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| Etiology or causes According to the US government's National Institute of Mental Health (NIMH), "There is no single cause for bipolar disorder—rather, many factors act together to produce the illness." "Because bipolar disorder tends to run in families, researchers have been searching for specific genes—the microscopic "building blocks" of DNA inside all cells that influence how the body and mind work and grow—passed down through generations that may increase a person's chance of developing the illness." "In addition, findings from gene research suggest that bipolar disorder, like other mental illnesses, does not occur because of a single gene." It is well established that bipolar disorder is a genetically influenced condition which can respond very well to medication (Johnson & Leahy, 2004; Miklowitz & Goldstein, 1997; Frank, 2005). Typical medicines used in the treatment of both Bipolar I & Bipolar II are: haloperidol, chlorpromazine,risperidone, clozapine, quetapine, olanzapine, perphanenazine, lithium, valproate, carbamezapine and lamictal. Psychological factors also play a strong role in both the psychopathology of the disorder and the psychotherapeutic factors aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing prodromal symptoms before full-blown recurrence, and, practicing the factors that lead to maintenance of remission (Lam et al, 1999; Johnson & Leahy, 2004; Basco & Rush, 2005; Miklowitz & Goldstein, 1997; Frank, 2005). Modern evidence based psychotherapies designed specifically for bipolar disorder when used in combination with standard medication treatment increase the time the individual stays well significantly longer than medications alone (Frank, 2005). These psychotherapies are Interpersonal and Social Rhythm Therapy for Bipolar Disorder, Family Focused Therapy for Bipolar Disorder, Psychoeducation, Cognitive Therapy for Bipolar Disorder and Prodrome Detection. All except psychoeducation and prodrome detection are available as books. Brain scientist Husseini K. Manji M.D. of the NIMH states that at their most basic level, the bipolar disorders involve problems in brain structure and function. He stated that these structural changes respond very well to treatment with lithium and valproate in a University of California, Los Angeles Neuropsychiatric Institute (NPI) Grand Rounds Talkgiven in 2003 (requires Real Player and a high-speed internet connection). Early in the course of the illness brain structural abnormalities may lead to feelings of anxiety and lower stress resilience. When faced with a very stressful, negative major life event, such as a failure in an important area, an individual may have their first major depression. Conversely, when an individual accomplishes a major achievement they may experience their first hypomanic or manic episode. Individuals with bipolar disorder tend to experience episode triggers involving either interpersonal or achievement-related life events. An example of interpersonal-life events include falling in love or, conversely, the death of a close friend. Achievement-related life events include acceptance into an elite graduate school or by contrast, being fired from work (Miklowitz & Goldstein, 1997). Veteran brain researcher Robert Post M.D. of the U.S. NIMH proposed the "kindling" theory which asserts that people who are genetically predisposed toward bipolar disorder experience a series of stressful events, each of which lowers the threshold at which mood changes occur. Eventually, the mood episode starts (and becomes recurrent) by itself. Not all individuals experience subsequent mood episodes in the absence of positive or negative life events, however. Individuals with late-adolescent/early adult onset of the disorder will very likely have experienced childhood anxiety and depression. Childhood onset bipolar disorder should be treated early because according to Joseph Calabrese of Case Western Reserve University, childhood forms of the illness may be easier to treat than adult forms of the illness. (See his University of California, Los Angeles NPI Grand Rounds Talk on rapid-cycling in October 2003.) It is becoming increasingly clear that bipolar and unipolar mood disorders have a genetic component. For example, a family history of bipolar spectrum disorders can impart a genetic predisposition towards developing a bipolar spectrum disorder. Since bipolar disorders are polygenic (involving many genes), there are apt to be many unipolar and bipolar disordered individuals in the same family pedigree. This is very often the case (Barondes, 1998). Anxiety disorders, clinical depression, eating disorders, premenstrual dysphoric disorder, postpartum depression, postpartum psychosis and/or schizophrenia may be part of the patient's family history and reflects a term called "genetic loading". Bipolar disorder is more than just biological and psychological. Since "many factors act together to produce the illness", bipolar disorder is called a multifactorial illness, because many genes and environmental factors conspire to create the disorder (Johnson & Leahy, 2004). Since bipolar disorder is so heterogeneous, it is likely that people experience different pathways towards the illness (Miklowitz & Goldstein, 1997). Two personal descriptions of the bipolar