Thursday, May 31, 2007

The HOT or NOT "Social Attention" Study

OR, "why men are much greater consumers of pornography than women."

Dr Petra? Dr Petra...? Paging Dr Petra... Too bad she's on vacation, she would certainly have a field day with this news story (and the original research that spawned it):
Why men like to gaze on the female form
By Roger Highfield, Science Editor

Men find photos of the opposite sex much more "rewarding" than women, new research claims today.

According to the study men take the same pleasure out of looking at an attractive female form as they do from having a curry or making money whereas women do not take any significant reward from looking at pictures of men.

The survey published in the journal Proceedings of the Royal Society B said that brain scan studies show that "reward centres" are triggered in men when they gaze at a woman's face or body whereas they are not in females. It also shows men are more likely to make an effort to view pictures of the opposite sex and pay out money.

The findings shed light on why men are much greater consumers of pornography than women and why sales of Playboy have always exceeded those of Playgirl, according to Dr Benjamin Hayden at the Centre for Neuroeconomic Studies, Duke University School of Medicine, Durham, North Carolina.

. . .

Yes, the experiment by Hayden and colleagues (2007) actually did use images taken from the HOT or NOT site:

Two databases were generated containing over 2000 male and 2000 female images. All images were downloaded from the Hotornot web site ( in July 2006. This publicly accessible web site allows anyone to post a photo and receive average attractiveness ratings from the browsing public. We selected images that had only a single central subject with a clearly visible face. We eliminated photos which were blurry or small, photos with animals or displays of wealth, photos in which emotionally salient objects such as guns, snakes or motorcycles were visible, photos with subjects in provocative sexual positions or with nudity and photos in which the subjects appeared to be younger than 18 years old.

We ignored the web site's posted ratings and reassessed attractiveness in a laboratory environment. Eleven males each rated all 2000 female photographs in the female database. Eleven females each rated all 2000 male photographs in the male database. Raters were not used as test subjects in subsequent experiments. Ratings were made on a PC using a program that displayed each photo for 1s and then waited for a rating. Raters could press a button to view each photograph again. The instructions asked raters to rate each image for attractiveness on a scale from 1 to 10.

Note that none of the images were pornographic in nature, but that didn't stop Mr. Highfield from extrapolating the results to purchases of Playboy. The Daily Telegraph article also leads you to believe it's a neuroimaging study, but it's not.
Hayden BY, Parikh PC, Deaner RO, Platt ML. Economic principles motivating social attention in humans. Proc Biol Sci. 2007 May 8; [Epub ahead of print].

We know little about the processes by which we evaluate the opportunity to look at another person. We propose that behavioural economics provides a powerful approach to understanding this basic aspect of social attention. We hypothesized that the decision process culminating in attention to another person follows the same economic principles that govern choices about rewards such as food, drinks and money. Specifically, such rewards are discounted as a function of time, are tradable for other rewards, and reinforce work. Behavioural and neurobiological evidence suggests that looking at other people can also be described as rewarding, but to what extent these economic principles apply to social orienting remains unknown. Here, we show that the opportunity to view pictures of the opposite sex is discounted by delay to viewing, substitutes for money and reinforces work. The reward value of photos of the opposite sex varied with physical attractiveness and was greater in men, suggesting differential utility of acquiring visual information about the opposite sex in men and women. Together, these results demonstrate that choosing whom to look at follows a general set of economic principles, implicating shared neural mechanisms in both social and non-social decision making.
It won't be long before we see the fMRI version.

ADDENDUM: for a discussion of this paper by an economist, see purple motes.

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Tuesday, May 29, 2007

C'mon, Aren't Faces REALLY Special?

A recently published paper in Nature Neuroscience by Thierry and colleagues (2007) claimed that faces really aren't that special after all, particularly where the N170 component is concerned. The Neurocritic covered this article (perhaps a little too UNcritically) back in March: Are Faces Special? Fellow bloggers at The Phineas Gage Fan Club and Cognitive Daily also posted about the paper. What did it claim to show? Let's review some material from a previous post.
An ever-controversial topic in the field of high-level vision and object recognition is the question of whether faces have a privileged status relative to other objects, processed by a special modular region of ventral temporal cortex called the fusiform face area (Kanwisher et al., 1997; Kanwisher & Yove, 2006; McKone et al., 2007), or whether faces are just one example of a stimulus class that requires substantial expertise in order to distinguish between similar exemplars (Gauthier et al., 1999, 2000; Gauthier & Bukach, 2007). A new article in Nature Neuroscience tackles this issue and comes up with a surprising answer.

Thierry and colleagues (2007) recorded event-related potentials (ERPs), which are synchronized brain waves time-locked to the occurrence of particular stimuli or events. In particular, the N170 component is thought to be a highly specific ERP response to faces (as opposed to other objects) that shows a peak at 170 msec after stimulus presentation (Bentin et al, 1996).

