the Bactrian camel and prefrontal cortex: evidence from somatosensory function

I’ve been swamped with work lately, and don’t expect to see the light at the end of the tunnel for a few more weeks, so there won’t be any serious blogging here for the foreseeable future. But on a completely frivolous note, someone reminded me the other day of a cognitive neuroscience paper title generator I wrote a few years ago and had forgotten about. So I brushed it off and added a small amount of new content, and now it’s alive again here. I think it’s good for a few moments of entertainment, and occasionally produces a rare gem–like the one in the title of this post, or my all-time favorite, Neural correlates of nicotine withdrawal in infants.

Feel free to post any other winners in the comments…

trouble with biomarkers and press releases

The latest issue of the Journal of Neuroscience contains an interesting article by Ecker et al in which the authors attempted to classify people with autism spectrum disorder (ASD) and health controls based on their brain anatomy, and report achieving “a sensitivity and specificity of up to 90% and 80%, respectively.” Before unpacking what that means, and why you probably shouldn’t get too excited (about the clinical implications, at any rate; the science is pretty cool), here’s a snippet from the decidedly optimistic press release that accompanied the study:

“Scientists funded by the Medical Research Council (MRC) have developed a pioneering new method of diagnosing autism in adults. For the first time, a quick brain scan that takes just 15 minutes can identify adults with autism with over 90% accuracy. The method could lead to the screening for autism spectrum disorders in children in the future.”

If you think this sounds too good to be true, that’s because it is. Carl Heneghan explains why in an excellent article in the Guardian:

How the brain scans results are portrayed is one of the simplest mistakes in interpreting diagnostic test accuracy to make. What has happened is, the sensitivity has been taken to be the positive predictive value, which is what you want to know: if I have a positive test do I have the disease? Not, if I have the disease, do I have a positive test? It would help if the results included a measure called the likelihood ratio (LR), which is the likelihood that a given test result would be expected in a patient with the target disorder compared to the likelihood that the same result would be expected in a patient without that disorder. In this case the LR is 4.5. We’ve put up an article if you want to know more on how to calculate the LR.

In the general population the prevalence of autism is 1 in 100; the actual chances of having the disease are 4.5 times more likely given a positive test. This gives a positive predictive value of 4.5%; about 5 in every 100 with a positive test would have autism.

For those still feeling confused and not convinced, let’s think of 10,000 children. Of these 100 (1%) will have autism, 90 of these 100 would have a positive test, 10 are missed as they have a negative test: there’s the 90% reported accuracy by the media.

But what about the 9,900 who don’t have the disease? 7,920 of these will test negative (the specificity3 in the Ecker paper is 80%). But, the real worry though, is the numbers without the disease who test positive. This will be substantial: 1,980 of the 9,900 without the disease. This is what happens at very low prevalences, the numbers falsely misdiagnosed rockets. Alarmingly, of the 2,070 with a positive test, only 90 will have the disease, which is roughly 4.5%.

In other words, if you screened everyone in the population for autism, and assume the best about the classifier reported in the JNeuro article (e.g., that the sample of 20 ASD participants they used is perfectly representative of the broader ASD population, which seems unlikely), only about 1 in 20 people who receive a positive diagnosis would actually deserve one.

Ecker et al object to this characterization, and reply to Heneghan in the comments (through the MRC PR office):

Our test was never designed to screen the entire population of the UK. This is simply not practical in terms of costs and effort, and besides totally  unjustified- why would we screen everybody in the UK for autism if there is no evidence whatsoever that an individual is affected?. The same case applies to other diagnostic tests. Not every single individual in the UK is tested for HIV. Clearly this would be too costly and unnecessary. However, in the group of individuals that are test for the virus, we can be very confident that if the test is positive that means a patient is infected. The same goes for our approach.

Essentially, the argument is that, since people would presumably be sent for an MRI scan because they were already under consideration for an ASD diagnosis, and not at random, the false positive rate would in fact be much lower than 95%, and closer to the 20% reported in the article.

