Αμφισβήτηση για τη διάγνωση της Διπολικής Διαταραχής στις ΗΠΑ
| Στη σημερινή καταχώρηση, παρατίθενται δύο άρθρα που αναφέρονται αμφότερα στην αμφισβήτηση για την απόδοση της διάγνωσης διπολικής διαταραχής στις ΗΠΑ. Το πρώτο, που είναι σημερινό θέμα από το in.gr πραγματεύεται την αύξηση κατά 40% της απόδοσης διπολικής διαταραχής ιδαίτερα σε εφήβους... Το δεύτερο άρθρο, άμεσα σχετιζόμενο, είναι από τη λίστα radpsy net και εκ τούτου στα αγγλικά, και συζητάει εις βάθος το ζήτημα της απόδοσης αυτής της διαγνωστικής κατηγορίας, με βάση τα κριτήρια του DSM. Μεγάλο και το σημερινό ποστ... Ανάλογα με τα κριτήρια Υπό αμφισβήτηση η έξαρση διπολικής διαταραχής στις ΗΠΑ | ||
 Τα Νέα | ||
| Τα όρια της ασθένειας είναι συχνά αυθαίρετα | ||
| ||
Ανάλυση που δημοσιεύεται την Τρίτη δείχνει ότι οι επισκέψεις εξωτερικών ασθενών κάτω των 19 ετών στους οποίους διαγνώστηκε διπολική διαταραχή εκτοξεύτηκαν από τις 20.000 το 1994 στις 800.000 το 2003, με παράλληλη αύξηση στη χρήση αντιψυχωσικών από παιδιά. Στους ενήλικες, οι διαγνώσεις διπλασιάστηκαν στο ίδιο διάστημα. Δύο εξηγήσεις υπάρχουν για τη δραματική αυτή αύξηση, σημειώνει ο Μαρκ Όλφσον του Πανεπιστημίου Κολούμπια και επικεφαλής των ερευνητών. Είτε οι γιατροί αποτύγχαναν παλαιότερα να αναγνωρίσουν σωστά τη διαταραχή στους νέους, είτε είναι σήμερα υπερβολικά πρόθυμοι να προχωρήσουν σε διάγνωση. Η διπολική διαταραχή, παλαιότερα γνωστή ως μανιοκατάθλιψη, χαρακτηρίζεται από εναλλαγή περιόδων κατάθλιψης και μανίας (αφύσικα ανεβασμένης διάγνωσης). Τα συμπτώματα μπορεί να διαφέρουν στα παιδιά και ορισμένοι γιατροί δεν πιστεύουν ότι μπορεί να γίνει διάγνωση πριν από την ενηλικίωση. Τα αίτιά της παραμένουν άγνωστα, ωστόσο πιστεύεται ότι είναι εν μέρει κληρονομική. Οι ερευνητές επισημαίνουν την ανάγκη για «μελέτες αξιοπιστίας», στις οποίες θα εξεταστεί η ακρίβεια των διαγνώσεων σε παιδιά και έφηβους. Η μελέτη δημοσιεύεται στο Archives of General Psychiatry. |
Και το δεύτερο άρθρο:
By James Phelps, MD,
URL: http://www.psychiat rictimes. com/showArticle. jhtml?articleId= 191504355
July 2006, Vol. XXIII, No. 8
Psychiatric diagnosis is currently based on a system of categories, much like the Linnaean classification in biology. However, a seemingly opposite diagnostic system is emerging, usually dubbed the �dimensional view,� in which related psychiatric conditions such as major depressive disorder (MDD) and bipolar disorder (BD) are seen as end points of a spectrum.
With this expansion of the concept of BD to include intermediate forms (ie, manifestations between clearly unipolar and clearly bipolar cases), concerns have arisen about the potential for overdiagnosis of BD1 and the blurring of our understanding.2 However, diagnostic error thus far has been skewed in the direction of underdiagnosis.3
The concept of overdiagnosis or underdiagnosis presumes some �natural types� that we diagnosticians are correctly or incorrectly classifying. Indeed, the term �classify� implies that we are looking at native classes. This is, for example, the process used by an ornithologist to identify a particular bird: scientists use visible traits such as size, color, beak shape, wing bars, eye rings, and other field signs. They may also observe preferences such as habitat (ground or high trees), interactions (flocking or pairing), diet (seeds, worms, or fish), and even behavior over time (eg, migration or wintering-over) .
