My Own Bipolar Kerfuffle

August 5, 2012

I have a confession to make.  I don’t know what “bipolar disorder” is.  And as a psychiatrist, I’ll admit that’s sort of embarrassing.

Okay, maybe I’m exaggerating when I say that I don’t know what bipolar disorder is.  Actually, if you asked me to define it, I’d give you an answer that would probably sound pretty accurate.  I’ve read the DSM-IV, had years of training, took my Boards, treated people in the midst of manic episodes, and so on.  The problem for me is not the “idea” of bipolar disorder.  It’s what we mean when we use that term.

I recognized this problem only recently—in fact, just last month, as I was putting together the July/August issue of the Carlat Psychiatry Report (now available to subscribers here).  This month’s issue is devoted to the topic of “Bipolar Disorder,” and two contributors, faculty members at prestigious psychiatry departments, made contradictory—yet perfectly valid—observations.  One argued that it’s overdiagnosed; the other advocated for broadening our definition of bipolar disorder—in particular, “bipolar depression.”  The discrepancy was also noted in several comments from our Editorial Board.

Disagreements in science and medicine aren’t necessarily a bad thing.  In fact, when two authorities interpret a phenomenon differently, it creates the opportunity for further experimentation and investigation.  In time, the “truth” can be uncovered.  But in this case, as with much in psychiatry, “truth” seems to depend on whom you ask.

Consider this question.  What exactly is “bipolar depression”?  It seems quite simple:  it’s when a person with bipolar disorder experiences a depressive episode.  But what about when a person comes in with depression but has not had a manic episode or been diagnosed with bipolar disorder?  How about when a person with depression becomes “manic” after taking an antidepressant?  Could those be bipolar depression, too?  I suppose so.  But who says so?  One set of criteria was introduced by Jules Angst, a researcher in Switzerland, and was featured prominently in the BRIDGE study, published in 2011.  His criteria for bipolarity include agitation, irritability, hypomanic symptoms for as short as one day, and a family history of mania.  Other experts argue for a “spectrum” of bipolar illness.

(For a critique of the BRIDGE study, see this letter to the editor of the Archives of General Psychiatry, and this detailed—and entertaining—account in David Allen’s blog.)

The end result is rather shocking, when you think about it:  here we have this phenomenon called “bipolar disorder,” which may affect 4% of all Americans, and different experts define it differently.  With the right tweaking, nearly anyone who comes to the attention of a psychiatrist could be considered to have some features suggestive of someone’s definition of bipolar disorder.  (Think I’m kidding?  Check out the questionnaire in the appendix of Angst’s 2003 article.)

Such differences of opinion lead to some absurd situations, particularly when someone is asked to speak authoritatively about this disorder.  At this year’s APA Annual Meeting for example, David Kupfer (DSM-IV Task Force Chair) gave a keynote address on “Rethinking Bipolar Disorder,” which included recommendations for screening adolescents and the use of preventive measures (including drugs) to prevent early stages of the illness.  Why was it absurd?  Because as Kupfer spoke confidently about this disease entity, I looked around the packed auditorium and realized that each person may very well have has his or her own definition of bipolar disorder.  But did anyone say anything?  No, we all nodded in agreement, deferring to the expert.

This problem exists throughout psychiatry.  The criteria for each diagnosis in the DSM-IV can easily be applied in a very general way.  This is due partly to fatigue, partly to the fact that insurance companies require that we give a diagnosis as early as the first visit, partly because we’re so reluctant (even when it’s appropriate) to tell patients that they’re actually healthy and may not even have a diagnosis, and partly because different factions of psychiatrists use their experience to create their own criteria.  It’s no wonder that as criteria are loosened, diagnoses are misapplied, and the ranks of the “mentally ill” continue to grow.

As editor of a newsletter, I’m faced with another challenge I didn’t quite expect.  I can’t come out and say that bipolar disorder doesn’t exist (which wouldn’t be true anyway—I have actually seen cases of “classic,” textbook-style mania which do respond to medications as our guidelines would predict).  But I also can’t say that several definitions of “bipolar” exist.  That may be perceived as being too equivocal for a respectable publication and, as a result, some readers may have difficulty taking me seriously.

