determine the extent to which the behavioural activation (BA) component of cognitive therapy (CT) could account for the benefits of CT in depressed patients. The results were consistent with activation theory, and long-term follow-up results suggested that BA was as effective at preventing relapse as CT. This article provides an overview of the current BA model and its underlying principles.
A Brief History of Behavioural Activation
Study results indicated that the BA component of Ct was just as effective as the entire CT process, which led researchers to investigate the topic further. The previously accepted cognitive theory of depression required clients to confront and modify negative core schemas in order to effect change in depression was under question, as it appeared that BA was not only necessary, but may also be sufficient.
This led scientists to go back and study the literature on depression. Based on the principles of Skinner, Ferster proposed a completely behavioural model of depression, placing an emphasis on a functional analysis of behaviour in the understanding of depression. Additionally, he highlighted the importance of increased avoidance and escape behaviours and decreased positively reinforced behaviours in depressed people. Lewinsohn, on the other hand, proposed a behavioural model in which depression comes form an increase in aversive events or a decrease in pleasurable events. In this model, depression was assumed to be causally related to an increase in punishment or a decrease in reward.
These models did not lead to purely behavioural treatments. Over time, cognitive aspects were added into the treatment regime, including cognitive resrtucturing interventions in combination with relaxation therapy. Behavioural treatments were viewed as components of cognitive treatments, with the aim of modifying cognitive structures, and behavioural therapy had strayed from it's original intended roots.
While CT had been shown to be effective in the treatment of depression in laboratory studies, many researchers in the field were still skeptical and wanted to look at the therapy in more detail. This led to the development of BA as a treatment in its own right.
Behavioural Activation and the Demedicalisation of Depression
The BA model for the treatment of depression is unlike other conventional models, as it places a significant importance on context and individual, internal dysfunction. These individual defect models are representations of the science of our times, and include biological, genetic, and cognitive defects. Individual illness models focus on pathology within the organism, whereas a functional models look outside of the organism to establish relations between behavior and environment. However, it is important to note that functional models do not exclude genetic or biological components of depression. While many studies have investigated the relationship between neurotransmitter imbalance and depression, studies remain inconclusive about the specific biological dysfunction that may account for the success of treatments, as well anything related to causation on this topic.
The BA model, similarly, does not discount biological or genetic factors related to depression, but suggests that an emphasis placed solely or largely on biology ignores many important factors of consideration, such as contextual factors. This is evident in the doubling of the incidence of depression since the Second World War, which cannot be explained by biology and genetics alone, as well as the existence of various sub-types of depression, where genetics plays a greater role in some, but not others.
Looking at the demographics on depression, it is clear that contextual external factors are an important part of the pathology of depression. Traumatic life events, life stressors, and whether or not one is married all play a role in an individual's relationship to depression, concluding that depression cannot be explained by purely biological factors. Common treatments often include the use of anti-depressants, which come with their own set of side-effects and may not be the best method of treatment for depression.
The Basics of Behavioural Activation
BA begins with the assumption that triggers for depression are more often found in the lives or environment of the sufferer, rather than within the sufferer himself. Thus, BA is based fundamentally on a distinctly behavioural model of depression, one where external factors play a causal role in depression. BA looks at events in an individual's life and his or her responses to those events once the individual has become depressed. Depressed individuals often express avoidance behaviours, as they try to cope with unconditioned responses to events in their lives. Inactivity, withdrawal, and inertia are also common symptoms of depression. BA takes these symptoms and pays attention to the role of these behaviours in the context of an individual's life.
For example, avoidance behaviours, such as staying in bed due to lethargy, prevents people with depression from the potential of coming into contact with anti-depressive situations and behaviours. The results of this avoidant behaviour are often secondary behaviours, such as not showing up to work on time. BA works to counter both primary and secondary behaviours, by working toward guided activities to increase the probability of clients contacting positive reinforcements in their lives.
Closely related to avoidance patterns are routine disruptions, which have also been shown to have a negative impact on people with depression. The concept of social zeitgebers, refers to indicators in our lives that regulate our biological rhythms. Zeitstörers, on the other hand, are time disruptors, things that disrupt this routine. This concept may be highly relevant in the treatment of depression, as our bodies eventually become dependent on these routines. Disruption of these routines can cause us to be out of sync with our environments, and can negatively contribute to already existing depression within an individual. One important part of BA is returning to, or redefining these routines.