The DSM system is like that of the ornithologist. The purpose of the diagnostic interview is to gather observations, for which the DSM serves as a �field guide,� organizing the observed findings by category of illness. But just as in ornithology, over time an experienced clinician relies less and less on the specific DSM rules and progressively more on pattern recognition. A good bird watcher distinguishes a woodpecker from a hawk not so much by specific field signs but from an overall gestalt�rapid synthesis of a whole complex of findings (eg, location in the tree, position on the branch, size, shape, color, behavior, call). Likewise, an experienced clinician might strongly suspect that a patient has BD based on observations on an inpatient unit, even before an interview.
Unlike birding, however, experience gives clinicians the ability to recognize intermediate cases that blur the boundaries of the classification system. Indeed, this lack of discrete boundaries has been studied quantitatively in at least 2 research settings, both of which showed a continuum of symptoms in patients with DSM-diagnosed MDD and BD. Some patients with MDD have no symptoms suggestive of BD, others have a few such symptoms, and still others have many with no gaps in this progression that might serve as a natural point of cleavage between the conditions.4
The same result was obtained by Benazzi5 in a study designed specifically to look for such gaps. Similarly, Mackinnon and Pies6 recently presented an elegant model for rapid-cycling and mixed-state BD, demonstrating that mood, energy, and creativity/speed- ofthought symptoms fluctuating asynchronously can create a continuum of forms of the illness. Although this model has not yet been subjected to rigorous study, it accords well with clinical impressions, just as Jamison7 summarized over a decade ago: �The clinical reality of manic-depressive illness is far more lethal and infinitely more complex than the current psychiatric nomenclature . . . would suggest.�
IS THE DSM INCORRECT?
Is the DSM system incorrect, then? Is BD really just one end of a mood spectrum continuum? The key word here is really: notice that again we are presuming to model reality. We are assuming there is a correct way of explaining, such that there could be overrecognition and underrecognition of bipolarity. Yet we still lack biologic underpinnings for these models. A truly valid nosologic system will ultimately be anchored by understanding etiology�from genetic susceptibilities through molecular differences to anatomic and/or physiologic changes. We are witnessing exciting progress in this regard. For example, recent work by Tsankova and colleagues8 on regulation of brain-derived neurotrophic factor transcription by histone methylation and acetylation in response to social defeat stress further calcifies neuroplasticity, an important bone in the skeleton of mood disorder pathology.
Must we wait for the rest of the skeleton to form to see how bipolar and unipolar mood disorders really are related? (Is there truly a joint in there somewhere?) One hopes not�critical clinical decisions rest on these distinctions. Many patients do not respond, or do not sustain their response, to antidepressant treatment. What percentage of them have an underlying bipolar component as the basis for that failed treatment? Who is at risk for a dangerous reaction to antidepressants? How can we recognize subthreshold bipolarity if, as shown in the most recent iteration of the United States National Comorbidity Survey, it can cause as much disability as diabetes or asthma?9
Many have suggested that the DSM should include a broader range of bipolarity, including Klerman's 10 categories I through VI; Akiskal and Pinto's11 I through IV, including 1½, 2½, 3½; and the recent bipolar spectrum disorder proposed by Ghaemi and colleagues.12 A review for the International Society for Bipolar Disorders' position paper series on bipolar diagnosis13 concludes that 3 groups of patients should be considered for such an extension of the categoric system, including:
- Subthreshold cases, as suggested by the National Comorbidity Survey Replication Study (NCS-R)9 and the Zurich cohort.14
- Patients with multiple soft signs of bipolarity, as defined by Ghaemi and colleagues,12 even if they lack detectable hypomania.
- Patients with antidepressant- induced hypomania or mania.
Or, might it be better to view bipolarity as an illness dimension, one that can be present to varying degrees? This approach has been adopted, at least as a working approach awaiting further study, by the bipolar clinic at Harvard's teaching hospital, where instead of asking, �Does this patient have bipolar disorder or not?� clinicians are taught to ask �How much bipolarity might this patient have?�15 Among other diagnostic tools (available at www.manicdepressive .org), the clinic uses the Bipolarity Index, a 100-point scale with 20 points for hypomania or mania, but an additional 80 points for other features (eg, family history, age at onset, course of illness, response to medications) .16
What problem do we need to solve right now? When should antidepressants be used?