Bentin et al. (1996)
In the new NN paper, Thierry et al. argue that previous studies of the N170 component did not adequately control for variability across stimulus classes, i.e., face stimuli have been much more similar to each other than the non-face stimuli.
The bottom line was that if interstimulus perceptual variance was adequately controlled across stimulus classes, the specificity of N170 for faces went away. [But an even earlier component, P1, popped up to discriminate between faces and cars. This wasn't adequately explained.]

But wait! There are problems with this paper -- as outlined by Bruno Rossion from the Face Categorisation Lab in Belgium -- not the least of which is that Thierry et al. didn't adequately control for interstimulus variance in their own study! His reply (and perhaps others) will appear in a future issue of Nature Neuroscience. Watch his web site (and this space) for an update as it occurs. As for now, you can read Bruno's comments here.


Thierry G, Martin CD, Downing P, Pegna AJ (2007). Controlling for interstimulus perceptual variance abolishes N170 face selectivity. Nature Neuroscience 10:505-511.

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Sunday, May 27, 2007

Weird Psychiatric Disorder Day

This morning's brief movie capsule didn't explain either delusional parasitosis or folie à deux. Wikipedia says that
Delusional parasitosis is a form of psychosis in which sufferers hold a delusional belief they are infested with parasites.
Mind Hacks has the best description of this bizarre condition in The curious case of Morgellons disease:
Morgellons is claimed to be a new form of skin disease by its sufferers but has been largely ignored by the medical community and some have claimed it is, in reality, a psychotic syndrome akin to delusional parasitosis.
Michael Shannon's character in Bug suffered from delusions that far exceeded mere aphid infestation, and he easily persuaded his drunk, drug-using, desperate and lonely new girlfriend (Ashley Judd) that the tiny bugs were real, so that she spiraled down with him in a folie à deux:
(literally, "a madness shared by two") is a rare psychiatric syndrome in which a symptom of psychosis (particularly a paranoid or delusional belief) is transmitted from one individual to another. ... Recent psychiatric classifications refer to the syndrome as shared psychotic disorder (DSM-IV) (297.3) and induced delusional disorder (folie à deux) (F.24) in the ICD-10, although the research literature largely uses the original name.
The director was William Friedkin, of The Exorcist fame, so be prepared for some over-the-top gory scenes of self-mutilation and self-dentistry (as well as some dark humor and romantic love).

Bug (2006) - Brian F. O'Byrne, Michael Shannon

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Delusional Parasitosis AND Folie a Deux!

In one movie! In a word, Bug.

Bug (2006) - Michael Shannon, Ashley Judd

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Thursday, May 24, 2007

Synesthetes Show Greater Connectivity in the Inferior Temporal Cortex

Ah ah
Something ain't right
I'm gonna get myself
I'm gonna get myself
I'm gonna get myself connected

--Stereo MC's, Connected

SYNESTHESIA can be defined as unusual conscious experience, in which stimulation of one sensory modality leads to a sensory experience in a second, unstimulated sensory modality. For example, seeing letters might lead some people to see colors.
Previous neuroimaging studies have observed activations in V4 (a color processing region of visual cortex) when "colored hearing" synesthetes listened to spoken words (Nunn et al., 2002; Paulesu et al., 1995) and when grapheme-color synethetes viewed letters (Hubbard et al., 2005; Sperling et al., 2006). It has long been hypothesized (Ramachandran & Hubbard, 2001), but never proven, that people with synesthetic abilities have an unusual degree of connectivity between the brain regions involved in coding two (or more) sensory modalities. A brand new study by Rouw and Scholte (2007) used diffusion tensor imaging, a magnetic resonance imaging method that provides images of white matter tracts, to demonstrate just that. Although the authors found increased anisotropy in multiple areas [explained by hand-waving], indicative of greater connectivity, they emphasized the differences in inferior temporal cortex because of its role in processing color and letter/word stimuli.
Increased diffusion anisotropy reflects increased or more coherent connectivity due to microstructural aspects such as degree of myelination, axonal diameter, and density and coherence in fiber orientation as well as macrostructural features such as intravoxel fiber-tract coherence.

Figure 2. Increased brain activation and increased anisotropy in the inferior temporal cortex in grapheme-color synesthetes. The white matter skeleton (green) is projected on an MNI brain (grayscale). Greater BOLD signal (blue) as well as greater anisotropy (yellow) underlie synesthetic experiences in color-grapheme synesthesia. [from Rouw & Scholte, 2007]
Rouw R & Scholte HS (2007). Increased structural connectivity in grapheme-color synesthesia. Nature Neuroscience. Published online: 21 May 2007.

Diffusion tensor imaging allowed us to validate for the first time the hypothesis that hyperconnectivity causes the added sensations in synesthesia. Grapheme-color synesthetes (n = 18), who experience specific colors with particular letters or numbers (for example, 'R is sky blue'), showed greater anisotropic diffusion compared with matched controls. Greater anisotropic diffusion indicates more coherent white matter. Anisotropy furthermore differentiated subtypes of grapheme-color synesthesia. Greater connectivity in the inferior temporal cortex was particularly strong for synesthetes who see synesthetic color in the outside world ('projectors') as compared with synesthetes who see the color in their 'mind's eye' only ('associators'). In contrast, greater connectivity (as compared with non-synesthetes) in the superior parietal or frontal cortex did not differentiate between subtypes of synesthesia. In conclusion, we found evidence that increased structural connectivity is associated with the presence of grapheme-color synesthesia, and has a role in the subjective nature of synesthetic color experience.
Or, as this witty headline puts it, it's a...
Red-letter day for brain connectivity
More neural connections may explain synesthesia
Staff Writers 21/05/2007 11:24:24

People with grapheme-colour synesthesia - who see a cascade of colours associated with individual letters when looking at a page of text - appear to have more neural connections in areas of the brain involved in word processing and binding perceptions together, a new study shows.

