Section Learning Objectives
- Classify the symptoms of depression.
- Identify and describe the two types of depressive disorders.
- Identify the disorders that are commonly comorbid with depressive disorders.
- Describe the epidemiology of depressive disorders.
- Discuss the factors that contribute to depressive disorders.
- Describe treatment options for depressive disorders.
6.1.1 Clinical Description
184.108.40.206 Symptoms of Depressive Disorders
Symptoms of depression can generally be categorized into four categories to include mood, behavioral, physical and cognitive symptoms.
While clinical depression can vary in its presentation among individuals, most if not all individuals with depression will report significant mood disturbances such as a depressed mood (e.g., feeling sad, hopeless, discouraged) and/or feelings of anhedonia, which is the loss of interest or pleasure in previously interesting activities. These feelings occur transiently in all of us and therefore they must be present most of the day, nearly every day to be considered as symptoms of depression.
Fatigue and/or decreased energy are a symptom of depression that can make even the simplest of tasks (e.g., showering, getting off the couch to get the T.V. remote) seem difficult. Behavioral issues such as decreased physical activity and reduce productivity – both at home and at work – can result from this fatigue and cause disruptions in daily functioning (e.g., difficulty maintaining social interactions and employment responsibilities).
Changes in sleep patterns are common in those experiencing depression. This can occur at various points throughout the night – either difficulty falling asleep (initial insomnia), waking up in the middle of the night (middle insomnia), or even waking too early and not being able to fall back asleep before having to wake for the day (terminal insomnia). Excessive sleeping can also occur (hypersomnia).
Additional physical symptoms such as a change in weight or eating behaviors are also a symptom of depression. Some individuals who are experiencing depression report a lack of appetite, often forcing themselves to eat something during the day. On the contrary, others eat excessively, often seeking “comfort foods” such as those high in carbohydrates. Due to these changes in eating behaviors, there may be associated changes to weight. Changes in weight of more than 5% of one’s body weight are considered a symptom of depression.
Finally, psychomotor agitation, which is the purposeless physical movement of the body (i.e. pacing around a room, tapping toes, restlessness etc.) and the opposite psychomotor retardation (e.g., slowed speech, thinking and movement) are symptoms of depression.
It should not come as a surprise that there are serious disruptions in cognitions as individuals with depressive disorders typically hold a negative view of themselves and the world around them. They are quick to blame themselves when things go wrong, and rarely take credit when they experience positive achievements. Feelings of worthlessness and guilt are common symptoms of depression. These distorted cognitions can create a negative feedback loop and further contribute to feelings of depression. Finally, thoughts of suicide and self-harm do occasionally occur in those with depressive disorders and are considered one of the most severe symptoms of depression.
Individuals with depressive disorders also report difficulty thinking, making decisions, and/or concentrating on tasks. This is supported by research that has found individuals with depression perform worse than those without depression on tasks of memory, attention, and reasoning (Chen et al., 2013).
220.127.116.11 Types of Depressive Disorders
The two most common types of depressive disorders are: major depressive disorder (MDD) and persistent depressive disorder (PDD). PDD (previously known as Dysthymia) is thought to be a more chronic, and potentially less severe form depression. More specifically, although symptoms for MDD and PDD are nearly identical, the duration and number of symptoms required to diagnose the two disorders differ substantially. First, while symptoms of MDD must persist for a minimum of two weeks to make a diagnosis, symptoms of PDD must persist continuously for a minimum of two years for a diagnosis. Second, five symptoms are required to diagnose MDD, while only two are required for a diagnosis of PDD.
As with most of the disorders listed in the DSM 5, diagnoses of both MDD and PDD require that the symptoms cause significant distress or impairment. Moreover, the clinician needs to rule out that the symptoms are caused by something secondary (e.g., a medical condition, a substance, a schizophrenia spectrum disorder) and establish that the individual has never have had a manic or hypomanic episode before a diagnosis of MDD or PDD can be made.