One response to this reply–which is in fact Heneghan’s response in the comments–is to point out that the pre-test probability of ASD would need to be pretty high already in order for the classifier to add much. For instance, even if fully 30% of people who were sent for a scan actually had ASD, the posterior probability of ASD given a positive result would still be only 66% (Heneghan’s numbers, which I haven’t checked). Heneghan nicely contrasts these results with the standard for HIV testing, which “reports sensitivity of 99.7% and specificity of 98.5% for enzyme immunoassay.” Clearly, we have a long way to go before doctors can order MRI-based tests for ASD and feel reasonably confident that a positive result is sufficient grounds for an ASD diagnosis.

Setting Heneghan’s concerns about base rates aside, there’s a more general issue that he doesn’t touch on. It’s one that’s not specific to this particular study, and applies to nearly all studies that attempt to develop “biomarkers” for existing disorders. The problem is that the sensitivity and specificity values that people report for their new diagnostic procedure in these types of studies generally aren’t the true parameters of the procedure. Rather, they’re the sensitivity and specificity under the assumption that the diagnostic procedures used to classify patients and controls in the first place are themselves correct. In other words, in order to believe the results, you have to assume that the researchers correctly classified the subjects into patient and control groups using other procedures. In cases where the gold standard test used to make the initial classification is known to have near 100% sensitivity and specificity (e.g., for the aforementioned HIV tests), one can reasonably ignore this concern. But when we’re talking about mental health disorders, where diagnoses are fuzzy and borderline cases abound, it’s very likely that the “gold standard” isn’t really all that great to begin with.

Concretely,  studies that attempt to develop biomarkers for mental health disorders face two substantial problems. One is that it’s extremely unlikely that the clinical diagnoses are ever perfect; after all, if they were perfect, there’d be little point in trying to develop other diagnostic procedures! In this particular case, the authors selected subjects into the ASD group based on standard clinical instruments and structured interviews. I don’t know that there are many clinicians who’d claim with a straight face that the current diagnostic criteria for ASD (and there are multiple sets to choose from!) are perfect. From my limited knowledge, the criteria for ASD seem to be even more controversial than those for most other mental health disorders (which is saying something, if you’ve been following the ongoing DSM-V saga). So really, the accuracy of the classifier in the present study, even if you put the best face on it and ignore the base rate issue Heneghan brings up, is undoubtedly south of the 90% sensitivity / 80% specificity the authors report. How much south, we just don’t know, because we don’t really have any independent, objective way to determine who “really” should get an ASD diagnosis and who shouldn’t (assuming you think it makes sense to make that kind of dichotomous distinction at all). But 90% accuracy is probably a pipe dream, if for no other reason than it’s hard to imagine that level of consensus about autism spectrum diagnoses.

The second problem is that, because the researchers are using the MRI-based classifier to predict the clinician-based diagnosis, it simply isn’t possible for the former to exceed the accuracy of the latter. That bears repeating, because it’s important: no matter how good the MRI-based classifier is, it can only be as good as the procedures used to make the original diagnosis, and no better. It cannot, by definition, make diagnoses that are any more accurate than the clinicians who screened the participants in the authors’ ASD sample. So when you see the press release say this:

For the first time, a quick brain scan that takes just 15 minutes can identify adults with autism with over 90% accuracy.

You should really read it as this:

The method relies on structural (MRI) brain scans and has an accuracy rate approaching that of conventional clinical diagnosis.

That’s not quite as exciting, obviously, but it’s more accurate.

To be fair, there’s something of a catch-22 here, in that the authors didn’t really have a choice about whether or not to diagnose the ASD group using conventional criteria. If they hadn’t, reviewers and other researchers would have complained that we can’t tell if the ASD group is really an ASD group, because they authors used non-standard criteria. Under the circumstances, they did the only thing they could do. But that doesn’t change the fact that it’s misleading to intimate, as the press release does, that the new procedure might be any better than the old ones. It can’t be, by definition.