Hubbard EM, Arman AC, Ramachandran VS, Boynton GM. (2005). Individual differences among grapheme-color synesthetes: brain-behavior correlations. Neuron 45:975-85.

Nunn JA, Gregory LJ, Brammer M, Williams SC, Parslow DM, Morgan MJ, Morris RG, Bullmore ET, Baron-Cohen S, Gray JA. (2002). Functional magnetic resonance imaging of synesthesia: activation of V4/V8 by spoken words. Nat Neurosci. 5:371-5.

Paulesu E, Harrison J, Baron-Cohen S, Watson JD, Goldstein L, Heather J, Frackowiak RS, Frith CD. (1995). The physiology of coloured hearing. A PET activation study of colour-word synaesthesia. Brain 118:661-76.

Ramachandran VS & Hubbard, EM. (2001). Psychophysical investigations into the neural basis of synaesthesia. Proc. R. Soc. Lond. B 268:979–983.

Rich AN, Williams MA, Puce A, Syngeniotis A, Howard MA, McGlone F, Mattingley JB. (2006). Neural correlates of imagined and synaesthetic colours. Neuropsychologia 44:2918-25.

If you make sure you're connected
The writing's on the wall
But if your mind's neglected
Stumble you might fall
Stumble you might fall
Stumble you might fall

--Stereo MC's, Connected

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Monday, May 21, 2007

Neurobiological Correlates of Melbourne-Sydney Rivalry

You think I made this up? I can't find the article online yet, but here's the abstract.
Velakoulis D, Fornito A, Walterfang M, Malhi G, Yucel M, Pantelis C. (2007). A tale of two cities: a neuroimaging investigation of Melbourne-Sydney rivalry comparing cortical thickness in healthy adults. Australas Psychiatry 15(1):67-71.

OBJECTIVE: We sought to identify neurobiological correlates of Melbourne-Sydney rivalry through neuroimaging measures of a key brain region involved in cognitive and emotional regulation. METHOD: Twenty subjects from each city were recruited from two large neuroimaging databases, and were scanned on a GE Signa 1.5 T magnetic resonance imaging scanner. Cortical thickness of the anterior cingulate cortex (ACC) was measured using a tessellated mesh method, after image segmentation. These measures were compared with key sporting, financial and academic variables. RESULTS: Residents of Melbourne had a significantly thicker ACC (p less than 0.0001) than Sydney residents, and this difference remained significant when age and intracranial volume were controlled for (p = 0.001). This difference mirrored that in variables measuring wealth, sporting and academic success. CONCLUSIONS: The thinner ACC seen in Sydney-siders may reflect the effects of increased stress due to elevated property prices, relative lack of sporting success and other variables. An alternative explanation is that a thinner ACC is the result of increasing cortical refinement and efficiency, and a marker of a more mature city. However, if these findings are a result of latitudinal effects, this may have significant implications for residents of more northern regions of the Australian continent.
[NOTE: the authors are from the Melbourne Neuropsychiatry Centre, University of Melbourne, Melbourne, Vic, Australia.]

Perhaps the current issue of Australasian Psychiatry is similar to the (semi-)joke issue published by the British Medical Journal around Christmas...

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NAcc Localization for DBS

The topographical location of the nucleus accumbens in relation to other brain structures on a horizontal plane 3 mm below the AC-PC plane (Schlaepfer et al., 2007).

As the previous post discussed, the nucleus accumbens (NAcc) is an experimental target for deep brain stimulation in severe forms of depression that have failed to respond to other treatments such as psychotherapy, antidepressants (and other drugs), and the ever-controversial electroconvulsive therapy, or ECT [see current edit wars at Wikipedia].

Position of deep brain stimulation electrodes

The location of the lowest contact of the stimulation electrode in a horizontal and coronal plane with projections of the left (green) and right (yellow) electrode path in the surgical planning stage. Stereotaxic coordinates are 1.5 mm rostral to the anterior edge of the anterior commissure, measured at the crossing point, 4 mm ventral and 7–8 mm lateral of the midline of the third ventricle. Burr holes were placed deep fronto laterally (Schlaepfer et al., 2007).