It is important to note that these are not the only depressive disorders recognized by the DSM 5. Indeed, the DSM 5 added two new depressive disorders – Disruptive Mood Dysregulation Disorder and Premenstrual Dysphoric Disorder. Since these are new disorders less is known about them and as such we will not consider them in any further detail here.
According to the DSM-5 (APA, 2013), the prevalence of MDD is approximately 7% within the U.S. (which represents the highest prevalence of depression in the world). The prevalence rate for PDD is much lower, with a 0.5% rate among adults in the U.S. There is a difference among demographics, with individuals in the 18- to 29- year-old age bracket reporting the highest rates of depression than any other age group. Similarly, depression is approximately 1.5 to 3 times higher in females than in males. The estimated lifetime prevalence for MDD in women is 21.3% compared to 12.7% in men (Nolen-Hoeksema, 2001).
Suicidality in depressive disorders is much higher than in the general public. Males and those with a past history of suicide attempts/threats are most at risk for attempting suicide.
I’m sure it does not come as a surprise that studies exploring depression symptoms among the general population show a substantial pattern of comorbidity with other mental disorders (Kessler, Berglund, et al., 2003). In fact, in a large-scale research study nearly three-fourths of participants with lifetime MDD also met criteria for at least one other DSM disorder (Kessler, Berglund, et al., 2003). Among those that are the most common are anxiety disorders, ADHD, and substance abuse.
Given the extent of comorbidity among individuals with MDD, researchers have tried to identify which disorder precipitated the other. The majority of the studies have identified most cases of depression occur secondarily to another mental health disorder suggesting that the onset of depression is a direct result of the onset of another disorder (Gotlib & Hammen, 2009).
Research throughout the years continues to provide evidence that depressive disorders have some biological cause. Most individuals who develop depression have some predisposition to develop a depressive disorder. Among the biological factors are genetic factors, biochemical factors, endocrine factors, and brain structure.
As with other disorders, researchers often explore the prevalence rate of depressive disorders among family members, in efforts to determine whether there is some genetic component. If there is a genetic predisposition to developing depressive disorders, one would expect a higher rate of depression within families than that of the general population. Research supports this as there is nearly a 30 percent increase in the risk of depression in relatives of individuals diagnosed with depression, compared to 10 percent of the general population (Levinson & Nichols, 2014).
Another way to study the genetic component of a disorder is via twin studies. One would expect identical twins to have a higher rate of the disorder as opposed to fraternal twins, as identical twins share the same genetic make-up whereas fraternal twins only share that of siblings, roughly 50%. A large-scale study found that there was nearly a 46% chance that if one identical twin was diagnosed with depression, that the other was as well. In contrast, the fraternal twin rate was only 20%. This study provided enough evidence that there is a strong genetic link in the development of depression (McGuffin et al., 1996).
Finally, scientists have more recently been studying depression at a molecular level, exploring possibilities of gene abnormalities underlying depressive disorders. While much of the research is speculative due to sampling issues and low power, there is some evidence that depression may be tied to the 5-HTT gene on chromosome 17, as this is responsible for the activity of serotonin (Jansen et al., 2016).
As you will read in the treatment section, there is strong evidence of a biochemical deficit in depression. More specifically, low activity levels of norepinephrine and serotonin, have long been documented as contributing factors to developing depressive disorders. This was actually discovered accidentally in the 1950’s when monoamine oxidase inhibitors (MAOIs) were given to patients with tuberculosis, and miraculously, their depressed moods were also improved. Soon thereafter, medical providers found that medications used to treat high blood pressure, by causing a reduction in norepinephrine, also caused depression in their patients (Ayd, 1956).
While these initial findings were premature in the identification of how neurotransmitters affected the development of depressive symptoms, they did provide insight as to what neurotransmitters were involved. Researchers are still trying to determine exact pathways; however, it does appear that both norepinephrine and serotonin are involved in the development of symptoms, whether it be between the interaction between them, or their interaction with other neurotransmitters (Ding et al., 2014).
