Bipolar Disorder - Symptoms, Diagnosis, and Treatment - Essay Example

Bipolar Disorder: Symptoms, Diagnosis, and Treatment The term 'bipolar disorder ' is used to describe patterns of manic or hypomanic behavior (with elevated, expansive or irritable moods) that may or may not alternate with episodes of clinical depression. The word 'hypomania' comes from the Greek and means 'less than mania'. Occasionally, people show a mixture of both high and low features at the same time, or switch during the day, giving a mixed picture. Bipolar disorder is thought to be primarily caused by biological factors. It is strongly inherited. Marie-Paule Austin, et al, 2002 It is now common to distinguish Bipolar I and Bipolar II disorders from one another, but distinctions between the two are not clear-cut, whether examined in formal diagnostic manuals or considered more informally in clinical practice. In general terms, Bipolar I disorder corresponds to the earlier term 'manic depressive illness' (Marie-Paule Austin, et al, 2002). Here, episodes of highs or lows are more severe and persistent, functioning is impaired and psychotic features may be present. In the past, people with severe bipolar disorder may have been admitted to an asylum where they could have remained manic for many months or depressed for many years and then spontaneously remitted, indicating that there is a pattern to even the most severe expressions of the condition. Bipolar II is less severe (so that highs are more likely to be described as 'hypomanic' rather than 'manic'); it is not usually associated with psychotic features and tends to be briefer. The North American DSM-IV diagnostic manual specifies that hypomanic episodes must last at least four days, but many researchers and clinicians are confident that some individuals with true Bipolar II can have highs and lows lasting hours rather than days. The diagnostic manuals generally rule that mood and behavioral changes must be evident to others (e.g. family members) but there are many people with true bipolar disorder (I and II) who fail to show observable features—even when psychotic—so that imposing 'observable change' may miss some individuals. The term 'mixed state' refers to times when individuals meet the criteria for both manic and depressive episodes (Marie-Paule Austin, et al, 2002). Historically, The necessity of identifying mild forms of disorder is generally recognized, complete consensus on the nature of the relation of mild to full syndromal disorder does not exist. However, in the affective disorders, historically precedented by Kraepelin's ( 1921) position on this issue, there has been increasing support for viewing subsyndromal forms as directly related to full syndromal forms ( Akiskal, 1981a, 1981b, Akiskal et al., 1977). The work on the cyclothymia- bipolar I relationship demonstrates this position most convincingly. Not only has cyclothymia been found to merge behaviorally imperceptibly with the bipolar II (and sometimes bipolar I) form of bipolar disorder ( Akiskal et al., 1977), but also equivalent rates of bipolar disorder have been found in the first- and second-degree relatives of cyclothymic and bipolar I patients ( Akiskal et al., 1977). Others have demonstrated an excess of cyclothymia and dysthymia in the biological offspring of affectively ill probands ( Akiskal, 1981b). Furthermore, in at least seven pedigrees, cyclothymic probands have provided the link for the transmission of full syndromal bipolar disorder in three consecutive generations ( Akiskal et al., 1977). In addition, one study ( Akiskal et al., 1977) found that an equivalent proportion of cyclothymics and bipolar I patients experienced induction of hypomanic episodes by tricyclic antidepressants, a phenomenon that may serve as a marker for the bipolar genotype ( Bunney, 1978). Finally, in 2- to 3-year follow-up studies, nonpatient ( Depue et al., 1981; Klein & Depue, 1984) and outpatient ( Akiskal et al., 1977) cyclothymics evidenced more severe episodes, indicating that cyclothymia is characterized by an increased risk for developing a full syndromal bipolar disorder. It is findings such as these, and data from others showing cyclothymic behavioral disturbance as a precursor to full syndromal bipolar disorder, that led to the inclusion of cyclothymia in the affective disorders section of DSM-III. The extent to which other mild affective forms are related to full syndromal affective disorders is less well known, al- though initial evidence in support of a specific type of dysthymia- bipolar disorder association has been reported ( Akiskal, 1981a). The importance of this work is that it supports a continuum model of behavioral disturbance between cyclothymia and