experience The following is a quote from a successfully treated individual with bipolar disorder (from the U.S. National Institute of Mental Health): Manic-depression distorts moods and thoughts, incites dreadful behaviors, destroys the basis of rational thought, and too often erodes the desire and will to live. It is an illness which is biological yet looks and feels psychological, one that is unique in conferring advantage and pleasure, yet one that brings in its wake almost unendurable suffering and, not infrequently, suicide. I am fortunate that I have not died from my illness, fortunate in having received the best medical care available, and fortunate of having the friends, colleagues, and family that I do. In her book, Touched With Fire, Kay Redfield Jamison, Ph.D., writes: The clinical reality of manic-depressive illness is far more lethal and infinitely more complex than the current psychiatric nomenclature, bipolar disorder, would suggest. Cycles of fluctuating moods and energy levels serve as a background to constantly changing thoughts, behaviors, and feelings. The illness encompasses the extremes of human experience. Thinking can range from florid psychosis, or "madness", to patterns of unusually clear, fast and creative associations, to retardation so profound that no meaningful mental activity can occur. Behavior can be frenzied, expansive, bizarre, and seductive, or it can be seclusive, sluggish, and dangerously suicidal. Moods may swing erratically between euphoria and despair or irritability and desperation. The rapid oscillations and combinations of such extremes result in an intricately textured clinical picture. History of the bipolar disorders Varying moods and energy levels have been a part of the human experience since time immemorial. The words Depression (previously melancholia) and Mania have their etymologies in Ancient Greek. The word melancholia is derived from ‘melas’, meaning black, and ‘chole’, meaning bile, 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. 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). The idea of a relationship between mania and melancholia can be traced back to at least the 2nd century AD. Soranus of Ephedrus (98-177 AD) described mania and melancholia as distinct diseases with separate aetiologies; 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; Akiskal 1996). 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; Marneros 2001). The contemporary psychiatric conceptualisation of manic-depressive illness is typically traced back to the 1850s. Marneros (2001) describes the concepts emerging out of this period as the “rebirth of bipolarity in the modern era”. On January 31st 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent oscillations between mania and depression. Two weeks later, on the 14th February 1854, Jean-Pierre Falret presented a description to the Academy on what was essentially the same disorder. This illness was designated folie circulaire (‘circular insanity’) by Falret, and folie à double forme (‘dual-form insanity’) by Baillarger (Sedler 1983). Emil Kraepelin (1856-1926), a German psychiatrist considered by many (including Hagop Akiskal M.D.) to be the father of the modern conceptualization of bipolar disorder, categorized and studied the natural course of untreated bipolar patients long before mood stabilizers were discovered. Describing these patients in 1902, he coined the term "manic depressive psychosis." He noted in his patient observations that intervals of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals in which the patient was able to function normally. After World War II, Dr John Cade, Psychiatrist, Bundoora Repatriation Hospital, Melbourne, Australia was investigating the effects of various compounds on veteran patients with manic depressive psychosis. In 1948, Dr John Cade discovered that Lithium Carbonate could be used as a successful treatment of manic depressive psychosis. This was the first time a compound or drug had been discovered that proved to be a successful treatment of any psychiatric condition. The discovery was perhaps the beginning of psychopharmacological treatments of psychiatric conditions. The discovery preceded the discovery of phenothiazines for the treatment of schizophrenia, and the discovery of benzodiazepines for the treatment of anxiety states, by about 4 years. The term "manic-depressive illness" first appeared in 1958. 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. Epidemiology of bipolar disorder Clinical depression and bipolar disorder are currently classified as separate illnesses; some researchers are increasingly viewing them as part of an overlapping spectrum that also includes anxiety and psychosis. The National Comorbidity Survey replication is a study concerning international and U.S. rates of bipolar spectrum disorder. There are two audio talks. The first talk is entitled "The Bipolar Spectrum: Epidemiology and Clinical Perspectives" by Kathleen Merikangas Ph.D. of the NIMH 1st talk. The second talk is entitled "Prevalence and Effects of Mood Disorders on Role Performance in the United States" by Ronald Kessler Ph.D. from Harvard Medical School 2nd talk. According to Hagop Akiskal, M.D., at the one end of the spectrum is bipolar type schizoaffective disorder and at the other end is unipolar depression (recurrent or not recurrent) with the anxiety disorders present across the spectrum. Also included in this view is premenstrual dysphoric disorder, postpartum depression and postpartum psychosis. This view helps to explain why many people who have the illness do not have first-degree relatives with clear-cut "bipolar disorder", but who have family members with a history of these other disorders. In a 2003 study, Hagop Akiskal M.D. and Lew Judd M.D. re-examined data from the landmark Epidemiologic Catchment Area study from two decades before. The original study found that 0.8 percent of the population surveyed had experienced a manic episode at least once (the diagnostic threshold for bipolar I) and 0.5 a hypomanic episode (the diagnostic threshold for bipolar II). By tabulating survey responses to include sub-threshold diagnostic criteria, such as one or two symptoms over a short time period, the authors arrived at an additional 5.1 percent of the population, adding up to a total of 6.4 percent of the entire population who can be thought of as having a bipolar spectrum disorder. This and similar recent studies have been interpreted by some prominent bipolar disorders researchers as evidence for a much higher prevalence of bipolar disorders in the general population than previously thought. However these re-analyses should be interpreted cautiously because of substantive as well as methodological study limitations. Indeed prevalence studies of bipolar disorder are carried out by lay interviewers (that is, not by expert clinicians/psychiatrists who are more costly to employ) who follow fully structured/fixed interview schemes; responses to single items from such interviews may suffer limited validity. Furthermore, a well known statistical problem arises when ascertaining disorders and conditions with a relatively low population prevalence or base-rate such as bipolar disorder: even assuming that lay interviews diagnoses are highly accurate in terms of sensitivity and specificity and their corresponding area under the ROC curve (that is, AUC, or area under the receiver operating characteristic curve), a condition with a relatively low prevalence or base-rate is bound to yield high false positive rates, which exceed false negative rates; in such a circumstance a limited positive predictive value, PPV, yields high false positive rates even in presence of a specificity which is very close to 100% (Baldessarini, Finklestein, Arana, 1983). To simplify, it can be said that a very small error applied over a very large number of individuals (that is, those who are *not affected* by the condition in the general population during their lifetime; for example, over 95%) produces a relevant, non negligible number of subjects who are incorrectly classified as having the disorder or any other condition which is the object of a survey study: these subjects are the so-called false positives; such reasoning applies to the 'false positive' but not the 'false negative' problem where we have an error applied over a relatively very small number of individuals to begin with (that is, those who are *affected* by the condition in the general population; for example, less than 5%). Hence, a very high percentage of subjects who seem to have a history of bipolar disorder at the interview are false positives for such a medical condition and apparently never suffered a fully clinical syndrome (that is, bipolar disorder type I): the population prevalence of bipolar disorder type I, which includes at least a lifetime manic episode, continues to be estimated at 1% (Soldani, Sullivan, Pedersen, 2005). A different but related problem in evaluating the public health significance of psychiatric conditions has been highlighted by Robert Spitzer of Columbia University: fulfillment of diagnostic criteria and the resulting diagnosis do not necessarily imply need for treatment (Spitzer, 1998). As a consequence, subjects who experience bipolar symptoms but not a full blown, impairing bipolar syndrome should not be automatically considered as patients in need of treatment. Recent studies have indicated that at least 50% of adult sufferers report manifestation of symptoms before the age of 17. Moreover, there is a growing consensus that bipolar disorder originates in childhood. In young children the illness is now referred to as pediatric bipolar disorder. Today about 0.5% of children under 18 are believed to have the condition. For children, the main concern is that bipolar disorder needs to be diagnosed correctly and treated properly because it can look like unipolar depression, ADHD or conduct disorder. If a child with bipolar disorder is misdiagnosed and treated with antidepressants or stimulants, the child may become violent, suicidal, homicidal or otherwise severely destabilized. Young children, adolescents and adults each express the illness differently according to child and adolescent bipolar disorders expert Demitri Papolos M.D. and the Child and Adolescent Bipolar Foundation. There is, however, controversy about this last point Bipolar disorder manifests in late life as well. Some individuals with hyperthymic temperament (or "hypomanic" personality style) who experience depression in later life appear to have a form of bipolar disorder. Much more needs to be elucidated about late life bipolar disorder. |