Ultimately, if we want to develop brain-based diagnostic tools that are more accurate than conventional clinical diagnoses, we’re going to need to show that these tools are capable of predicting meaningful outcomes that clinician diagnoses can’t. This isn’t an impossible task, but it’s a very difficult one. One approach you could take, for instance, would be to compare the ability of clinician diagnosis and MRI-based diagnosis to predict functional outcomes among subjects at a later point in time. If you could show that MRI-based classification of subjects at an early age was a stronger predictor of receiving an ASD diagnosis later in life than conventional criteria, that would make a really strong case for using the former approach in the real world. Short of that type of demonstration though, the only reason I can imagine wanting to use a procedure that was developed by trying to duplicate the results of an existing procedure is in the event that the new procedure is substantially cheaper or more efficient than the old one. Meaning, it would be reasonable enough to say “well, look, we don’t do quite as well with this approach as we do with a full clinical evaluation, but at least this new approach costs much less.” Unfortunately, that’s not really true in this case, since the price of even a short MRI scan is generally going to outweigh that of a comprehensive evaluation by a psychiatrist or psychotherapist. And while it could theoretically be much faster to get an MRI scan than an appointment with a mental health professional, I suspect that that’s not generally going to be true in practice either.

Having said all that, I hasten to note that all this is really a critique of the MRC press release and subsequently lousy science reporting, and not of the science itself. I actually think the science itself is very cool (but the Neuroskeptic just wrote a great rundown of the methods and results, so there’s not much point in me describing them here). People have been doing really interesting work with pattern-based classifiers for several years now in the neuroimaging literature, but relatively few studies have applied this kind of technique to try and discriminate between different groups of individuals in a clinical setting. While I’m not really optimistic that the technique the authors introduce in this paper is going to change the way diagnosis happens any time soon (or at least, I’d argue that it shouldn’t), there’s no question that the general approach will be an important piece of future efforts to improve clinical diagnoses by integrating biological data with existing approaches. But that’s not going to happen overnight, and in the meantime, I think it’s pretty irresponsible of the MRC to be issuing press releases claiming that its researchers can diagnose autism in adults with 90% accuracy.

ResearchBlogging.orgEcker C, Marquand A, Mourão-Miranda J, Johnston P, Daly EM, Brammer MJ, Maltezos S, Murphy CM, Robertson D, Williams SC, & Murphy DG (2010). Describing the brain in autism in five dimensions–magnetic resonance imaging-assisted diagnosis of autism spectrum disorder using a multiparameter classification approach. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (32), 10612-23 PMID: 20702694

what the general factor of intelligence is and isn’t, or why intuitive unitarianism is a lousy guide to the neurobiology of higher cognitive ability

This post shamelessly plagiarizes liberally borrows ideas from a much longer, more detailed, and just generally better post by Cosma Shalizi. I’m not apologetic, since I’m a firm believer in the notion that good ideas should be repeated often and loudly. So I’m going to be often and loud here, though I’ll try to be (slightly) more succinct than Shalizi. Still, if you have the time to spare, you should read his longer and more mathematical take.

There’s a widely held view among intelligence researchers in particular, and psychologists more generally, that there’s a general factor of intelligence (often dubbed g) that accounts for a very large portion of the variance in a broad range of cognitive performance tasks. Which is to say, if you have a bunch of people do a bunch of different tasks, all of which we think tap different aspects of intellectual ability, and then you take all those scores and factor analyze them, you’ll almost invariably get a first factor that explains 50% or more of the variance in the zero-order scores. Or to put it differently, if you know a person’s relative standing on g, you can make a reasonable prediction about how that person will do on lots of different tasks–for example, digit symbol substitution, N-back, go/no-go, and so on and so forth. Virtually all tasks that we think reflect cognitive ability turn out, to varying extents, to reflect some underlying latent variable, and that latent variable is what we dub g.

In a trivial sense, no one really disputes that there’s such a thing as g. You can’t really dispute the existence of g, seeing as a general factor tends to fall out of virtually all factor analyses of cognitive tasks; it’s about as well-replicated a finding as you can get. To say that g exists, on the most basic reading, is simply to slap a name on the empirical fact that scores on different cognitive measures tend to intercorrelate positively to a considerable extent.

