Depression

Detailing Depression

Throughout our lives there are experiences, such as ending a relationship or losing a loved one, that cause us to become sad or get the “blues.” Many people may assume that they have depression, yet may not have all the symptoms that warrant a diagnosis of clinical depression, or unipolar depression (Comer, 2005). However, some have severe depression along with “mania …, a state of breathless euphoria, or at least frenzied energy, in which people may have an exaggerated belief that the world is theirs for the taking; together characterizing bipolar disorder” (Comer, 2005, p. 193). How common is unipolar depression and bipolar disorder and what symptoms indicate that a person has either mood disorder? The biological, psychological, and sociocultural models of depression provide possible causes which will be referenced throughout the discussions. Since I am currently experiencing depression, received a clinical diagnosis, and I am disabled, we will discuss the risk of depression amongst the disabled, and possible treatment options for both mood disorders.

Unipolar Depression Symptomology and Diagnosis

            The adult population in the United States suffering from mild forms of depression ranges between 3 to 5 percent, while those suffering from severe unipolar depression ranges between 5 to 10 percent (Comer, 2005). Globally, 17% of all adults may experience a severe episode of unipolar depression in their lives and half recover within six weeks, while 90% recover within a year (Comer, 2005).The biological model has provided studies on the cause of a genetic predisposition toward depression to support with 20% of twins in the study sharing the experience of depression and have also identified that low activity of the neurotransmitters norepinephrine and serotonin play a part in developing depression (Comer, 2005).

Depression may include such symptoms as feelings of despair, anger, worthlessness, indecisiveness, and uncontrollable crying. A week ago, I found myself in uncontrollable episodes of crying accompanied with feelings of anxiety, agitation, emptiness, loneliness, despair, and isolation with a brief suicidal thought (which is extremely rare for me). It seemed as though this had come out of no where, but symptoms had existed in a less apparent form prior to my depressive episode and were brought on by stress from lacking supportive relationships. “In fact, researchers have found that depressed people experience a greater number of stressful life events during the month just before the onset of their disorder than do other people during the same period of time” (Comer, 2005, p. 197). Symptoms of unipolar depression affect the emotional, motivational, behavioral, cognitive, and physical functions, usually building upon one another, of a person’s life (Comer, 2005).

The emotional symptoms I experienced a week ago characterize unipolar depression, but along with my additional motivational, behavioral, and cognitive symptoms my psychiatrist felt it warranted using the biological treatment of Paroxetine, or Paxil, a second generation antidepressant that increases serotonin activity by preventing its reuptake without affecting norepinephrine or other neurotransmitters (Comer, 2005). I explained that I had socially isolated myself for three years while doing my academics and upon recently learning the importance of socialization for developing one’s personality, I had a new found desire to be around people only to find myself nervous, frustrated, self-conscious, agitated, sad, and lacking in social skills when trying to interact with friends. My motivational symptoms were derived from my social isolation and although I now desire to socialize, my psychiatrist feared that I may become easily discouraged if these symptoms were not biologically treated. Being confined to a wheelchair and my social isolation collectively contributed to my depressive behavioral symptoms of being less active and less productive (Comer, 2005). The behavioral model would explain the cause as a lack of perceived social rewards due to my social isolation and treatment may consist of creating a weekly schedule of pleasurable activities while ignoring my negative behaviors and praising (rewarding) my constructive behavior (Comer, 2005).

However, my disability alone set the stage for my cognitive symptoms of depression. From the sociocultural model, my disability comes with hidden prejudice and stereotypes that society provides, making me feel inadequate, undesirable, inferior, and some times evil (Comer, 2005). In fact, as an adolescent I caused an accident that hurt my old best friend, and his father persisted on giving me a speech on how he knew that I must have a lot of hate in my heart; I begun to wonder if I did have a lot of hate and evil, but I now know that he was just ignorant. “Evidence is abundant that the disabled typically have not received equal consideration for positions or promotions even [when the] capacity to perform is not an issue” (Turner & Noh, 1988, p. 29).