At the risk of sounding grandiose, I may be experiencing what our field’s leadership must experience on a regular basis.  Academic psychiatrists make their living by conducting research, publishing their findings, and, in most cases, specializing in a given clinical area.  It’s in their best interest to assume that the subjects of their research actually exist.  Furthermore, when experts see patients, they do so in a specialty clinic or clinical trial, which reinforces their definitions of disease.

This can become a problem to those of us seeing the complicated “real world” patients on the front lines, especially when we look to the experts for answers to such questions as whether we should use antipsychotics to treat acute mania, or whether antidepressants are helpful for bipolar depression.  If their interpretations of the diagnoses simply don’t pertain to the people in our offices, all bets are off.  Yet this, I fear, is what happens in psychiatry every day.

In the end, I can’t say whether my definition of bipolar disorder is right or not, because even the experts can’t seem to agree on what it is.  As for the newsletter, we decided to publish both articles, in the interest of maintaining a dialogue.  Readers will simply have to use their own definition of “bipolar disorder” and “bipolar depression” (or eschew them altogether)—hopefully in ways that help their patients.  But it has been an eye-opening experience in the futility (and humility) of trying to speak with authority about something we’re still trying desperately to understand.

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Is The Joke On Me?

May 12, 2012

I recently returned from the American Psychiatric Association (APA) Annual Meeting in Philadelphia.  I had the pleasure of participating on a panel discussing “psychiatrists and the new media” with the bloggers/authors from Shrink Rap, and Bob Hsiung of dr-bob.org.  The panel discussion was a success.  Some other parts of the conference, however, left me with a sense of doubt and unease.  I enjoy being a psychiatrist, but whenever I attend these psychiatric meetings, I sometimes find myself questioning the nature of what I do.  At times I wonder whether everyone else knows something I don’t.  Sometimes I even ask myself:  is the joke on me?

Here’s an example of what I mean.  On Sunday, David Kupfer of the University of Pittsburgh (and task force chair of the forthcoming DSM-5) gave a talk on “Rethinking Bipolar Disorder.”  The room—a cavernous hall at the Pennsylvania Convention Center—was packed.  Every chair was filled, while scores of attendees stood in the back or sat on the floor, listening with rapt attention.  The talk itself was a discussion of “where we need to go” in the management of bipolar disorder in the future.  Dr Kupfer described a new view of bipolar disorder as a chronic, multifactorial disorder involving not just mood lability and extremes of behavior, but also endocrine, inflammatory, neurophysiologic, and metabolic processes that deserve our attention as well.  He emphasized the fact that in between mood episodes, and even before they develop, there are a range of “dysfunctional symptom domains”—involving emotions, cognition, sleep, physical symptoms, and others—that we psychiatrists should be aware of.  He also introduced a potential way to “stage” development of bipolar disorder (similar to the way doctors stage tumors), suggesting that people at early stages might benefit from prophylactic psychiatric intervention.

Basically, the take-home message (for me, at least) was that in the future, psychiatrists will be responsible for treating other manifestations of bipolar disorder than those we currently attend to.  We will also need to look for subthreshold symptoms in people who might have a “prodrome” of bipolar disorder.

A sympathetic observer might say that Kupfer is simply asking us to practice good medicine, caring for the entire person rather than one’s symptoms, and prevent development or recurrence of bipolar illness.  On the other hand, a cynic might look at these pronouncements as a sort of disease-mongering, encouraging us to uncover signs of “disease” where they might not exist.  But both of these conclusions overlook a much more fundamental question that, to me, remains unanswered.  What exactly is bipolar disorder anyway?