What’s not so clear is what the implications of g are for our understanding of how the human mind and brain works. If you take the presence of g at face value, all it really says is what we all pretty much already know: some people are smarter than others. People who do well in one intellectual domain will tend to do pretty well in others too, other things being equal. With the exception of some people who’ve tried to argue that there’s no such thing as general intelligence, but only “multiple intelligences” that totally fractionate across domains (not a compelling story, if you look at the evidence), it’s pretty clear that cognitive abilities tend to hang together pretty well.

The trouble really crops up when we try to say something interesting about the architecture of the human mind on the basis of the psychometric evidence for g. If someone tells you that there’s a single psychometric factor that explains at least 50% of the variance in a broad range of human cognitive abilities, it seems perfectly reasonable to suppose that that’s because there’s some unitary intelligence system in people’s heads, and that that system varies in capacity across individuals. In other words, the two intuitive models people have about intelligence seem to be that either (a) there’s some general cognitive system that corresponds to g, and supports a very large portion of the complex reasoning ability we call “intelligence” or (b) there are lots of different (and mostly unrelated) cognitive abilities, each of which contributes only to specific types of tasks and not others. Framed this way, it just seems obvious that the former view is the right one, and that the latter view has been discredited by the evidence.

The problem is that the psychometric evidence for g stems almost entirely from statistical procedures that aren’t really supposed to be use for causal inference. The primary weapon in the intelligence researcher’s toolbox has historically been principal components analysis (PCA) or exploratory factor analysis, which are really just data reduction techniques. PCA tells you how you can describe your data in a more compact way, but it doesn’t actually tell you what structure is in your data. A good analogy is the use of digital compression algorithms. If you take a directory full of .txt files and compress them into a single .zip file, you’ll almost certainly end up with a file that’s only a small fraction of the total size of the original texts. The reason this works is because certain patterns tend to repeat themselves over and over in .txt files, and a smart algorithm will store an abbreviated description of those patterns rather than the patterns themselves. Which, conceptually, is almost exactly what happens when you run a PCA on a dataset: you’re searching for consistent patterns in the way observations vary along multiple variables, and discarding any redundancy you come across in favor of a more compact description.

Now, in a very real sense, compression is impressive. It’s certainly nice to be able to email your friend a 140kb .zip of your 1200-page novel rather than a 2mb .doc. But note that you don’t actually learn much from the compression. It’s not like your friend can open up that 140k binary representation of your novel, read it, and spare herself the torture of the other 1860kb. If you want to understand what’s going on in a novel, you need to read the novel and think about the novel. And if you want to understand what’s going on in a set of correlations between different cognitive tasks, you need to carefully inspect those correlations and carefully think about those correlations. You can run a factor analysis if you like, and you might learn something, but you’re not going to get any deep insights into the “true” structure of the data. The “true” structure of the data is, by definition, what you started out with (give or take some error). When you run a PCA, you actually get a distorted (but simpler!) picture of the data.

To most people who use PCA, or other data reduction techniques, this isn’t a novel insight by any means. Most everyone who uses PCA knows that in an obvious sense you’re distorting the structure of the data when you reduce its dimensionality. But the use of data reduction is often defended by noting that there must be some reason why variables hang together in such a way that they can be reduced to a much smaller set of variables with relatively little loss of variance. In the context of intelligence, the intuition can be expressed as: if there wasn’t really a single factor underlying intelligence, why would we get such a strong first factor? After all, it didn’t have to turn out that way; we could have gotten lots of smaller factors that appear to reflect distinct types of ability, like verbal intelligence, spatial intelligence, perceptual speed, and so on. But it did turn out that way, so that tells us something important about the unitary nature of intelligence.

This is a strangely compelling argument, but it turns out to be only minimally true. What the presence of a strong first factor does tell you is that you have a lot of positively correlated variables in your data set. To be fair, that is informative. But it’s only minimally informative, because, assuming you eyeballed the correlation matrix in the original data, you already knew that.

