Friday, February 26, 2010

Did Artist Käthe Kollwitz Have Alice in Wonderland Syndrome?

"Rare migraineurs have strange symptoms where the diagnosis may be lurking just down a rabbit hole" (Evans & Rolak, 2004).

Alice in Wonderland syndrome is an unusual perceptual phenomenon most often caused by migraine headaches, but also seen in association with epilepsy and Epstein-Barr virus. The most well-known symptoms are:
  • Alteration of body image: the sizes of parts of the body are perceived incorrectly.
  • Alteration of visual perception: the sizes of external objects are perceived incorrectly.
In their review, Evans and Rolak (2004) noted that:
Patients are aware of the illusory nature of their perceptions and are sometimes reluctant to admit to them for fear of being thought insane. This sensation of formed body distortions, a type of metamorphopsia, appears to be caused by migrainous ischemia. Most authorities believe, based in part on direct electrical stimulation studies of the brain, that these body distortions ... arise primarily in the posterior parietal lobe, especially in the nondominant [right] hemisphere. Migrainous ischemia and irritability in this area produces the bodily distortions.
Extensive [permanent] damage to the right parietal lobe can result in hemispatial neglect, where the patient ignores the contralateral (left) side of space, including the left side of the body. The visual illusions of metamorphopsia (as opposed to body distortions) have been associated with altered blood flow in the right temporo-occipital region (Heo et al., 2004).

Vaughan Bell, primary author of the Mind Hacks blog, revealed that he experienced Alice in Wonderland syndrome as a child but grew out of it as an adult (see Three impossible things before breakfast). He linked to a Guardian article by journalist Rik Helmsley, who described his symptoms in detail:
Floors either curved or dipped, and when I tried walking on them, it felt as though I was staggering on sponges. When I lay in bed and looked at my hands, my fingers stretched off half a mile into the distance...

I graduated and took a job as a system administrator in a new town, but instead of going away, my symptoms just got worse. Everything was now distorted, all the time. Walking down the road, parked cars appeared the size of Corgi models, while I'd feel disproportionately tall. At work, my chair seemed enormous, while I seemed to have shrunk.
The German expressionist artist Käthe Kollwitz may have suffered from AIWS, according to a recent article by Graeme Drysdale (2009). Kollwitz was known for her etchings, drawings, and woodcuts that portrayed graphic levels of suffering due to poverty, illness, and war. Her work often contained distorted depictions of hands and heads.

Poverty, 1893-94 (or Misery), by Käthe Kollwitz

Drysdale's hypothesis is that Kollwitz's art was heavily influenced by AIWS symptoms caused by migraine or epilepsy:
In her diary, Kollwitz self-described symptoms of Alice in Wonderland Syndrome during her childhood. She complained of episodes where objects appeared to grow larger or smaller and perceptual distortions where she felt she was diminishing in size. This may explain why Kollwitz’s artistic style appeared to shift from naturalism to expressionism, and why her artistic subjects are often shaped with large hands and faces. The distortion present in her visual art may have less to do with a deliberate emphasis of the artist’s feelings and more to do with her perceptual experience.

Die Witwe I (The Widow I), 1922-3. Woodcut on paper.

In her diary, she described frightening visual hallucinations:
‘Then there was a horrible state I fell into when objects would begin to grow smaller. It was bad enough when they grew larger, but when they grew smaller it was horrifying’.
So it's possible that the expressionistic distortions in the work of Käthe Kollwitz were brought on by Alice in Wonderland syndrome. To me that seems more plausible than psychoanalytic speculation on the role of "oral birth fantasies, sex fantasies and suppressed emotion."


Drysdale, G. (2009). Kaethe Kollwitz (1867-1945): the artist who may have suffered from Alice in Wonderland Syndrome. Journal of Medical Biography, 17 (2), 106-110 DOI: 10.1258/jmb.2008.008042

Evans RW, Rolak LA. (2004). The Alice in Wonderland Syndrome. Headache 44:624-5.

Heo K, Cho YJ, Lee SK, Park SA, Kim KS, Lee BI. (2004). Single-photon emission computed tomography in a patient with ictal metamorphopsia. Seizure 13:250-3.

Johnny Depp as the Mad Hatter, in Tim Burton's adaptation of Alice in Wonderland.