As described in Chapter 2, the endocrine system is a collection of glands responsible for regulating hormones, metabolism, growth and development, sleep, and mood among other things. Some research has implicated hormones, particularly cortisol (a stress hormone), in the development of depression (Owens et al, 2014). Additionally, elevated levels of melatonin (a hormone released when it is dark outside to assist with the transition to sleep), may also be related to depressive symptoms, particularly a specific type of depression commonly referred to as seasonal affective disorder which is prominent in northern latitudes where there is less sunlight in the winter.
Seeing as neurotransmitters are involved in depressive disorders, it should not be a surprise that brain anatomy is also involved. While exact anatomy and pathways are yet to be determined, research studies implicate the prefrontal cortex, the hippocampus, and the amygdala. More specifically, drastic changes in blood flow throughout the prefrontal cortex have been linked with depressive symptoms. Similarly, a smaller hippocampus, and consequently, a fewer number of neurons, have also been linked to depressive symptoms (this may also help to account for some of the memory problems commonly reported in depression). Finally, heightened activity and blood flow in the amygdala (the brain area responsible for the fight or flight response), are also consistently found in individuals with depressive symptoms.
The cognitive model, arguably the most conclusive model with regards to depressive disorders, focuses on the negative thoughts and perceptions that may contribute to and maintain symptoms of depression. One theory often equated with the cognitive model of depression is learned helplessness. The concept of learned helplessness was developed based on Seligman’s (1972) laboratory experiment involving dogs. In this study, Seligman restrained dogs in an apparatus and routinely shocked the dogs regardless of their behavior. The following day, the dogs were placed in a similar apparatus; however, this time the dogs were not restrained and there was a small barrier placed between the “shock” floor and the “safe” floor. What Seligman observed was that despite the opportunity to escape the shock, the dogs flurried for a bit, and then ultimately laid down and whimpered while being shocked. Based on this study, Seligman concluded that the animals essentially learned that they were unable to avoid the shock the day prior, and therefore, learned that they were helpless in avoiding the shocks. When they were placed in a similar environment but had the opportunity to escape the shocks, their learned helplessness carried over and they continued to believe they were unable to escape the shocks.
The concept of learned helplessness has been linked to humans through research on attributional styles (Nolen-Hoeksema, Girgus & Seligman, 1992). There are two types of attributional styles – positive and negative. A negative attributional style focuses on the internal, stable, and global influences of daily life, whereas a positive attributional style focuses on the external, unstable, and specific influences of the environment. Research has found that individuals with a negative attributional style are more likely to experience depression. This is likely due to their negative interpretation of daily events. For example, if something bad were to happen to them, they would likely conclude that it is their fault (internal), bad things always happen to them (stable), and bad things happen all the time. Unfortunately, this maladaptive thinking style often takes over their global view of themselves and the world, thus making them more vulnerable to depression.
In addition to attributional style, Aaron Beck also attributed negative thinking as a precursor to depressive disorders (Beck, 2002, 1991, 1967). Often viewed as the grandfather of Cognitive-Behavioral Therapy, Beck went on to coin the terms maladaptive attitudes, cognitive triad, errors in thinking, and automatic negative thoughts – all of which combine to explain the cognitive model of depressive disorders.
Maladaptive attitudes, or negative attitudes about oneself, others, and the world around them are often present in those experiencing depression. These attitudes are inaccurate and often global. For example, “If I fail my exam, the world will know I’m stupid.” Will the entire world really know you failed your exam? Not likely. Because you fail the exam, are you stupid? No. Individuals with depressive symptoms often develop these maladaptive attitudes regarding everything in their life, indirectly isolating themselves from others. The cognitive triad also plays into the maladaptive attitudes in that the individual interprets these negative thoughts about themselves, their experiences, and their futures. An example would be getting dumped and thinking “I am worthless, no one loves me or treats me well, and my future is hopeless,” rather than concluding that they were a bad match with the person.