I realize that’s an extraordinarily embarrassing question for a psychiatrist to ask.  And in all fairness, I do know what bipolar disorder is (or, at least, what the textbooks and the DSM-IV say it is).  I have seen examples of manic episodes in my own practice, and in my personal life, and have seen how they respond to medications, psychotherapy, or the passage of time.  But those are the minority.  Over the years (although my career is still relatively young), I have also seen dozens, if not hundreds, of people given the diagnosis of “bipolar disorder” without a clear history of a manic episode—the defining feature of bipolar disorder, according to the DSM.

As I looked around the room at everyone concentrating on Dr Kupfer’s every word, I wondered to myself, am I the only one with this dilemma?  Are my patients “special” or “unique”?  Maybe I’m a bad psychiatrist; maybe I don’t ask the right questions.  Or maybe everyone else is playing a joke on me.   That’s unlikely; others do see the same sorts of patients I do (I know this for a fact, from my own discussions with other psychiatrists).  But nobody seems to have the same crisis of confidence that I do.  It makes me wonder whether we have reached a point in psychiatry when psychiatrists can listen to a talk like this one (or see patients each day) and accept diagnostic categories, without paying any attention to the fact that they our nosology says virtually nothing at all about the unique nature of each person’s suffering.  It seems that we accept the words of our authority figures without asking the fundamental question of whether they have any basis in reality.  Or maybe I’m just missing out on the joke.

As far as I’m concerned, no two “bipolar” patients are alike, and no two “bipolar” patients have the same treatment goals.  The same can be said for almost everything else we treat, from “depression” to “borderline personality disorder” to addiction.  In my opinion, lumping all those people together and assuming they’re all alike for the purposes of a talk (or, even worse, for a clinical trial) makes it difficult—and quite foolish—to draw any conclusions about that group of individuals.

What we need to do is to figure out whether what we call “bipolar disorder” is a true disorder in the first place, rather than accept it uncritically and start looking for yet additional symptom domains or biomarkers as new targets of treatment.  To accept the assumption that everyone currently with the “bipolar” label indeed has the same disorder (or any disorder at all) makes a mockery of the diagnostic process and destroys the meaning of the word.  Some would argue this has already happened.

But then again, maybe I’m the only one who sees it this way.  No one at Kupfer’s talk seemed to demonstrate any bewilderment or concern that we might be heading towards a new era of disease management without really knowing what “disease” we’re treating in the first place.  If this is the case, I sure would appreciate it if someone would let me in on the joke.


Abilify for Bipolar Maintenance: More Hard Questions

May 31, 2011

Much attention has been drawn to a recent PLoS Medicine article criticizing the evidence base for the use of Abilify as maintenance treatment for bipolar disorder.  The major points emphasized by most critics are, first, that the FDA approved Abilify for this purpose in 2005 on the basis of flawed and scanty evidence and, secondly, that the literature since that time has failed to point out the deficiencies in the original study.

While the above may be true, I believe these criticisms miss a more important point.  Instead of lambasting the FDA or lamenting the poor quality of clinical research, we psychiatrists need to use this as an opportunity to take a closer look at what we treat, why we treat, and how we treat.

Before elaborating, let me summarize the main points of the PLoS article.  The authors point out that FDA approval of Abilify was based on only one “maintenance” trial by Keck et al published in 2007.  The trial included only 161 patients (only 7 of whom, or 1.3% of the total 567 who started the study, were followed throughout 26 weeks of stabilization and 74 follow-up weeks of maintenance).  It also consisted of patients who had already been stabilized on Abilify; thus, it was “enriched” for patients who had already shown a good response to this drug.  Furthermore, the “placebo failures” consisted of patients who were abruptly withdrawn from Abilify and placed on placebo; their relapses might thus be attributed to the researchers’ “randomized discontinuation” design rather than the failure of placebo.  (For more commentary, including follow-up from Bristol-Myers Squibb, Abilify’s manufacturer, please see this excellent post on Pharmalot.)

These are all valid arguments.  But as I read the PLoS paper and the ongoing discussion ever since, I can’t help but think, so what??  First of all, most psychiatrists probably don’t know about the PLoS paper.  And even if they did, the major questions for me would be:  would the criticism of the Keck et al. study change the way psychiatrists practice?  Should it?