Course of Treatment
Within one general structure, BA has several components, as outline below:
Establishing a therapeutic relation between client and therapist and presenting the model
In the first session of therapy, the treatment model is presented to the client, both in discussion and in a written letter. The client is then encouraged to express any concerns about the model or as any questions. While this model presentation occurs early in treatment, it is often the case that the presentation of the model must be repeated in subsequent sessions.
The presentation of the model includes explanations of the relationship between mood, activity, and environment, as well as the vicious cycle of depressed mood, decreased activity level, and subsequent consequences, outlined previously in this paper. In part of this explanation, it is important for the client to understand that increased activation is a way to break out of this cycle, and that theraoeutic goals must be goal-directed, rather than mood-directed. That is, one of the goals of introducing the BA model is to dispel the myth that changes must first happen in mood in order for behavioural changes to occur.
Another emphasis of BA is the importance of focused activation, that is, simply increasing activity at random is not an effective course of treatment for depression. Instead, BA encourages clients to increase behaviours that are positively reinforcing, activities that are likely to disrupt the spiral of depression. BA must, thus, be tailored to each individual client's life in order to be effective.
Conveying optimism is also important in the presentation of the BA model. By conveying a sense of understanding for the difficulties caused my depression, such as a lack of energy and motivation, therapists can establish a sense of empathy, and at the same time, allow the client to see that waiting for his or her mood to change will likely result in being trapped in a depressive spiral.
Finally, the role of the therapist is explained to the client. In BA, it is emphasised that the therapist serves as a coach or trainer, someone who works collaboratively with clients to solve the client's problems, rather than the therapist just prescribing tools for the client to use, or the client figuring it out on his or her own.
Developing treatment goals
As mentioned above, BA therapy should be a collaboration between therapist and client. After the model has been presented to the client, therapist and client work together to identify secondary problem behaviours (such as avoidance patterns,) as well as larger life issues that may contribute to the client's depression. This information is then used to form both short term and long term goals.
Clients often have non-specific goals, such as "feeling better' or "being more social." It is the therapist's job to guide the client towards focused, specific, and operational goals that are more achievable and measurable than these initial vague goals.
They also often have difficult distinguishing between long- and short term goals. A long-term goal can be defined as a goal that cannot be attained through immediate action, and that requires progressive steps to achieve. Within a 16-week treatment period, it is only possible to focus on one or two long term goals. Most of BA focuses on helping clients increase their activation with short-term goals by detailing the steps required i order to reach these goals and acting as a coach or mentor to the client as they follow these steps.
Conducting a functional analysis of daily events
In conducting a functional analysis of the client's behaviours, BA focuses on the specific triggers for depression and the client's responses to those triggers. It is important to not environmental influences and past learning histories characterised by low levels of positive reinforcement and/or aversive control. In general, the functional analysis seeks to answer five questions:
What triggered the depression?
What particular depressive symptoms does the client experience?
What is the client's coping response to depression?
To what extent do avoidance patterns exacerbate the depression?
What routines are disrupted?
This functional analysis guides the course of treatment and teaches clients how to conduct functional analyses on themselves.
Treatment review and relapse prevention
After some time spent in therapy, clients will have learned how to determine environmental factors that influence their depression. In order to remain an effective course of treatment, it is important that the original goals formed are reviewed. In the final session of therapy, therapists sit with the clients, assess the progress made over the therapeutic period, and formulate a relapse prevention/response plan with the client.
Activation Strategies in a Typical BA Regimen
Simply encouraging clients to be more active will not work as a form of therapy. In BA, clients sit with therapists t o identify which activities would be helpful to the client in increasing positive reinforcement. The client and therapists try out several activities in a "trial an error" manner, and if an activity appears to help improve the client's mood, the client is encouraged to do more of that activity.
Activity logs monitoring the activity performed, the time spent on that activity, and the client's mood/observations during that activity are often used in BA. When activities appear to have an impact on mood, therapists discuss why that may be, allowing the client to delve deeper into what kinds of solutions may help in their depression.
Assignments usually follow a gradient of difficulty, beginning with easy tasks, such as keeping an activity log, and moving on to more complicated goals, such as joining a social group.
