Interesting study from Princeton psychologist Daniel Oppenheimer, called "Consequences of Erudite Vernacular Utilized Irrespective of Necessity:Problems With Using Long Words Needlessly." (I should mention I have not read, and can't find, an actual copy of this study.)

Took a selection of writing samples (grad school applications, sociology dissertations etc), and changed each of the words to more complex/longer synonyms.  Then he gave these samples to 71 students and asked them to judge the intelligence of the authors.  The more complex and flowery the language, the  dumber the author was assumed to be. 

 

Think about it... 

From  collision detection

This time by one of our own (academic psychologist, Harvard) in an Op-Ed, entitled, "I'm Ok, You're Biased."

 

The premise is summarized here:

Doctors scoff at the notion that gifts from a pharmaceutical company could motivate them to prescribe that company's drugs, and Supreme Court justices are confident that their legal opinions are not influenced by their financial stake in a defendant's business, or by their child's employment at a petitioner's firm. Vice President Dick Cheney is famously contemptuous of those who suggest that his former company received special consideration for government contracts.

 

Which would be an ok, if not tired, set up, except for the very next sentence:

Voters, citizens, patients and taxpayers can barely keep a straight face. 

It's the populism of the message that is laughable.  So doctors, lawyers, Supreme Court Justices and others have no idea that they're biased, but the average joe does?  Seems pretty unlikely.  But-- maybe they are biased and it's okay.

And the proposed solution, of course, is the same knee jerk ineffectual nonsense proposed before:

In short, doctors, judges, consultants and vice presidents strive for truth more often than we realize, and miss that mark more often than they realize. Because the brain cannot see itself fooling itself, the only reliable method for avoiding bias is to avoid the situations that produce it.

 

There's that determinism so popular among those who feel powerless. 

I hope that the irony of the NY Times, through a psychologist, preaching about objectivity is not lost on anyone.  It is so bad at that paper that both the right and the left simultaneously blast it for overt bias.  No wonder that the NY Times stock has lost 50% of its value in two years.

Why not discuss the bias of journalists?  Or, more importantly, why are they assumed immune from it?  This isn't an idle political question, it is the very essence of this debate.

I'll state it explicitly:  first, the reason it doesn't matter if doctors are biased (and why it matters very much if journalists are) is because medicine is supposed to be a science. If it is a science-- receptors and all-- then it shouldn't matter what I think, it should matter what is true.  I can delude myself and say that seizure drugs are mood stabilizers for the long term; but that doesn't make it true.  But if you want to actually see if it is true, you have to look it up.  And don't come back with "one negative study doesn't disprove its efficacy."  This is science again: it's not up to me to disprove its efficacy, it's up to you to prove it has any.

So the real question isn't bias, it's whether medicine in general is paying attention to its own data.  Do we read our own studies, or hope the "thought leaders" will, and then write us a synopsis?  Do we believe it because Harvard said so? Is this science, or a cult of personality?

 

Second, when discussing medicine, the question of bias is not the important one. Yyou have to ask what the harm is.  Thie bias isn't harmful to science because science should be able to stand on its own.  The bias is only harmful to patients-- so the real question we should be asking is not if there is bias, but if it harms patients.  Ready: pretend a family doc gets paid $800,000 by Pfizer to prescribe only Lipitor, no Zocor, Mevacor, etc.  What, exactly, is the harm?  It's not snake oil: in all the anti-pharma controversy, no one is accusing them of selling a product that doesn't do what they say it does.  So unless you can tell me which patient shouldn't get Lipitor, but should get Zocor, then you can't argue this hurts the patient.  I'm not saying it isn't sneaky, or unethical.  But unless you can show the harm, you can't say it's harmful.  That's what's relevant.

 

But we're not really worried about patients, are we?  That's a screen.  What this is all about is our own impotence; anger against people who are perceived to have power.  We don't even actually believe our own nonsense.  This is the same argument against Vice President Cheney.  If everyone is so sure that the Iraq war was about oil and Halliburton, why didn't everyone buy Exxon and Halliburton stock back in 2002?  It's fun to criticise, I know.  But belief without follow through is pointless.  If you're not willing to act on your own beliefs, why should anyone else even listen to your crazy beliefs?

 

I'm not saying doctors and politicians aren't biased.  I'm saying we should worry about the things that actually matter.  Want to start somewhere, Daniel Gilbert? Academic medicine, and the journals that are their propaganda arms.  These people aren't scientists, they are science journalists.  And they are very much biased. Don't believe me?   Call me when you look up everyone's supporting references.

 

 

Because they're not. 

Odd article in Clinical Psychiatry News about the Match.

Although it doesn't come out and say it, it basically laments the fact that there are so many foreign medical graduates in psychiatry.  Which is weird, because there aren't. 