Let’s think about psychiatric illness for a moment.  Most disorders are characterized by an initial, abrupt onset or “episode.”  These acute episodes are usually treated with medications (plus or minus psychotherapy or other psychosocial interventions), often resulting in rapid symptomatic improvement—or, at the very least, stabilization of those symptoms.

One big, unanswered (and, unfortunately, under-asked) question in psychiatry is, then what?  Once a person is stabilized (which in some cases means nothing more than “he’s no longer a danger to himself or others”), what do we do?  We don’t know how long to treat patients, and there are no guidelines for when to discontinue medications.  Instead we hear the common refrain:  depression, schizophrenia, and bipolar disorder, are lifelong illnesses—”just like hypertension or diabetes”—and should be treated as such.

But is that true?  At the risk of sounding like a heretic (and, indeed, I’d be laughed out of residency if I had ever asked this question), are there some cases of bipolar disorder—or schizophrenia, or depression, for that matter—which only require brief periods of psychopharmacological treatment, or none at all?

The conventional wisdom is that, once a person is stabilized, we should just continue treatment.  And why not?  What doctor is going to take his patient off Abilify—or any other mood stabilizer or antipsychotic which has been effective in the acute phase—and risk a repeat mood episode?  None.  And if he does, would he attribute the relapse to the disease, or to withdrawal of the drug?  Probably to the disease.

For another example of what I’m talking about, consider Depakote.  Depakote has been used for decades and is regarded as a “prototypical” mood stabilizer.  Indeed, some of my patients have taken Depakote for years and have remained stable, highly functional, and without evidence of mood episodes.  But Depakote was never approved for the maintenance treatment of bipolar disorder (for a brilliant review of this, which raises some of the same issues as the current Abilify brouhaha, read this article by The Last Psychiatrist).  In fact, the one placebo-controlled study of Depakote for maintenance treatment of bipolar disorder showed that it’s no better than placebo.  So why do doctors use it? Because it works (in the acute phase.)  Why do patients take it?  Again, because it works—oh, and their doctors tell them to continue taking it.  As the old saying goes, “if it ain’t broke, don’t fix it.”

However, what if it is broke[n]?  Some patients indeed fail Depakote monotherapy and require additional “adjunctive” medication (which, BTW, has provided another lucrative market for the atypical antipsychotics).  In such cases, most psychiatrists conclude that the patient’s disease is worsening and they add the second agent.  Might it be, however, that after the patient’s initial “response” to Depakote, the medication wasn’t doing anything at all?

To be sure, the Abilify study may have been more convincing if it was larger, followed patients for a longer time, and had a dedicated placebo arm consisting of patients who had not been on Abilify in the initial stage.  But I maintain that, regardless of the outcome of such an “improved” trial, most doctors would still use Abilify for maintenance treatment anyway, and convince themselves that it works—even if the medication is doing absolutely nothing to the underlying biology of the disease.

The bottom line is that it’s easy to criticize the FDA for approving a drug on the basis of a single, flawed study.  It’s also easy to criticize a pharmaceutical company for cutting corners and providing “flawed” data for FDA review.  But when it comes down to it, the real criticism should be directed at a field of medicine which endorses the “biological” treatment of a disorder (or group of disorders) whose biochemical basis and natural history are not fully understood, which creates post hoc explanations of its successes and failures based on that lack of understanding, and which is unwilling to look itself in the mirror and ask if it can do better.


How Lithium Works (Maybe)

February 17, 2011

“Half of what we have taught you is wrong.  Unfortunately, we don’t know which half.”

— attributed to a Harvard Medical School dean at commencement, sometime in the 20th century

The above, possibly apocryphal, statement is often invoked to illustrate how dynamic the field of medicine can be, and how what we thought we once knew beyond a shadow of a doubt, sometimes turns out to be dead wrong.  It’s also a celebration of scientific progress; as we revise our pathophysiological models, we can develop more targeted therapeutics.