Cognitive distortions, also known as errors in thinking, are a key component in Beck’s cognitive theory. Beck identified 15 errors in thinking that are most common in individuals with depression. Among the most common are catastrophizing (believing things are far worse than they actually are), jumping to conclusions, and overgeneralization. I always like to use my dad as an example for overgeneralization – whenever we go to the grocery store, he always comments about how whatever line he chooses, at every store, it is always the slowest/takes the longest. Does this happen every time he is at the store? I’m doubtful, but his error in thinking makes him perceive this to be true.
Finally, automatic negative thoughts, or a constant stream of negative thoughts, also lead to symptoms of depression as individuals regularly think in a pessimistic manner. While some cognitions are manipulated and interpreted in a negative view, Beck stated that there are another set of negative thoughts that occur automatically, such as these. Research studies have continually supported Beck’s maladaptive thoughts, attitudes, and errors in thinking as fundamental issues that contribute to and help maintain depressive disorders (Possel & Black, 2014; Lai et al., 2014). Furthermore, as you will see in the treatment section, cognitive strategies are among the most effective forms of treatment for depressive disorders.
The behavioral model explains depression as a result of a change in the number of rewards and punishments one receives throughout their life. This change can come from work, intimate relationships, family, or even the environment in general. Among the most influential in the field of depression is Peter Lewinsohn. He stated depression occurs in most people due to the reduced positive rewards in their life. Because they are not being positively rewarded, their constructive behaviors occur more infrequently until they stop engaging in the behavior completely (Lewinsohn et al., 1990; 1984). An example of this is a student who continues to receive bad grades on exams despite studying for hours. Over time, the individual will reduce the amount of study time, thus continuing to earn poor grades.
In the sociocultural theory, the role of family and one’s social environment play a strong role in the development of depressive disorders. These topics will be explored next.
Depression is commonly found to be related to a lack of social support. This is supported by research showing that separated and divorced individuals are three times more likely to experience depressive symptoms than those who are married or even widowed (Schultz, 2007). While there are many factors that lead a couple to separate or even end their marriage, some relationships end due to a spouse’s mental health issues, particularly depressive symptoms. Depressive symptoms have been positively related to increased interpersonal conflicts, reduced communication, and intimacy issues, all of which are often reported in causal factors leading to a divorce (Najman et al., 2014). The relationship between depression and marital problems appears to be bidirectional with stress and marital discord leading to increased rates of depression in one or both spouses (Nezlek et al., 2000). Further, while some research indicates that having children provides a positive influence in one’s life, it can also lead to stress both within the individual, as well as between partners due to the division of work and potential differences in discipline strategies and beliefs. Research studies have shown that women who had three or more young children who also lacked a close confidante and outside employment, were more likely than other mothers to become depressed (Brown, 2002).
While depression is experienced across the entire world, one’s cultural background may influence what symptoms of depression are presented. Common depressive symptoms such as feeling sad, lack of energy, anhedonia, difficulty concentrating and thoughts of suicide are the hallmark in most societies, but other symptoms may be more specific to one’s nationality. More specifically, individuals from Asian cultures often focus on the physical symptoms of depression – tiredness, weakness, sleep issues, and there is less of an emphasis on the cognitive symptoms. Individuals from Latino and Mediterranean cultures often experience problems with “nerves” and headaches as primary symptoms of depression (APA, 2013).
Within the United States, many researchers have explored potential differences across ethnic or racial groups in both rates of depression, as well as presenting symptoms of those diagnosed with depression. These studies continually fail to identify any significant differences between ethnic and racial groups; however, one major study has identified a difference in the rate of recurrence of depression in Hispanic and African Americans (Gonzalez et al., 2010). While the exact reason for this is unclear, the researchers propose a lack of treatment opportunities as a possible explanation. According to Gonzalez and colleagues (2010), approximately 54% of depressed Caucasian Americans seek out treatment, compared to the 34% and 40% Hispanic and African Americans, respectively. The fact that there is such a large discrepancy in the use of treatment between Caucasians and minority Americans suggests that minorities are not receiving the effective treatment necessary to resolve the disorder, thus leaving them more vulnerable for repeated depressive episodes.
