Depression is a sneaky thief, slipping into a life gradually and robbing it of meaning one loss at a time. The losses are imperceptible at first, but eventually weigh so heavily that the person’s life becomes empty. Once begun, the course of depression varies with the individual and with the form of illness. Untreated, it can last weeks, months or even years. (Ainsworth, 2000, p1)
Referred to as the “common cold of psychopathology”, (Blaney & Millon, 2009, p230), our textbook states depression is associated with a complexity of conceptual understandings. Commonly thought of from a laymen’s perspective as a concept that refers to feelings of sadness, it is also a serious potentially disabling diagnostic category within the DSM (Blaney & Millon, 2009). So with all this said, how might one define the concept?
Depressive disorders are characterized by persistent depressed mood or loss of interest (normally for at least two weeks) and at least four other symptoms such as change in eating patterns or appetite, sleep disturbance, psychomotor agitation or retardation, fatigue or loss of energy, feelings of worthlessness or guilt, difficulty in concentration, and suicidal thoughts, plans, or attempts. (Depression, 2005)
For the purposes of this paper, we focus on unipolar dimension with above-described symptomatology. In the next section, we will examine several proposed etiological perspectives from which to better understand this disorder.
Currently there are a variety of theoretical perspectives with which to better understand the underlying causality of depression. In fact, research as of late reflects an ever-increasing understanding of the complex multifactorial nature of the causal factors underlying depression. It appears that an individual’s temperament and biological vulnerabilities interact with interpersonal problems, life events, and environmental factors in a cyclical and complex manner. Apparently as many etiological perspectives allude to, we define our life events and are influenced by them as well. Of relevance for this paper, are the specific etiologies that relate to the three psychotherapy models we examine for depression. Therefore, it must be kept in mind, that while these etiological factors are listed below separately, they are interrelated in a complex manner, (Blaney & Millon, 2009).
Life Event Models.
As our textbook states: “One might suppose that one reason people get depressed is that bad things happen to them.” (Blaney & Millon 2009, p233). In fact research shows that while this is true, the reality is a bit more complex. Essentially, the effect of these life events is as a result of how the individual is affected by it long term. In other words, these life events are simply often a trigger for the onset of depressive episodes, but the recurrent maintenance of a depressive disorder diagnosis, is the result of individual vulnerabilities.
Another proposed etiology can be found in research that shows a individuals who suffer from depression, tend to suffer from a high degree of interpersonal problems (Reinke, et al, 2007). It appears from this perspective the etiological focus is upon the specific manner in which one’s social environment responds to displays of hopelessness, and withdrawal, and irritability (Reinke, et al, 2007). From this standpoint, someone suffering from depression takes in these reactions as a reinforcement of their negative belief systems. Therapy methods aimed at addressing this issue, are focused on improving the social skill deficits commonly seen in depressed individuals (Blaney & Millon, 2009, p239)
Cognitive models of depression focus on a person’s thinking as a primary source of vulnerability for suffers (Blaney & Millon, 2009, p239). A person’s cognitive world essentially defines the manner with which information is processed and underlying flavor of life events. According to Beck’s Cognitive Theory of Depression, individuals organize experience around self-schemas (Blaney & Millon, 2009, p239). With depressed individuals, these self-schemas just happen to be fraught with an array of cognitive distortions. Stressful life events exacerbate these schematic perceptions, and increase a person’s vulnerability to depression.
Therapies for Depression.
With this overview of etiological perspectives, it is now possible to move forward with a discussion of three therapies for depression. What follows is a discussion of cognitive behavioral therapy, interpersonal therapy, and rational emotive therapy. A cursory overview of these treatment methods as forms of psychotherapy for depression will be provided.
Cognitive Behavioral Therapy.
Cognitive therapy for depression addresses the schematic cognitive models with which individuals use to understand life experiences (Blaney & Millon, 2009; Corsini, 2011). The key issues of focus one’s thoughts, emotions, and beliefs that define their perspective. What makes is actually quite intriguing about this therapy method, is the wealth of research it is based on. Most notable among this research is the work of Aaron T. Beck, who helped define the cognitive state of depressed individuals (Corsini, et al, 2011). In addition to developing a useful groundwork to better understand the self-schemas associated with depression, he also created useful testing-tools such as the Beck Depression Inventory (Reinke, et al, 2007). Essentially, it appears a cognitive triad, consisting of unexamined beliefs of self, others and the future predominate depressed states. These unexamined beliefs appear to result in unexamined thought processes result in a negative view of life. In cognitive therapy, interventions are aimed at helping the individual re-examining this underlying cognitive foundation. Through thought monitoring, and self-examination clients can be empowered to better understand and address this self-schema.