My recent bout of depression was also brought about by my cognitive pessimism concerning my conflicting relationship with my wife along with my social life and after discussing this with the only friend I could, I was not given any support and he even took my wife’s side immediately without considering anything from my perspective; sociocultural studies have shown that depressed people lacking social support stay depressed longer than depressed individuals with a supportive spouse or warm friendships (Comer, 2005). According to Comer (2005), “the psychodynamic theorists who emphasize relationships [claim] that depression results when people’s relationships leave them feeling unsafe and insecure … [, though] certain features of the psychodynamic explanation are nearly impossible to test” (Comer, 2005, p. 203). More specifically, the cognitive model would point to my self-blame for the social isolation and the negative cognitive triadic thinking about my experiences, myself, and my future that exacerbated my depressive episode (Comer, 2005). This brought about a sense of hopelessness and helplessness that spurred my crying spells and physical symptoms of eating more and sleeping more (Comer, 2005).

Cognitive therapy usually requires fewer than 20 sessions and consists of four phases that provide encouragement to become more active, confident, and to develop a detailed schedule of pleasurable hourly activities; education on how to recognize and record automatic thoughts once they have achieved some emotional relief from the first phase; realization of flawed automatic thoughts, explanation of how illogical thinking processes contribute to these thoughts, and how the person’s style of interpreting events consists of bias in an attempt to change it; help to change the primary attitude that led up to depression by questioning an attitude’s validity (Comer, 2005). There are two sociocultural treatments: couple therapy teaches communication and problem-solving skills to minimize conflict, while interpersonal psychotherapy (IPT) commonly looks to identify and resolve any conflicting expectations of each other that may be causing an interpersonal role dispute, develop social support and skills needed to accompany an interpersonal role transition, help identify social insecurity as interpersonal deficits preventing intimate relationships and develop social effectiveness, and if needed, develop new ways of remembering a person of interpersonal loss so that a patient may move on and seek new relationships (Comer, 2005).

According to Comer (2005), to be diagnosed with a major depressive episode one must have at least five of the following symptoms nearly every day during the same two week period: depressive mood most of the day, loss of interest or pleasure in almost all activities most of the day, a significant loss or gain in appetite or weight, insomnia or hypersomnia, fatigue or loss of energy, feeling worthless or excessive guilt, reduction in ability to concentrate, recurrent thoughts of death or suicide, a suicide attempt, or a specific plan for committing suicide, and significant distress or impairment from symptoms. A major depressive disorder is diagnosed in the presence of a major depressive episode without a history of a manic or hypomanic episode (Comer, 2005).

Danger of Depression for the Disabled

According to Turner and Noh (1988), studies revealed that the risk of developing depression is three times higher for men with physical disabilities regardless of age, education, marital status, area of residence, or level of income and the findings supported that disability sets up a constant strain that may have important mental health implications. As a child, my mother had a habit of doing things for me because she felt my life was difficult enough and in the process brought about learned helplessness, a concept of the cognitive model (Comer, 2005). The psychodynamic model would claim that my mother pushed me toward excessive dependence which produced my depressive symptoms once I felt that I lacked social support (Comer, 2005).

Turner and Noh (1988) claim that “higher levels of mastery and social support are associated with lower depression, while higher levels of stressful events and [constant] strain are associated with increased depression” (p. 30). Compared to an abled person, my sense of mastery is lacking due to my mother’s pity for my physical limitations, and my recent depressive episode came about when I felt that I had no social support during conflicts in my marriage; collectively contributing to increased depression. Within my marriage I was feeling that I could not always rely on my wife to consider our life circumstances over everything else and her family’s negative influence provides a constant strain that prevents her from developing a less stressed, defensive, and angry personality; therefore, ultimately preventing both of us from escaping this type of harmfully destructive personality. Turner and Noh (1988) support that greater difficulty in meeting routine needs and securing satisfactions produces more severe strain that contributes to increased depression for the disabled.