As we consider revisions to the current diagnostic system, we should remember the problem we are trying to solve. At present, the DSM system works well at the extremes of diagnosis: mania identifies BD well when recognized as such. (Numerous factors can impede this recognition, such as lack of insight on the part of the patient or lack of sufficient search on the part of the clinician; neither is the fault of the DSM system.) Conversely, an adult with a single episode of major depression following severe psychosocial stress with no family history of BD will be widely recognized as having MDD. These fully expressed, recognizable cases�shown in the Figure (See Psychiatric Times, July 2006, p. 76) as points E and A�will be treated with mood stabilizers and antidepressants, respectively.
Point D in the Figure (See Psychiatric Times, July 2006, p. 76) represents identifiable BD II, with fully expressed hypomania. The DSM system of diagnosis works reasonably well for such a patient. Our problem comes with intermediate forms. Point C represents subthreshold cases per the NCS-R. Some psychiatrists would call this BD not otherwise specified (BD NOS; ie, bipolar but not meeting BD II criteria). However, others would regard this as a form of depression, perhaps atypical but not bipolar because DSM criteria for hypomania are not met.
The same disagreement arises�and perhaps with more strength�at point B, where only a few bipolar-minded clinicians might persist in calling this BD NOS, and most psychiatrists would call it MDD. Obviously, from a spectrum viewpoint there are almost an infinite variety of other intermediate cases (but let us not digress into Zeno's paradox!).
Some clinicians are already using a spectrum view of diagnosis, but many are not. The resulting division of opinion was demonstrated dramatically in a 2005 Webcast presented by Harvard faculty, with an audience of hundreds of psychiatrists.17 The program focused on a patient with clear symptoms of depression, as well as anger, anxiety, sleep problems, and alcohol use. His case was clearly selected to present features of MDD yet suggests possible BD II. His symptoms were presented in considerable detail to focus on this differential. After the Harvard experts concluded in favor of a unipolar diagnosis, the audience was asked to voice their opinion� bipolar or unipolar? Two thirds chose bipolar. Not only did they disagree with the experts, they were substantially divided among themselves. What an embarrassment for our field.
Notice that on this disagreement hinges a critical, relatively immediate decision. Suppose a patient presents with depression. Suppose the important elements in a standard differential diagnosis have been excluded: substance use or hypothyroidism and other suborganic causes such as Parkinson disease or B12 deficiency (some would include personality disorders, but that is a complex issue18). Suppose the patient strongly prefers a medication approach to psychotherapy and is unlikely to adopt an exercise program as the primary intervention. If the patient is electing a pharmacologic approach for managing depression, should the clinician begin with an antidepressant or consider a mood stabilizer with antidepressant clout?
We can debate whether the line between unipolar and bipolar should be drawn farther to the left on the continuum. We can debate whether there really is a continuum. These debates have persisted for years. (The term �soft bipolar spectrum� was first used in 1987.19) Perhaps in a few years the DSM-V will include one more intermediate form (eg, BD III). Yet here we sit in the field of psychiatry with a system of diagnosis that forces us to disagree with one another in public. This system may even be doing harm by forcing misclassification of patients as unipolar, leading to dangerous adverse effects from antidepressants. All of this, because we persist in clinging to a categoric system for a continuum of symptoms.
To address this dilemma now, instead of waiting for the DSM-V, we could reframe our current division of opinion in new, more manageable terms. Thus, when considering a medication approach to depression, which findings warrant changing our current default assumption from antidepressants to mood stabilizers? This reframing alone will not solve our problem; some psychiatrists would require clear-cut mania or hypomania, setting the bar for this shift in strategy between points C and D in the Figure (See Psychiatric Times, July 2006, p. 76). Others would extend use of mood stabilizers as far as C and others even to B. Several well-known researchers have even suggested that some patients at Point A (ie, no observable signs or history of hypomania) might warrant consideration for mood stabilizers. The bipolar spectrum disorder proposed by Ghaemi and colleagues12 suggests that even patients who have never had hypomania, only multiple soft signs�such as a first degree relative with BD, depression onset between ages 15 and 19, and subsequent repeated brief episodes�may still have enough bipolarity to present some risk if treated with antidepressants alone.
