Turns out that  Plan B emergency contraception does not reduce pregnancy rates.  Big surprise.  But the one difference was that those with easy access took it more often.  (News article here.)  So I stand behind my earlier question: why do oral contraceptives require a prescription, but this doesn't?

Coupled with the fact that 50% of abortions are done by women who have already had one abortion at least, and 18% are on their third or greater,  and you have a social policy problem on your hands.  While everyone is busy with political nonsense, we are missing an important segment of the population that is simply not taking responsibility for their behavior.  Having three or more abortions in the United States has exactly nothing to do with abortion rights or women's health issues or access to contraception.

Oh, but it will be okay, won't it?  OB/GYN will lead the charge?   Sure.  Context is everything: in the same issue of Obstetrics and Gynecology from which the above study came is an editorial by Douglas Laube, MD, President of ACOG.  He suggests that OB/GYN has lost its way: med schools are not attentive to "differences in gender biology" (seriously.)  And he suggests doing something about it:

I will create a task force to assess whether our specialty should adapt behavioral assessment techniques to evaluate candidates’ suitability as women’s health care providers.

I wonder if "suitability" will include social/political beliefs?

Well, he does quote Isaiah Berlin, who

"set in motion a vast and unparalleled revolution in humanity’s view of itself." 

Unparalleled?

"His lectures helped to destroy the traditional notions of objective truth and validity of ethics..."  

So, even if true (it's not,) is that supposed to be a good thing? 

He's also upset that America doesn't pay its elementary school teachers enough.

Oh, and he closes his editorial with a quote "by the prophet Muhammed." Outstanding.

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Addendum:  Let me explain what I mean by that last sentence, again, it's context:  he's not a  Muslim.  He is (was) a Lt. Commander in the Naval Reserve.  Are you telling me that in all of literature, the only quotation he could find to express his point is that one?  Does he have a copy of the Hadith handy?   What would you say if Mubarak (Pres. of Egypt) closed a speech with a quote from Augustine's Confessions?  This is obviously a ploy, a pretense, he wants to show he transcends the childishness of politics and religion, he's about humanity.

That's where it all falls apart, that's where it stops being science and starts being dangerous.

I looked through six other articles/addresses by him; he seems to be a rigorous and thoughtful clinician and educator-- but-- and this is the but that is killing medicine and society-- he, like so many other doctors, wants to be a social policy analyst.  No, no, for the love of God, no.

In researching something else, I learned that Imitrex may actually treat the headache associated with subarachnoid hemorrhage-- which is a bad thing, because you're still going to die.

Subarachnoid hemorrhage, the "worst headache of your life"-- comes on suddenly, lasts for hours (even days, yes, days), worse in light or with sounds, but not affected by movement-- is the result of an aneurysm (usually middle cerebral artery) popping.  CT is positive in 95% of cases if taken early-- the longer time passes, the less sensitive CT becomes. 

A case report of a woman whose headache improved with Imitrex (6mg SQ) but still ultimately died.  The authors said this was the only case report they found, but in the same issue is another such case report (improved after 6mg SQ and died later that day) , and  a year later some British guys reported three other  migraine patients who came in with undiagnosed SAH and their headache got better after getting Imitrex.  (Two got 6mg, the other got 3x100mg).  They were correctly diagnosed only after they came back with headache and meningeal signs, and got CTs.

The editor of the first journal notes that sumatriptan is not "migraine-specific" and is effective in treating other head pains (such as viral meningitis, and, I discovered, orgasm headaches *.)  The authors of the earlier SAH report hypothesize that since triptans block transmission at the   trigeminal nucleus caudalis, any pain from the meninges should be blocked.  (In bacterial meningitis, the pain relief may also be augmented by the 5HT1D and B agonism, which (in mice) reduces inflammation, decreases intracranial pressure, and reduces white blood cells in the CSF(!)) This may be only true in acute meningitis, as failure in two meningitis patients may have been the result of sensitization of the caudalis neurons (where triptans are supopsed to block input) and spontanueous activity. (So get your triptans early.)

The obvious message here, given the efficacy iin SAH with such low doses of Imitrex, is that one should not assume efficacy is diagnostic of a migraine. Triptans seem to be efficacious across a variety of trigeminal neuropathies; which, like everything else in medicine, is good and bad.