As mentioned above, people with depression often get stuck in avoidance patterns in order to alleviate their immediate discomfort. This usually falls under the TRAP model: a trigger, such as demands at work, illicit a response, such as a depressed mood or a sense of helplessness, which in turn, causes an avoidance pattern, such as staying at home. In encouraging a client to break the avoidance pattern, the client is encouraged to replace avoidance patterns with alternate coping mechanisms, such as using graded tasks to improved the situation.
Many clients resist the notion that disruptions in routines make depression worse. Clients are encouraged to take an experimental approach to determining a set routine and schedule. This often involves the use of activity logs, previously mentioned in this article.
Attention to Experience
For many clients with depression, a great deal of time and energy is spent on focusing on the misery in his or her life. In BA, this behaviour is addressed, however it is addressed in a manner that continues to focus on activating the client. Instead of using cognitive interventions to challenge the client's beliefs, BA focuses on developing interventions that block ruminative behaviours and maximise exposure to naturally-occurring positive environmental reinforcement.
Overcoming Obstacles in Treatment
Depressed clients are often passive and may experience difficulties in taking action on goals developed in therapy. In such cases, the therapist must work with the client to get over the hump. One fundamental step is to ensure that the client agrees with the model of treatment. If the client does not agree, it is very unlikely that BA therapy will be effective, as the client must take in active role in his or her therapy. The strategies mentioned above, using activity logs, and graded tasks can encourage a client to be an active contributor to his or her treatment.
Article: Science, serotonin, and sadness
Wrobel, S. (2007). Science, serotonin, and sadness: the biology of antidepressants: A series for the public. The FASEB Journal, 21(13), 3404-3417.
Fluoxetine was trademarked as Prozac in 1988, arriving in the U.S.A. This new drug was critically acclaimed at the time and is still used by millions of people across nations. In the past, depression was viewed as a disease of the mind, soul and the heart and individuals who suffered it felt stereotyped and ashamed. Prozac changed that, by acting on the biochemical mechanism in the brain.
Prozac and other drugs that affect the reuptake process of serotonin (SSRI) weren't the first drugs that treated depression, but were the first to be designed specifically after the realization of how the brain and neurotransmitters work.
People with depression have reduced levels of serotonin in their brains. Selective serotonin reuptake inhibitor drugs correct this imbalance by not allowing the neurons to retake the serotonin, and thus leaving more of this neurotransmitter (NT) available for the brain to use. This created a new term, which the public knows, as "chemical imbalance" and changed the way it perceived depression.
Building on past clinical research, SSRI drugs raised more questions and opportunities for the future.
What is depression?
Often regarded as the common cold of psychotherapy, depression affects 5%-8% of the world population and prevents people from enjoying their lives, sometimes leading to suicidal thoughts and acts. Depression, in addition to the emotional and physical pain it causes, has a cost of 70 billion dollars per year for the economy.
Thankfully though, 80-90% of severely depressed patients can be treated with a combination of drugs and therapy. We owe the existence of these pharmacological interventions to the physicians and scientists who fought through years of research and did not give up at the first sign of unexpected results.
Depression: the real thing
Depression is endogenous, meaning that it has no clear precipitating event. Without treatment, symptoms of depression can persist for weeks, months, or years; however with adequate treatment those who suffer from depression often find relief. Anyone, at any age, can suffer from depression - worldwide, 5-8% of the population suffers from major depression, while 20% of the population has been affected by milder forms. Women are twice as likely as men to develop depression, probably due to hormones, and are particularly at risk after childbirth. However, men have been found to be four times as likely to commit suicide than women. The accepted explanation for depression is an imbalance in neurotransmitters, particularly serotonin. There is also a genetic component, as depression has been shown to run in families.
There are several forms of depression:
Major depressive disorder is severe enough to interfere with the ability to function in daily life, such as in sleep, work, and eating. Symptoms include feeling sad or fatigued for a long period of time, loss of interest in hobbies, feelings of guilt and hopelessness, and persistent physical ailments (such as digestive disorders and chronic pain) that do not respond to treatment.
Dysthymia is a less severe form of major depressive disorder, but can still affect daily function. People with dysthymia can also have major depressive episodes.
Bipolar disorder is characterised by cycling mood changes between mania and depression. While manic phases are happy and positive, thinking, social behaviour and judgment can still be impaired throughout. Left untreated, bipolar disorder can develop to psychosis.