As previously discussed, there is a significant difference between rates of depression in men and women, with women being twice as likely to experience an episode of depression than men (Schuch et al., 2014). There are a few speculations of why there is such an imbalance in the rate of depression across genders.
The first theory – artifact theory – posits that the difference between genders is due to clinicians or diagnostic systems being more sensitive to diagnosing women with depression than men. While women are often thought to be more “emotional,” easily expressing their feelings and more willing to discuss their symptoms with clinicians and physicians, men often withhold their symptoms or present with more traditionally “masculine” symptoms of anger or aggression. While this theory provides a possible explanation for the gender differences in the rate of depression, research has failed to support this theory suggesting that men and women are equally likely to seek out treatment and discuss their depressive symptoms (McSweeney, 2004; Rieker & Bird, 2005).
The second theory – hormone theory – suggests that variations in hormone levels trigger depression in women more than in men (Graziottin & Serafini, 2009). While there is biological evidence supporting the changes in hormone levels during various phases of the menstrual cycle and their impact on women’s ability to integrate and process emotional information, research has failed to support this theory as the reason for higher rates of depression in women (Whiffen & Demidenko, 2006).
The third theory – life stress theory – suggests that women are more likely to experience chronic stressors than men, thus accounting for their higher rate of depression (Astbury, 2010). Women are at an increased risk for facing poverty, lower employment opportunities, discrimination, and poorer quality of housing than men, all of which are strong predictors of depressive symptoms (Garcia-Toro et al., 2013).
The fourth theory – gender roles theory – suggests that social and or psychological factors related to traditional gender roles also influence the rate of depression in women. For example, men are often encouraged to develop personal autonomy, seek out activities that interest them, and display achievement-oriented goals, while women are encouraged to empathize and care for others, often fostering an interdependent functioning, which may cause women to value the opinion of others more highly than do their male counterparts.
The final theory – rumination theory – suggests that women are more likely than men to ruminate, or intently focus and dwell on their depressive symptoms, thus making them more vulnerable to developing depression at a clinical level (Nolen-Hoeksema, 2012). Several studies have supported this theory and shown that rumination of negative thoughts is positively related to an increase in depression symptoms (Hankin, 2009).
While many theories have been proposed to explain the gender discrepancy in depression, no one single theory has produced enough evidence to fully explain why women experience depression more than men. Due to the lack of evidence, gender differences in depression remains a highly researched topic, while simultaneously being one of the least understood phenomena in the clinical psychology world.
Given that MDD is among the most frequent and debilitating psychiatric disorders, it should not be surprising that the research on the treatment of depression is quite extensive. Among its treatment options, the most efficacious treatments include antidepressant medications, Cognitive-Behavioral Therapy (CBT; Beck et al., 1979), Behavioral Activation (BA; Jacobson et al., 2001), and Interpersonal Therapy (IPT; Klerman et al., 1984). Although CBT is the most widely known and used treatment for depression, there is minimal evidence to support one treatment modality over the other; rather treatment is generally dictated by therapist competence, availability, and client preference (Craighhead & Dunlop, 2014).
Antidepressant medications are often the most common first-line attempt at treatment for depression for a few reasons. Oftentimes an individual will present with symptoms to their primary caregiver (a medical doctor) who will prescribe some line of antidepressant medication. Medication is often seen as an “easier” treatment for depression as the individual can take the medication at their home, rather than attending weekly therapy sessions. However, this also leaves room for adherence issues as a large percentage of individuals do not take their prescription medication as indicated by their physician. Further, antidepressant medications take 3-6 weeks to begin to take effect.
There are a few different classes or antidepressant medications, each categorized by their structural or functional relationships. It should be noted that no specific antidepressant medication has been proven to be more effective in treating MDD than others (APA, 2010). In fact, many people try several different types of antidepressant medications until they find one that is effective for them, with minimal side effects.