As discussed earlier, etiologically, depressed individuals tend to suffer from a greater degree of interpersonal issues. It appears, that a person’s way of coping in response to stressful life events, tends to also influence the nature of their interactions with others.
Cognitively, the individual becomes excessively self-focused, self crtitical, pessimistic, and more aware of discrepancies between personal standards and actual accomplishments. Behaviorally, the person withdraws, has more social difficulties and becomes less motivated. These cognitive and behavioral consequences combine to spiral the individual into an ever-deepening state of depression. (Blaney & Millon, 2009; 237).
Interpersonal therapy, is a form of brief therapy that is based heavily on empirical research. In this respect, it is well suited in today’s mental health environment. It is focused on addressing underlying attachment histories that are often associated with the interpersonal difficulties of depressed individuals. Conceptually, it is based on a biopsychosocial causal model of depression. Essentially, according to this perspective, depression is the byproduct of biological factors, individual temperament, attachment history, which can all be placed within the context of their social relationships (Corsini, et al, 2011).
As a brief therapy, it is phasic and goal directed starting off with assessments and interventional design (Reinke, et al, 2007).. Involving client education, this allows a cline to better understanding of interpersonal patterns, and an adoption of the sick role. With this understanding in place, a collaborative and goal-directed approach can ensue, to improve a person’s interpersonal coping patterns (Reinke, et al, 2007).
Rational Emotive Therapy
Developed by Albert Ellis, rational emotive behavioral theory “holds that when a charged emotional consequence (C) follows a significant activating event (A), event A may seem to, but actually does not cause C. Instead emotional consequences are largely created by B – the individual’s belief system” (Corsini & Wedding, 2011, p196). Unique amongst other therapy methods, this therapy approach focuses on one’s individual belief system. Whereas many other methods are focused on addressing the activating events and/or emotional consequences, few appear to address the belief systems that interrelate these two factors.
MDD vs. BD
Major Depressive Disorder (MDD)
A diagnosis of MDD requires a depressed mood and loss of pleasure/interest for at least two weeks (American Psychiatric Association, 2013). Other symptoms include low self-esteem, feelings of guilt, sleep difficulties, fatigue, loss of energy, inability to concentrate, and weight loss (American Psychiatri Association, 2013). Preston, et al, (2013) list six major groups of antidepressants, including: (1) Tricyclic antidepressants, (2) Selective serotonin reuptake inhibitors (SSRI’s), (3) Serotonin and Norepinephrine Reuptake Inhibitors (SNRI’s), (4) Norepinephrine Reuptake Inhibitors (NRI’s), (5) Monamine Oxidase Inhibitors (MAOI’s), and (6) atypical antidepressants (p173).
Bipolar Disorders (BD)
The DSM-5 manual includes a chapter titled “Bipolar and Related Disorders” (American Psychiatric Association, 2013, p123). “Diagnoses included in this chapter are: bipolar 1 disorder, bipolar 2 disorder, cyclothymic disorder” (American Psychatric Association, 2013), and disorders related to substance use and medical conditions. These diagnoses have in common episodes of depression intermingled with either hypomania or mania. In contrast to depression, described above, mania involves racing thoughts, elevated mood, and distractability (American Psychiatric Association, 2013). Differentiating between MDD and BD is critical because each has unique treatment considerations. Before discussing this it will be important to briefly review the types of medications utilized with each disorder.
Tricyclics: Tricyclics work by increase the activity of serotonin and monamines by blocking the reuptake of these neurotransmitters, and allowing them to remain in effect for a longer time period. Since these drugs effect many neurotransmitter systems, they produces a long list of unwanted side effects, (anticholinergic, adrenergic, and antihistamic), and are lethal in small doses (Preston, et al, 2013, p175). For this reason they are not the first choice in the treatment of depression.
SSRI’s: Sertonin is an inhibitory neurotransmitter produced within the neuron that is unable to cross the blood-brain barrier (Lambert & Kinsley, 2011). The prefrontal cortex utilizes serotonin in an effort to regulate emotions in the limbic system. SSRI’s act as antidepressants by blocking the reuptake of serotonin. Since the action of SSRI’s are much more selective than Tricyclic antidepressants, they have fewer side effects. Side effects include GI “upset, sweating, anxiety, insomonia, headache, restlessness and sexual dysfunction” (Preston, et al, 2013, p175). Despite these benefits, it is important to note their action is delayed, and clients may need to wait 4-6 weeks before noticing an improvement.