In this regard, psychiatry is no different from any other field of medicine.  We don’t know (yet) what we don’t know, but once we do, our treatments will improve.  At the same time, we need to be careful how we use this new information, lest it give us a false sense that we “know” something we don’t.

I thought of this question when I encountered a headline earlier today at psychcentral.com“How Lithium Works Finally Explained.” Talk about a tantalizing headline!  First used clinically in the late 1800s (and later “rediscovered” in the 1940s), and still used extensively as a mood stabilizer in bipolar disorder and as adjunctive treatment for major depression, lithium is one of the most widely prescribed medications in all of medicine.  Many patients report a very good response to lithium, and its efficacy has not been surpassed by the multitude of other mood stabilizing agents introduced in the last 40 years.

But there’s just one problem.  Nobody really knows how lithium works.  It’s an ion (similar to sodium), so it doesn’t bind to a receptor or transporter, like most other psychiatric drugs.  It doesn’t seem to affect membrane potential (and therefore neuron excitability), and it doesn’t seem to target any particular region of the brain, much less those thought to be involved in mood disorders.  It may inhibit intracellular messengers (the phosphatidylinositol pathway) or it might inhibit cellular differentiation (via the Wnt signaling pathway).  Maybe it blocks sodium ion transport.  Maybe it interacts with nitric oxide.  No one knows.  And yet it works.

So it was with great interest that I read the original paper cited in the Psychcentral article.  It’s a “mega-analysis,” published in the February 15 issue of Biological Psychiatry, of 321 bipolar patients in 11 centers worldwide who underwent MRI scans and were compared to non-bipolar controls.  Half of the bipolar patients were taking lithium.  To summarize the results, patients taking lithium had larger hippocampal and amygdala volumes than those not taking lithium, and patients with a longer history of bipolar disorder had reduced cerebral volumes.

The data, then, seem to be consistent with the idea of lithium as having a “trophic” effect—i.e., as a promoter of neuronal growth, at least in some brain structures.  But that’s about all we can say.  Whether this has anything to do with intracellular signaling or the Wnt pathway, or with any known nerve growth factors, is beyond the scope of this study.

So despite the exciting headline claiming to identify the “mechanism of lithium,” this is simply an observation, much like the observation about how antipsychotics may decrease brain volumes, about which I wrote last week.  It suggests further research to understand lithium’s effect on these regions.  But it may not be clinically relevant.

Lithium is a widely used drug because it works.  Period.  These new data add to our knowledge about bipolar disorder, but to assume that they help us understand bipolar patients any better than we did before, is incorrect.  Moreover, it may lead us to draw false conclusions about our patients (i.e., “he’s not responding to lithium so his hippocampus must be atrophied”) or, worse, reject or disregard data that don’t fit with our hypothesis.  I’d much rather prescribe a drug because I have years of experience using it, and have heard hundreds of patients endorse its benefit, rather than adhere to an incorrect theory, even a theory with “face validity” like lithium promoting nerve cell growth and differentiation.  In fact it’s not too hard to find arguments against this theory:  for starters, consider lithium’s teratogenic effects during human embryonic development.

Anyone who wants an accurate explanation for how a psychiatric drug works is, unfortunately, out of luck.  The serotonin hypothesis is a perfect example:  SSRIs work in a lot of patients, and the serotonin hypothesis helps to guide treatment, but it might be absolutely incorrect.  How many alternate explanations have we ignored because we want to believe that our model must be right?

We can, and should, continue to use SSRIs to treat depression, and lithium to treat bipolar disorder.  But we should be aware that our explanations of their mechanisms are mere hypotheses—nothing more.  And, moreover, that these hypotheses may be contradicted or proven wrong.  Because we don’t know which half of our knowledge is the correct half.