By comparison, another research group has shown up to 6 months of improvement treating BD II with antidepressant monotherapy, which would appear to contradict the concerns about this practice. However, Amsterdam and Shults20 did indeed see an increase in mania scores (Young Mania Rating Scale [YMRS]) in patients treated with fluoxetine. Although they dismiss it as �not clinically meaningful,� the YMRS is not very sensitive to subtle hypomania; thus finding any increase with this instrument may warrant concern.
In general practice, however, most physicians are �lumpers��when using a medication approach, they treat depression with antidepressants. Indeed, physicians verge on lumping even bipolar depression into the same approach: as of 2003, as many as 80% of community psychiatrists' patients with BD were taking antidepressants.21 So perhaps a more operational reframing of the diagnostic dilemma might be summarized by a single question: presuming, as discussed above, that a proper differential diagnosis of depression has been conducted and a medication approach is now to be initiated, how many antidepressants should be tried in a patient lacking DSM indications of BD (and, therefore, �unipolar�), before trying a mood stabilizer?
In current practice, we routinely try multiple antidepressants, do we not? But for a patient with a family history of BD, perhaps the transition in strategy should come earlier. And for a patient with many soft signs of bipolarity, perhaps the transition should come after a single antidepressant trial� or even before. This is the principle value of the spectrum concept: it makes you think. It adds bipolarity to the differential of apparently unipolar depression, even when a thorough search for hypomania has yielded little. (Credit for this concept goes to Jack Katzow, MD, my colleague on the International Society for Bipolar Disorders' spectrum subcommittee. )
Should we simply expand the range of patients for whom one can rationally consider mood stabilizers? All of the atypical antipsychotics have been used with some evidence of efficacy,22 but few formal randomized trials have been conducted. Interestingly, 2 important randomized trials were not published. Data from these studies show that lamotrigine failed to improve the course of treatment-resistant patients with unipolar disorder,23 even though one would think such a group would represent an enriched sample of soft bipolarity. These data obviously give us pause in considering the breadth of applicability of lamotrigine. Furthermore, olanzapine in this population caused the same weight gain problems we know all too well.24
Clinicians also consider medication risks when choosing among options. In my opinion, we may be underestimating the risk of antidepressants relative to those of mood stabilizers (a very broad and complex group, none of which meet the most rigorous definition of this term25). When, for a given patient, antidepressants lack efficacy as evidenced by a series of failed but presumably wellconducted treatments, what should we do next (besides reconsidering the differential yet again)? In my opinion, clinicians�and patients�may be slow to consider mood stabilizers because of the greater perceived risks of such medications. This deserves study, certainly. In the meantime, let's exam-ine what we know so far about these relative risks.
RISKS OF TREATMENTS, COMPARED
The Table compares the short- and long-term risks (significant implications, not just side effects) of these agents, focusing on mood stabilizers that have at least some data supporting antidepressant efficacy.
Every mood stabilizer can, at least rarely, cause death. Most have several other significant long-term risks. By comparison, antidepressants carry less direct risk of death, unless one counts the hotly debated risk of increasing suicidality. Instead, a variety of destabilizing effects have been associated with antidepressants, although the data are scant and debated (for a review, see Phelps26).
Of even greater concern, at least theoretically, is the potential for the antidepressants to worsen an underlying BD�a process generally referred to as �kindling.� Readers are likely well aware that this is a model, a framework for thought, not a research-tested concept. Nonetheless, it is an important concept to consider. Yet kindling concern is rarely raised when discussing the use of antidepressants for BD, perhaps because the data by which to evaluate this risk are almost nonexistent.
For example, Grunze27 criticized the American reticence to use antidepressants in BD, but his review does not mention kindling as a potential risk. By comparison, El-Mallakh and Karippot28 concluded a review on antidepressant use in BD: �Long-term use may destabilize the illness, leading to an increase in the number of both manic and depressed episodes; induce rapid cycling (at least 4 episodes a year); and increase the likelihood of a mixed state.�
A case report of an apparent antidepressant- induced mood instability in a patient with unipolar disorder following 7 years of euthymic response to an antidepressant raises broader concerns,29 akin to the �acid syndrome� (antidepressant- associated chronic irritable dysphoria.)30 Using nationwide register studies, Kessing and Andersen31 have demonstrated that the average risk of recurrence increases with the number of episodes in depressive and bipolar affective disorders.
