Manic Depression Research Paper

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Many lay people use the name manic depression to refer to a disorder that is more formally called bipolar disorder within the diagnostic system of the American Psychiatric Association. In this formal diagnostic system, there are three forms of bipolar disorder. Bipolar I disorder, the most severe form, is defined by a single episode of mania. Manic episodes are characterized by a period of expansive, elevated, or irritable moods, along with such symptoms as diminished need for sleep, rapid speech, grandiosity, agitation or increased activity, racing thoughts, and increased engagement in pleasurable activities that have potential to cause trouble. The symptoms must last for at least one week and create severe impairment. Bipolar II disorder is a milder form of the disorder, defined on the basis of hypomania and recurrent depression. Hypomania is characterized by the same set of symptoms as mania, but symptoms must only last for four days and do not create severe impairment. Cyclothymia is defined by frequent ups and downs that are not severe enough to meet the criteria for hypomania or mania.

Two measures commonly used to verify diagnoses within research studies include Michael B. First and M. Gibbons’s 2004 Structured Clinical Interview for DSMIV (Diagnostic and Statistical Manual of Mental Disorders, 4th ed.), and Jean Endicott and Robert L. Spitzer’s 1978 Schedule for Affective Disorders and Schizophrenia. No biological markers are available to aid with diagnosis.

About 1 percent of the population experiences bipolar I disorder; it was estimated in 2005 by Ronald C. Kessler et al. that bipolar II disorder also affects approximately 1 percent of the population. Cyclothymia may affect 4 percent of the population, according to a 2004 study by E. J. Regeer et al. The vast majority of people with a single episode of mania will experience another episode during their lifetime, many within five years, reported Michael J. Gitlin et al. in 1995. A 2002 report by Lewis L. Judd et al. said that mild symptoms lingering between episodes are common. The median time of onset for this disorder has been estimated at twenty-five years of age, according to the report by Kessler et al., but at least 25 percent of affected people report that episodes began by age seventeen.

It is well established that bipolar disorder is biologically based: heritability accounts for as much as 85 percent of whether people develop mania, according to a 2003 report from Peter McGuffin et al. Neurobiological research in 2003 by Craig A. Stockmeier suggests that a set of brain regions, modulated by dopamine and serotonin, are involved in the disorder. Psychosocial variables, including negative life events, negative cognition, and family hostility and criticism can increase the risk of depressive episodes within this disorder, per several reports (Butzlaff and Hooley 1998; Monroe et al. 2001; Alloy et al. 2000). Sleep loss and events involving goal attainment can predict increases in mania over time (Johnson 2005a, 2005b; Malkoff-Schwartz et al. 1998, 2000).

Historically, treatments for this disorder, including psychotherapy alone or hospitalization, were not very effective. The discovery of lithium’s mood-stabilizing effects led to dramatic gains in outcome. The dominant treatment approach is mood-stabilizing medication. The first-line treatment recommendation remains lithium, but if side effects are difficult to tolerate, anticonvulsant medications are also useful mood stabilizers. Antidepressants are often added to combat depression, but not without a mood stabilizer because antidepressants can provoke manic symptoms when administered alone (Altshuler et al. 1995; Goldberg and Whiteside 2002). Antipsychotic medications can address psychotic or agitation symptoms. Research in 2004 by Sheri L. Johnson and Robert L. Leahy indicates that family or individual talk therapy can be helpful supplements to medication.