full syndromal bipolar affective disorders. The basic assumption of this model is that the episodic characteristics and the core behavior comprising the primary features of cyclothymic disorder are qualitatively similar to, although quantitatively less severe than, those of bipolar I disorder. Such a model is not, however, incompatible with the notion of a genetic-biologic distinction between normalcy and cyclothymia ( Depue & Monroe, 1983; Depue et al., 1981; Gottesman & Shields, 1971). There are two major implications of the continuum model. First, because the behavioral and episodic features that characterize bipolar I disorder are assumed to be qualitatively similar to those of cyclothymia, these may be used to identify cyclothymia, although issues concerning the milder intensity, shorter duration, and any potential dissimilarity of course in cyclothymes must be addressed. Second, the behavioral and episodic features that distinguish bipolar I and normal phenotypes also are assumed to distinguish cyclothymic and normal phenotypes, although the discrimination problem is much greater in the latter case. Taken together, these two implications provide the framework for a paradigm in which cyclothymic individuals are identifiable as having bipolar affective disorder on the basis of their behavioral patterns. As several studies have demonstrated ( Akiskal et al., 1977; Depue et al., 1981; Kraepelin, 1921), a sizable portion of the cyclothymic population is at increased risk for developing bipolar I or II disorder in the future. Hence, behavioral identification of cyclothymia is placed within a risk framework, and so the entire approach may be referred to as the behavioral high-risk paradigm ( Depue et al., 1981). The features of the behavioral high-risk paradigm as applied to bipolar affective disorder are as follows. Onset of bipolar subsyndromal behavioral disturbance (cyclothymia) usually occurs during early or mid-adolescence (14 years of age on the average: Akiskal et al., 1977; Depue et al., 1981). For individuals experiencing subsyndromal onset, two major outcomes seems possible: (a) the continuation of cyclothymic disorder at similar, reduced, or increased levels of severity; or (b) the onset of some form of full syndromal bipolar disorder, where initial untreated episodes occur at about 24 years of age on the average ( Akiskal et al., 1977; Depue & Monroe, 1978). Considering the ages of subsyndromal and full syndromal onsets together, this yields an approximately 10-year identification period during which individuals comprising the cyclothymia risk pool could be potentially identifiable on the basis of full syndromal behavioral and episodic features. Of course, the goal in using the paradigm is to identify cyclothymes as early in the identification period as possible. It is because behavioral identification holds the promise of great economy that its use is so alluring to researchers. In cases where the behaviors comprising the risk index can be validly assessed in the form of a self-report inventory, as described following the behavioral paradigm is extremely efficient as a first stage case-identification procedure (Depue et al., 1981; Goldberg, 1972). There are, however, many problems in applying a high-risk paradigm based on a behavioral index. Bipolar affective disorder displays the features of a common disorder. As such, when considered across its full spectrum, it presents with a phenotype that varies greatly in intensity. At more extreme intensities, identification of the bipolar phenotype is not generally problematic. At very mild intensities, however, the bipolar phenotype will merge almost imperceptibly with the normal phenotype (e.g., where mild cyclothymes are behaviorally indistinguishable from highly variable normal). As one attempts to identify milder and milder cases, the threshold between case and noncase becomes increasingly arbitrary. This problem of discriminability inherent to many common disorders is greatly magnified by the use of behavior as the risk indicator, because behavior is far removed from the action of the genes underlying the proposed distinction between normal and pathological phenotypes. Family history. Statistics show that many bipolars are related to individuals with affective disorders. Hirshfield and colleagues ( 1986) found that from 60 to 65 percent of bipolars had family members with some history of major depression or bipolar illness. Prevalence. Mood disorders in children have long been under diagnosed in the United States because of the belief that a child's emotional and personality immaturity militates against such a disorder ( Weller and Weller 1991). Only in the past decade has the existence of bipolar disorder