 

As the article correctly indicates, there were 1037 slots available.  983 (95%) were filled.  U.S.  med school graduates  comprised 62%.

 

The article says:

Another issue that concerns some psychiatrists is "a continued and sustained reliance" on international medical graduates to fill residency slots.

What's so wrong about this perspective is that it misses how slots get filled.  The slots don't "exist" and need filling.  Slots exist because there's a demand for them.  And they get filled by FMGs because they had been filled by FMGs the year before.  For example: in 2005, U.S. grads filled 63.6% of the slots.  In 2006, it is 62%. 

 

So the question isn't why so many FMGs go into psychiatry.  It is a) what is it about U.S. medical education that doesn't prompt U.S. grads to go into psychiatry; and b) do we really need this many psychiatrists?

 

What we should be thankful for, and Dr. Weissman indicates this, is that by taking in FMGs to residency slots, we don't have to pay to educate them in U.S. medical schools.     Basically, it's free money: some other country paid to educate them, and now they work here.  Good for us.

 

But this should lead us to the next question: why send them to medical school at all?  Many argue that foreign medical schools are not as good as U.S. ones.  Fine-- then why are they allowed in residencies?  And if they are, then you can't say you need a U.S. "level" of education, either.     And if an NP can prescribe, and a psychologist can prescribe, you similarly can't obligate we all go to medical school.

 

So either we need U.S. med schools, or we don't.  There are ramifications to either choice.  Choose.

You can find the distribution of residency matches here. 

A Healthcare Savings Account allows you to put aside $2700/yr, or $5040/yr/family, tax-free, for healthcare expenses.  So what?  So sit down.

First, a primer on deductible medical expenses.  The IRS allows you to deduct  the amount you spent on approved healthcare, minus 7.5% of your gross adjusted income.  In other words, take your gross adjusted income (i.e. how much you make minus deductions) and multiply by .075.  Subtract this amount from your total medical expenses: that's how much you can deduct.

You make $100,000.  You incurred $4000 in medical expenses.

0.075 x 100000 = 7500.  7500-4000=3500.  You can deduct 3500 from your taxes.

In the above example, if you only incurred $2000 in medical expenses, you can't deduct  anything.  Think of the 7.5% as a sort of-- deductible.

Healthcare Savings Accounts are different, and complementary.  In the above example, the $4000 of medical expenses was (hopefully) made with money you earned and paid taxes on.   If you're in a 35% tax bracket, you actually had to make $5400 to come up with that $4000.  So you had to pay $1900 in taxes; and another $500 is a wash (7.5% deductible).  So your illness cost you $1900 in addition to whatever the actual medical care cost.

But in George Bush's America, not only can you deduct medical expenses, but you can also put away money tax free for use in healthcare. 

Many progressive types will complain that this doesn't solve the healthcare crisis, and they are right.  But that's because HSA aren't about healthcare, they are about savings; they are another way of sheltering income from taxes.  What they are, in effect, is 401(k)s.

Say you retire. You'll draw on your 401(k), which was funded by $14000/yr contributions, to pay for food, vacations, cable, whatever-- and healthcare.  With an HSA, you can save $14000 AND $2700 a year, and use it as necessary when you retire.  If you have medical expenses, you can just use the HSA money; the 401(k) money is for everything else. 

So you can now save $16700 a year.  AND you can deduct your medical expenses (above 7.5%)

And by the way, money in an HSA is fully investible, like a 401(k). 

But what happens if you get hit by a truck (i.e. you have catastrophic medical expenses?)

Each HSA is linked with a "High Deductible Health Plan" (HDHP).  They have high yearly deductibles of $1k-$2k, depending on the plan (which you can use saved HSA money to pay) but have maximum deductibles of about $5000 (or $10,000 per family.)  In other words, you always have to pay at least $1000, but not ever more than $5000.
 

Each plan also has a monthly premium you have to pay (around $90) but about 60% is placed into your HSA (called "Premium Pass Through"-- you are in essence paying money to yourself, and the rest to the plan.)  Each plan has different premiums, minimum and maximum deductibles, and penalties/enticements to use network services.  These are summarized here, and in slightly more detail here.

Look, you can argue the social policy ramifications of this all day.  But don't look a gift horse in the mouth.

By the way, you may be fascinated to know what is an allowable medical deduction.

• Abortions
• Acupuncture
• Home improvements for health reasons (elevators, widening a doorway,"lowering" kitchen cabinets)
• Fertility enhancement
• Lead paint removal
• Legal fees to get healthcare
• Medical conferences and transportation (if the conference is about your/your family's illness)
• Psychoanalysis
• Transportation to healthcare services (gas, bus, etc)
• Weight loss programs
• Wigs
• Vasectomies

And enough with the notion that medication compliance is a good proxy for overall efficacy.