Theoretical motivations behind the procedure:
We believe that DBS to the ventral striatum, and in particular, the nucleus accumbens, will be a promising and efficacious treatment of severe depression. Our hypothesis is based on three lines of reasoning: (1) the ventral striatum is heavily implicated in both normal and abnormal reward processes, (2) the nucleus accumbens acts as a 'motivation gateway' between limbic systems involved in emotion and systems involved in motor control, and (3) the ventral striatum is uniquely located to modulate activity in other regions of the brain.
The case histories of the three patients included in the trial are predictably, well, depressing in their inability to obtain relief from any other form of treatment:
Patient 01 is a 66-year-old woman suffering from major depression since age 21. The current depression episode was her sixth, and lasted for 17 months. During the current episode, the patient failed seven antidepressant medication trials, and augmentation with five different neuroleptics also failed. The patient did not respond to both an adequate trial of psychotherapy and 13 treatments of bilateral ECT. At study entry the patient was severely depressed, with a Hamilton Depression scale (HDRS24) score of 38. At study entry she was treated with 90 mg duloxetine, 1 mg risperidone, 10 mg diazepam, 75 mg L-thyroxin, and 75 mg melperone.

Patient 02
is a 37-year-old unemployed university graduate (economics). The current episode was his second, and began 9 years ago. Seventeen different antidepressant medication treatments have failed, as did augmentation with five neuroleptics and lithium. The patient had four courses of unsuccessful ECT treatments with at least 10 treatment sessions (twice unilateral, twice bilateral), and psychotherapy was tried, again to no avail. At study entry he was treated with 50 mg quietapine and 75 mg amitryptiline.

Patient 03 is the 37-year-old monozygotic twin brother of patient 02; unipolar major depression had developed in both patients in almost exactly the same way at the same time, he had the same professional education and current state as his brother. His current episode began 11 years ago, and this patient has been unsuccessfully treated with at least eight antidepressant medications, and augmentation with at least three neuroleptics and with lithium failed. The patient had two ECT treatment courses (one unilateral and one bilateral), comprising 10 and 15 treatment sessions, respectively, with no success, and psychotherapy also failed. ... At study entry they were severely depressed (HDRS24 score of 31 and 32). At study entry he was treated with 50 mg quietapine, 150 mg amitryptiline, and 75 mg L-thyroxin.
The stimulator was turned on and off in a double-blind fashion, and...

Clinical ratings improved in all three patients when the stimulator was on, and worsened in all three patients when the stimulator was turned off. These effects were immediate and bi-directional (eg when the stimulator was turned off, depression ratings immediately worsened, and when the stimulator was turned on, depression ratings immediately improved).

The figure to the left shows that each patients' score on depression rating scales, MADRAS (Montgomery-Åsberg Depression Rating Scale) and HDRS24 (Hamilton Depression Rating Scale, 24-item version) -- shown in red and green lines, respectively -- fell when the stimulator was on (shown in purple line and indicated by gray shading).

Finally, PET imaging was performed before and after stimulation to examine which brain areas responded to the treatment. Predictably, after one week of stimulation, greater blood flow was observed in the NAcc. Metabolism also increased in dorsolateral and dorsomedial prefrontal cortex and in the amygdala [?? - which one might expect is overactive already in depression; see Drevets, 1999] but decreased in ventrolateral and ventromedial prefrontal cortex, caudate, and thalamus.

Caveats? Limitations?
These findings should be taken as very preliminary at the clinical level. We certainly do not suggest that DBS to the nucleus accumbens is a 'magic bullet' procedure that will cure depression.

Drevets WC. (1999). Prefrontal cortical-amygdalar metabolism in major depression. Ann NY Acad Sci. 877:614-37.

Schlaepfer TE, Cohen MX, Frick C, Kosel M, Brodesser D, Axmacher N, Joe AY, Kreft M, Lenartz D, Sturm V. Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression. Neuropsychopharmacology 2007 Apr 11; [Epub ahead of print]

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Friday, May 18, 2007

More About the Nucleus Accumbens

When the cortex has received and processed a sensory stimulus indicating a reward, it sends a signal announcing this reward to a particular part of the midbrain–the ventral tegmental area (VTA)–whose activity then increases. The VTA then releases dopamine not only into the nucleus accumbens, but also into the septum, the amygdala, and the prefrontal cortex.

The nucleus accumbens then activates the individual’s motor functions, while the prefrontal cortex focuses his or her attention.
And now we return to our continuing [plodding] coverage of the 2007 meeting of the Cognitive Neuroscience Society.

In today's installment, we'll learn about:

Deep Brain Stimulation in the Nucleus Accumbens for Major Depression

Previously, The Neurocritic has written about deep brain stimulation of area 25 in the ventral anterior cingulate cortex as a treatment for intractable depression:

The Sad Cingulate

Sad Cingulate on 60 Minutes and in Rats

I hadn't heard of the nucleus accumbens (NAcc) as a DBS target region, but it makes sense from the standpoint of anhedonia (inability to experience pleasure from normally pleasurable life events) in major depression. Why not stimulate the "pleasure center" when you're feeling blue? Extensive research in animals and humans has demonstrated "hedonic hot spots" (Pecina et al., 2006) in the NAcc that respond to food and pharmaceutical and financial and... er uh sexual rewards (Knutson & Cooper, 2005).