been recognized in childhood and adolescence. Bipolar disorder is believed to afflict 2.5 million Americans ( Fried 1995). Precise estimates among the pre-adult population are unclear owing to the disorder's rarity in this age group. While less common than depressive disorder, it is a condition that merits study, for it is destructive, often psychotic, and frequently lethal. Gender. Bipolarity occurs equally in males and females. Although depressive episodes are more prevalent among women, manic episodes occur with equal frequency in both genders. Age of onset. As clinicians may not be prepared to recognize children with bipolar disorder, and as parents have little information available to them ( Spivack 1994), understanding of the prevalence and the time of onset is unclear. The belief that bipolar disorders usually begin in late adolescence or early adulthood, rarely in childhood or early adolescence, is still held by many mental health professionals. More research and practical information are needed to clarify the onset issue. Cause. Bipolar disorder, a biological, inherited disorder ( Spivack 1994), is not usually diagnosed until adolescence. Early signs may suggest another condition, or it may be interpreted without the benefit of a bigger picture, such as family history. Course. Many adolescents admitted to hospitals with severe depression later show a clinical course compatible with bipolar disorder. When bipolar disorder occurs in childhood or adolescence, it is associated with suicide and rapid cycling between depressive and manic phases. Episodes of bipolarity last from two to four months. The average time between symptoms is 33 months. Left untreated, a person with bipolar disorder can expect to have at least 10 manic or major depressive episodes in a lifetime, and cycling between episodes may increase in frequency. Treatment can help shorten the episodes and lessen the severity of symptoms. It is critical to bipolar disorder to identify appropriate levels of services for this complex condition. Medication, intensive personal and family therapy, environmental interventions, special education, and hospitalization may all be required at one time or another or concurrently. Psychotherapy helps a youngster understand herself or herself adapt to stresses, rebuild self-esteem, and improve relationships. Swinging from the pits to the heights is a serious problem, and bipolarity is a serious psychiatric disorder. Such signs represent the duality with which the individual struggles, including dramatic motoric, cognitive, and emotional shifts. It is, thus, understandable that adolescents with bipolar disorder may experience dissociativeness, a feeling that they are outside of their own bodies, watching themselves. Frequently they report feelings of fragmentation, which may be a response to the intensity of manic emotions. The seriousness of bipolar disorder is also reflected in suicide statistics. "The thing that doesn't get emphasized enough is the fact that manic-depressive illness kills people. There's an extremely high suicide rate attached to it. It's the most important thing about the illness" ( Jamison quoted in Fried 1995, p. 13). Diagnostic Considerations The major diagnostic issue raised by the referring therapist is whether Mr. H presents with a bipolar disorder. This diagnosis must be considered seriously because of a positive family history of bipolar disorder and because there is strong evidence that bipolar disorder is highly heritable (Goodwin & Jamison, 1990). Evaluation of the presence of a bipolar disorder rests heavily on obtaining a detailed history both of the patient's presenting symptoms and of any past episodes of depression and/or mania. In other words, reliable diagnosis requires both a careful cross-sectional and longitudinal assessment (Goodwin & Jamison, 1990). The reason for this is that a bipolar disorder typically involves marked fluctuations in mood between euphoria and depression. Thus, a patient will present quite differently if seen in a depressed, manic, mixed, or euthymic state. For example, a patient may not manifest the elevated mood, hyperactivity, grandiosity, pressured speech, and flight of ideas associated with mania when depressed and may not appear sad, anergic, anhedonic, or guilt-ridden during the manic phase of the illness. This description has important implications for interpreting personality test data when considering whether an individual meets diagnostic criteria for a bipolar disorder. Specifically, test data provides information both about an individual's current state, such as mood, as well as longstanding, stable characteristics, such as personality style or self-image. One must take into account that