 

All of these horrible psychiatry studies-- CATIE, Lamictal and Depakote maintenance trials, etc-- keep telling us how long patients stay on medications, because they say this means the drugs are working.  The authors think that if a drug is working, they patient will stay on it.  But you would think this only if you didn't actually treat many patients.  I can make a similar argument that staying on a medication is inversely related to efficacy-- because when a patient feels better, they simply stop taking their meds.  

 

Think about antibiotics.  People don't finish the full 14 day course, precisely because they feel well.  If they felt sick, they would probably take them longer than 14 days.  In fact, people overuse these antibiotics even when its a virus, despite the antibiotic having no efficacy at all.    They will demand an antibiotic even though know that it shouldn't be doing anything.

 

Same with pain meds.  Oh, that's an acute problem?  How about the chronic problems of diabetes and hypertension.  People will skip/miss/forget doses when they feel asymptomatic, and will be more compliant when they have symptoms associated with these illnesses (e.g. headache, dizziness, etc.)

 

Look, I'm not telling you that compliance and efficacy aren't related.  I am saying that if you want to measure efficacy, don't use compliance as a proxy-- go measure actual efficacy.   And don't tell me it's too hard.  You got $67 million for this study.  Find a way.

if CATIE is so important, and was funded by the NIMH (i.e. taxpayer dollars), why isn't it available free on the CATIE or NIMH websites?  Or anywhere else?  Snakes.  All of you are snakes.

1.  You know, if you're going to be rigorous about BID dosing schedules because the FDA requires it, why so liberal with total dosing for Zyprexa?  A mean dose of Zyprexa is 20.8 is way (150%) above FDA guidelines.  For comparison, that would have meant dosing Geodon at 240mg, Seroquel at 1000mg, and Risperdal at 6mg.  BTW: a mean of 20.8mg means that a lot of people were dosed with MORE than 20.8mg (max=30mg).

2.  The miracle here isn't that Zyprexa won, but that Zyprexa 20mg barely won against Geodon 114mg.

3.  Why Trilafon (perphenazine)?  Originally you thought all conventionals were the same; so why not Haldol?  Or Mellaril?  You say it's because it had lower rates of EPS and TD, which is fine, but then why exclude TD patients from that arm?

4.  So you excluded patients with tardive dyskinesia from the perphenazine group (fine) but then had the nerve to say people tolerated it as well as other meds?  Do you think maybe people who have TD may have different tolerances to meds?  Different EPS?  Different max doses?  That they're just different?

5.  You can't generalize from an obviously slanted "typical" arm to all other typicals.  If you chose Trilafon over Haldol because of better tolerability a priori, you can't now say that "typicals" have equal tolerability to atypicals.  Why not pick two typicals of differing potencies (like Mellaril and Haldol) and infer from there?

6.  Do you actually believe-- does anyone believe-- that any of these patients are compliant with BID regimens?  Especially with sedating meds like Seroquel?


The secret to understanding CATIE 2 is to understand that there are two CATIE 2s.

CATIE2-Efficacy: People who dropped out of CATIE 1 because their med didn't work were randomized to Clozail, Zyprexa, Risperdal or Seroquel.  On average, new Clozaril switches stayed on 10 months, everyone else only 3.  44% of Clozaril stayed on for the whole 18 month study; only 18% of the others completed the study.

CATIE2-Tolerability: People who dropped out of CATIE 1 because of side effects (not efficacy) were randomized to Zyprexza, Risperdal, Seroquel, and Geodon (not Clozaril.)  Risperdal patients stayed on for 7 months, Zyprexa for 6, Seroquel for 4 and Geodon for 3.

CATIE2-Efficacy is fair.  If you fail a drug, you're likely to do better on Clozaril than anything else.

CATIE2-Tolerabilty makes no sense at all.  The reason Geodon was used is because it has "very different" side effects.  Hmm. How?  "In particular, ziprasidone [Geodon] was known not to cause weight gain."  But this assumes that the intolerability of the first antipsychotic was its weight gain.

Most importantly is this: if a patient couldn't tolerate their first antipsychotic, how likely is it that it was effective?  In other words, if it wasn't tolerable, it wasn't efficacious-- these patients could have been in CATIE2-Effectiveness study.  So how did they choose?

Easy: they gave the patient the choice: Geodon or Clozaril?  Out of 1052, half left altogether.  99 went into the Clozaril study (CATIE2-Effectiveness) and 444 went into Geodon (CATIE2-Tolerability.)  Of the 444 in the Tolerability trial, 41% were actually labeled first drug non-responders.  38% were labeled as not tolerating their first drug, but of those, who knows how many were also nonresponders?

And 74% dropped out again.

If you take the 444 in the Tolerability study and divide them into two groups:

• those who left CATIE1 because of lack of efficacy: then switching to Zyprexa or Risperdal kept them on their meds longer.  (Which makes no sense again: this is the same thing as the CATIE2-Effectiveness, where (except for Clozaril) there was no difference between Seroquel, Zyprexa and Risperdal.)
• those who left CATIE 1 because of lack of tolerability, then it made no difference what you switched to.

Sigh.

 

And what's with the blinding?  In every other study with a clozapine arm, you equalize the weekly blood draws by making everyone have to submit to them.  But in this case, they unblinded clozapine so as not to have to subject all these people to blood sticks.  Except they were subjecting them already-- they were checking blood levels.

And where was perphenazine?  "[CATIE1] did not anticipate this unexpected result [that perphenazine would be as efficacious] that challenged the widely accepted (but never proven) belief that the newer atypical antipsychotic medications are better than all older antipsychotic medications" and so was not considered for CATIE2.  Apart from the fact that it is simply untrue that anyone thought the atypicals were more efficacious than the typicals, it is furthermore untrue that that the authors did not "anticipate this unexpected result."  In 2003, after basically doing Medline meta-analysis, they found that "not all of them were substantially different from conventionals such as perphenazine."

What's funny about these guys is how they conveniently lump all typicals together but arguing for differential effects of  individual atypicals; then argue typicals are different from each other to justify picking Trilafon; and then say atypicals are different from each other ("not all of them were different") but typicals are all pretty much the same ("conventionals such as perphenazine.")

 

Bottom line:

 

The stated purpose of CATIE2 was to help clinicians decide which drug to switch to if patients a) failed their first drug; b) couldn't tolerate their first drug.

The divorce rate in America is 40-50%. Say you get divorced, and a friend says, I have two women for you, Jane and Mary.   If the problem with your first wife was that she didn't turn you on, you should marry Jane.  If the problem with your ex was that she was annoying, you should marry Mary.

 

What's going to happen here is that your second marriage, to either girl, is doomed.  Certainly more than the national average of 50%.    How long is it going to take before your second wife doesn't turn you on either?  How long before you find stuff intolerable about her?    The answer is, more likely than your first marriage-- say, 75%-- because the problem isn't your wives, it's you.  You've framed the question in an idiotic and arbitrary manner.  You don't get married to get turned on OR to be with someone who isn't annoying.  You want the marriage to have both simultaneously, and much more.  These things are not separable.  This is CATIE2.  A meaningless dichotomy-- efficacy and tolerability are not separate, let alone opposites-- used to create a false paradigm of medication selection.

As you may know, when prescribing Clozaril (clozapine), a complete blood count with differential (CBC w/ diff) has to be checked every two weeks, because of the risk of agranulocytosis.

The FDA has relaxed these requirements: now, you have to check weekly for the first six months; then every two weeks for six months, then only monthly after that.  You have to show WBC >3500/ml, and ANC>2000/ml.  (That's white blood count and absolute neutrophil count.)

Don't think for a millisecond this was done because the FDA did a rigorous re-evaluation of safety data.   This is the FDA that black boxed antidepressants for suicide and antipsychotics-- oh, sorry, only atypical antipsychotics, even though typicals are as bad, if not worse-- for death in patients with dementia related psychosis.

What's stupid about this is that agranulocytosis is the least of anyone's problems.  In the Clozaril National Database (1990-1994) (1), there were 99,502 patients.  382 (0.4%) got agranulocytosis, and 12 died (that's 0.001%).  The number of clozaril related deaths (all kinds) was more than 400.

In an Italian study, the rates of neutropenia are about 0.9%, and agranulocytosis 0.7% (2)

They are, however, dying in not insignificant numbers by other things.

Consider a Maryland finding: of the 2046 clozaril patients from 1990-2000, three died of new onset diabetic ketpacidosis. (0.15%) None had had diabetes. (3)  Or the Israeli study (4) that found that 4/561 clozaril patients had sudden death--  10 years younger, healthier, and 4 times the rate of  non-clozaril treated sudden deaths.  NB: no one died from agranulocytosis.

How about myocarditis: 8000 patients over 6 years: 15 myocarditis, 8 cardiomyopathy; 6 died.  That's 0.3%  5 of the 6 deaths occurred in first month  (that's right: month). (2)  Given the rapidity of death, the authors speculate it's an acute hypersensitivity reaction (i.e. IgE/Type I).

A review of Pubmed/MEDLINE from 1970-2004  found rates of fatal myocarditis/cardiomyopathy to be between 0.015% and 0.188%.

An oft cited article by Walker examined 67072 clozapine patiens from 1991-1993, and found that of the 396 deaths, the most common cause was pulmonary embolism.  (FYI: Zornberg found that exposure to low potency antipsychotics massively increases the PE risk to (OR 24 for low potency, 3 for high potency; not dose related, usually occurred in first three months.) 

In contrast to Hagg's finding of 12 cases of PE/DVT, and a frequency of about 0.03%, another study of 13000 inpatients over 6 years found 5 PEs, i.e. a rate of 0.038%; but this was no different than typical neuroleptics of non-treated.

Look, I'm not saying to ignore agranulocytosis.  I'm saying that when your patient's heart explodes, you can't say, "but the FDA only said CBCs!"  You need to be checking EKGs.  And when the lawyer asks you how most people die when on clozapine, it'll look really bad when you give the wrong answer.

Here is a suicide statistic:

"Suicide is the eighth leading cause of death in men."

That's useless, because there is no context. Other useless statements are: the risk is higher in psychiatric illness; the risk is higher the more previous attempts; men have higher rates of sucide than women, etc.

Here are some statistics (1999, 2001 and 2003-- they're all the same) which may help you.

In the US in 2001, 30,622 people died from suicide.   Yes.  That few.

24,672 were men. 5950 were women. (That's 80/20). In the whole world (WHO 2000), it was about 815,000.

5395 were over 65. (85/15 males to females)
3971 were 15-24. (85/15 males to females)

So 70% of all suicides are adults.
73% of all suicides are white males (20,000+). To put it in perspective, in 2003, the number of black women who suicided was 358.
Guns were involved in 55% of all suicides; 60% of the men's, and 73% of the elderly's, and 54% of youth's.

In other words, mostly white adult males die.

White men over 85 have the highest rate given their popualtion (54/100,000), vs. an overall rate of 10.7/100,000 (.01%) But this number of suicides is so small that the statistic doesn't help you.

So the real risk factors are white males with a gun.

I should also point out that 30,622 is a really small number of people-- even though it is almost as many as homicides (20k) and AIDS deaths (14k) combined.

How about suicide attempts that don't result in death?

Well, there are a lot: in 2002, 132,353 were hospitalized for a suicide attempt, and 116,639 were seen in an ER and released. But here's the thing: they didn't die.

The problem with our suicide assessment is that it screens for attempts, not death. And while non-psychiatrists might be surprised to hear this, a whole lot of people commit impulsive suicidal acts with no or little interest in actually dying. Psychiatry cannot do much to stop these acts, nor should it be responsible to do so. A psychiatrist should be no more responsible to prevent these parasuicidal acts than an endocrinologist is to guarantee that the patient takes their insulin. If psychiatric illness-- that's major Axis I-- so impairs their reason that they don't know what they're doing, can't stop, etc-- then it's our responsibility, just like, given that same patient, it's the endocrinologist's.  Otherwise, it is not.

We spend a lot, a lot, of money and time hospitalizing people who are not going to die. A not insignificant portion are outright malingerers, and everyone knows it. The rest may be at risk, but they may not be best served in a hospital.

So we can either spend our time and resources on preventing suicide attempts, or on preventing the 30k actual suicide deaths. It's not the same thing.

For those who live and breathe the abortion debate, it may be worthwhile to personalize the issue and see if anything changes. Certainly, Rick Santorum has done this.

If you do not already know the story, Senator Santorum told it himself on Fresh Air in September 2004. Briefly, at approximately 20 weeks gestation, he and his wife learned the fetus had a terrible disorder that would likely result in the fetus’ demise. They had three choices: carry the fetus to term, when it would inevitably die; abort the fetus; or try a risky surgery on the fetus (which was still inside the womb) which had a low probability of success. The Santorums, true to their faith and their principles, reasoned thusly: if this was a five year old child, there would be no debate. They went with the surgery.

As tragedies go, this was a big one, as the surgery failed, the fetus died, and the mother suffered complications. However, the story clearly indicates how one should reason if one believes life begins at conception. This is the point for the Senator; it is illogical to argue any differently. If we are debating the abortion issue, this is a hard argument to rebut.

But I am not, here on this blog, interested in the abortion issue specifically; I am interested in another question. It is this:

Who pays for this surgery?

It is not an academic question. Senator Santorum has the benefit of almost infinite medical resources. If we are going to force Medicaid patients to make a similar choice, we have to ask this practical question.

Many are not going to like having, depending on your perspective, a moral or privacy question reduced to money; but that is precisely the problem. Accountability. In the end, someone has to pay.

Only the schizoid will argue that abortion should not be an option even when the mother’s life is in mortal danger; and only the amorally unrealistic will fail to realize that there is something psychologically wrong with a woman who has had three, four, five abortions. (This is not so unusual: it is 18% of all abortions.) You may think it is your right to have as many abortions as you need, and you may be right; but there is still something wrong with you.

Not permitting abortions requires an explanation of how we're going to pay for surgeries like the Santorums's. And if you want to keep abortions legal, you have to tell me how we're going to pay for them; or for any complications that result from them.

Either healthcare is a right, like due process; or it isn’t, like driving. Either one you pick, you must be accountable for the consequences of your selection, for example, its effect on the abortion question; similarly, your stance on abortion must include an discussion of cost. Even if this is,a fter all, a moral question, someone still has to pay for it. I recognize this tarnishes the purity of the academic dialogue. It’s not pretty, it’s not clean, but it’s reality. And if you think that money is not a relevant factor here, then it almost certainly means you are not going to be the one who will have to pay.

This applies to other questions beyond abortion, of course. If someone discovers a cure for AIDS, but it costs ten million dollars, does everyone get to have it?

When the universal healthcare nuts draft a plan that includes how they are going to pay for the unintended consequences of an insufficiently reasoned abortion provision (or restriction), give me a call. Until then, wovon man nicht sprechen kann....

Homeland Security Official Charged in Online Seduction

The system has failed.

Plot synopsis: DHS press secretary is caught in online sting, as he has sexual online chats to what he thinks is a 14yo girl but is really a cop.

Seriously, what's wrong with these people? Do you need a 14yo so badly, at any cost, you're willing to tell them you actually work for Homeland? Is that supposed to turn on 14 year old girls?

You would think the deputy press secretary of Homeland Security would know that he could be easily caught on the internet trying to solicit sex from a minor, or at least that the Department would know what he is doing on their computers. But he doesn't, for two reasons: a) he's stupid; b) in fact, the Department doesn't know what he is doing, because the Department is stupid.

I'll do you one better: no one traffics kiddie porn on IRC if they have half a brain in their head. You want to traffic kiddie porn? Make your connections over online games like WoW, Everquest, or Halo. In the case of the former two, the chat conversation works as well as irc, and in the case of the latter, it's voice traffic. In no case is the transcript or anything else logged. I bet there's more weird crap happening in online games than you'd want to know.

Add to that freenet, which is basicaly encrypted decentralized bittorrent with invite-only peers, and you've got a pretty robust digital underground.

CNS Spectr. 2006 Mar;11(3):179-86.

The authors examined the difference between two (theoretical) subtypes of OCD symptoms. Based on the earlier work of Lee and Kwon, obsessions can be divided into autogenous and reactive.

Autogenous: occur without identifiable or likely stimuli; repetitive; disturbing;
Examples: "sexual, aggressive, or immoral thoughts, images, or impulses." The sudden obsession to rape; or seeing a red shirt, which signifies raping.
Coping strategy: suppress these thoughts

Reactive: caused by identifiable external stimuli, including thoughts of contamination, asymmetry, loss; are realistic;
Coping strategy:reduce anxiety (e.g. wash hands.)

They found some interesting differences:

Autogenous obsessives were more likely to be male, and older (34) and have older ages of onset (27);

Reactive obsessives were more likely female (60/40), younger (27) and younger age of onset (19).

No difference in either group in education or marital status; nor were there any major psychiatric comorbidities.

But autogenous obsessives rarely (1%) dissociated; reactives did dissociate (10%).

A few points. That aggressive/sexual thoughts go with males is no surprise. But that they are found in the older people is interesting. If you can see how primitive thinking occurs in reactive OCD, it makes sense they would get their symptoms at a younger age. It is known that cleaning and checking obsessions are associated with an earlier age of onset.

The prevalence of dissociation in reactive patients- or the absence of it in autogenous patients-- had already been suspected. Checking and symmetry symptoms (associated here with reactive type) had already been found to be more commonly associated with dissociation. (Personal diversion: my own clinical experience with pedophiles supports this-- that those with sexual obsessions are fully conscious of them; obsess over them, are familiar with every nuance. They know to molecular detail what the child looks like, how it moves; and are totally aware of their own behavior at every step of the molestation, even when they pretend a quasi-dissociative experience as a defense. They wouldn't dissociate during the acts because, in effect, it defeats the purpose of committing the act.)

Additionally, in other studies, Lee and partners (Telch, Kwon, etc) found that autogenous obsessions were more associated with schizotypal personality than to other OCD symptoms themselves (while reactive obsessions had no association with schizotypal.) 1 The authors use this finding to support the idea that autogenous obsessions represent cognitive issues, while reactive represent behavioral ones; autogenous obsessives obsess; reactive obsessives are compulsives. This is further supported another study finding that on Rorshach, autogenous obsessives, like schizophrenics, have severe thought disorder, while reactive obsessives do not.2 The belief that merely thinking a thought could make it true (formally called the likelihood bias of though-action fusion) sounds like the magical thinking in schizotypal, and in fact TAF is seen in schizotypals 4 1. It would be interesting if it could be investigated in autogenous obsessives versus reactive obsessives separately, the hypothesis being that autogenous obsessives display likelihood TAF, while reactives do not.

Clinically, it may be fair to say that people with autogenous type obsessions share schizotypal features, and cognitive/perceptual distortions, while reactive obsessions go with OCPD features and compulsive behaviors. So, do antipsychotics help autogenous obsessives (and not (or better than) reactive obsessives?)

In line with this, there is some evidence that schizophrenics and OCDs share some neurodevelopmental pathology. For example, using fractal dimension and CSF volume, one could accurately categorize schizophrenics or OCD patients, vs controls, with 90% accuracy.3 It would be interesting to see if these obsessives, based on brain pathology alone, could be distinguished between autogenous and reactive types. I suspect the answer will be yes.

1. J Anxiety Disord. 2005;19(7):793-805. Epub 2005 Jan 5.
2. J Clin Psychol. 2005 Apr;61(4):401-13.

3. Neurosci Lett. 2005 Aug 12-19;384(1-2):172-6.

4. Behav Res Ther. 2005 Jan;43(1):29-41.

and turn out to be wrong.

There's been something of a controversy raging over the best place to get accurate information.

Specifically, there's a free, user-written encyclopedia called wikipedia at http://www.wikipedia.org that competes with the
Encyclopedia Britannica. The idea is that anyone who uses wikipedia can edit any story. So if you happen to be reading an article that has an error in it (for example, if it says the Constitution was ratified in 1798) you can correct it with a few clicks (e.g. you change it to 1789). Aside from controversial topics (where articles are edited constantly to favor one
opinion or the other), the "hard facts" articles on science, culture or history are fairly decent. Or so they seem at first glance.

The controversy is this: Britannica's editor in chief went on record (in a newspaper article I can't find) stating that Britannica is a better, more reliable source of "knowledge" because it's a closed controlled editing environment, where articles are researched, edited, and reviewed internally by academics who are experts in their respective fields.

Wikipedia responded saying it doesn't need all that editorial oversight because any error in an article is corrected relatively quickly by an expert in the field.

The essence of the argument is "top-down" (Britannica) vs. grass-roots/bottom-up (wikipedia), or,  to put it more succintly, does the existence of a gatekeeper for knowledge improve the quality, accuracy, and veracity of knowledge?

The debate matters for two reasons: (1) at some point people have to agree on the basic facts of whatever they are talking about, and (2) there needs to be a place where you can find the core true facts about any subject.

So anyway, the medical journal Nature decided to compare the two sources of knowledge:

http://www.nature.com/news/2005/051212/full/438900a.html

Now you may ask what the hell business is it of Nature's (a quasi-medical journal) to do this (review the accuracy of encyclopedias), but that's my point and I'll get to that in a second.

Anyway, surprise surprise, Nature says that in the case of science articles, wikipedia is better. This was not unexpected - wikipedia claimed all along that it amounted to enabling peer-review of its articles by readers, and Nature, of course, is all about peer-review.

Britannica responded, finding errors in Nature's methodology (warning: pdf ahead, but it's worth reading if you think for a second Nature should be trusted to do anything):

http://corporate.britannica.com/britannica_nature_response.pdf

concluding that the study was bogus, and that Britannica had far fewer errors and omissions than Nature claimed.

 

What interests me here is not the accuracy of Wikipedia vs. Britannica, but why Nature feels it is in any position to examine this.

Here is Nature's response to Britannica's criticisms:

http://www.nature.com/nature/journal/v440/n7084/full/440582b.html

Here's the line to focus on:

"Britannica complains that we did not check the errors that our reviewers identified...but there is a more important point to make. Our reviewers may have made some mistakes — we have been open about our methodology and never claimed otherwise — but the entries they reviewed were blinded: they did not know which entry came from Wikipedia and which from Britannica."

For the record, Nature says this is how the test was
conducted:

"Each pair of entries was sent to a relevant expert
for peer review. The reviewers, who were not told
which article came from which encyclopaedia, were
asked to look for three types of inaccuracy: factual
errors, critical omissions and misleading statements. 42 useable reviews were returned."

And this, my scientician friends, is why medicine isn't a science. Nature is saying that its methodology is sound because the entries they reviewed were blinded - BUT WHO ARE THE PEER REVIEWING EXPERTS, WHO SELECTED THE ENTRIES, AND ACCORDING TO WHAT CRITERIA?

 

You cannot excerpt an article describing something and then test the excerpt for omissions. Furthermore, the excerpting is not blinded, and the person excerpting things may have a different opinion of what can be safely left out than the person doing the review.

Nature's mistake is assuming that the expert is always right. If the expert disagrees with Britannica, then Britannica is wrong.  You should be able to test the accuracy of an entire encyclopedia article *by giving it to multiple experts*. Not the other way around, multiple articles to one expert. The hypothesis is "do experts think the article is correct", and you test it by find the percentage of experts that think it is/isn't. 

What is truly ironic is that while Nature likes to hold itself out as an open source for medical knowledge (and thus more like Wikipedia), it is in fact a gatekeeper of knowledge like Britannica. When Nature publishes an article, the belief of the scientific community is that the article is correct *because it's in Nature*. But Nature is the journal of statistical regression sciences - medicine, global warming, etc., i.e. disciplines where there is no right answer or it's impossible to know the right answer because you are observing only a small percentage of all the variables being affected.  It tests associations, not causality. 

Keep this in mind when a journal like Nature also makes policy proclamations ("global warming needs to be stopped") or creates artificial hierarchies by its coverage (substantially more articles on HIV than malaria, so HIV becomes more "important" than malaria, etc.)

I had a patient with a chief complaint of deja vu, so I looked it up. (BTW: turned out to be undiagnosed dementia in my patient's case.)

Best article I found was Wild E. J Neurol. 2005 Jan;252(1):1-7. Summarized (and all below references come from Wild's paper):

Definition: "any subjectively inappropriate impression of familiarity of a present experience with an undefined past." (Neppe, 1983)

Wild explains that the definition here is importantly specific: "subjectively inappropriate" means that the patient understands the familiarity is impossible (i.e. this is not a delusion.) "Undefined past" is a non-existent past, and the patient never pinpoints it (because it never happened).

Some theories:

Wigan (1985), Jensen (1868) and Maudsley (1889): a "loss of synchronicity" between two hemispheres of brain, so that they are working "separately but synchronously." Jensen also suggests it is familiarity of one part of the experience generalized to the whole.

Gestalt psychology: object-affect entities. An experience causes an affect, which is identical to the affect assocaited with an unrelated event in the past. Your brain interprets it as a rememberance of the object (as opposed to the affect.)

De Nayer:"tape recorder hypothesis:" you are remembering the event and recollecting the event at the extact same time.

Freud: the situation is similar to a suppressed fantasy, so the fantasy activates as a wish to make improvements in the current situation, so in essence it is the wish to turn back time.

Biology:

Associations with temporal lobe epilepsy suggested that that was the relevant neuroanatomy, but some interesting experiments suggest that deja vu is associated with limbic structures (especially hippocampus and amygdala) and not the temporal neocortex itself. Bancaud (1994) tried to synthesize the available information and proposed that the perception is encoded in the temporal neocortex and remembered in the hippocampus; affective memory is supplied by the amygdala. Then, these relate back to the temporal neocortex as a daja vu. Thus, a situation, as it is experienced and "recorded" (see De Nayer) activates deeper memory structures.

All of this appears to be lateralized to the to the temporal lobe ipsilateral to the dominant hand (which is really the non-dominant hemisphere-- it crosses). In fact, the point of all this was to use the symptom of deja vu to predict where a seizure focus would be. (Unfortuantely, a PET scan study could not confirm this lateralization.)
Because of the prominent association of deja vu with autosomal dominant "partial epilepsy with auditory features" a genetic contribution is suggested. This gene is the LGI1/epitempin gene (10q24).

Assessment should rule out depersonalization or flashbacks. If deja vu is short or infrequent, it is probably normal; but if recurrent, prolonged, or associated with physical sensations, consider TLE. If associated with anxiety or depression, consider psychiatric causes.

Other articles:

A study of 24 epileptics receiving direct stereotactic electrical stimualtion of the brain found that stimualtion of the entorhinal cortex produced more deja vu than the amygdala or hippocampus, while the perirhinal cortex was associated with the recollection of memories.

A prospective study of TLE patients and their "auras" (called simple partial seizures, i.e. seizures with no loss of consciousness, and include deja vu, weird tastes, etc)) found that the SPSs, deja vu, a warm sensation, a cephalic sensation, taste hallucination, and a "strange" sensation predicted an abnormal amygdala ipsliateral to the seizure focus. Though fear was the most common for all TLE patients, the single best predictor of an abnormal amygdala was... deja vu. As described by Wild, this occurred most commonly on the right (i.e. ipsilateral to handedness, or nondominant for language.)
A study of 14 patients with varying frontal lobe damage were tested for a number of memopry parameters; those with incorrect "feeling-of-knowing" had damage in the right prefrontal cortex.

Although deja vu is supposedly distinct from psychosis, and not related to dopamine, there's a case report of a 39yo physician-patient who took amantadine and phenylpropanolamine to ward off the flu, and got intense deja vus. They stopped when he stopped the medications. The authors find other case reports finding the same.

An interesting case report (two cases, actually) found that, contrary to the popular understanding that the deja vu shares some similarity to an actual past event, on formal testing these two patients had recollections which were unlikely related to previous familiarity ("incorrectly recognised low frequency words."). They then created justifications, i.e. they confabulated the recollections.

As an aside, there are 85 articles in Pubmed with the words "deja vu all over again" in the titles. Almost none actually had anything to do with deja vu. That's creativity for you.