----

* Orgasm headache: apparently triptans can treat or prevent "orgasmic headaches."  The funniest line is in the abstract of that paper:   "In patients who chose to predict their sexual activity, short-term prophylaxis with oral triptans 30 min before sexual activity might be a therapeutic option.."

In the same JCP issue in which atrocities were committed, McGirr and friends looked at 351 Canadian  consecutive suicides, and then performed a psychological autopsy to find out what had been wrong with them.

Almost all of the women killed themselves with two methods: overdose (46%); surprisingly,  hanging (38%).  For men, it was hanging (53%) or firearm a distant second (16%).  I don't know what's going on in Montreal, but it's different than LA.  (Less guns?  More trees?)

In comparison to men, women were more likely to be college grads and have jobs, to have a lifetime history of depression or anxiety, but less likely to have ever abused alcohol (26% females vs 44% males).

In the six months prior to the suicide,

Depression:   males 52%; females 56%

Anxiety: males 10%; females 15%

Alcohol: males 31%; females 18%. 

So there it is, more than half of suicides were depressed at the time of the hanging/shooting/OD.

Which is fine, but there is one statistic the authors neglected to report:

Number of patients who had been in psychiatric treatment at the time of death: 10. 

The number 10 doesn't appear in the study, and repeated attempts to get the actual number from the authors were failures: "we don't have systematic data."  Ok: the same group put out another study: out of 422 suicides, 28% had been to psychiatry in the past year.  Let me translate: 70% had not. 

If a tree falls in the forest, and no one hears it fall, shouldn't we get some guys out to the forest? 

---

Addendum: in the Oct 2006 Am J Pub Health, the authors find that suicide rates have been decreasing-- dramatically-- especially for the elderly since 1985 (from 21/100k to 16/100k) and youth since 1995 (14/100k to 10/100k).  But it's worth repeating that the number of actual suicides is still very small.

Long but necessary.

I have written endlessly about how language controls psychiatric thought, and that it will be impossible for psychiatry to progress while semiotics trumps science.  Here is a recent example:

In the Oct 2006 JCP, there is an article about the efficacy of Depakote ER for acute mania. 

As I read the introduction to this useless paper, I get kicked in the throat by this:

"Currently approved treatments of the acute manic phase of bipolar disorder can be categorized primarily as mood stabilizers (e.g. divalproex sodium, lithium, and carbamazepine) or as atypical antipsychotics (i.e. aripiprazole, olanzapine, quetiapine, risperidone, and ziprasidone.(5)"

Note carefully that the authors have taken a set of medications and artificially divided them into "mood stabilizers" OR "antipsychotics." Ok, well, wouldn't it be great if reference 5 actually justified this?  Using data or logic?  Well, it doesn't. 

But the damage has been done.  Unless you have a computer with FIOS and three monitors and are reading every reference, a quick skim registers that there is a reference, which you assume has been checked, and move on.  In fact, the authors here don't even feel that a reference is necessary-- everyone knows what a mood stabilizer is.  It's too basic to even reference.

So, is there any reason that seizure drugs are "mood stabilizers" (read: prophylactic) while antipsychotics are not?  For antipsychotics, is there anything about their pharmacology, half-life, color, or pill size that a priori exclude them from the "mood stabilizer" category while including the seizure meds?

The artificiality of the terminology is confirmed when you actually look at the data: the only drugs listed here which actually are "mood stabilizers" are lithium, olanzapine and aripirazole (over 6 months).

A study may eventually show Depakote is a mood stabilizer after all, but that's not my point. My issue is that in the absence of data or logical necessity, how can we take an arbitrary set of names and make unjustified deductions?

This is the semiotic trap of psychiatry.  It doesn't actually matter what the data says (e.g. Depakote is not a mood stabilizer, Zypexa is), what matters is the language, the categories.  This isn't science.  Just because there are graphs and chi-squareds, doesn't make it science.   There's no science here at all.  At best it is linguisitics.  At worst, propaganda.

I'm not saying they are lying.  It's worse than that.  It's the structure of psychiatry.  It's a subtle manipulation of reality to make people believe what you "already know" to be true.  They are trying to convey a perspective, not report a finding. For example, later on the authors try to make the point that higher levels correlate with efficacy, but go too high and you get toxicity:

One analysis noted that serum valproate concentrations between 45-125 ug/ml were associated with efficacy, while serum valproate concentrations > 125 ug/ml were associated with an increased frequency of adverse effects. 19

This isn't what reference 19 says, exactly.  What it says is that 45 is a pivot point; below it is not as good as above it.  But it doesn't say that higher and higher levels give you better and better  efficacy.  What makes the omission of this rather important clarification all the more perplexing is that reference 19 was written by the same authors as this article.