some psychological characteristics are state variables that change over time, whereas others are trait variables that remain constant over time. Thus, very different profiles would be expected if a patient with a bipolar disorder were tested while in a depressed as opposed to a manic or euthymic state (Nichols, 1988). One cannot conclude from a protocol indicating the presence of depression that a patient has a unipolar opposed to a bipolar disorder. This distinction can only be made on the basis of a careful exploration of the onset, symptoms, duration, and clinical course of past and present episodes of affective disturbance. Types of Mania. There are three types of mania: hypomania, acute mania, and delirious mania. Of these three, hypomania is the least disturbed and most common. It features supercharged mood, overactive behavior, and poor judgment, unwillingness to listen to reason, grandiosity, and desire to control. Called "mild mania," the hypomanic phase is considered to be the one silver lining among the disorder's many thunderous clouds. During hypomania there is increased energy, expansiveness, risk taking, and fluency of thought, which can lead to periods of superhuman productivity (Fried 1995). It is focused frenzy. Thus, evident in bipolar disorder is enjoyment of the "rushes" of mania and the desire to avoid the down times. In a pursuit of highs and avoidance of lows, these patients may have repeated legal troubles and children show academic underachievement. Work Cited Marie-Paule Austin, Kerrie Eyers, Sue Grdovic, Dusan Hadzi-Paviovic, Gin Malhi, Philip Mitchell, Gordon Parker, David Straton, Kay Wilhelm; Dealing with Depression: A Commonsense Guide to Mood Disorders, Allen & Unwin, 2002 Akiskal H. S. (1981a). Dysthymic and cyclothymic disorders: A paradigm for high-risk research in psychiatry. Brook Lodge Symposium, UpJohn Company, Kalamazoo, MI. Akiskal H. S. (1981b). Subaffective disorders: Dysthymia, cyclothymia and bipolar II disorders in the "borderline" realm. Psychiatric Clinics of North America, 4, 25 - 46. Akiskal H. S., Djenderdejian A. H., Rosenthal R. H., & Khani M. ( 1977). Cyclothymic disorder: Validating criteria for inclusion in the bipolar affective group. American Journal of Psychiatry, 134, 1227-1233. Bunney W. E., Jr. ( 1978). Psychopharmacology of the switch process in affective illness. In M. H. Lipten , A. Dimascio, & K. F. Killam (Eds.), Psychopharmacology: A generation of progress (pp. 1249-1260). New York: Raven. Depue R. A., & Evans R. ( 1981). The psychobiology of depressive disorders: From pathophysiology to predisposition. In B. A. Maker (Ed.), Progress in experimental personality research (Vol. 10, pp. 1 - 114 ). New York: Academic. Depue R. A., & Monroe S. M. ( 1978). The unipolar-bipolar distinction in the depressive disorders. Psychological Bulletin, 85, 1001-1030. Depue R. A., & Monroe S. M. ( 1983). Psychopathology research. In M. Heisen, A. Kazelin, & A. Bellack (Eds.), Clinical psychology handbook (pp. 239-264). New York: Pergamon. Depue R. A., Slater J. F., Wolfstetter-Kausch H., Klein D., Goplerud E., & Farr D. ( 1981). A behavioral paradigm for identifying persons at risk for bipolar depressive disorders: A conceptual framework and five validation studies. Journal of Abnormal Psychology, 90, 381-437. Goldberg D. P. ( 1972). The detection of psychiatric illness by questionnaire. New York: Oxford University Press. Gottesman I. I., & Shields J. ( 1972). Schizophrenia and genetics: A twin study vantage point. New York: Academic. C. Robin Boucher, Students in Discord: Adolescents with Emotional and Behavioral Disorders; Greenwood Press, 1999 Hirshfield. R. M.A., et al. 1986. "Personality of recovered patients with bipolar affective disorders". Journal of Affective Disorders 11 : 81-89. Weller E., and Weller R. A. 1991. Mood disorders in children. In J. M. Wiener (Ed.), Textbook of child & adolescent psychiatry. Washington, DC: American Psychiatric Press. Fried S. 1995. "Creative tension". Washington Post Magazine. April 16: 1013, 27-32. Spivack G. R. 1994. "When ADHD is not ADHD". Families Newspaper 3 ( 10): 8. Klein D., Depue R., & Slater J. (in press). "Inventory identification of cyclothymia in the offspring of bipolar patients". Archives of General Psychiatry. Kraepelin E. ( 1921). Manic-depressive illness and paranoia. Edinborough: E & S Livingstone. Ronald J. Ganellen; Integrating the Rorschach and the Mmpi-2 in Personality Assessment, Lawrence Erlbaum Associates, 1996 Nichols D. S. (1988). "Mood disorders". In R. L. Greene (Ed.), The MMPI: Use with specific populations (pp. 74-129). Philadelphia: Grune & Stratton. Goodwin F. K., & Jamison K. R. (1990). Manic-depressive illness. New York: Oxford. Read More