Lessons of Rebecca Riley

February 2, 2011

I’ve been following the Rebecca Riley case in Massachusetts, although not as closely as I would like to, since I find the details so incredibly disturbing.  For those of you who aren’t familiar with it, four year-old Rebecca died in 2006 after an overdose of the psychotropic medications clonidine, Depakote, and Seroquel.  Her parents were convicted of murder in 2010 even though they argued that they were simply “following the instructions” of Rebecca’s child psychiatrist, Dr Kiyoko Kifuji of Tufts Medical Center.  Dr Kifuji had diagnosed Rebecca with bipolar disorder and prescribed three powerful medications to her, starting at the age of 2.

It has also come to light that Rebecca’s parents had exploited the social service system to obtain federal disability benefits for their three children– Rebecca and two older siblings, who were also diagnosed with bipolar disorder and ADHD by Dr Kifuji.  Also, Dr Kifuji’s medical license was suspended for two years after Rebecca’s death, although she eventually returned to practice medicine at Tufts, where she still sees patients.  Finally, Tufts settled a malpractice suit with the family last week for $2.5 million.

Many news stories disturb me, but this one makes me particularly angry, because all parties share part of the blame.  Obviously, I did not evaluate Rebecca myself (and, in the interest of full disclosure, I am not a child psychiatrist, nor have I even raised a two-year-old of my own), but the facts of the case, as I understand them, fill me with contempt for just about everyone involved.  Everyone that is, except for Rebecca.

The objects of my rage?  Let’s go down my list, one at a time:

  • Dr Kiyoko Kifuji – Even if we grant the possibility that bipolar disorder can be diagnosed in a two year-old (a questionable premise, even according to the experts), the evidence suggests that Dr Kifuji permitted Rebecca’s parents to give the medications as they saw fit (and agreed with their decisions to increase doses), authorized prescriptions over the phone without evaluating Rebecca, and was cautioned by pharmacies that Rebecca’s parents were going through meds more quickly than expected.  Social workers and a school nurse also alerted Dr Kifuji to the fact that Rebecca seemed oversedated and “like a floppy doll,” but Dr Kifuji allegedly made no adjustments to Rebecca’s treatment plan.
  • Michael and Carolyn Riley (Rebecca’s parents) – Seven abuse and neglect complaints were filed with the Massachusetts Dept of Children and Families, starting in 2002, alleging that the Rileys seemed unable to care for their children; apparently they, too, were also taking doses of medications that, at times, impaired their judgment.  Furthermore, it has come to light that everyone in the Riley family (except Rebecca) had applied for, and received, federal disability payments, in what appears to be a deliberate attempt to defraud the system to earn extra income.  They had filed an application for Rebecca, which was denied, but the Rileys appealed the decision.  However, after Rebecca’s death, in a jailhouse interview in September 2007, Carolyn Riley confessed to Katie Couric that she was not sure whether Rebecca had bipolar disorder after all: “maybe she was just hyper for her age.”
  • Massachusetts Department of Children and Families– While not directly responsible for Rebecca’s death, the warning signs were clearly visible that the Rileys were unfit to care for their children, including the abuse and neglect complaints noted above, as well as specific complaints from Rebecca’s therapist that, on a home visit, Carolyn Riley seemed “drugged and unable to care for [her] children.”  Agencies like this are incredibly overburdened and underfunded, but when they drop the ball, as they did in this case, lives may be at stake.
  • The psychiatric profession – As I’ve written on this blog, we as a discipline have not only expanded diagnostic criteria for mental illness (and are continuing to do so), but sometimes err on the side of over-diagnosis and over-treatment, rather than exploring alternate explanations for behavior or less potent treatment options.  One may argue that Dr Kifuji was practicing within the accepted standard of care.  Because I am not a child psychiatrist, I cannot comment on that, but there has been a 40-fold increase in diagnosis of childhood bipolar disorer from 1994 to 2003, which only a few in our profession have questioned or challenged.
  • The pharmaceutical industry – Drug companies are easy targets for frustration and rage, but in this case it could be argued that it was the inappropriate use of three commonly used (and frequently effective) medications which led to Rebecca’s death.  Two of the three medications she was taking (clonidine and valproic acid) are off-patent, so no one can accuse a drug company of “pushing” a medication on Rebecca for the sake of profit.  Nevertheless, efforts by Big Pharma to promote and expand the use of their medications can unfortunately bias some providers to overuse their agents, and the promotion of drugs while downplaying the risk of adverse effects is inexcusable.  (Even so, in my opinion, we doctors need to be held responsible for what we prescribe and why.)
  • Massachusetts Board of Registration of Medicine – Dr Kifuji entered a “voluntary agreement” to stop practicing psychiatry from February 2007 to September 2009.  The Board conducted an investigation into the case but “closed the complaint against Dr Kifuji without discipline.”  She has since returned to practice.  In my experience, I have seen state medical boards revoke licenses from doctors whose misbehaviors were not nearly as (allegedly) egregious as Dr Kifuji’s, or which involved only their personal lives and not patient care.  When I see the reports of this case and recognize that Dr Kifuji still practices psychiatry (in the same location and with the same patient population) I am concerned about the double standard being practiced by licensing bodies.
  • Tufts Medical Center – Obviously, Kifuji’s care was provided by an institution that also shares some responsibility for the ethical and beneficent provision of medical care. At the same time, it is shocking that Kifuji has retained her faculty position at Tufts.  Again, in my experience, hospitals and other institutions tend to be overly conservative when there is even the question of inappropriate behavior by one of their providers, if only to maintain good public relations.  Perhaps her employment will be terminated or limited now that a malpractice settlement has been reached, but it does strike me as one of those cases in which I see nothing that Tufts could gain by Dr Kifuji’s continued employment.
  • Malpractice Attorneys – Another easy (but valid) target.  Even assuming that malpractice was committed and the charges were valid, the fear of cases of this magnitude may make doctors less likely to treat the cases which actually do require aggressive care (and also contributes to defensive medicine, resulting in greater health care costs).  One might ask, however, whether the case, brought on behalf of Rebecca’s estate, had any merit, since her parents had already been convicted of her murder.  But as with most things in life, where there’s an opportunity for a payout, there are those who will spring into action:  A settlement of $2.5 million at 35% contingency fee, plus other expenses = $875K +.  And maybe the lawyer will be the guardian of funds, or set up a trust for Rebecca’s siblings, for an additional fee.  As a doctor wrote on a different website, “Three years of law school suddenly sounds like a better investment than medical school, internship, residency, and fellowship training.”