Alice: "If I had a world of my own, everything would be nonsense. Nothing would be what it is, because everything would be what it isn't. And contrary wise, what is, it wouldn't be. And what it wouldn't be, it would. You see?"

'But I don't want to go among mad people,' Alice remarked.
'Oh, you can't help that,' said the Cat: 'we're all mad here. I'm mad. You're mad.'
'How do you know I'm mad?' said Alice.
'You must be,' said the Cat, 'or you wouldn't have come here.'

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Wednesday, February 24, 2010

Neuromarketing the Neurology of Facebook

Facebook brain activation - visual cortex (photo by Marc Van Rymenant)

First, we had the fictitious Neurology of Twitter study, sponsored by The Neurocritic. Now it appears there's been an actual (unpublished) fMRI study of viewing Facebook pages, conducted by Netway, a neuromarketing firm.
A global premiere: travel in the mind of Facebook users

In the digital world, where business results are ever more top of the list, user experience is one of the key factors of success.

. . .

In plain English: we can see which zones of the brain are activated when a user is performing a task.

If we can identify the activated zones of the brain, we also know the answer to the following questions:

  • Doesn’t the screen have too many elements?
  • Which parts of the screen are analysed the most by the brain?
  • Do users recognize the used visuals?
  • Do the call-to-action elements incite action?
  • Do users understand the content?

And if we do that, we can objectively measure the user experience.
I would retort that it's not possible to answer those questions by examining fMRI results alone. Eye tracking and user behavior are essential. And the danger of extrapolating user experience from the pattern of brain activity? The logical fallacy of reverse inference, flogged repeatedly on this blog. One cannot directly infer the participants' cognitive or emotional state from the observed pattern of brain activity in neuroimaging experiments (Aguirre, 2003; Poldrack, 2006).

Let's examine some of Netway's conclusions. From looking at the figure above, they say:
In the case of Facebook we see the right visual cortex has a higher level of activation. This indicates the visual elements at the left side of the interface generate more brain activity than the right-side elements.
That generally happens if the density of visual stimuli in the left visual field is greater than in the right visual field, or if there is some difference in basic perceptual features. You don't need fMRI to tell you that. Commenter Theo Vosse explains further:
Sorry, but this is nonsense. Even the low-level visual analysis is wrong. That there is more activity in one part of the visual cortex than in another only means that there is a difference in contrast, color or brightness between the left and right sides. Furthermore, since fMRI is pretty slow, this is averaged over the different places of focus, so it might just mean that people focus more on one side of the monitor than on the other. Or something completely different. You can’t tell, because you have no proper baseline.
Then we hear a bit about the dorsal ("where" pathway) and ventral ("what" pathway) visual streams. But Netway really goes awry and starts reading tea leaves when they reach the prefrontal cortex.

Facebook brain activation - semantic activation (photo by Marc Van Rymenant)

The Brodmann 44 zone is involved in recovering information in our semantic memory. This means a surfer watches the elements and this system will activate a network of knowledge about a certain word or an object.

The information that is recovered in the long-term memory during a Facebook site visit activates the semantic network. People will know what they see and that activates a set of linked information (I know this person, it is a friend of…, …).

We see the Brodmann 45 zone is not activated. If this had been the case, it would have meant the recovered information didn’t activate strong associations. That would mean the content is not very well known or not very often used by our brain.

There is absolutely no evidence for such a distinction between these two regions of the inferior frontal gyrus (not that it's entirely clear what was meant here). BA44 is activated by strong semantic associations and BA45 by weak semantic associations? That is nonsense... Neuromarketing companies do not have to subject their studies to peer review, and in fact it's detrimental to expose their proprietary methods. So buyer beware! But if corporations want to pay for such tenuous insights, I can't feel too sorry for them.


Aguirre GK (2003). Functional Imaging in Behavioral Neurology and Cognitive Neuropsychology. In: T.E. Feinberg & M.J. Farah (Eds.), Behavioral Neurology and Cognitive Neuropsychology. New York: McGraw Hill.

Poldrack RA (2006). Can cognitive processes be inferred from neuroimaging data? Trends in Cognitive Sciences 10: 59-63.

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Thursday, February 18, 2010

Hard-Hitting Interview of Louann Brizendine in ELLE Magazine

Dr. Louann Brizendine, author of The Female Brain (2006), will have a new book published on March 23, 2010. It's cleverly titled..............