Bibliography:

  1. Alloy, Lauren , Lyn Y. Abramson, Michael E. Hogan, et al. 2000. The Temple-Wisconsin Cognitive Vulnerability to Depression Project: Lifetime History of Axis I Psychopathology in Individuals at High and Low Cognitive Risk for Depression. Journal of Abnormal Psychology 109: 403–418.
  2. Altshuler, Lori , Robert M. Post, Gabriele S. Leverich, et al. 1995. Antidepressant-induced Mania and Cycle Acceleration: A Controversy Revisited. American Journal of Psychiatry 152: 1130–1138.
  3. American Psychiatric 2000. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). 4th ed., text rev. Washington, DC: Author.
  4. Butzlaff, Ronald , and Jill M. Hooley. 1998. Expressed Emotion and Psychiatric Relapse: A Meta-analysis. Archives of General Psychiatry 55: 547–552.
  5. Endicott, Jean, and Robert Spitzer. 1978. A Diagnostic Interview: The Schedule for Affective Disorders and Schizophrenia. Archives of General Psychiatry 35 (7): 837–844.
  6. First, Michael , and M. Gibbon. 2004. The Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I) and the Structured Clinical Interview for DSM-IV Axis II Disorders (SCID-II). In Comprehensive Handbook of Psychological Assessment. Vol. 2: Personality Assessment, eds. Mark J. Hilsenroth and Daniel L. Segal, 134–143. Hoboken, NJ: Wiley.
  7. Gitlin, Michael , Joel Swendsen, Tracy L. Heller, and Constance Hammen. 1995. Relapse and Impairment in Bipolar Disorder. American Journal of Psychiatry 152: 1635–1640.
  8. Goldberg, Joseph F., and Joyce Whiteside. 2002. The Association between Substance Abuse and Antidepressantinduced Mania in Bipolar Disorder: A Preliminary Study. Journal of Clinical Psychiatry 63: 791–795.
  9. Johnson, Sheri 2005a. Life Events in Bipolar Disorder: Towards More Specific Models. Clinical Psychology Review 25: 1008–1027.
  10. Johnson, Sheri 2005b. Mania and Dysregulation in Goal Pursuit. Clinical Psychology Review 25: 241–262.
  11. Johnson, Sheri , and Robert L. Leahy, eds. 2004. Psychological Treatment of Bipolar Disorder. New York: Guilford.
  12. Judd, Lewis , Hagop S. Akiskal, Pamela J. Schettler, et al. 2002. The Long-Term Natural History of the Weekly Symptomatic Status of Bipolar I Disorder. Archives of General Psychiatry 59: 530–537.
  13. Kessler, Ronald , Wai Tat Chiu, Olga Demler, and Ellen E. Walters. 2005. Prevalence, Severity, and Comorbidity of 12Month DSM-IV Disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry 62 (6): 617–627.
  14. Malkoff-Schwartz, Susan, Ellen Frank, Barbara Anderson, et al. 1998. Stressful Life Events and Social Rhythm Disruption in the Onset of Manic and Depressive Bipolar Episodes: A Preliminary Inv Archives of General Psychiatry 55: 702–707.
  15. Malkoff-Schwartz, Susan, Ellen Frank, Barbara Anderson, et al. 2000. Social Rhythm Disruption and Stressful Life Events in the Onset of Bipolar and Unipolar E Psychological Medicine 30: 1005–1016.
  16. McGuffin, Peter, Fruhling Rijsdijk, Martin Andrew, et al. The Heritability of Bipolar Affective Disorder and the Genetic Relationship to Unipolar Depression. Archives of General Psychiatry 60: 497–502.
  17. Monroe, Scott , Kate Harkness, Anne D. Simons, and Michael E. Thase. 2001. Life Stress and the Symptoms of Major Depression. Journal of Nervous and Mental Disease 189: 168–175.
  18. Regeer, J., M. ten Have, M. L. Rosso, et al. 2004. Prevalence of Bipolar Disorder in the General Population: A Reappraisal Study of the Netherlands Mental Health Survey and Incidence Study. Acta Psychiatrica Scandinavica 110 (5): 374–382.
  19. Stockmeier, Craig 2003. Involvement of Serotonin in Depression: Evidence from Postmortem and Imaging Studies of Serotonin Receptors and the Serotonin Transporter. Journal of Psychiatric Research 37: 357–373.

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