What you don’t know, and can’t know, on the basis of a PCA, is what underlying causal structure actually generated the observed positive correlations between your variables. It’s certainly possible that there’s really only one central intelligence system that contributes the bulk of the variance to lots of different cognitive tasks. That’s the g model, and it’s entirely consistent with the empirical data. Unfortunately, it’s not the only one. To the contrary, there are an infinite number of possible causal models that would be consistent with any given factor structure derived from a PCA, including a structure dominated by a strong first factor. In fact, you can have a causal structure with as many variables as you like be consistent with g-like data. So long as the variables in your model all make contributions in the same direction to the observed variables, you will tend to end up with an excessively strong first factor. So you could in principle have 3,000 distinct systems in the human brain, all completely independent of one another, and all of which contribute relatively modestly to a bunch of different cognitive tasks. And you could still get a first factor that accounts for 50% or more of the variance. No g required.

If you doubt this is true, go read Cosma Shalizi’s post, where he not only walks you through a more detailed explanation of the mathematical necessity of this claim, but also illustrates the point using some very simple simulations. Basically, he builds a toy model in which 11 different tasks each draw on several hundred underlying cognitive tasks, which are turn drawn from a larger pool of 2,766 completely independent abilities. He then runs a PCA on the data and finds, lo and behold, a single factor that explains nearly 50% of the variance in scores. Using PCA, it turns out, you can get something huge from (almost) nothing.

Now, at this point a proponent of a unitary g might say, sure, it’s possible that there isn’t really a single cognitive system underlying variation in intelligence; but it’s not plausible, because it’s surely more parsimonious to posit a model with just one variable than a model with 2,766. But that’s only true if you think that our brains evolved in order to make life easier for psychometricians, which, last I checked, wasn’t the case. If you think even a little bit about what we know about the biological and genetic bases of human cognition, it starts to seem really unlikely that there really could be a single central intelligence system. For starters, the evidence just doesn’t support it. In the cognitive neuroscience literature, for example, biomarkers of intelligence abound, and they just don’t seem all that related. There’s a really nice paper in Nature Reviews Neuroscience this month by Deary, Penke, and Johnson that reviews a substantial portion of the literature of intelligence; the upshot is that intelligence has lots of different correlates. For example, people who score highly on intelligence tend to (a) have larger brains overall; (b) show regional differences in brain volume; (c) show differences in neural efficiency when performing cognitive tasks; (d) have greater white matter integrity; (e) have brains with more efficient network structures;  and so on.

These phenomena may not all be completely independent, but it’s hard to believe there’s any plausible story you could tell that renders them all part of some unitary intelligence system, or subject to unitary genetic influence. And really, why should they be part of a unitary system? Is there really any reason to think there has to be a single rate-limiting factor on performance? It’s surely perfectly plausible (I’d argue, much more plausible) to think that almost any complex cognitive task you use as an index of intelligence is going to draw on many, many different cognitive abilities. Take a trivial example: individual differences in visual acuity probably make a (very) small contribution to performance on many different cognitive tasks. If you can’t see the minute details of the stimuli as well as the next person, you might perform slightly worse on the task. So some variance in putatively “cognitive” task performance undoubtedly reflects abilities that most intelligence researchers wouldn’t really consider properly reflective of higher cognition at all. And yet, that variance has to go somewhere when you run a factor analysis. Most likely, it’ll go straight into that first factor, or g, since it’s variance that’s common to multiple tasks (i.e., someone with poorer eyesight may tend to do very slightly worse on any task that requires visual attention). In fact, any ability that makes unidirectional contributions to task performance, no matter how relevant or irrelevant to the conceptual definition of intelligence, will inflate the so-called g factor.

If this still seems counter-intuitive to you, here’s an analogy that might, to borrow Dan Dennett’s phrase, prime your intuition pump (it isn’t as dirty as it sounds). Imagine that instead of studying the relationship between different cognitive tasks, we decided to study the relation between performance at different sports. So we went out and rounded up 500 healthy young adults and had them engage in 16 different sports, including basketball, soccer, hockey, long-distance running, short-distance running, swimming, and so on. We then took performance scores for all 16 tasks and submitted them to a PCA. What do you think would happen? I’d be willing to bet good money that you’d get a strong first factor, just like with cognitive tasks. In other words, just like with g, you’d have one latent variable that seemed to explain the bulk of the variance in lots of different sports-related abilities. And just like g, it would have an easy and parsimonious interpretation: a general factor of athleticism!