The poster presented at the meeting actually had nothing to do with the clinical efficacy of DBS in the NAcc, but the fact that electrodes were implanted there allowed the authors (Cohen et al., 2007, based in Germany) to record neuronal activity from the human NAcc, quite a rare opportunity. In their experiment, EEG activity (local field potentials) was recorded in the NAcc while the patients performed a reward-based learning task (choose a coin: one rewards 75% of the time, the other 25%) with periodic reversals of the contingencies. Frequency information and event-related potentials (ERPs) were extracted from the data (see below).

Michael Cohen1, Nikolai Axmacher2, Roshan Cools3, Doris Lenartz4, Christian Elger2, Volker Sturm4, Thomas Schlaepfer2.

1UC Davis, 2University of Bonn, Germany, 3University of Cambridge, 4University of Cologne, Germany — The nucleus accumbens acts as a "gateway" between motivation and action: It receives inputs from limbic structures involved in emotion (i.e., amygdala and orbitofrontal cortex) and projects to structures involved in action selection and behavioral control (i.e., basal ganglia output structures). Studying the human nucleus accumbens is difficult because of limitations in spatial and temporal resolution of neuroimaging techniques such as PET and fMRI. To overcome these limitations, we recorded local field potentials from the nucleus accumbens of patients undergoing Deep Brain Stimulation for treatment of major depression. Electrodes were implanted into the nucleus accumbens, and before stimulation began, externalized leads were used to record electrical potentials. We recorded these potentials while patients engaged in a reward-based reversal learning task, in which patients could maximize their rewards by learning to adapt their behavior to changes in reinforcement contingencies. Behaviorally, patients quickly adapted their decision-making to maximize rewards, demonstrating that reinforcement learning circuits remained intact. ERPs from around 300-400 ms following feedback differentiated wins from losses, and predicted whether patients would choose the same or the opposite decision option on the following trial as on the current trial. Frequency decomposition revealed enhanced power in the gamma frequency band from 100-400 ms following feedback onset, and increased alpha band activity following wins compared to losses. The spatial and temporal resolution of these electrophysiological recordings provide novel insights into the function of the nucleus accumbens' role in using reinforcement information to guide behavior.
What about the clinical aspects? Did the patients improve after DBS? Yes. Although a very preliminary study in only 3 patients, all showed clinical improvement when the stimulator was on, compared to when it was off (Schlaepfer et al., 2007).
Schlaepfer TE, Cohen MX, Frick C, Kosel M, Brodesser D, Axmacher N, Joe AY, Kreft M, Lenartz D, Sturm V. Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression. Neuropsychopharmacology. 2007 Apr 11; [Epub ahead of print]

Deep brain stimulation (DBS) to different sites allows interfering with dysfunctional network function implicated in major depression. Because a prominent clinical feature of depression is anhedonia-the inability to experience pleasure from previously pleasurable activities-and because there is clear evidence of dysfunctions of the reward system in depression, DBS to the nucleus accumbens might offer a new possibility to target depressive symptomatology in otherwise treatment-resistant depression. Three patients suffering from extremely resistant forms of depression, who did not respond to pharmacotherapy, psychotherapy, and electroconvulsive therapy, were implanted with bilateral DBS electrodes in the nucleus accumbens. Stimulation parameters were modified in a double-blind manner, and clinical ratings were assessed at each modification. Additionally, brain metabolism was assessed 1 week before and 1 week after stimulation onset. Clinical ratings improved in all three patients when the stimulator was on, and worsened in all three patients when the stimulator was turned off. Effects were observable immediately, and no side effects occurred in any of the patients. Using FDG-PET, significant changes in brain metabolism as a function of the stimulation in fronto-striatal networks were observed. No unwanted effects of DBS other than those directly related to the surgical procedure (eg pain at sites of implantation) were observed. Dysfunctions of the reward system-in which the nucleus accumbens is a key structure-are implicated in the neurobiology of major depression and might be responsible for impaired reward processing, as evidenced by the symptom of anhedonia. These preliminary findings suggest that DBS to the nucleus accumbens might be a hypothesis-guided approach for refractory major depression.
To be continued....


Pecina S, Smith KS, Berridge KC. (2006). Hedonic hot spots in the brain. Neuroscientist 12:500-11.

Knutson B, Cooper JC. Functional magnetic resonance imaging of reward prediction. (2005). Curr Opin Neurol. 18:411-7.

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Wednesday, May 16, 2007

Triple Track Razor...

Image from: Cubic Awareness Online
Richard Janczarski, webmaster

"Religious beliefs are irrational and invalid. They cannot be considered to be true. Their supernatural elements are superfluous, lacking real basis: therefore, Occam's Razor rejects them."
(Occam's Razor is a rational principle. For more rationality, see The Rational Belief.)"

...''Because you'll believe anything.''
ONCE upon a time, razors with multiple blades were a joke. The first broadcast of "Saturday Night Live" included a mock commercial for the "Triple Track," a three-bladed razor, featuring the slogan: "Because you'll believe anything."