But the damage has been done, again.  Now you think you have read a statement in support of what you already assumed to be true.  So you push the level.

You may argue that I am misinterpreting the author's words, that he never implied that efficacy had a linear relationship with level.  Ok: prior to reading this blog, did you think that there was?  Where did you learn that?  Did you pull it out of the ether?  No-- you skimmed articles like these that left you with half-truths, and never questioned it because everyone knows this already.

Let me show you what I mean.  Here's the relationship of the Depakote level to maintenance treatment:

Higher serum levels were modestly but significantly correlated with less effective control of manic symptoms in a maintenance study (26). The study therefore supports a somewhat lower serum level range for maintenance treatment than for treatment of mania.

Did you know that?  That the efficacy decreases as the level increases?  I'm not asking if you believe it, I'm asking if you had ever heard it.  Because if the answer is no, then there is something very, very wrong with the way we convey our knowledge. *

-------------------

*Contrary to the opinions of former girlfriends, I am not an idiot.  I can plausibly explain this odd finding: the most manic patients got higher and higher doses, so the least responsive ended up getting the highest doses and levels.  So it looks like higher levels were associated with decreased efficacy, when really the highest doses went to the sickest people.  Ok, good explanation.  But this supports my earlier point: you can't take something which requires a post hoc justification and use it to make a leap in logic to conclude something else.

The real problem of a critique of our own cultural models is to ask, when we see a unicorn, if by any chance it is not a rhinoceros.

 

Previously, I had written an (what I thought to be outstanding) article about suicide documentation.  The main point was a refocusing of the note away from Objective and towards Assessment.  It now occurs to me that what I was really trying to get at is the lost art of writing a psychiatric formualtion of a patient.

The reason we don't do formulations anymore-- they're not even taught in most residencies, certainly not in mine or now to the residents I supervise-- is because it's not clear what the formulation is supposed to do.  Doctors get overwhelmed by the psychodynamics of it and can't seethe practical utility.  Someone brought them twenty ingredients but didn't tell them what they were cooking. 

A formulation is different than a diagnosis or description of the patient.  The formulation seeks to convey the relevant parts of a patient so that you can predict how a patient might behave in future circumstances.   By way of example, a formulation is similar to a "profile" in crime movies.  When they say things like, "he's going to want to tie the women with piano wires, because he's a schizophrenic who was forced to sleep in a tuba..." that's a formulation (sort of-- you get the idea.)

The formulation helps prediction by linking the various aspects-- seemingly unrelated, perhaps-- of a patient's existence.  It's the stuff you know is relevant, but DSM and standard psychiatry have no room for.  What does it mean if I tell you an inpatient brought with her fuzzy bunny slippers?  That's goes in the formulation.  A statement such as, "the strong family history of bipolar disorder,  along with his chronic alcohol abuse and prior suicide attempts, and the pending divorce and custody battle, and his recent apostasis from Catholicism put him at higher risk for suicide" is the type of sentence I want in the Assessment-- and it is precisely a short example of a "biopsychosocial" formulation. 

Note the importance of having all factors together, as opposed to individually.  It sets up the logic; it lets the reader know, immediately and obviously, what you were thinking.   This is very different than writing in one part of the note, "Fam Hx: strong bipolar;" and in another part of the note, "Chronic alcohol abuse;  history of multiple suicide attempts;" and in another place, "patient divorcing, and custody trial is next month."  Putting it that way, in the classic H&P format, forces the reader to have to infer.   Put in a biopsychosocial formulation, and the reader gets it instantly without even reading the rest of the H&P.  That's what you want.

Interestingly, the term "biopsychosocial" was coined by George Engel, psychoanalyst(?), who in 1977 made the startling observation, "The dominant model of disease today is biomedical, and it leaves no room within its framework for the social, psychological, and behavioral dimensions of illness."

[It] would seem that psychiatry would do well to emulate its sister medical disciplines by finally embracing once and for all the medical model of disease.  But I do not accept such a premise.  Rather, I contend that all medicine is in crisis, and, further, that medicine's crisis derives from the same basic fault as psychiatry's, namely, adherence to a model of disease no longer adequate for the scientific tasks and social responsibilities of either medicine or psychiatry.