Of course, in a trivial sense, you’d be right to call it that. I doubt anyone’s going to deny that some people just are more athletic than others. But if you then ask, “well, what’s the mechanism that underlies athleticism,” it’s suddenly much less plausible to think that there’s a single physiological variable or pathway that supports athleticism. In fact, it seems flatly absurd. You can easily think of dozens if not hundreds of factors that should contribute a small amount of the variance to performance on multiple sports. To name just a few: height, jumping ability, running speed, oxygen capacity, fine motor control, gross motor control, perceptual speed, response time, balance, and so on and so forth. And most of these are individually still relatively high-level abilities that break down further at the physiological level (e.g., “balance” is itself a complex trait that at minimum reflects contributions of the vestibular, visual, and cerebellar systems, and so on.). If you go down that road, it very quickly becomes obvious that you’re just not going to find a unitary mechanism that explains athletic ability. Because it doesn’t exist.

All of this isn’t to say that intelligence (or athleticism) isn’t “real”. Intelligence and athleticism are perfectly real; it makes complete sense, and is factually defensible, to talk about some people being smarter or more athletic than other people. But the point is that those judgments are based on superficial observations of behavior; knowing that people’s intelligence or athleticism may express itself in a (relatively) unitary fashion doesn’t tell you anything at all about the underlying causal mechanisms–how many of them there are, or how they interact.

As Cosma Shalizi notes, it also doesn’t tell you anything about heritability or malleability. The fact that we tend to think intelligence is highly heritable doesn’t provide any evidence in favor of a unitary underlying mechanism; it’s just as plausible to think that there are many, many individual abilities that contribute to complex cognitive behavior, all of which are also highly heritable individually. Similarly, there’s no reason to think our cognitive abilities would be any less or any more malleable depending on whether they reflect the operation of a single system or hundreds of variables. Regular physical exercise clearly improves people’s capacity to carry out all sorts of different activities, but that doesn’t mean you’re only training up a single physiological pathway when you exercise; a whole host of changes are taking place throughout your body.

So, assuming you buy the basic argument, where does that leave us? Depends. From a day-to-day standpoint, nothing changes. You can go on telling your friends that so-and-so is a terrific athlete but not the brightest crayon in the box, and your friends will go on understanding exactly what you meant. No one’s suggesting that intelligence isn’t stable and trait-like, just that, at the biological level, it isn’t really one stable trait.

The real impact of relaxing the view that g is a meaningful construct at the biological level, I think, will be in removing an artificial and overly restrictive constraint on researchers’ theorizing. The sense I get, having done some work on executive control, is that g is the 800-pound gorilla in the room: researchers interested in studying the neural bases of intelligence (or related constructs like executive or cognitive control) are always worrying about how their findings relate to g, and how to explain the fact that there might be dissociable neural correlates of different abilities (or even multiple independent contributions to fluid intelligence). To show you that I’m not making this concern up, and that it weighs heavily on many researchers, here’s a quote from the aforementioned and otherwise really excellent NRN paper by Deary et al reviewing recent findings on the neural bases of intelligence:

The neuroscience of intelligence is constrained by — and must explain — the following established facts about cognitive test performance: about half of the variance across varied cognitive tests is contained in general cognitive ability; much less variance is contained within broad domains of capability; there is some variance in specific abilities; and there are distinct ageing patterns for so-called fluid and crystallized aspects of cognitive ability.

The existence of g creates a complicated situation for neuroscience. The fact that g contributes substantial variance to all specific cognitive ability tests is generally thought to indicate that g contributes directly in some way to performance on those tests. That is, when domains of thinking skill (such as executive function and memory) or specific tasks (such as mental arithmetic and non-verbal reasoning on the Raven’s Progressive Matrices test) are studied, neuroscientists are observing brain activity related to g as well as the specific task activities. This undermines the ability to determine localized brain activities that are specific to the task at hand.