So many opportunities for Rebecca’s life to have turned out differently.  And so much blame to go around.  Unfortunately, the only one without any culpability at all is Rebecca herself.


Bipolar in the eye of the beholder

January 4, 2011

 

So whom is the joke on here?

I found this video on one of the several blogs I subscribe to.
(Okay, I’ll admit it, I’m a sucker for these Xtranormal videos.)

It seems to be composed from the point of view of the jaded psychiatric consumer patient, disturbed at the fact that her fairly unremarkable complaints are interpreted by her psychiatrist as symptoms of bipolar disorder, and how every problem’s solution seems to be a medication adjustment.

Indeed, most mental health conditions include, among their symptoms, common concerns like insomnia, poor attention/concentration, feelings of sadness, or (my personal favorite) “stress.”  But the truth is that bipolar disorder (the topic of this video) is a serious illness which can, at times, be incapacitating and threaten one’s livelihood or even one’s life.  Sleeplessness and “talking fast,” in and of themselves, do not make a bipolar diagnosis.

Watching the video as a psychiatrist, however, I’m reminded of the other side of the issue; namely, that patients will frequently come in with fairly ordinary complaints and profess that they must be “bipolar” or “depressed” or “anxious” and require medication.  Sometimes this self-assessment is accurate, but other times it’s more appropriate to exercise restraint.

The truth remains that, while in some physician-patient encounters the doctor tries to diagnose and treat on the basis of few symptoms, at other times the patient actually wants the diagnosis and/or the drug.  Which gives rise to the age-old
“slippery slope” in psychiatry, in which we deal with behaviors existing on a spectrum from normal to pathological.  Where does “wellness” end and “illness” begin?  And who makes this decision?


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