As some of you remember, The Female Brain was roundly criticized for its inaccuracies. Foremost among them: "A woman uses about 20,000 words per day while a man uses about 7,000." In a thoroughly researched series of posts, Mark Liberman of Language Log explained there was no evidence at all for that claim:
I looked through the book to try to find the research behind the 20,000-vs.-7,000-words-per-day claim, and I looked on the web as well, but I haven't been able to find it yet. Brizendine also claims that women speak twice as fast as men (250 words per minute vs. 125 words per minute). These are striking assertions from an eminent scientist, with big quantitative differences confirming the standard stereotype about those gabby women and us laconic guys. The only trouble is, I'm pretty sure that both claims are false.
In anticipation of the new book, ELLE writer Diana Kapp did a nice job with her article on:
The Male Brain

Neuropsychiatrist Louann Brizendine on her inevitably best-selling new book

By Diana Kapp February 12, 2010 6:30 p.m

You might want to try to keep your own personal pet caveman in the dark on this one, but in her inevitably best-selling new book, The Male Brain (Broadway Books), neuropsychiatrist Louann Brizendine, MD, officially, scientifically lets guys off the hook for skirt-chasing, conking out after sex, avoiding emotionality—even spending Sundays glued to ESPN...

Despite accusations leveled in publications from Nature to The New York Times that Brizendine engaged in weak science in The Female Brain, The Male Brain is, like its predecessor, a breezy and loosey-goosey girlfriend-gab take on the state of gender-based brain science. Brizendine often relies on unreplicated or small-scale experiments, studies, and surveys to draw sweeping, possibly oversimplified conclusions about gender and human nature and to spin small distinctions and differences in the data into vive la différence.
Kapp also conducted a critical interview with Dr. Brizendine in which she asked some difficult questions. For instance:
ELLE: You write that “our brains are much more plastic and changeable than scientists believed a decade ago,” yet most of your book stacks up examples of hardwired differences. You say the nature-nurture debate is dead, yet your book seems to cast you in the nature camp.
LB: Nature-nurture is dead because they’re really the same thing. Nature is the thing we must understand first, in terms of how things get wired in utero and the phases of brain development. The piece that used to be called nurture is genetically driven changes that come with things like stress, hormonal differences, neglect, abuse, drugs, or toxic substances. Understanding the genetics we’re born with and how they get modified by our upbringing and environment is the key.
ELLE: The journal Nature said about The Female Brain that you fail “to meet even the most basic standards of scientific accuracy and balance” and accused you of making sex differences in brain structure seem almost to make men and women two different species.
LB: If that’s what people are getting out of my book, that’s an incorrect view. There are many more similarities than there are differences. I’m not trying to write scientific treatises. I’m writing for people who are intelligent but don’t do science. In doing honor to its complexity, I think I’ve hit the mark in some respects and missed the mark in others. Scientifically, looking at gender differences is in its infancy. It’s only really important in medicine to study diseases, for example. Gender differences per se are of less interest.
Perhaps Diana Kapp should be a book reviewer for Nature. And I wonder if ELLE will be hiring neurobloggers soon...

ADDENDUM: In a comment, Sanjay Srivastava has pointed to a brief 2007 Science paper (Mehl et al.) that was published after Lieberman's original critique:
Are women really more talkative than men?

Women are generally assumed to be more talkative than men. Data were analyzed from 396 participants who wore a voice recorder that sampled ambient sounds for several days. Participants' daily word use was extrapolated from the number of recorded words. Women and men both spoke about 16,000 words per day.

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Monday, February 15, 2010

Vegas casino develops technique for unobtrusive radiofrequency ablation of the amygdala

Figure 1. Schematic diagram of the radiofrequency ablation device, adapted from surgical oncology procedures to apply a focal high frequency alternating current to the region of the amygdala.

Alternatively, a gamma knife-like TMS application, slyly incorporated into a metal detector, temporarily deactivates the amygdala when each customer enters the casino.

Figure 2. Adjustable transcranial magnetic stimulation (TMS) helmet incorporated into a Metor 200 Walk-Thru Metal Detector.