Selective serotonin reuptake inhibitors (SSRIs)
SSRI’s are among the most common medications used to treat depression due to their relatively benign side effects. Additionally, the required dose to reach therapeutic levels is low compared to the other medication options. Possible side effects from SSRI’s include but are not limited to nausea, insomnia, weight gain, and reduced sex drive. SSRIs improve symptoms of depression by blocking the reuptake of serotonin and/or norepinephrine (SNRIs) in presynaptic neurons, thus allowing more of these neurotransmitters to be available for the postsynaptic neurons. While this is the general mechanism through which all SSRIs work, there are minor biological differences among different types of medications within the SSRI family. These minor differences are actually beneficial to clients in that there are a few treatment options to maximize medication benefits and minimize side effects.
Although originally developed to treat schizophrenia, tricyclic antidepressants were adapted to treat depression after failing to manage symptoms of schizophrenia (Kuhn, 1958). The term tricyclic came from the molecular shape of the structure which has three rings. Tricyclic antidepressants are similar to SSRIs in that they work by affecting the brain chemistry, altering the availability of neurotransmitters. More specifically, they block the absorption or reuptake of serotonin and norepinephrine, thus increasing their availability for postsynaptic neurons. Tricyclic antidepressants have been shown to be more effective in treating traditionally resistant depression and PDD. While effective, tricyclic antidepressants have been increasingly replaced by SSRIs due to SSRI’s reduced side effects. While the majority of side effects of tricyclics are minimal – dry mouth, blurry vision, constipation –others can be serious – sexual dysfunction, weight gain, tachycardia, cognitive and/or memory impairment, to name a few. Tricyclic antidepressants should not be used in cardiac patients as they have been shown to exacerbate cardiac arrhythmias (Roose & Spatz, 1999).
Monoamine Oxidase Inhibitors (MAOIs)
The utility of MAOIs was found serendipitously after producing antidepressant effects in a tuberculosis patient in the early 1950’s. Although they are still prescribed, they are not typically the first line medications due to potentially lethal interactions when ingested with common substances like cheese and wine and safety concerns with hypertensive crises. Because of this, individuals on MAOIs have strict diet restrictions in efforts to reduce their risk of hypertensive crises (Shulman, Herrman & Walker, 2013).
How do MAOI’s work? In basic terms, monoamine oxidase is released in the brain to remove excess norepinephrine, serotonin, and dopamine. MAOIs essentially prevent the monoamine oxidase (hence the name monoamine oxidase inhibitors) from removing these neurotransmitters, thereby leading to an increase in these neurotransmitters (Shulman, Herman & Walker, 2013) associated with depression. While these drugs are effective, they come with serious side effects. In addition to the hypertensive episodes, they can also cause nausea, headaches, drowsiness, involuntary muscle jerks, reduced sexual desire, and weight gain to name a few (American Psychiatric Association, 2010). Despite these side effects, studies have shown that individual’s prescribed MAOI’s for depression have a treatment response rate of 50-70% (Krishnan, 2007). Overall, despite their effectiveness, MAOIs are likely the best treatment for later staged, treatment-resistant depression in individuals who have exhausted other treatment options (Krishnan, 2007)
It should be noted that occasionally, antipsychotic medications are used for individuals with MDD; however, these are limited to individuals presenting with psychotic features.
Cognitive Behavioral Therapy (CBT)
CBT was founded by Aaron Beck in the 1960’s and is a widely practiced therapeutic tool used to treat depression. The basics of CBT involve what Beck called the cognitive triad – cognitions (thoughts), behaviors, and emotions. Beck believed that these three components are interconnected, and therefore, affect one another. It is believed that CBT can improve emotions in individuals with depression by changing both cognitions and behaviors, which in return will improve mood/emotion. Common cognitive interventions with CBT include monitoring and recording thoughts, identifying cognitive errors, examining the evidence supporting/negating cognitions, and creating rational alternatives to maladaptive thought patterns. Behavioral interventions of CBT include activity planning, pleasant event scheduling, task assignments, and coping skills training.
Cognitive behavioral therapy generally follows three phases of treatment:
- Phase 1: Increasing pleasurable activities. Similar to behavioral activation (read below), the clinician encourages the client to identify and engage in activities that are pleasurable to the individual. The clinician is able to help the client identify the activity and plan when they will engage in that activity.
