Posted by Mr.Scott on March 25, 2002, at 18:49:28
In reply to Do I really have bipolar II?, posted by Kristin on March 23, 2002, at 14:32:33
I surely have mild bipolar disoder, but have never lost sleep not once! Only have I slept too much...
Just think of it as mild Bipolar disorder which like heart disease can come in many shapes and sizes. Don't fret over the diagnosis (easier said than than done I know!), just keep an open mind about treatment. I don't have a link but here is an interesting article, and believe me I have MANY MANY more..
Scott
The Bipolar Spectrum: A Valid Forme Fruste?
by S. Nassir Ghaemi, M.D.
Closely related to the question of my previous column-whether or not bipolar disorder (BD) is misdiagnosed-is the issue of how to define bipolar disorder. For most of this century, American psychiatry's definition of manic-depressive illness has tended to be rather narrow (while those of schizophrenia and depression have been correspondingly broad). Over the last two decades, the diagnostic limits of schizophrenia have been narrowed greatly and those of affective disorders (including BD) broadened somewhat. This trend has led to increasing discussion of the concept of a "bipolar spectrum." Is this concept valid and useful?
Historically, the original conceptions underlying BD always reflected the controversy over whether to view the illness broadly or narrowly. (This history is best reviewed in Baldessarini [2000], and Goodwin and Jamison [1990]). In the mid- to late 19th century, leaders in French psychiatry identified mania and depression; they tended to diagnose manic-depressive conditions narrowly, with many subgroupings. In the late 19th and early 20th century, the German psychiatrist Emil Kraepelin first argued for a neat division of all psychotic syndromes into schizophrenia (narrowly conceived and limited to a small number of individuals in the population) and manic-depressive illness (broadly conceived and including what today we would call recurrent major depression). Kraepelin's work gained much influence for a few decades, but it was soon eclipsed by the rise of interest in Freud. Freud had little interest in diagnosis, and thus the controversy between Kraepelin's broad view and the earlier narrower French perspective ebbed. In the 1950s and 1960s, some European psychiatrists resuscitated the earlier French conceptions and made the distinction between bipolar (mania being present) and unipolar (mania not present) affective illnesses. Genetic and outcome research supported this model and led to its acceptance in American nosology with DSM-III in 1980. More recently, BD has been further divided into type I (mania present) and type II (hypomania present, a milder form of manic symptoms) in DSM-IV.
Thus, if one begins with Kraepelin's original broad concept of manic-depressive illness, mainstream psychiatry has moved to a more narrow description of BD (type I or II) and unipolar depression. For the last half century, this has meant that most clinicians have not diagnosed BD unless a patient was frankly, overtly and unequivocally manic (usually extremely agitated, psychotic and hospitalized). The tendency has been for everyone else to receive a diagnosis of unipolar depression or schizophrenia. This scenario is a source of some wonder. The textbooks say, and everyone claims to agree, that unipolar depression and schizophrenia are diagnoses of exclusion. One is supposed to rule out past mania before diagnosing unipolar depression in a nonpsychotic depressed individual; one is also supposed to rule out mania before diagnosing schizophrenia in a psychotic individual. Yet, in each case, since mania has only been diagnosed when extreme and severe, it is my opinion that the tendency is to underdiagnose BD. (See my previous columns for empirical studies that support this notion.)
The concept of the bipolar spectrum is, in many senses, a reversion to the original Kraepelinian perspective. Today, when referring to the bipolar spectrum, the clinician is first making the statement that mania is not necessary for the diagnosis of bipolar disorder. Hypomania would do, being defined as milder manic symptoms lasting a few days or more that are not associated with any significant social or occupational dysfunction. This last qualifier is extremely important. With hypomania, one has no difficulties; in fact, one is functioning more effectively in life. I believe that hypomania is the only diagnosis in DSM-IV that does not have, as one of its criteria, the presence of significant social or occupational dysfunction. This makes type II BD (hypomania and depression) unique-the defining diagnostic feature (hypomania) occurs when someone is feeling well. This, of course, often makes it difficult for individuals and clinicians to recognize. The problem with bipolar II disorder, consequently, is not hypomania, but the inevitable depressions that precede or follow it.
Bipolar II disorder is becoming more and more accepted as a valid diagnosis, although it remains a quite unreliable one, i.e., clinicians often do not agree on what to call hypomania and what to call normal mood. In my opinion, most clinicians are culturally biased to overdiagnose normality and underdiagnose hypomania.