But can precipitating mania or hypomania with an antidepressant kindle an underlying bipolarity so as to make the patient's long-term course worse than it otherwise would have been? We must ask ourselves this question, even though at present we have no systematic studies of such long-term effects, and such research would be tremendously difficult to conduct. For now and likely for the foreseeable future (perhaps until we have a biomarker to follow over time), this leaves us reliant on case reports and clinical suspicions�a very weak basis for complex treatment decisions.
Therefore, a full appraisal of the risks of antidepressants is not possible at present. A biomarker of antidepressant exacerbation that could be used to project risk would be extremely helpful. Already there is a potential candidate, since inheriting 2 short versions of the serotonin transporter gene may substantially increase this risk (not all studies have supported the connection, but 2 are strongly positive32,33). In the meantime, differences in opinion regarding how much risk antidepressants pose in patients with BD might be a significant factor explaining why some BD specialists are inclined to avoid them as much as possible, whereas others feel they are being underused. Could some� much?�of the debate about the socalled bipolar spectrum boil down to our different perception of antidepressant risks?
Perhaps we could address that question through attitudinal research. Ironically, psychiatrists' understanding of bipolarity may not be the most important determinant of just which patients will receive antidepressants� because we are not the most frequent antidepressant prescribers.
PRIMARY CARE PROVIDERS
Rather than psychiatrists or even psychotherapists, primary care providers (PCPs) are clearly the front line of depression treatment in the United States. In a further irony, while psychiatrists are increasingly considering a spectrum approach to bipolar diagnosis, PCPs are being encouraged by colleagues,34 psychiatrists,35 and the pharmaceutical industry36 to use a categoric tool, the Mood Disorders Questionnaire (MDQ).
Although most physicians knew this once, many have forgotten that accurate use (the �predictive value�) of a test like the MDQ depends heavily on clinicians' pretest hunch (ie, the prior probability of BD).37 Yet developing a discriminating hunch comes from understanding bipolar presentations, from BD I mania through hypomania to the 11 soft signs that form the criteria for bipolar spectrum disorder and the Bipolarity Index, as previously discussed. Such training is rare for PCPs, although an online primer has been available and refined over the past 5 years.37 PCPs are besieged by various efforts to educate them on many topics, and thus the extent to which even continuing medical education can reach them is limited. When we have their ear, as when discussing a consultation, we can teach them to systematically assess 4 areas they already query, in addition to the fifth dimension of bipolarity they will see reflected in the MDQ (hypomania):
- Family history (several versions of the MDQ also assess this, albeit minimally).
- Age at onset of first depression.
- Course of illness (many recurrences vs few, length of episodes, rapid onset/offset) .
- Response to previous antidepressants: agitation, insomnia, irritability.
To summarize for them the spectrum perspective in concrete, applicable terms, we could suggest (after reviewing with them the full differential) that the more bipolar soft signs one detects, the earlier one should consider switching from an antidepressant- based strategy to a mood-stabilizer" based strategy. However, we must admit that there is no agreed-on or empirically established cutoff point to guide this decision, and indeed there may not be such a point of natural cleavage: bipolar disorder may not be a species, as in ornithology, despite the implications of the DSM.
CONCLUSION
Despite the advantages of a spectrum view, particularly in matching clinical experience, the DSM's, categoric approach, with its greater internal structure and validated diagnoses, is also a valuable part of our clinical thinking. We can adopt an approach long used in physics, where 2 apparently exclusive ways of viewing the electromagnetic spectrum are used simultaneously: light is a wave and a particle.
For psychiatrists, this means using the DSMand the spectrum views in complementary fashion, like bifocals in a pair of glasses�carrying both lenses with us, switching back and forth to find the one that best brings an individual patient into focus. Our patients have illnesses that are both waves�varying continuously over a spectrum�and particles�with discrete characteristics that can help us identify who is likely to do well with an antidepressant and who merits caution. As in physics, complementarity helps manage uncertainty. This dual-lens perspective might allow the focus of our debate to shift toward further identifying characteristics that predict adverse reactions to antidepressants (away from debates about the breadth of bipolarity). So far these factors include 11 soft signs.11
Many of our primary care colleagues, however, are struggling to identify any nonmanic version of BD, such as BD II. For them, the MDQ as a screening tool is probably better than no screening tool at all. However, there will be significant misclassification unless they are quickly educated on bipolar phenomenology, which must be used to anchor their interpretation of the MDQ results. Other PCPs are ready to move beyond a categoric view; they need a cautious de-emphasis of the MDQ, with increased emphasis on recognizing intermediate bipolar spectrum variations.