Chance discovery meets scientific explanation
The history of neuropharmacology helps us understand that mental disorders are diseases of the brain. But in order to learn more about these disorders, scientists had to work hard to understand the brain and the nervous system. The physical and biochemical processes went beyond the scope of dualism, and scientists were forced to re-examine what they once accepted as a truth: that mind and boy were separate.
In the early 20th century, scientists established a basic understanding of how neurotransmitters convey signals through nerves. In the late 1940s and early 1950s, scientists several important neurotransmitters, as well as their levels and relation to certain behaviours:
Norepinephrine: constriction of blood vessels, increase heart rate and blood pressure
Dopamine: shortage of this NT is involved in Parkinson's Disease
Serotonin: deeply connected to depression
Despite their research attempts, the first drugs to treat depression were discovered by chance in patients who were taking the drugs for other purposes. These drugs were far from perfect, but it was a pleasant surprise to observe that they worked for all patients with depression
Thorazine: A story of keen observation
In 1952, a chance discovery of a drug that worked against schizophrenia was made.
While in the search for anti-malarial products, French scientists (from the pharmaceutical firm, Rhone-Poulenc) researched phenothiazine, the basic foundation of methylene blue, which eventually lead to the discovery of its antihistaminic effects.
While the old compounds were too toxic for humans, a newly developed phenothiazine compound had positive effects on patients with Parkinson's, alluding that it had effects on the neurological system. In an attempt to minimise circulatory shock, Laborit, a French naval surgeon, discovered that promethiazine caused patients to relax and become sedated and began using it in combination with anesthesia. An improved version of the drug, chlorpromazine, was already in clinical trails and became a staple in Laborit's toolkit. He began encouraging his colleagues to use the drugs on psychiatric patients, often mixed with barbiturates or other sedatives. The effect of chlorpomazine was unclear until much later, when it was given to manic psychiatric patients on its own.
Later, the American pharmaceutical company, Smith-Kline & French (now Glaxo-Smith&Kline) brought the drug to the United States as Thorazine, and although they were unaware of how it worked, it relieved patients from their psychosis.
Thorazine was considered a "miracle drug" and is responsible for the discharge of more than half a million patients who were previously committed to mental asylums.
"Psychic Energizers": Tuberculosis leads to unexpected discovery and MAOIs
Having vast quantities of Hydrazine post WWII, in 1951 chemists at Hoffman-La Roche created the drugs isoniazid and iproniazid by structurally manipulating hydrazine, a chemical once used by the German military to propel rockets. Both were used to treat tuberculosis (TB). The psychiatrist, Nathan Kline, claimed that the drug improved patients' mood and brought them happiness; and in 1957, after the release of several scientific papers describing the use of the drugs to treat depression, it became an accepted method of treatment for over 400 000 patients.
Iproniazid and other similar compounds were called "monoamine oxidase inhibitors" (MAOIs) because they worked by inhibiting monoamine oxidase, an enzyme that destroys monoamines, such as norepinepherine and serotonin. Iproniazid disappeared from use soon after, as it caused jaundice in many patients.
From Thorazine to Tricyclics
After the huge success of Thorazine, scientists had hope that a related drug like imipramine would be even more effective against psychosis. Unfortunately, this was not the case, however in 1958, Swiss clinical psychiatrist, Ronald Kuhn, discovered that imipramine caused drastic changes in depressed patients, causing their moods to improve. Eventually, in the 1950;s and 60's, Ciba-Geigy, a pharmaceutical manufacturer released Tofranil, the market brand of imipramine. Tofranil is considered a tricyclic antidepressant (TCA), because of it's structure, with three rings of atoms. Later, another TCA, Elavil was released, and by the 1970's, TCA's became the World Health Organisation's number one recommendation for the treatment of depression. TCAs would keep this status until the arrival of SSRIs.
Problems with lack of selectivity
While effective in treating depression, there were still several problems with MAOIs and TCAs. The most important one was that they did not alter neurotransmitters selectively, so while the symptoms of depression were eliminated, these drugs still caused unwanted side effects that were sometimes dangerous. MAOIs were discovered to cause migraines and high blood pressure, due to its interaction with tyramine, a substance found in foods like cheeses, wines, chocolate, and smoked or pickled meat. These side effects did not necessarily have an immediate onset and could last more than two weeks after the patients stopped taking the medication.
