The metaphysics of a Jazz Thing

A fantastic study has just been released by open-access science journal PLoS One that investigated the neuroscience of jazz improvisation.

Jazz musicians were put inside an fMRI brain scanner and were asked to do complete a number of different musical exercises using a specially adapted magnet-friendly keyboard.

The musicians were asked to demonstrate musical scales, a pre-practised fixed piece, and an improvisation exercise while their brains were scanned.

A summary of the study by the John Hopkins medical school team gives the main results:

The scientists found that a region of the brain known as the dorsolateral prefrontal cortex, a broad portion of the front of the brain that extends to the sides, showed a slowdown in activity during improvisation. This area has been linked to planned actions and self-censoring, such as carefully deciding what words you might say at a job interview. Shutting down this area could lead to lowered inhibitions, Limb suggests.

The researchers also saw increased activity in the medial prefrontal cortex, which sits in the center of the brain’s frontal lobe. This area has been linked with self-expression and activities that convey individuality, such as telling a story about yourself.

Some years ago, psychiatrist Sean Spence suggested that Jazz music may have been born owing to the ‘the father of Jazz’, Buddy Bolden, having schizophrenia and suffering from associated frontal lobe impairments.

Spence argued that reduced frontal lobe function meant that Bolden could only improvise, as he didn’t have the cognitive control to stick to pre-learnt pieces.

At the time improvisation was considered a sign that you couldn’t play ‘proper music’ well enough, but Bolden took improvisation to a new level with wondrous flights of fancy and, as the legend goes, jazz was born. That’s not the whole story of course, but it’s possibly an ingredient.

While these new findings don’t give us much of a lead on whether this might have been the genuine beginning of jazz music, it’s interesting that the idea that reduced frontal lobe function ‘frees up’ the over-inhibited playing of set pieces, is consistent.

Link to PLoS One article on the cognitive neuroscience of Jazz.
Link to study summary.
Link to BBC News on Spence’s theory.

Behavioural Obamanomics

Theories are made great by those whom they inspire. Perhaps then, it is not surprising that the fresh new face of the US presidential race has been inspired by behavioural economics, one of the fresh new faces of cognitive science.

The New Republic magazine has an article on how the Obama campaign have adopted behavioural economics – the science of how people actually reason about money, as opposed to how they should – as their mainstay of economic policy.

Unsurprisingly, The New Republic, generally a centre-left publication, hold out great hope for the partnership of this new science and an Obama government.

You can find subtle evidence of this influence across numerous Obama proposals. For example, one key behavioral finding is that people often fail to set aside money for retirement even when their employers offer generous 401(k) plans. If, on the other hand, you automatically enroll workers in 401(k)s but allow them to opt out, most stick with it. Obama’s savings plan exploits this so-called “status quo” bias.

What is more interesting though is that cognitive science is starting to make inroads into policy development outside the traditional area of defence (where psychology, and more recently neuroscience, have traditionally been key in driving defence spending).

Link to The New Republic article ‘The Audacity of Data’.
Link to intro to behavioural economics (both via MeFi).

Chuck Close and perceptual Science

I just discovered the wonderfully perceptive artist Chuck Close did a cover for Science magazine back in 1999.

Close was renowned for doing huge super-realistic paintings of portrait photographs that seem more real than real. When you get up close you notice that he’s painted in insanely small details, like individual hairs that stretch into the background and blur as they become out of focus in the original photograph.

Painting this sort of detail on such a huge scale makes you question how real photographs really are, as it gives them an surreal quality despite looking like wonderful likenesses. It’s an uncanny perceptual effect.

In 1988, Close suffered a stroke in his spinal artery, restricting his movement and confining him to a wheelchair.

Close was determined to continue painting and thought about how he could still paint with his inability to do fine detail because of his damaged nervous system.

His later paintings, like the one featured on this cover, break down images almost into perceptual units. As you move away from them, they coalesce into photorealistic images.

His paintings lose a lot when you can’t see them in their original towering sizes, so if you ever get the chance to his work ‘live’, don’t miss it.

He’s a wonderful ‘perceptual explorer’ and a wry commentator on our photo obsessed age.

Link to BBC News article on Chuck Close cover.
Link to search of his pictures (just stunning).

The 7even sins of memory

PsyBlog has just finished its series on the ‘seven sins of memory’ that fade and distort what we try to remember, based on memory researcher Dan Schacter’s book on the same name.

The ‘seven sins’ are:

1. Transience
2. Absent-Mindedness
3. Blocking
4. Misattribution
5. Suggestibility
6. Bias
7. Persistence

And PsyBlog looks at each one, discussing what research has told of us about this particularly memory difficulty and how it affects our record of things past.

If you’re interested in reading more, Schacter’s 1999 book comes highly recommended.

Link to PsyBlog on the ‘Seven Sins of Memory’.

New antidepressants all bark and no bite?