--Nick Berns, Skin Deep; Shaving With Five Blades When Maybe Two Will Do
Chris at Developing Intelligence has an interesting post on Why The Simplest Theory Is [Almost] Never The Right One, in which he suggests that Occam's Razor isn't a very useful principle in the life sciences, developmental psychology, or cognitive neuroscience. A heated and lively discussion ensues in the comments.
Sweet and divine
Razor of mine
Sweet and divine
Razorblade shine

--Foo Fighters, Razor
What is Occam's Razor?
Occam's razor (sometimes spelled Ockham's razor) is a principle attributed to the 14th-century English logician and Franciscan friar William of Ockham. The principle states that the explanation of any phenomenon should make as few assumptions as possible, eliminating, or "shaving off," those that make no difference in the observable predictions of the explanatory hypothesis or theory.
[As an aside, I always thought that parsimony was overrated...]

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Tuesday, May 15, 2007


Television evangelist Falwell dies at 73

By SUE LINDSEY, Associated Press Writer

LYNCHBURG, Va. - The Rev. Jerry Falwell, the folksy, small-town preacher who used the power of television to found the Moral Majority and turn the Christian right into a mighty force in American politics during the Reagan years, died Tuesday at 73.

. . .

Tinky Winky
Over the years, Falwell waged a landmark libel case against Hustler magazine founder Larry Flynt over a raunchy parody ad, and created a furor in 1999 when one of his publications suggested that the purse-carrying "Teletubbies" character Tinky Winky was gay.
Not to make light of anyone's death (and condolences to his family and friends), but Falwell was known for blaming...
the pagans, and the abortionists, and the feminists, and the gays and the lesbians who are actively trying to make that an alternative lifestyle, the ACLU, People For the American Way, all of them who have tried to secularize America.
...for the attacks of 9/11/01.
I point the finger in their face and say 'you helped this happen.'
And Tinky Winky too.

UPDATE: Tinky Winky says bye-bye to Jerry Falwell

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Monday, May 14, 2007

Is It Bad To Gamble When Sleep Deprived?

In the annals of the incredibly obvious, researchers have shown that "late-night gambling is a risky game":

Obviousman by Wiley Miller
Blame boneheaded bets on your tired brain
Scientists pinpoint why late-night gamblers lose big time

By Linda Carroll

. . .

Scientists set up experiments in which people have a choice between a high-risk gamble with the opportunity for a big payout and a low-risk option that offers the prospect of more moderate gain. They compared the decisions made by well-rested gamblers and those who’ve been up for hours on end.

Sure enough, the studies showed that when sleep is curtailed, people are drawn to risky, but high-paying, options.
Was it really that incredibly obvious? No. That is not what the study by Venkatraman et al. (2007) showed at all:
There was no significant difference in risk preference between the 2 states. Subjects earned an average bonus of $35.50 (SD = $6.71) for the rested-wakefulness session and $35.70 (SD = $10.08) for the sleep-deprivation session.
To be fair, though, the authors did brain scans on these sleepy gamblers to assess changes in gain/loss sensitivity with sleep deprivation, and other media outlets were a little less tabloid-ish with their headlines (and more accurate in their reporting):
Sleep Deprivation Can Threaten Competent Decision-making

. . .

The authors found that the nucleus accumbens, an area in the brain involved with the anticipation of reward, becomes selectively more active when high risk-high payoff choices were made under conditions of sleep deprivation. Further, the number of high risk decisions did not increase with sleep deprivation, but the expectation of being rewarded for making the high risk gamble was elevated. Allied to this finding was the observation that there was an attenuated response to losses in the insula, a part of the brain involved with evaluating the emotional significance of an event.
Stay tuned for more on the nucleus accumbens!


Vinod Venkatraman, YM Lisa Chuah, Scott A Huettel, Michael WL Chee (2007). Sleep Deprivation Elevates Expectation of Gains and Attenuates Response to Losses Following Risky Decisions. Sleep 30:603-609

Johnny Depp in Fear and Loathing in Las Vegas

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Friday, May 11, 2007

The Overuse Theory of Alzheimer's Disease

"Past and Future Self" by Austin Houldsworth
Exploring the parallels between an expanding/contracting universe and human development.
Shown at the 2006 Darklight Festival (among other places). View the 1 min video at perpetual art machine.

As part of the symposium on Projecting the Past Into the Future: The Cognitive Neuroscience of Prospective Thought, Randy L. Buckner from the Howard Hughes Medical Institute at Harvard University spoke about his previously published hypothesis (Buckner et al., 2005; Buckner & Vincent, 2007) on how "overuse" of the default brain network contributes to the development of Alzheimer's disease [see also an earlier paper by Greicius et al., 2004]: the high metabolism of the "default mode" areas induces a toxic cellular cascade that can lead to the formation of plaques.

To quickly review, the default mode of brain function (Raichle et al., 2001) engages a certain network of brain regions (posterior cingulate and precuneus and medial prefrontal cortex) during "rest." These regions become DEactivated when people are engaged in the typical types of cognitive tasks they're asked to do in a scanner. So it's really only a "resting state" when compared to performing some active task. When asked to rest and stare at a plus sign, you may think about what you'll do over the weekend or remember where you went for dinner last night.