The other part of the bipolar spectrum would be the category of NOS (not otherwise specified). (The evidence for the following discussion is best detailed in Akiskal [1996].) This could include individuals with a family history of type I BD and those who have hypomania only on antidepressants. Other potential "soft signs" of BD include atypical (increased sleep and appetite) and psychotic depressive episodes (both are more common in bipolar than unipolar depression); early age of onset of depressive illness; many brief recurrent depressive episodes (Kraepelin included them in his concept of manic-depressive illness); transient antidepressant response ("poop-out," meaning acute improvement but later relapse); and "hyperthymic" baseline personality when not depressed (a kind of chronic hypomania that is not brief and episodic but rather seems to be one's basic personality). A single soft sign is not diagnostic of the bipolar spectrum, but the more soft signs that exist, the increased likelihood that it is bipolar spectrum rather than unipolar depressive illness.
This broad bipolar spectrum view stems from observations regarding treatment response with lithium and antidepressants and, thus, has practical utility. Bipolar spectrum patients may be less likely to respond to antidepressants (thus representing part of that pool of people diagnosed with treatment-resistant depression) and may be more likely to respond to mood stabilizers (alone or along with antidepressants) (Akiskal, 1996).
If valid, the bipolar spectrum concept would have the advantage of redressing the imbalance in diagnostic perspectives and influencing clinicians to diagnose milder cases of mania and hypomania. An increase in diagnosis of the bipolar spectrum would also narrow down the diagnostic range of unipolar depression to more realistic and accurate levels. This is the perspective of individuals, myself included, who are attracted to the concept of the bipolar spectrum.
What can be said against the bipolar spectrum? First, there is little research to validate or invalidate it. To some extent, this is a circular problem: Since the field has generally ignored anything but classic bipolar I disorder, researchers and grant-giving agencies are often wary of giving money for research on a new and poorly documented concept such as the bipolar spectrum. I ran into this problem a few years ago when gabapentin (Neurontin), a new medication approved by the U.S. Food and Drug Administration for epilepsy, was to be studied for use in psychiatric conditions. I suggested that the drug be studied in type II bipolar depression along with, or perhaps instead of, type I BD. In my early clinical experience, I found limited efficacy for the medication in type I BD, but found suggested efficacy in type II bipolar illness. If gabapentin had mild to moderate mood-stabilizing effects, it might not work in type I BD, but it might have benefits in the milder parts of the bipolar spectrum (Ghaemi et al., 1998). This suggestion was not accepted on the grounds that the diagnosis of bipolar II disorder was unreliable (clinicians often disagree in defining hypomania), and that the diagnosis itself was too vague to be worth studying. Another factor may have been that the FDA has never recognized any bipolar diagnosis other than mania, and thus studying hypomania or the bipolar spectrum would not necessarily meet with any support on the part of federal regulators when seeking a treatment indication. Gabapentin went on to be ineffective in double-blind research on bipolar I disorder (Pande, 1999), and controlled research in the bipolar spectrum was never conducted.
The other major criticism made of the bipolar spectrum-in my opinion, the one with the most merit-is that the spectrum concept waters down the definition of bipolar disorder so much that it would impair biological research (Baldessarini, 2000). In general, for biological studies into the etiology and pathophysiology of a disease, it is necessary for the clinical definition of the condition to be as precise and homogeneous as possible. Since the spectrum concept is, by definition, broad and heterogeneous, it might impair the ability of biological studies to find the underlying problems leading to BD. This is a real concern.
One solution would be a "two-hat" answer. Wearing the researcher's hat, I would continue to focus on narrow, clearly defined bipolar I disorder. Wearing the clinician's hat, I would broaden my view to include the bipolar spectrum. Is this proposed solution inconsistent? Yes, but as Emerson long ago pointed out, consistency is not necessarily a component of truth. Whatever the biological etiology, the clinical manifestations of that etiology can vary immensely, especially as those manifestations might be influenced by varied environmental and other factors. This has long been recognized in medicine, where the concept of the forme fruste has long been invoked to describe mild, subtle forms of specific diseases.
Does bipolar disorder have a forme fruste? Probably. But we need to do more work on describing, defining and validating its characteristics.
Dr. Ghaemi is a research psychiatrist in the Psychopharmacology Program at Cambridge Hospital and an instructor in psychiatry at Harvard Medical School.
References
Akiskal HS (1996), The prevalent clinical spectrum of bipolar disorders: beyond DSM-IV. J Clin Psychopharmacol 16(2 suppl 1):4S-14S.
Baldessarini RJ (2000), A plea for the integrity of the bipolar disorder concept. Bipolar Disorders 2(1):3-7.
Ghaemi SN, Katzow JJ, Desai SP, Goodwin FK (1998), Gabapentin treatment of mood disorders: a preliminary study. J Clin Psychiatry 59(8):426-429.
Goodwin FK, Jamison KR (1990), Manic-Depressive Illness. New York: Oxford University Press.
Pande AC (1999), Combination treatment in bipolar disorder (abstract). Bipolar Disorders 1(suppl 1):17.
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