- Phase 2: Identifying automatic negative thoughts. During this stage, the clinician provides psychoeducation about the automatic negative thoughts that can maintain symptoms of depression. The client learns to identify these thoughts on their own and maintains a thought journal of these cognitions to review with the clinician in session.
- Phase 3: Challenging automatic negative thoughts. Once the individual is consistently able to identify these negative thoughts on a daily basis, the clinician is able to help the client identify how these thoughts are maintaining their depressive symptoms. It is at this point that the client begins to have direct insight as to how their cognitions contribute to their disorder. Finally, the client is taught to challenge the negative thoughts and replacing them with positive thoughts.
CBT typically requires 10-20 sessions and it not only assists in recovery from depression but it also assists in preventing relapse. Evidence shows lower relapse rates following CBT (20-35%) compared to controls who received no treatment (70%) and those who were on antidepressant medications and stopped taking them (50%).
Rates of relapse following any treatment for MDD are often associated with individuals whose onset was at a younger age (particularly adolescents), those who have already experienced multiple major depressive episodes, and those with more severe symptomology, especially those presenting with severe suicidal ideation and psychotic features (APA, 2013).
Behavioral Activation (BA)
BA is similar to the behavioral component of CBT in that the goal of treatment is to alleviate depression and prevent future relapse by changing an individual’s behavior. Founded by both Ferster (1973) and Lewinsohn and colleagues (Lewinsohn, 1974; Lewinsohn, Biglan, & Zeiss, 1976) the goal of BA is to increase the frequency of behaviors so that individuals have opportunities to experience greater contact with sources of reward in their lives. In order to do this, the clinician assists the client by developing a list of pleasurable activities that s/he can engage in outside of treatment (i.e. going for a walk, going shopping, having dinner with a friend). Additionally, the clinician assists the client in identifying negative behaviors – crying, sleeping too much, avoiding friends – and monitoring them so that they do not impact the outcome of their pleasurable activities. Finally, the clinician works with the client on effective social skills. The thought is that if the negative behaviors are minimized and the pleasurable activities are maximized, the individual will receive more positive rewards or reinforcement from others and their environment, thus improving their overall mood.
Interpersonal Therapy (IPT)
IPT was developed by Klerman, Weissman, and colleagues in the 1970’s as a treatment arm for a pharmacotherapy study of depression (Klerman & Weissman, 1994). The treatment was created based on data from post World War II individuals who expressed a significant impact on their psychosocial life events. Klerman and colleagues noticed a significant relationship between the development of depression and complicated bereavement, role disputes, role transitions, and interpersonal deficits in these individuals (Weissman, 1995). The idea behind IPT therapy is that depression compromises interpersonal functioning, which in return, makes it difficult to manage stressful life events. The basic mechanism of IPT is to establish effective strategies to manage interpersonal issues, which in return, will ameliorate depressive symptoms. There are two main principles of IPT. First, depression is a common, medical illness, with a complex and multi-determined etiology. Since depression is a medical illness, it is also treatable and is not the individual’s fault. Second, depression is connected to a current or recent life event. The goal of IPT is to identify the interpersonal problem that is connected to the depressive symptoms and resolve this crisis so the individual can improve his/her life situation while relieving depressive symptoms.
18.104.22.168 Multimodal Treatment
While both pharmacological and psychological treatment alone is very effective in treating depression, a combination of the two treatments may be helpful for individuals who have not achieved wellness in a single modality.
Multimodal treatments can be offered in three different ways: treatments can be instigated concurrently, treatments can be instigated done sequentially, or stepped treatments can be offered (McGorry et al., 2010). With a stepped treatment, pharmacological therapy is often used initially to treat depressive symptoms. Once the client reports some relief in symptoms, the psychosocial treatment is added to address the remaining symptoms. While all three methods are effective in managing depressive symptoms, matching clients to their treatment preference may produce better outcomes than clinician driven treatment decisions.