This discussion will be continued in a second article to be published in a future issue of Psychiatric Times.
| Table
Risks of mood stabilizers and antidepressants | |||||||
| Short-term potential risks | Long-term potential risks | ||||||
| Mood stabilizers | |||||||
| Lithium | Lithium toxicity, rare renal failure | Thyroid dysfunction, weight gain, renal impairment | |||||
| Divalproex sodium | Rare pancreatitis, hepatic failure (almost confirmed) | Weight gain, polycystic ovarian syndrome? | |||||
| Olanzapine, quetiapine, risperidone | Neuroleptic malignant syndrome, ketoacidosis | Weight gain, diabetes, tardive dyskinesia | |||||
| Lamotrigine | Stevens-Johnson syndrome | Small continued risk of Stevens-Johnson syndrome | |||||
| Antidepressants | Increased suicidal ideation and action? | Induces mania or hypomania Destabilizing effects, including induction of rapid cycling Induction of mixed states Kindling? | |||||
Dr Phelps has been practicing psychiatry for more than 15 years and specializes in treating bipolar disorder. He recently published Why Am I Still Depressed? Recognizing and Managing the Ups and Downs of Bipolar II and Soft Bipolar Disorder.
Dr Phelps states that he has received grants and honoraria from GlaxoSmithKline, Astra- Zeneca, and Abbott Laboratories.
Drugs Mentioned in This Article
Divalproex sodium (Depakote)
Fluoxetine (Prozac)
Lamotrigine (Lamictal)
Lithium (Eskalith, Lithobid)
Olanzapine (Zyprexa)
Quetiapine (Seroquel)
Risperidone (Risperdal)
References
1. Patten SB. Does almost everybody suffer from a bipolar disorder? Can J Psychiatry. 2006;51:6-8.
2. Baldessarini RJ. A plea for integrity of the bipolar disorder concept. Bipolar Disord. 2000;2:3-7.
3. Ghaemi SN, Sachs GS, Chiou AM, et al. Is bipolar disorder still underdiagnosed? Are antidepressants overutilized? J Affect Disord. 1999;52:135- 144.
4. Cassano GB, Rucci P, Frank E, et al. The mood spectrum in unipolar and bipolar disorder: arguments for a unitary approach. Am J Psychiatry. 2004;161: 1264-1269.
5. Benazzi F. Bipolar II disorder and major depressive disorder: continuity or discontinuity? World J Biol Psychiatry. 2003;4:166-171.
6. Mackinnon DF, Pies R. Affective instability as rapid cycling: theoretical and clinical implications for borderline personality and bipolar spectrum disorders. Bipolar Disord. 2006;8:1-14.
7. Jamison KJ. Touched With Fire. New York: Simon and Schuster; 1993.
8. Tsankova NM, Berton O, Renthal W, et al. Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action. Nat Neurosci. 2006;9:519-525.
9. Kessler R. Prevalence and effects of mood disorders on role performance in the United States. Presented at: International Society of Bipolar Disorder Annual Meeting; June 2005; Pittsburgh.
10. Klerman GL. The spectrum of mania. Compr Psychiatry. 1981;22:11-20.
11. Akiskal HS, Pinto O. The evolving bipolar spectrum. Prototypes I, II, III, and IV. Psychiatr Clin North Am. 1999;22:517- 534.
12. Ghaemi SN, Ko JY, Goodwin FK. "Cade's disease" and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder. Can J Psychiatry. 2002;47:125- 134.
13. Phelps JR, Angst J, Katzow J, Sadler JZ. Validity and utility of the bipolar spectrum model. Bipolar Disorders. In press.
14. Angst J, Gamma A, Benazzi F, et al. Toward a redefinition of subthreshold bipolarity: epidemiology and proposed criteria for bipolar-II, minor bipolar disorders and hypomania. J Affect Disord. 2003; 73:133-146.
15. Saenger E. The Bipolarity Index as a tool for assessment and creating rapport: an expert interview with Gary Sachs, MD. Medscape Psychiatry & Mental Health. 2005. Available at: http://www.medscape .com/viewarticle /503893. Accessed March 28, 2006.
16. Massachusetts General Hospital, Bipolar Clinic Web site. Affective Disorders Evaluation. Available at: http://www.manicdep ressive.org/ images/blankade. pdf, Accessed March 28, 2006.