This default network shows a high level of resting activity (Buckner et al., 2005).

amyloid beta-containing plaques in the brain of a person who had Alzheimer's disease.
One possibility is that lifetime cerebral metabolism associated with regionally specific default activity predisposes cortical regions to AD-related changes, including amyloid deposition, metabolic disruption, and atrophy.

taken from Figure 6 (Buckner et al. , 2005): Convergence and hypothetical relationships across molecular, structural, and functional measures. Each image represents the projection of data ... onto the cortical surface of the left hemisphere. Three patterns emerge. First, regions showing default activity in young adults are highly similar to those showing amyloid deposition in older adults with AD, including both posterior cortical regions and anterior regions. Second, atrophy and metabolism disruption in AD prominently affect the posterior cortical regions also affected by amyloid deposition and less so the anterior regions. Third, the regions affected in AD and those active in default states in young adults overlap memory networks showing retrieval success effects during recognition in young adults.

Figure 7 (Buckner et al. , 2005): A schematic illustration of one possible configuration of lifelong events that lead to AD. Conducive metabolic conditions, associated with default mode activity patterns, may lead to regionally specific amyloid deposition. In turn, atrophy and dementia may then result. This metabolism cascade should be considered a hypothesis.

Plausible or not?? The posterior cortical areas are especially affected, but medial prefrontal cortex not so much. And what is the toxic cellular cascade that leads to amyloid deposition?


Buckner RL, Snyder AZ, Shannon BJ, LaRossa G, Sachs R, Fotenos AF, Sheline YI, Klunk WE, Mathis CA, Morris JC, Mintun MA. (2005). Molecular, structural, and functional characterization of Alzheimer's disease: evidence for a relationship between default activity, amyloid, and memory. J Neurosci. 25:7709-17.

Buckner RL, Vincent JL. (2007). Unrest at rest: Default activity and spontaneous network correlations. Neuroimage Jan 25; [Epub ahead of print]

Greicius MD, Srivastava G, Reiss AL, Menon V. (2004). Default-mode network activity distinguishes Alzheimer's disease from healthy aging: evidence from functional MRI. Proc Natl Acad Sci 101:4637-42.

Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA, Shulman GL. (2001). A default mode of brain function. Proc. Natl. Acad. Sci. 98: 676–682.

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Thursday, May 10, 2007

Imagining the Past, Remembering the Future

Symposium Session 4 at the CNS 2007 Annual Meeting was on Projecting the Past Into the Future: The Cognitive Neuroscience of Prospective Thought.
Summary: Humans spend a significant amount of time envisioning possible future events, yet the bulk of cognitive neuroscience research has focused on how humans re-experience past happenings. Such an oversight is surprising as future-oriented thought makes it possible for humans to anticipate events, formulate strategies based on previous experiences, and override momentary needs in pursuit of longer-term goals. In this symposium we present findings that suggest the brain evolved sophisticated mechanisms for envisioning the future. Schacter's work suggests that to deal effectively with the future people utilize the psychological and neural processes involved in remembering the past. Based on her recent findings, McDermott suggests that the ability to envision future events involves the simulation of behavior and the reinstatement of visuo-spatial contexts. Buckner will present data suggesting that one fundamental function of the brain is simulating alternative strategies and perspectives. Finally, Bar presents a framework linking perception, memory and predictions and argues that the mind is constantly anticipating "what's next" based on analogies with past experiences. As a package, these findings suggest that one core component of human cognition is anticipating possible future scenarios based on memories of past events.
The Neurocritic wrote about this topic (and the papers by Addis et al., 2007 [Schacter Lab], Szpunar et al., 2007 [McDermott Lab], and Hassabis et al., 2007 [Maguire Lab]) back in February. Was anything new presented? Not too much. The audience laughed [audibly] when Kathleen McDermott described the experimental control condition for imagining one's own future (imagine former President Clinton doing...) and how participants could easily imagine him in various scenarios. I snorted [inaudibly] when she admitted that interpretation of her results [i.e., activation of posterior cingulate cortex, parahippocampal gyrus, and occipital regions reflect autobiographical memory and spatial navigation] relies on reverse inference1. McDermott did describe a new study with an alternate control condition asking the participants to imagine themselves in an unfamiliar future situation (e.g., scuba diving, bullfight, jungle), so that self-referential (not Clinton-referential) processing was involved in all three conditions. The original result was replicated (Future familiar = Past familiar > Future novel).

Schacter mentioned a paper under review that looked at the effects of aging on the level of detail produced when imagining future events. This experiment followed from the findings of Levine et al. (2002), which demonstrated that older adults show a reduced level of contextual (episodic) detail when recalling autobiographical events; instead, they rely more on "semantic details not connected to a particular time and place" than do young adults. The new Schacter et al. results found the same thing in elderly participants imagining the future.

For his conclusion, Schacter acknowledged that no regions of the brain were more active for remembering the past vs. imagining the future in his study (Addis et al., 2007). It's a confounded comparison: we should imagine an alternate past instead of recalling an existing one.

