![]() | Only 14 pages are availabe for public view |
Abstract Bipolar disorder, formerly known as manic–depressive disorder, has intrigued scholars dating back to ancient Greece, yet it remains enigmatic in many ways. Hypomania, with its euphoria, energy, and productivity, has been described as a powerful elixir, and there is no other psychiatric condition in which people report craving the return of symptoms. Literature, arts, and history have been shaped by the remarkable creativity of individuals with bipolar disorder, including Vincent van Gogh, Martin Luther, Robert Schumann, Pytor Illyich Tchaikovsky, and the Pulitzer Prize winners John Berryman, Amy Lowell, and Anne Sexton (Goodwin & Jamison, 1990; Jamison, 1996). Kraepelin (1921) described the course of this illness systematically more than 80 years ago. He noted the heterogeneity in the types of symptoms, the pattern of episodes, and the level of functioning. His descriptions of symptoms are strikingly concordant with the terms used to describe bipolar disorder in DSM-IV-TR, and many of his diagnostic distinctions remain well supported today. Similarly, issues he raised regarding the heterogeneity of this diagnosis remain prominent. The coexistence of other Axis I disorders with bipolar disorder complicates psychiatric diagnosis and treatment. Conversely, symptom overlap in DSM-IV diagnoses hinders definition and recognition of true co-morbidity. Psychiatric co-morbidity is often associated with earlier onset of bipolar symptoms, more severe course, poorer treatment compliance, and worse outcomes related to suicide and other complications. Medical co-morbidity may be exacerbated or caused by pharmacotherapy of bipolar symptoms (Ranga, 2005). Bipolar disorder is not associated consistently with substantial changes in the number or density of neurons in any particular brain region, although lower density of glial cells has been found in some postmortem studies (Vawter, Freed, & Kleinman, 2000). Compared to research on structural abnormalities, more focus is being placed on understanding the level of activity in different brain regions, particularly during episodes. To full fill the aim of this study the essay was divided into: i. Chapter I: in which we reviewed the historical roots bipolar disorder and the various type of classification discussing it and the development of the bipolar spectrum. ii. Chapter II: in which we tried to cover all medical and psychiatric comorbidity. We stressed on the importance of discovering any comorbidy which affect the course, prognosis, and management of the bipolar spectrum. iii. Chapter III: in which we reviewed various neurobiological theories regarding bipolar spectrum disorder. we tried to cover alterations in brain structure, alterations in brain function, functional brain circuits, alterations in brain chemistry, neurochemical changes, neuroendocrine changes, signaling networks: the cellular cogwheels underlying long-term neuroplasticity, clinical correlates. |