Plus ca change...

Engel, like others, had understood that somatic symptoms such as pain, weakness, etc, and autonomic symptoms such as reflux, tachycardia, etc could be symbolic expressions of emotion or conflict.   How could the Objective portion of a note ever explain why you discharged a person with acute bilateral leg paralysis?  It can't-- but a biopsychosocial formualtion can.

As per Engel, the main question such a biopsychosocial model seeks to answer is why some patients experience an "illness" while others experience a "problem of living."  Importantly, the patient himself doesn't often know: the patient defines it as an illness recursively by whether or not he "needs" a doctor, and not by an actual understanding of what's wrong with him.  It's the doctor's job to decide whether it is actually an illness or a life problem, and then properly re-educate and re-train the patient.

Note that in my post about suicide documentation, the hypothetical patient was not malingering.  He believed he needed to be hospitalized because he was suicidal.  But when you discharge such a patient from the ER, you are thinking that the person will not die-- the suicidality is an expression of something else.  This is Engel's dichotomy.  The patient thinks one thing, you think another-- it's your job to explain to the patient what's really going on, AND explain to the reader why you did what you did. 

Typically, formulations are taught, in my opinion, backwards, so students "don't get it."   You're taught to start with what's going on now, then describe what historical factors that made the patient who he is  (including genetics, upbringing, social stressors, meds, etc),; then psychodynamic explanations, and then your proposed treatment and how you predict the patient will respond.   I think it is easier to go backwards.  First, decide what you think is going to happen in the future (will commit suicide, won't relapse, is a mania risk, etc) and then explain what it is about his past and present that makes you think this.  In this way, you're writing the formulation with a purpose.

"Joe came to the ER for suicidality after he got drunk after getting divorce papers.

Joe takes rejection very hard, and characteristically when the rejection is new, he doesn't spend time to think things through.  He exhibits poor judgment (give examples here or in Objective), is impulsive (examples), and also does things which further reduce his judgment and raise his impulsivity (like get drunk.)

Joe has several narcisissitic features . For example, importantly, his suicidality is directed at his ex-wife.  The point of the attempt is that she find out, that she know he is feeling hurt.  If it was guaranteed that she would never find out, he would not attempt suicide because it would have lost its meaning.  He needs her, or at least someone, to acknowledge his pain, and see him as the person he is trying to portray.   As we talked,  I made it clear that I did see he was hurt, and I understood the rejection--how it not only was a loss of a wife, but also a hint that he himself was unworthy of her.  We discussed that she was entitled to leave him, but that she could not deterine his value."

etc, etc.  You see how even without an Objective portion, the narrative in the Assessment is quite clear. The reader understands what you were seeing and thinking.

Addendum 11/15/06:  Fair is fair.  I found an even better review by one Eric Chudler, PhD at Univ. of Washington, called Neuroscience for Kids.  (don't laugh).  I didn't review all the links, but it is certainly more comprehensive than what I have here.

You know how everyone says that people go insane when there's a full moon? Well, I looked it up.

Most studies finding a link vbetween violence and the moon were done in the 1970s.  For example, a 1978 study found a lunar relationhsip to everything-- suicides, asssaults, MVAs, and psych ER presentations, with both homicides and assaults both occurring more often around the full moon.  Then again, you have to be suspicious of any study that actually tells you they actually used a computer.

But by the 1990s, this lunar relationship was on the way out.  Consider a 1997 study in Italy found no relationship between community psych contacts and the moon phases. A 1998 Australian study found no relationship between violent episodes in inpatient psychiatric patients and the moon phases.  A Spanish 2002 study found no link between ER presentations for violence and the moon's luminosity.  A German 2005 study found only the weakest link between completed suicide and the moon (the new moon, mostly.) A 1992 Canadian study reviewed 20 studies covering 30 years and found no link to attempts or completed suicides and lunar phases.  And, to prove a point, a gigantic Austrian study in 2003 found no relationship between lunar parameters (phases or sideric) and any ER presentations.

Which brings me to one point-- do Americans do anything other than drug studies? Well, one non-clinical study was done in Texas and found no link between prisoner violence and lunar phases.