I hope I’ve convinced you by this point that the neuroscience of intelligence doesn’t have to explain why half of the variance is contained in general cognitive ability, because there’s no good evidence that there is such a thing as general cognitive ability (except in the descriptive psychometric sense, which carries no biological weight). Relaxing this artificial constraint would allow researchers to get on with the interesting and important business of identifying correlates (and potential causal determinants) of different cognitive abilities without having to worry about the relation of their finding to some Grand Theory of Intelligence. If you believe in g, you’re going to be at a complete loss to explain how researchers can continually identify new biological and genetic correlates of intelligence, and how the effect sizes could be so small (particularly at a genetic level, where no one’s identified a single polymorphism that accounts for more than a fraction of the observable variance in intelligence–the so called problem of “missing heritability”). But once you discard the fiction of g, you can take such findings in stride, and can set about the business of building integrative models that allow for and explicitly model the presence of multiple independent contributions to intelligence. And if studying the brain has taught us anything at all, it’s that the truth is inevitably more complicated than what we’d like to believe.

in praise of (lab) rotation

I did my PhD in psychology, but in a department that had close ties and collaborations with neuroscience. One of the interesting things about psychology and neuroscience programs is that they seem to have quite different graduate training models, even in cases where the area of research substantively overlaps (e.g., in cognitive neuroscience). In psychology, there seem two be two general models (at least, at American and Canadian universities; I’m not really familiar with other systems). One is that graduate students are accepted into a specific lab and have ties to a specific advisor (or advisors); the other, more common at large state schools, is that graduate students are accepted into the program (or an area within the program) as a whole, and are then given the (relative) freedom to find an advisor they want to work with. There are pros and cons to either model: the former ensures that every student has a place in someone’s lab from the very beginning of training, so that no one falls through the cracks; but the downside is that beginning students often aren’t sure exactly what they want to work on, and there are occasional (and sometimes acrimonious) mentor-mentee divorces. The latter gives students more freedom to explore their research interests, but can make it more difficult for students to secure funding, and has more of a sink-or-swim flavor (i.e., there’s less institutional support for students).

Both of these models differ quite a bit from what I take to be the most common neuroscience model, which is that students spend all or part of their first year doing a series of rotations through various labs–usually for about 2 months at a time. The idea is to expose students to a variety of different lines of research so that they get a better sense of what people in different areas are doing, and can make a more informed judgment about what research they’d like to pursue. And there are obviously other benefits too: faculty get to evaluate students on a trial basis before making a long-term commitment, and conversely, students get to see the internal workings of the lab and have more contact with the lab head before signing on.

I’ve always thought the rotation model makes a lot of sense, and wonder why more psychology programs don’t try to implement one. I can’t complain about my own training, in that I had a really great experience on both personal and professional levels in the labs I worked in; but I recognize that this was almost entirely due to dumb luck. I didn’t really do my homework very well before entering graduate school, and I could easily have landed in a department or lab I didn’t mesh well with, and spent the next few years miserable and unproductive. I’ll freely admit that I was unusually clueless going into grad school (that’s a post for another time), but I think no matter how much research you do, there’s just no way to know for sure how well you’ll do in a particular lab until you’ve spent some time in it. And most first-year graduate students have kind of fickle interests anyway; it’s hard to know when you’re 22 or 23 exactly what problem you want to spend the rest of your life (or at least the next 4 – 7 years) working on. Having people do rotations in multiple labs seems like an ideal way to maximize the odds of students (and faculty) ending up in happy, productive working relationships.

A question, then, for people who’ve had experience on the administrative side of psychology (or neuroscience) departments: what keeps us from applying a rotation model in psychology too? Are there major disadvantages I’m missing? Is the problem one of financial support? Do we think that psychology students come into graduate programs with more focused interests? Or is it just a matter of convention? Inquiring minds (or at least one of them) want to know…