Diagnosing and Treating Mania and Bipolar Disorder

Manic episodes are characterized by either powerful happy or irritable emotions, increased motivation for constant excitement, involvement, and companionship through an overwhelming, domineering, and excessive social style, behavior becomes very active and speech is rapid and loud, and show poor judgment and planning while sometimes maintaining a self-esteem of grandiosity in the cognitive realm (Comer, 2005); according to Comer (2005), diagnosis of a manic episode requires the persistence of at least three of these symptoms for at least a week along with significant distress or impairment.

With 1.0 and 1.5 percent of all adults suffering this disorder, diagnosis for bipolar I disorder requires “1. The presence of a manic, hypomanic, or major depressive episode. 2. Currently in a hypomanic or major depressive episode, history of a manic episode. 3. Significant distress or impairment” (Comer, 2005, p. 218). Those with bipolar I disorder can have mixed episodes that switch from manic to depressive episodes throughout the same day or have alternation of a month of depressed episodes followed by a month of manic episodes (Comer, 2005). Diagnosis of bipolar II disorder requires “1. The presence of a hypomanic or major depressive episode. 2. If currently in a major depressive episode, history of a hypomanic episode. If currently in a hypomanic episode, history of a major depressive episode. No history of a manic episode. 3. Significant distress or impairment” (Comer, 2005, p. 218); in this form of bipolar disorder, hypomanic (mildly manic) episodes alternate with major depressive episodes over time and without treatment emotional episodes usually continue (Comer, 2005). According to Comer (2005), numerous experiences with hypomanic symptoms along with mild depressive symptoms warrant the diagnosis of a milder form of bipolar disorder, cyclothymic disorder found in 0.4 percent of the population carrying the potential to develop into a bipolar I or II disorder.

According to Comer (2005), genetics have been determined as one biological cause for bipolar disorder, with 40% of the identical twins in family pedigree studies sharing the disorder. Decreased serotonin and norepinephrine activity may produce depressive symptoms while low serotonin activity and high norepinephrine activity may produce manic symptoms, collectively contributing to bipolar disorders (Comer, 2005). Another speculation is that the communicating neurons in the brain improperly transport ions which may “cause neurons to fire too easily (resulting in mania) or to stubbornly resist firing (resulting in depression)” (Comer, 2005, p. 221).

Researchers are uncertain as to how Lithium specifically treats bipolar disorders, however 60% with mania improve while taking it and a study found that discontinuing Lithium produces a 28 times greater risk of relapse (Comer, 2005). Although Lithium has a good success rate, some patients are more susceptible than others to its side effects and may benefit from the anti-seizure drugs Tegretol and Depakote, or a combination of both (Comer, 2005). In any case, Comer (2005) explains that bipolar disorders are treated with Lithium, Tegretol, and Depakote along with psychotherapy to develop a more effective social life.

Maintaining Mood Disorders

Even rarer within the total population than depression, bipolar disorders may not be as easily noticed. The key to recognizing this disorder is in identifying manic episodes that characterize bipolar disorder and understanding alternating and mixed episodes with depression. Psychotherapy alone is not as effective as when it is used in conjunction with Lithium, Tegretol, and/or Depakote in treating bipolar disorders.    

Considering the biological, psychological, and sociocultural models, depression can be genetically inherited through chemical imbalances of particular neurotransmitters, psychologically conditioned earlier in life to set the stage later in life, or develop as a result of cultural pressures. In my case of depression, cultural stereotypes and attitudes about physical disability increase the likelihood of my experiences with depression due to the influence on my self-image; my disability set the stage during my childhood for experiencing learned helplessness that the cognitive model looks to as a contributor to depression and also made it easy to experience the behavioral symptoms of being less active and less productive. Depending upon the level of impairment on every day life, behavioral-, cognitive-, and psycho-therapy along with biological medication is efficient for treating depression.

Reference

Comer, R. J. (2005). Fundamentals of abnormal psychology (4th ed.).New York: Worth.

Turner, R., & Noh, S. (1988). Physical Disability and Depression: A Longitudinal Analysis.

     Journal of Health & Social Behavior, 29(1), 23-37. Retrieved from

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