TCAs, like MAOIs, caused undesirable side effects due to the fact that they are non-selective, or "dirty" drugs. This means that they have an effect at sites in the neuron in addition to their intended sites of interaction. For example, its effect on the acetylcholine receptors caused conditions like dry mouth, constipation, and blurred vision. Another major problem with the use of TCAs is that the "clearing time" of the drugs varied from person to person, meaning that some patients could accumulate excessive amounts of the drugs in their bodies, even when taking modest doses. The symptoms of toxicity mimic those of depression, which sometimes led doctors to increase the dosage, making the problem worse. In some cases, the lethal dose for TCAs is only five times the therapeutic dose, and TCAs were the leading cause of death by overdose.
The path to selectivity
Julius Axelrod was interested in whether mental illness was caused by the imbalance of the hormone epinephrine. He began studying the enzymes released with norepinephrine, taking a close look at monoamine oxidase, an enzyme that was known to interfere with neurotransmitters. Many scientists at the time, including Axelrod, believed that monoamine oxidase destroyed neurotransmitters once they leave the neuron that produced it. However, going against this theory, one of Axelrod's colleagues discovered that even when monoamine oxidase was inhibited, norepinephrine was deactivated, indicating that it had another means of leaving the system. This very phenomenon could account for the fact that epinephrine was only ever detected at 3% in the body at any given time.
In order to investigate further, Axelrod designed an experiment that involved injecting radioactive norepinephrine into animals. First, he disabled monoamine oxidase in the animals' bodies; then he disabled their sympathetic system on one side of their bodies; and finally, he injected the radioactive norepinephrine. Axelrod found that norepinephrine was not present in the part where the sympathetic system was destroyed, but in the other side of the animals' bodies where the sympathetic system was intact, norepinephrine was present. Thus, the inactivation of this neurotransmitter could be accounted for by its uptake into the sympathetic nervous system.
In 1961, Axelrod declared that neurotransmitters go through a reuptake process, by which they are recaptured or taken back into the neuron, so that it can be recycled.
A neurotransmitter is either destroyed or goes through reuptake. In the following years, Axelrod and his colleagues discovered that TCAs block neurotransmitter reuptake, while other antidepressants inhibit the destruction of neurotransmitters by enzymes like MAO.
Basic biology to drug design: the SSRIs
Serotonin was connected to depression, as shown by its low concentrations in the cerebrospinal fluid of depressed patients. Treatment with precursors of serotonin revealed antidepressant qualities, and now, thanks to the discoveries of Axelrod, it was now possible to design a drug that could target specific neurotransmitter involved in depression (serotonin.)
Using newly established techniques, such as nuclear magnetic resonance and crystallographic analyses, scientists were able to analyze the structures of compounds and find their properties and biological activity. In 1960s, Bryan Molloy tried to find a new drug to treat depression, one that would not have such severe side effects, like those caused by TCAs and MAOIs. Molloy created a series of analogues, structural derivatives that may differ by at least one element, of the antihistamine, diphenhydramine.
Later one, Solomon Snyder, one of Axelrod's students, developed a method that would allow for the discrimination of the reuptake of serotonin, dopamine or norepinephrine in nerve cells. They centrifuged brain cells, separating out the nerve endings. It was found that the nerve endings continued to take up the neurotransmitters to which they were exposed, giving researchers a quick way of finding out which compounds might block neurotransmitters.
In 1972, fluoxetine was found to restrict the reuptake of serotonin. It was later trademarked by the name of Prozac in 1974. Fluoxetine succeeded in passing various clinical studies and had no known side-effects. Prozac was approved by the FDA in 1987, to be taken once a day to treat depression. It was also later found to be effective against OCD. In a short time after, five SSRIs were developed by other companies and used worldwide. The development of these SSRIs marked a shift in the pharmaceutical industry, one where the serendipitous process of discovery was replaced by rational drug development:
identifying the enzyme or receptor involved in a disease
identifying the molecular structure of that enzyme or receptor
designing and synthesising a molecule that will bind tightly to that enzyme or receptor, changing its behaviour in the desired manner.
While many cheered, others worried
SSRIs have little side effects, due to their inhibition of reuptake for specific neurotransmitters. Another advantage was that they could be started from Day 1 of therapy, in contrast to the earlier TCAs and MAOIs, which had to be initiated a low, less than therapeutic levels.