The new generation antidepressants are no better than placebo in mild-moderate depression according to a new analysis of published and unpublished trials that were submitted during the drugs’ approval.

The study is published in PLoS Medicine and despite the huge headlines it has generated, is not entirely surprising.

Psychologist Irving Kirsch, who led this new research, has conducted several previous studies looking at the effectiveness of SSRI antidepressant drugs and found similar results, although this is the first time that the study has factored in the severity of depression.

This study focused on the drugs fluoxetine (Prozac), venlafaxine (Effexor), nefazodone (Serzone), and paroxetine (Seroxat or Paxil) and used the US Freedom of Information Act to request data on (mainly) negative trials that haven’t been published to complement the data set from published trials.

In this new analysis, only in severe depression did these medications show a distinct improvement over placebo, and this, the authors suggest, is because of the reduced placebo effect in the severely depressed, rather than than the fact that the medication has a differential effect in those most affected by mood disorders.

It’s important to note that the study didn’t show that the drugs had no effect in mild-moderate depression. They were all associated with an improvement in depression, but this was no different from placebo (a powerful effect in itself).

It’s also important to note that this finding doesn’t apply to all antidepressant drugs, and that it doesn’t apply to the use of these four drugs in all situations. They are also commonly prescribed for anxiety disorders which weren’t investigated in this study.

However, this is another example of how drug companies’ attempts to obscure data from negative trials are coming back to haunt them.

The Times has one of the best write-ups but as usual, the PLoS article has a jargon-free summary included so you can get the findings from the source even if you’re not familiar with scientific writing.

UPDATE: An important clarification from PJ, taken from the comments:

I think that by saying “this was no different from placebo” you are being misleading. Strictly speaking it was statistically different from placebo but did not reach the NICE criteria for a clinically significant difference:

“a three-point difference in Hamilton Rating Scale of Depression (HRSD)scores or a standardized mean difference (d) of 0.50”

Thanks PJ!

Link to full-text of PLoS Medicine paper.
Link to Times write-up.

Psychosis and the coming glutamate revolution

Dopamine has been the big player in understanding schizophrenia since antipsychotic drugs were discovered. All current antipsychotics have their main effect by blocking dopamine function in the mesolimbic pathway and there’s now significant evidence that this is the location of one of the major dysfunctions.

It’s been clear for a while that this isn’t the whole story though. Ketamine and PCP, two glutamate-focused drugs that barely touch the dopamine system directly, are heavily linked to schizophrenia and can intensify psychotic symptoms.

Findings such as these have sparked a flurry of interest in understanding the role of glutamate in psychosis, and there’s now an intense interest in developing drugs that might target this system.

One of the key hopes is that these newer drugs will have fewer side-effects, as, in some, antipsychotics are have unpleasant and unhealthy adverse consequences.

The New York Times has just published a great article on the development of these new drugs, just in mid-testing stage, and on the neuroscience that motivates them.

People who use PCP often have the hallucinations, delusions, cognitive problems and emotional flatness that are characteristic of schizophrenia. Psychiatrists noted PCP’s side effects as early as the late 1950s. But they lacked the tools to determine how PCP affected the brain until 1979, when they found that it blocked a glutamate receptor, called the NMDA receptor, that is at the center of the transmission of nerve impulses in the brain.

The PCP finding led a few scientists to begin researching glutamate’s role in psychosis and other brain disorders. By the early 1990s, they discovered that besides triggering the primary glutamate receptors — NMDA and AMPA — glutamate also triggered several other receptors.

They called these newly found receptors “metabotropic,” because the receptors modified the amount of glutamate that cells released rather than simply turning circuits on or off. Because glutamate is so central to the brain’s activity, directly blocking or triggering the NMDA and AMPA receptors can be very dangerous. The metabotropic receptors appeared to be better targets for drug treatment.

The article talks about some of the new drugs in development, and the fact that this is where drug companies are placing their (quite substantial) bets at the moment.

Link to NYT article ‘Daring to Think Differently About Schizophrenia’.

The Lobotomist documentary available online

After being put back from January, the fantastic documentary on Walter Freeman and the rise and fall of the frontal lobotomy is finally available to view online.

Unfortunately, it’s been cut up into little chunks and is only available as a Quicktime or Windows Media stream, which makes it a pain to watch and completely inaccessible to anyone not using Windows or Mac.

Needless to say, a better quality version is available on some torrent servers as a sensibly packaged video file and the healthiest torrent seems to be this one.

It’s a fantastically well-researched and balanced documentary, looking at the history of the procedure, Freeman’s over-identification with the operation and its abandonment as the problems became clear.

The tale is tragic for many reasons, not least of which is Freeman’s flawed personality and unwillingness to admit that the lobotomy was not the miracle cure he initially claimed.

There’s plenty more background information on the programme website and the Neurophilosophy article on the history of the procedure has some more details.

Link to The Lobotomist website and streamed version.
Link to Mininova torrent.