History of bipolar disorder
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Cyclical variations in moods and energy levels have been recorded at least as far back as several thousand years. The words "melancholia" (an old word for depression) and "mania" have their etymologies in Ancient Greek. The word melancholia is derived from melas/μελας, meaning "black", and chole/χολη, meaning "bile" or "gall", indicative of the term’s origins in pre-Hippocratic humoral theories. Within the humoral theories, mania was viewed as arising from an excess of yellow bile, or a mixture of black and yellow bile.
- 1 The linguistic origins of mania in relation to bipolar disorder
- 2 Relationship between mania and melancholia
- 3 Origin of bipolar disorder as a mental illness
- 4 Initial treatment options
- 5 Progression from manic-depressive "reaction" to manic-depressive "illness"
- 6 Current classification of bipolar disorder
- 7 See also
- 8 References
The linguistic origins of mania in relation to bipolar disorder
The linguistic origins of mania, however, are not so clear-cut. Several etymologies are proposed by the Roman physician Caelius Aurelianus, including the Greek word ""ania", meaning to produce great mental anguish, and "manos", meaning relaxed or loose, which would contextually approximate to an excessive relaxing of the mind or soul (Angst and Marneros 2001). There are at least five other candidates, and part of the confusion surrounding the exact etymology of the word mania is its varied usage in the pre-Hippocratic poetry and mythologies (Angst and Marneros 2001).
Relationship between mania and melancholia
The idea of a relationship between mania and melancholia can be traced back to at least the 2nd century AD. Soranus of Ephesus (98–177 AD) described mania and melancholia as distinct diseases with separate etiologies; however, he acknowledged that “many others consider melancholia a form of the disease of mania” (Cited in Mondimore 2005 p. 49).
The earliest written descriptions of a relationship between mania and melancholia are attributed to Aretaeus of Cappadocia. Aretaeus was an eclectic medical philosopher who lived in Alexandria somewhere between 30 and 150 AD (Roccatagliata 1986;[which?] Akiskal 1996[which?]). Aretaeus is recognized as having authored most of the surviving texts referring to a unified concept of manic-depressive illness, viewing both melancholia and mania as having a common origin in "black bile" (Akiskal 1996;[which?] Marneros 2001[which?]).
Origin of bipolar disorder as a mental illness
A clear understanding of bipolar disorder as a mental illness was recognized by early Chinese authors. The encyclopedist Gao Lian (c. 1583) describes the malady in his Eight Treatises on the Nurturing of Life (Ts'un-sheng pa-chien).
Avicenna, a Persian physician and psychological thinker who wrote The Canon of Medicine in 1025, identified bipolar disorder as a manic depressive psychosis, which he clearly distinguished from other forms of madness (Junun) such as mania, rabies, and schizophrenia (Junun Mufrit or severe madness).
The basis of the current conceptualisation of manic-depressive illness can be traced back to the 1850s; on January 31, 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent oscillations between mania and depression, which he termed folie à double forme (‘dual-form insanity’). Two weeks later, on February 14, 1854, Jean-Pierre Falret presented a description to the Academy on what was essentially the same disorder, and designated folie circulaire (‘circular insanity’) by him.(Sedler 1983) The two bitterly disputed as to who had been the first to conceptualise the condition.
These concepts were developed by the German psychiatrist Emil Kraepelin (1856–1926), who, using Kahlbaum's concept of cyclothymia, categorized and studied the natural course of untreated bipolar patients. He coined the term manic depressive psychosis, after noting that periods of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals where the patient was able to function normally.
Distinction between Manic-depression involving psychotic states, and that which does not involve psychosis
The first diagnostic distinction to be made between manic-depression involving psychotic states, and that which does not involve psychosis, came from Carl Gustav Jung in 1903. Jung’s distinction is today referred to in the DSM-IV as that between ‘bipolar I’ (mania involving possible psychotic episodes) and ‘bipolar II’ (hypomania without psychosis). In his paper Jung introduced the non-psychotic version of the illness with the introductory statement, “I would like to publish a number of cases whose peculiarity consists in chronic hypomanic behaviour” where “it is not a question of real mania at all but of a hypomanic state which cannot be regarded as psychotic”. Jung illustrated the non-psychotic variation with 5 case histories, each involving hypomanic behaviour, occasional bouts of depression, and mixed mood states, which involved personal and interpersonal upheaval for each patient.
Initial treatment options
After World War II, Dr. John Cade, an Australian psychiatrist, was investigating the effects of various compounds on veteran patients with manic depressive psychosis. In 1949, Cade discovered that lithium carbonate could be used as a successful treatment of manic depressive psychosis. Because there was a fear that table salt substitutes could lead to toxicity or death, Cade's findings did not immediately lead to treatments. In the 1950s, U.S. hospitals began experimenting with lithium on their patients. By the mid-'60s, reports started appearing in the medical literature regarding lithium's effectiveness. The U.S. Food and Drug Administration did not approve of lithium's use until 1970.
Progression from manic-depressive "reaction" to manic-depressive "illness"
The term "manic-depressive reaction" appeared in the first American Psychiatric Association Diagnostic Manual in 1952, influenced by the legacy of Adolf Meyer who had introduced the paradigm illness as a reaction of biogenetic factors to psychological and social influences. Subclassification of bipolar disorder was first proposed by German psychiatrist Karl Leonhard in 1957; he was also the first to introduce the terms bipolar (for those with mania) and unipolar (for those with depressive episodes only).
In 1968, both the newly revised classification systems ICD-8 and DSM-II termed the condition "manic-depressive illness" as biological thinking came to the fore.
Current classification of bipolar disorder
The current nosology, bipolar disorder, became popular only recently, and some individuals prefer the older term because it provides a better description of a continually changing multi-dimensional illness.
Empirical and theoretical work on bipolar disorder has throughout history "seesawed" between psychological and biological ways of understanding. Despite the work of Kraepelin (1921) emphasizing the psychosocial context, conceptions of bipolar disorder as a genetically based illness dominated the 20th century. Since the 1990s, however, there has been a resurgence of interest and research into the role of psychosocial processes.
- Liddell, Henry George and Robert Scott (1980). A Greek-English Lexicon (Abridged Edition). United Kingdom: Oxford University Press. ISBN 0-19-910207-4.
- df "Bipolar disorders beyond major depression and euphoric mania" (PDF). cambridge.org. Retrieved 2008-02-16.
- Youssef, Hanafy A.; Youssef, Fatma A.; Dening, T. R. (1996). "Evidence for the existence of schizophrenia in medieval Islamic society". History of Psychiatry 7 (25): 55–62 . doi:10.1177/0957154X9600702503. PMID 11609215.
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- Jung, C.G., (1903) ‘On Manic mood disorder’ in Psychiatric Studies Vol-1, Collected works, second edition (1970) translated by R.F.C Hull. Routledge and Kegan Paul. pp.109-111
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- Goodwin & Jamison. p88
- Alloy, LB; Abramson, LY; Urosevic, S; Walshaw, PD; Nusslock, R; Neeren, AM (2005). "The psychosocial context of bipolar disorder: environmental, cognitive, and developmental risk factors.". Clinical Psychology Review 25 (8): 1043–75. doi:10.1016/j.cpr.2005.06.006. PMID 16140445.