--- 

So it is with violence and suicide.  But what about other behaviors?  I haven't had time to investigate the question, but two studies are suggestive.  One (British) 2000 study found a slight  increase in presentation to family practice clinics during full moons that was not due to psychiatric symptoms.  An Austrian 2003 study found a strong relationship between thyroid clinic appointments and dates around the full moon.  And a strange (British) 2003 study finding that women called a crisis center more frequently on the new moon. 

I did find an interesting (Greek) study finding an excess of seizures on full moons (34% vs. about 21% for the other phases.)   Importantly (and in contrast to suggestions by other studies) these were not pseudoseizures, because all patients were monitored.  The authors speculate either electromagnetic/gravitational effects (hey, it could happen) or an interaction between the intrinsic seizure threshold and the environment (i.e. you can change your own threshold.)

My interpretation of this is that the moon can't affect your behavior directly (duh), but one's relationship to lunar cycles could influence your behavior.  Take the classic wolf and full moon relationship.    Prey animals, such as rats, generally reduce their activity during the full moon (don't want to get caught, I guess.) Wild maned wolves (which eat rats) travelled significantly less during the full moon.  The authors' explanation was that prey is less available, so wolves would want to conserve energy.  Additionally, maybe one reason why so few studies are American is that we have a lot of artificial night light, so the moon has less or no influence, while elsewhere there is less artificial light?  Who knows.  I'm going to bed.

Here's a question: can an antipsychotic be an antidepressant?  Why, or why not?

The correct answer is that the question is invalid, because there is no such thing as an "antipsychotic" or an "antidepressant."  We (should) define them based on what they do, not what they are.  Therefore, Wellbutrin and Effexor are both antidepressants if and only if they both treat depression-- not because of some element of their pharmacologies, which are anyway different.  Strattera, on the other hand-- which has a pharmacology (in some ways) similar to Effexor-- is not an antidepressant, only because it doesn't treat depression.

Following, just because something is called an antidepressant, or antihypertensive, it doesn't necessarily take on all the other properties or side effects of the others in its "class."   Not all "antidepressants" have withdrawal syndromes (only SSRIs do).  Not all antihypertensives cause urination (only diuretics do.)  You wouldn't dare put a "class labeling" on "antihypertensives" of "diuresis."

So you see where I'm going with this-- except you don't. 

I've previously yelled about the inanity of "antipsychotic induced diabetes" or "antidepressant induced mania" when they ignore pharmacologies, doses, and, of course, actual data.

But today I saw something that I now understand to be one of the signs of the Apocalypse.  It is the new package insert of Seroquel, which just got a new indication for the treatment of bipolar depression.  The new PI reads:

Suicidality in children and adolescents - antidepressants increased the risk of suicidal thinking and behavior (4% vs 2% for placebo) in short-term studies of 9 antidepressant drugs in children and adolescents with major depressive disorder and other psychiatric disorders.  Patients started on therapy should be observed closely for clinical worsening, suicidality, or unusual changes in behavior.  Families and caregivers should be advised of the need for close observation and communication with the prescriber.  SEROQUEL® is not approved for use in pediatric patients. (see Boxed Warning)

Stating the obvious: in none of these 9 studies was any patient actually ever on Seroquel; Seroquel itself is not associated with a risk of suicide; it's not even been tested for major depressive disorder; and, well, this isn't very rigorous science, is it?

Just because a is now called an antidepressant, it carries the same risk as the SSRIs? (Whether even SSRIs have this risk is besides the point.)  Isn't that, well, racist?

This is not really about preventing suicide.  If we were worried about suicide, really, then why 24 hours before the FDA posted this warning, no one cared about Seroquel's doubling of the suicide rate?  Oh, because it doesn't actually double the suicide rate?  Die.

So the game is clearly not about science, it's about politics, it's about liability, it's about money. 

If this was honestly about about protecting children from suicide, we'd shrug our shoulders and say, "well, they're just very, very cautious, so we'll be careful and keep going."  But that's not what this is.  What this is factually inaccurate, misleading, and therefore more dangerous, more harmful.  In a simple example, this warning protects no one for a risk of suicide-- no potentially suicidal patient is going to look at this and say, "well, crap, I'm not taking this."  But it may prevent someone from taking it when they could actually benefit.  See?

This is Structuralism gone very badly awry, Saussure  just bought a pick axe and he's come looking for us all.