On the other hand, SSRIs did have some side effects, including sleep disturbance, sexual dysfunction, and weight gain. Additionally, the greatness of SSRIs proved to be a double-edged sword, as the more useful they became, the more freely therapists prescribed and used them. Some feared that SSRIs would be used in instances beyond the treatment of depression, for example in people who wanted to change their personalities. The use of SSRIs for the treatment of depression remains controversial: Children and adolescents on SSRIs have been found to have a two-fold increased risk of suicidal tendencies.
The promise of the future, building on the past
Even today, drugs like TCAs, as well as a number of designer are prescribed and used increasingly. Using genetic identification, scientists can create specific drugs for patients. These drugs are often used in combination with cognitive-behavioral therapies treat depression.
Article: Cognitive-behavioral treatment of depression
A three-stage model to guide treatment planning
Overholser, J. (2003). Cognitive-behavioral treatment of depression: A three-stage model to guide treatment planning. Cognitive And Behavioral Practice, 10(3), 231-239.
Depression is a complex disorder involving many different factors. Therapy may aid greatly if it is suited to the client's specific needs. Cognitive-Behavioral therapy is a three-stage model that integrates therapeutic treatments with a flexible structure that provides each patient with proper treatment to depression.
The core elements needed at the start of the therapy include establishing a therapeutic alliance, conducting a thorough assessment, and using differential diagnosis to guide the preliminary treatment plan.
The therapeutic relationship is largely established by events that occur during the first therapy session. It is essential for the therapist to provide a safe and supportive atmosphere that is based on trust and acceptance. The therapist can educate the client about depression in terms of its symptomatology, course and treatment.
Assessment serves a variety of functions, including: documenting the client's diagnosis, evaluating the severity of depression, developing ideas for a preliminary treatment plan, monitoring the client's progress over time, evaluating the effectiveness of treatment, and readjusting the treatment plan as needed.
Self-monitoring allows the clients to notice patterns in their mood states and reduce generalizing their days into one mood state. Clients use scales to record their mood changes throughout the week while identifying their mood type and it's intensity.
The therapist needs to establish a diagnosis of major depression according to the current diagnostic criteria. A central part of the initial assessment involves the differential diagnosis of depressive symptoms and syndromes. Differential diagnosis can help to guide the development of the preliminary treatment plan. This can help assess the need for medication.
As part of the initial evaluation, the therapist should develop a preliminary treatment plan. Therapist and client can identify several goals for treatment, emphasizing the value of building competence in areas that can help reduce depressive tendencies. Changing cognitions can promote changes in emotions and behaviors. Thus, a cognitive conceptualization can provide a framework to guide the ongoing processes of understanding the client's problems and planning the best treatment. Depressed clients are more likely to benefit from cognitive therapy when therapist and client agree on the treatment goals and therapy tasks.
During the second stage of treatment, different components are used for different clients. The therapist can select the modules most directly related to the client's symptoms.
For reduced activity – Behavioral activation strategies include guiding clients to monitor their daily activities, evaluating different activities for the degree of mastery and pleasure they produce, and assigning a variety of simple activities to be completed between sessions. The goal is to increase the frequency of pleasant and reinforcing activities in the client's typical day. Activities completed between sessions can provide opportunities for clients to notice the cognitions related to their negative moods.
For impaired social functioning – Therapy can help to increase the frequency of pleasant social activities in the client's typical week, improve basic social skills or assertiveness, reduce tendencies for social withdrawal when feeling depressed, and increase the amount of social support and intimacy that is experienced by the client. Clients can begin to identify and confront negative cognitions that disrupt social functioning.
For ineffective coping with recent stressors- Negative life events have been found to precede the onset of major depression. The therapist can help clients evaluate their recent coping strategies and identify effective as well as ineffective coping strategies. Clients can learn to reduce their reliance on indirect or avoidance coping strategies. Therapy can help clients learn how to tolerate negative mood states, express their emotions in constructive ways, and use these negative emotions as cues to stop, think, plan and review their coping options.
For deficient problem-solving skills – Some depressed clients display a rigid approach to problems, and tend to anticipate negative consequences from their attempts to solve the problem. As a starting point, clients need to develop an adaptive attitude toward life problems, accepting problems as a natural part of life. Some clients need to reduce their tendency to respond impulsively or emotionally and learn to think through the situation until a reasonable solution is found. The problem should be defined in terms of concrete goals that are both specific and realistic, often subdividing a complex interpersonal problem into manageable components.