SNRI’s: These dual action antidepressants block the reuptake of both serotonin and norepinephrine. Side effects include GI complaints, sexual dysfunction, drowsiness, nervousness, and insomnia.
MAOI’s: Monamine Oxidase Inhibitors work by inhibiting the action of monamine oxidase enzymes. These enzymes are responsible for breaking down catecholamine neurotransmitters and serotonin (Lambert & Kinsley, 2011). Side effects include “hypotension, dizziness, sedation, insomnia, weight gain, dry mouth and sexual dysfunction” (Howard, 2006, p10). Some MAOI’s are able to inhibit the action of these enzymes for up to 2-3 weeks after patient’s stop taking them (Howard, 2006). For this reason, they are considered quite powerful. These drugs are no longer a first choice in the treatment of depression since they are associated with a significant for drug interaction.
NRI & CRH Blockers – Two final medications mentioned in our course textbooks include NRI’s (Norepinephrine Reuptake Inhibitors) and CRH blockers (Corticotropin Releasing Hormone Blockers) (Lambert & Kinsley, 2011; Preston, et al, 2013). Since these medications are newer, less is known about them. NRI’s block the reuptake of norepinephrine, and enhance it effects in heightening vigilance and drive (Lambert & Kinsley, 2011, p276). This effect is helpful in addressing mood and cognition in depressed patients. CRH blockers, block the release of CRH within the HPA Axis, dampening the stress response (Broadbear, 2005). While little is know about the effectiveness of this drug, it is nonetheless briefly mentioned as yet another medication to help with depression.
Lithium: “Lithium is now firmly established as a safe and effective treatment for acute mania and for the prevention of manic-depressive episodes” (Preston, et al, 2013, p199). Surprisingly, while this medication remains as a “1st line agent” (Preston et al, 2013, p199) for BD, the mode of action for this drug is, as yet, unclear. It is, nonetheless, hypothesized that Lithium’s effectiveness is somehow related to its ionic state and ability to stabilize cell membranes (Preston, et al, 2013). It is very important to note that Lithium has a very narrow therapeutic window, putting clients at a higher risk for toxic overdose. Consequently, this medication is prescribed based on blood level, requiring ongoing monitoring from this standpoint. An extensive list of side effects is discussed in Preston, et al, (2013), indicating it influenes the renal, GI, endocrine, cardiovascular, hematological, and dermatological systems.
Anticonvusants & Antipsychotics: Anticonvulsants such as Depakote, Tegretol, and Lamictal, are also FDA approved for BD, despite the fact that their mode of action is not clearly defined (Preston, et al, 2013). Finally, Preston, et al, (2013) briefly mention Antipsychotics as yet another medication useful in the treatment of mania or mixed-mania. They also are associated with an added benefit of fewer extrapyramidal side effects.
Regarding BD, effective treatment starts with accurate diagnosis and an ability to differentiate between the various Bipolar Disorders. Treating bipolar depression is tricky, since antidepressants can cause a sufferer to switch to a manic state. Atypical depressive symptoms, psychosis, and a history of bipolar disorder, are key indicators of bipolar depression (Preston, et al, 2013). Understanding the severity of a client’s manic and depressive episodes, and the frequency of “switching” is important. Preston, et al, (2013) state that Lithium is the first drug of choice for mania. Additionally, a clear “rational for inclusion of anticonvulsants and 2nd Generation antipsychotics,” (Preston, et al, 2013, p198), is vital. Understanding and managing side effects is important alongside psychotherapy. Finally, as stated earlier, close monitoring of Lithiums every few months is important
Accurate diagnosis and understanding of a client’s symptoms is critical for effective treatment. SSRI’s and SNRI’s are the first choice as treatments for depression. It is important to notify clients, that it may be a several weeks before they experience a reduction in symptoms. Finally, while NRI’s and CRF blockers are newer, Tetracyclics and MAOI’s have severe side effects to be wary of, (as mentioned earlier). Rationale for the use of these medications should be clearly thought out, and therapists should closely monitor a client’s response to this medication regimen.
Regarding the choice of meds, the textbook mentions starting with examining a client’s responses to previous medications and re-examining their symptoms. Are there any other unexplained symptoms or comorbidities to consider? Additionally, it is important to ensure clients have had an adequate exposure to the medication (8-12 weeks), to ensure their response to treatment is fully evaluated (Preston, et al, 2013). Finally, since these clients are highly prone to discontinuing medication, psychoeducation and close monitoring are important.