What about Buckner and Bar? Certain aspects of their talks merit future posts of their own...

1 inferring the participants' emotional state from the observed pattern of brain activity.


Addis DR, Wong AT, Schacter DL. (2007). Remembering the past and imagining the future: Common and distinct neural substrates during event construction and elaboration. Neuropsychologia 45: 1378-1385.

Hassabis D, Kumaran D, Vann SD, Maguire EA. (2007). Patients with hippocampal amnesia cannot imagine new experiences. Proc Natl Acad Sci 104: 1726-31.

Levine B, Svoboda E, Hay JF, Winocur G, Moscovitch M. (2002). Aging and autobiographical memory: dissociating episodic from semantic retrieval. Psychol Aging 17:677-89.

Szpunar KK, Watson JM, McDermott KB. (2007). Neural substrates of envisioning the future. Proc. Natl. Acad. Sci. 104:642-7.

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Sunday, May 06, 2007

"Without A Theory The Facts Are Silent"

-- Friederich A. von Hayek

Hayek was the Nobel Prize winner in Economics in 1974 and co-originator of The Hayek/Hebb Synaptic Model. Haven't heard of the Hayek/Hebb Synaptic Model (it's just Hebbian learning, right)? Greg Ransom explains why.

Dr. Joaquin Fuster, distinguished Professor of Psychiatry and Biobehavioral Sciences at UCLA, won the George A. Miller Prize in Cognitive Neuroscience at the CNS 2007 Annual Meeting. He began his lecture with the above quote by Hayek and summarized his work on the network model of cortical cognition (e.g., Fuster, 1999, 2003), providing an historical overview of work on the Perception-Action Cycle (Fuster, 2004).

Fig. 1 (Fuster, 2004). Representational map of the human lateral cortex. (a) Schema of the hierarchical organization of memory and knowledge. (b) Approximate topographic distribution of memory networks, using the same color code as in (a).

In contrast to the outdated (Fuster, 2000) Modular Paradigm (in which cognitive functions and the contents of cognition are localized in discrete regions dedicated to the specific functions and domains), Fuster has long supported the Network Paradigm where higher cortical functions are distributed across brain regions, showing extensive intersection and overlap. In this scheme, one neuron can be part of many networks.

The thing about a lot of contemporary cog neuro research (including some presented at this conference) is that it conforms to the Modular Paradigm of extreme localization of function:
Cognitive neuroscience is not a new field, though its precise origin is difficult to trace. It was born whenever and wherever scientists began to ponder the logical relations between brain and mind and to explore those relations by observation and experiment. Most certainly, it was not born in Squaw Valley, California, where in the summer of 1993 a group of neuroscientists met to give it a name and to give themselves an agenda. [NOTE: this is not a snide remark, oh no]

. . .

...they presumably wanted the all-encompassing coverage to support their main agenda, which was the cognitive science of the cerebral cortex. That extended coverage diluted the agenda, but not enough to obscure a central concept that appears in various forms in many of the chapters. That concept is the cortical module of cognition: a discrete and continuous piece of cortical tissue specialized to serve one cognitive function or to represent one essential aspect of the information processed by it. ...

. . .

In the higher levels of that theoretical edifice, anatomists and physiologists met neuropsychologists, who were eager to localize in the brain their own constructs of cognitive function—mostly derived from studies of the effects of cortical damage. The result of the intellectual alliance of those three groups of scientists was, in the humble opinion of this reviewer, something not too distant from a new phrenology more or less legitimized by the scientific method. One of my purposes in this review is to caution the reader about some of the problems with the neuromodular principle of cognition and the methods used to support it. Another is to point out the pressing need for a more apt and useful model of cognitive organization in the cortex.

There is no greater impediment to a unified cognitive neuroscience than our inveterate Aristotelian tendency to consider cognitive functions as separate entities...

J.M. Fuster - Memory in the Cerebral Cortex: An Empirical Approach to Neural Networks in the Human and Nonhuman Primate. Cambridge, MIT Press, (paperback), 1999.

J.M. Fuster - The module: crisis of a paradigm (book review, "The New Cognitive Neurosciences" Second Edition, M.S. Gazzaniga, Editor-in-Chief, MIT Press). Neuron 26:51-53, 2000.

J.M. Fuster - Cortex and Mind: Unifying Cognition, Oxford University Press, 2003.

J.M. Fuster - Upper processing stages of the perception–action cycle. Trends in Cognitive Sciences, 8:143-145, 2004.

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Wednesday, May 02, 2007

The Neurocritic Does New York

The Neurocritic will be going to New York to attend the 14th Annual Meeting of the Cognitive Neuroscience Society.
With spring in the air, the 2007 meeting will have a new program line-up that is fresh and promises to pique the interests of all attendees. The meeting will be kicked off on Saturday, May 5, by the George A. Miller Prize in Cognitive Neuroscience Lectureship, which will be followed by a reception and the first poster session. Poster sessions will continue from May 6–8, with additional sessions added on Sunday and Monday to accommodate the increasing number of submissions (1,100 are expected this year).
Poster-making has superceded blog posting as of late...but stay tuned!

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