17. Massachusetts General Hospital, Psychiatry Academy. Mood Disorders at the Interface of Clinical Practice and Emerging Genetics. Module 1; Jan 2005. Available at: http://www.mghcme. com/show. event.php? s=psychlink_ module1_011205_ details&id=5. Accessed March 28, 2006.
18. Phelps JR. Bipolar "Versus" Borderline. Available at: http://www.psychedu cation.org/ depression/ borderline. htm. Accessed April 28, 2006.
19. Akiskal HS, Mallya G. Criteria for the "soft" bipolar spectrum: treatment implications. Psychopharmacol Bull. 1987;23:68-73.
20. Amsterdam JD, Shults J. Fluoxetine monotherapy of bipolar type II and bipolar NOS major depression: a double-blind, placebo-substitutio n, continuation study. Int Clin Psychopharmacol. 2005; 20:257-264.
21. Ghaemi SN, Hsu DJ, Soldani F, Goodwin FK. Antidepressants in bipolar disorder: the case for caution. Bipolar Disord. 2003;5:421-433.
22. Barbee JG, Conrad EJ, Jamhour NJ. The effectiveness of olanzapine, risperidone, quetiapine, and ziprasidone as augmentation agents in treatmentresistant major depressive disorder. J Clin Psychiatry. 2004;65:975- 981.
23. GSK Trial Register, Lamotrigine Studies #SCA20022, SCA20025. Available at: http://ctr.gsk. co.uk/Summary/ lamotrigine/ studylist. asp. Accessed April 30, 2006.
24. Andersen SW, Clemow DB, Corya SA. Long-term weight gain in patients treated with open-label olanzapine in combination with fluoxetine for major depressive disorder. J Clin Psychiatry. 2005;66: 1468-1476.
25. Bauer MS, Mitchner L. What is a "mood stabilizer"? An evidence-based response. Am J Psychiatry. 2004;161:3-18.
26. Phelps J. Antidepressants in Bipolar Disorder: The Controversies. 2006. Available at: http://www.psychedu cation.org/ bipolar/controve rsy.htm. Accessed May 11, 2006.
27. Grunze H. Reevaluating therapies for bipolar depression. J Clin Psychiatry. 2005;66:17-25.
28. El-Mallakh RS, Karippot A. Use of antidepressants to treat depression in bipolar disorder. Psychiatr Serv. 2002;253:580- 584.
29. Phelps JR. Agitated dysphoria after late-onset loss of response to antidepressants: a case report. J Affect Disord. 2005;86:277- 280.
30. El-Mallakh RS, Karippot A. Antidepressant- associated chronic irritable dysphoria (acid) in bipolar disorder: a case series. J Affect Disord. 2005;84: 267-272.
31. Kessing LV, Andersen PK. Predictive effects of previous episodes on the risk of recurrence in depressive and bipolar disorders. Curr Psychiatry Rep. 2005;7:413-420.
32. Masoliver E, Menoyo A, Perez V, et al. Serotonin transporter linked promoter (polymorphism) in the serotonin transporter gene may be associated with antidepressant- induced mania in bipolar disorder. Psychiatr Genet. 2006;16:25-29.
33. Mundo E, Walker M, Cate T, et al. The role of serotonin transporter protein gene in antidepressantinduc ed mania in bipolar disorder: preliminary findings. Arch Gen Psychiatry. 2001;58:539- 544.
34. Kaye NS. Is your depressed patient bipolar? J Am Board Fam Pract. 2005;18:271- 281.
35. Citrome L, Goldberg JF. The many faces of bipolar disorder. How to tell them apart. Postgrad Med. 2005;117:15- 16, 19-23.
36. AstraZeneca Pharmaceuticals. Resources for an Accurate Diagnosis. Available at: www.IsItReallyDepre ssion.com. Accessed March 28, 2006.
37. Phelps JR, Ghaemi SN. Improving the diagnosis of bipolar disorder: Predictive value of screening tests. J Affect Disord. 2006;92:141- 148.
Evidence-based References
Cassano GB, Rucci P, Frank E, et al. The mood spectrum in unipolar and bipolar disorder: arguments for a unitary approach. Am J Psychiatry. 2004;161: 1264-1269.
Ghaemi SN, Ko JY, Goodwin FK. �Cade's disease� and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder. Can J Psychiatry. 2002;47:125- 134.
Blogged with Flock
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου