Fight Club

OK, so Dinah inspired me with her "You're The Psychiatrist...." post. She does do this fairly regularly. She stumbled into an Ultimate Fighting event and came out wondering, "Why do people do this?"

I'll tell you why. I have some experience with fighters, both as a psychiatrist who works with violent people and as someone who has hung around black belts for about twenty years.

It's about competition, it's about adrenaline and excitement, it's about taking risks and not being afraid of the consequences. (I'm tempted to say 'it's a guy thing', but besides being a sexist comment it would also happen to be an untrue statement. At some of the martial arts competitions I've been to I can tell you there are a substantial number of women competing nowadays. And you should see their tattoos!) So it's a sport, although I have to say there's sometimes a fine blurred line between a sport and a crime. If there are rules, if there's a professional organization sponsoring the event, if you have to pay to get in and you get some kind of formal training, then it's a sport.

Then there are crimes. People who fight---without rules and without sports equipment----sometimes do it because they enjoy it. It releases tension, gets rid of pent up emotion, and sometimes it settles problems (whether it's a good way to settle problems is obviously a whole different question). Among prisoners the challenge is to see how "good" you are at it or to establish dominance and defend your turf. It's to enforce gang rules or to punish rulebreakers. Among the younger inmates (also called "hoppers" in prison slang, after hip-hop) the idea is that fighting is protective; by being willing to 'step out' you'll be less vulnerable and it will keep people away from you. Younger inmates also will prove themselves by going up against much bigger prisoners or correctional officers. (The much bigger, more experienced correctional officers can usually see this coming and can 'talk them down' or persuade them that it's really not a good thing to do.)

So that's what my experience has been and what I can say about the motivation of fighters. Street fighters eventually grow up or burn out. They figure out they won't always be the biggest baddest person on the block and that injuries accumulate over time. Then there's the rare person who never figures it out, and they stay locked up. One prisoner I met had been in a coma for several weeks as result of a street fight. I asked him what he had learned from the experience. His response:

"Next time I bring a gun."

Oy.

Perchance to Dream

I've been having trouble sleeping sometimes lately. Oh, who am I kidding? I've always had intermittent insomnia, lately it's bothering me more for some reason. I'm lucky: if I don't sleep well, I don't feel it the next day, and so I've learned not to worry so much about it. If I go a few days with restless nights, I start getting irritable, and then I usually sleep well for a bit until the cycle repeats. A friend insists I'd sleep better if I turned off the computer and TV by 10 or 11 pm. I'm usually IN bed by 11:30, and I'm not much of a TV watcher, so I don't think that's it-- I sometimes get on the computer after that if I can't sleep, but I've tried first. Then she said it's the Diet Coke I have with dinner. Fine, I've given up caffeine after 9 am. I've had no Diet Coke in almost two weeks. I don't miss it, but it's not making much difference. Some nights I sleep well, others I don't. Last night, by the way, Roy was in my dreams....

So with that as a prelude, the New York Times has an interesting piece on sleep medications. I prescribe sleep medications sometimes, and I really don't think they're a problem for short term issues-- someone who sleeps poorly because of an acute stressor. And SSRI's often disrupt sleep, for some people the combination of an SSRI with trazodone seems to be helpful for both sleep and depression. Getting back to the New York Times article, "Sleep drugs found mildly effective but wildly popular"-- Stephanie Saul writes,

But if the unusual pitch makes you want to try Rozerem, consider that it costs about $3.50 a pill; gets you to sleep 7 to 16 minutes faster than a placebo, or fake pill; and increases total sleep time 11 to 19 minutes, according to an analysis last year. If those numbers send you out to buy another brand, consider this, as well: Sleeping pills in general do not greatly improve sleep for the average person.

The article goes on to say that while total time asleep is increased by 25 minutes or so, that sleep satisfaction amongst insomniacs is greatly increased. The article goes on to theorize why that is, to talk about some specific problems with certain hypnotics, and to say that the perfect sleep agent hasn't been found.

And with this thought, I've changed the sidebar poll-- Please vote for your favorite sleep medication. In Roy's honor, I've tried to be a bit more complete. And once again, in my pursuit of useless data, I don't care who you are, if you take or prescribe it, or if you merely like the idea, just tell us your favorite.

Oh, and finally, I should have put this on my last post about the Red Sox, but if you didn't know it, Red Sox pitcher Curt Schilling is a blogger-- do check out 38pitches.com . Funny, but his posts get more comments than our Shrink Rap posts get. I wonder why.

Molecular Psychiatry: Schizophrenia Mouse Model

Here's another interesting knockout mouse model for schizophrenia. This was in the July 31 issue of Molecular Psychiatry, "Phospholipase C-1 knockout mice exhibit endophenotypes modeling schizophrenia which are rescued by environmental enrichment and clozapine administration," by McOmish et al., in Australia.

"Phospholipase C-1 (PLC-1) is a rate-limiting enzyme implicated in postnatal-cortical development and neuronal plasticity. PLC-1 transduces intracellular signals from specific muscarinic, glutamate and serotonin receptors, all of which have been implicated in the pathogenesis of schizophrenia. Here, we present data to show that PLC-1 knockout mice display locomotor hyperactivity, sensorimotor gating deficits as well as cognitive impairment. These changes in behavior are regarded as endophenotypes homologous to schizophrenia-like symptoms in rodents. Importantly, the locomotor hyperactivity and sensorimotor gating deficits in PLC-1 knockout mice are subject to beneficial modulation by environmental enrichment. Furthermore, clozapine but not haloperidol (atypical and typical antipsychotics, respectively) rescues the sensorimotor gating deficit in these animals, suggesting selective predictive validity. We also demonstrate a relationship between the beneficial effects of environmental enrichment and levels of M1/M4 muscarinic acetylcholine receptor binding in the neocortex and hippocampus. Thus we have demonstrated a novel mouse model, displaying disruption of multiple postsynaptic signals implicated in the pathogenesis of schizophrenia, a relevant behavioral phenotype and associated gene–environment interactions."

PLC-1 is one of those proteins involved in processing the signal after the receptor is activated. Think of the ignition in your car. If the key is the neurotransmitter, like serotonin (or medication, like Prozac) and the lock (or keyhole) is the receptor, then PLC-1 is one of the wires that connects the lock on the steering column to the starter, which gets the engine going. We are all so used to thinking that what is important is the action at the receptor, but it is easy to forget that there is this whole other layer of machinery that gets engaged once the receptor is activated.

These so-called second messenger systems use a cascade of Rube Goldberg connectors to make things happen. Just like a genetic error can cause a receptor to malfunction, so can errors in this second messenger cascade.

This particular enzyme is involved in the growth and connectivity of brain cells. The researchers show that mice who are engineered to not produce PLC-ß-1 develop cognitive problems which have similarities to those seen in humans with schizophrenia. Changes in the environment can minimize these problems, suggesting that this animal model could be used to test other treatments -- including medications that work very differently from what is out there now -- for potential use in this neurodevelopmental illness.