For cognitive biases – Depressed patients neglect the positive parts of their life and focus on the negative aspects. Minor stressors affect clients as if they were major, which causes them to over-react to negative events. Hopelessness, worthlessness and helplessness are mainly focused on in cognitive therapy. Information about clients' life events can be brought from negative emotions.
Using cognitive therapy allows to locate, confront, and minimize depressive thinking processes. Due to the automatic occurrence of a client's thoughts, the client is taken a distance away from his own perspective. A "structured diary" acts as a self-monitoring tool that guides clients through a cognitive awareness process. Clients learn to recognize, record and eliminate maladaptive thinking processes.
Helping the patients' find positive qualities in negative occurrences and helping them shorten the delay required to reduce negative thinking processes aids their progress profoundly.
For Negative view of self – Low self-esteem is known to be connected to depression. Exploring the client's view of self is recommended and should be started by presenting semi structured worksheets and standardized questionnaires.
It is recommended to explore the client's self from a broad perspective and understand their lifestyle, as a depressive client's usually focus on a narrow and negative selection of subjects from their lives', such as only work or school.
A negative view of self may result from the client's poor performance on a subject that is significant to him or by harsh standards of the client. By using faulty comparisons and having unrealistically high aspirations, patients feel inferior to others. By focusing patients on positive aspects of self and methods of self-reinforcement, therapists encourage their clients to improve themselves.
Other issues relevant to stage two – Occasionally, therapy needs to confront predispositions of depression and its symptoms, which can be caused by abuse during childhood, neglect or loss; these are typically caused by parents. Past events may be responsible for current maladaptive cognition in patients and tending to it can promote helpful insight in the patient.
Active therapy usually starts at the 2nd session and involves weekly therapy. Stage two ends when the client has shown significant improvement.
70% of the patients may recover from major depression within one year. However, depression is episodic and patients may relapse, with 75% of the patients having another depressive episode within 5 years of recovery.
Cognitive therapy has shown reduced rates of relapse in patients and less symptoms of depression after medication treatment.
An ongoing evaluation of depressive symptoms is initiated by the therapist following the warning of the client of resurfacing of depressive episodes. If warned preemptively clients may be able to identify their patterns of depressive symptoms and seek treatment.
Before therapy is terminated, the therapist seeks for risk factors. These risk factors may activate depressive relapse. After identifying these risk factors, patients prepare for mood lapses. Clients may use negative emotional states as a warning sign to start using the techniques they learned in therapy.
Therapy is used to provide the client with coping techniques for the near future and ways to deal with risky situations, while improving the patient's awareness and decision making to reduce automatic actions to events.
The patient must be aware that that negative thoughts are one side of the coin and they do not represent the true scenario. Approaching the event with humor or confidence may aid in the difficult situations.
Therapists may ask their patients to keep record of their therapy sessions, as this can be used by the patient to use these records as an instruction guide in case they are reengaged with negative thoughts. These records should show the positive aspects of the treatment and provide guidance in case the symptoms recur.
During stage three, therapy is terminated. The sessions may still be provided via phone calls or as occasional maintenance sessions. All depressed patients are addressed during the third stage.
Treatment of depression using the cognitive-behavioral model can be a broad tool for therapists. Each stage is addressed to different patients.
During the first stage, clients undergo an evaluation to diagnose their depression state and in order to build a treatment program.
During the second stage, the therapist conceives a treatment that fits each client's specific needs that remain within the bounds of psychotherapeutic research evidence. The sessions are made systematically and progress in accordance to the client's needs.
During stage three, relapse prevention is acquainted to the patient and measures are made throughout the entire treatment to help the patient cope with any recurring symptoms of depression.
This three-stage model integrates therapeutic treatments with a flexible structure that provides each patient with proper treatment to depression. The model may also be used to train therapists or provide support for therapists that use group formats.
- for free to follow other supporters, see more content and use the tools
- for €10,- by becoming a member to see all content
Why create an account?
- Your WorldSupporter account gives you access to all functionalities of the platform
- Once you are logged in, you can:
- Save pages to your favorites
- Give feedback or share contributions
- participate in discussions
- share your own contributions through the 7 WorldSupporter tools
Add new contribution