What was the inspiration for such ground-breaking technology?1 The revelation that two rare individuals with bilateral lesions of the amygdala2 did not care about losing large sums of money in a gambling task (De Martino et al., 2010). This comes as no surprise, really, since the same two patients (S.M. and A.P.) do not show fear in other contexts. Patient S.M. in particular has repeatedly demonstrated deficits in the perception of fear (reviewed in Adolphs, 2008). She's more likely to judge unfamiliar faces as trustworthy and approachable (Adolphs et al., 1998). Further, she fails to show a normal sense of distrust and "danger" (Tranel et al., 2006), and:
Her interpersonal behaviour is notable for a somewhat coquettish and disinhibited style. She tends to be friendly with her examiners, with a familiar style of interaction that goes a little beyond what is typical in conventional Midwestern culture.
In a related vein, her requirement for personal space is non-existent (Kennedy et al., 2009). On the other hand, she's impaired at making eye contact with people during conversations (Spezio et al., 2007). Although fearful facial expressions are a mystery, she can accurately judge fear from whole-body cues (Atkinson et al., 2007). Hmm. I find it puzzling when investigators publish a paper that stands in relative isolation from their previous work, as if the current result is so novel that it merits placement in a high-profile journal.

So what does all this uncited work have to do with "loss aversion", the well-studied behavioral economic phenomenon3 probed in the current study? The authors proposed that "the amygdala computes a signal of prospective loss that is integrated with other information to guide behavioral choice" (De Martino et al., 2010). How does this fit with the collection of findings mentioned above? Granted, constraints of the short, high-impact journal article format prevent in-depth discussion and integration, but presenting so many punctate disconnected pieces just to up your number of glamor publications can be viewed as a disservice to the field. In my opinion, it's important to make connections between the different functions carried out by a particular brain structure (or network of structures), rather than treating the computations performed in a specific task as somehow uninformed by these other "computations".

Adolphs et al. (2005) tied some of the disparate fear findings together when they linked S.M.'s lack of eye contact to her impaired recognition of fear from faces. But how does this connect with her propensity to throw money away in Vegas? More broadly, do pathological gamblers show amygdala-like deficits similar to S.M.? Probably not. Ultimately, the casinos don't care whether it's due to alterations in the striatum, the ventromedial prefrontal cortex, or the amygdala, they'd just like to attract customers with lowered loss aversion...


1 In case it's not completely obvious, these are fictional techniques.

2 The cause of the amygdala damage was Urbach-Wiethe disease, a rare genetic disorder with less than 300 reported cases.

3 To learn more about loss aversion in neurological patients, I refer the reader to this post in The Frontal Cortex.


Adolphs R. Fear, faces, and the human amygdala. (2008). Curr Opin Neurobiol. 18:166-72.

Adolphs R, Tranel D, Damasio AR. (1998). The human amygdala in social judgment. Nature 393:470-4.

Adolphs R, Gosselin F, Buchanan TW, Tranel D, Schyns P, Damasio AR. (2005). A mechanism for impaired fear recognition after amygdala damage. Nature 433:68-72.

Atkinson AP, Heberlein AS, Adolphs R. (2007). Spared ability to recognise fear from static and moving whole-body cues following bilateral amygdala damage. Neuropsychologia 45:2772-82.

De Martino, B., Camerer, C., & Adolphs, R. (2010). Amygdala damage eliminates monetary loss aversion. Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0910230107

Kennedy DP, Gläscher J, Tyszka JM, Adolphs R. (2009). Personal space regulation by the human amygdala. Nat Neurosci. 12:1226-7.

Spezio ML, Huang PY, Castelli F, Adolphs R. (2007). Amygdala damage impairs eye contact during conversations with real people. J Neurosci. 27:3994-7.

Tranel D, Gullickson G, Koch M, Adolphs R. (2006). Altered experience of emotion following bilateral amygdala damage. Cogn Neuropsychiatry 11:219-32.

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Saturday, February 06, 2010

Psychodynamic Psychotherapy in the Scanner?

Arrangement for psychotherapy fMRI studies using the couch of Sigmund Freud.

[No not really, although the authors did stretch the implications of their findings in the Discussion...]

Whether the proprietors of this blog want to admit it or not, neuropsychoanalysis appears to be a new field of study. What does psychoanalysis do to the brain? In a new Psychotherapy Research paper, Loughead et al. (2010) collected autobiographical relationship narratives from 16 healthy control participants free of any psychiatric or neurological ailments. These types of vignettes were used as stimuli because "people in psychotherapy spontaneously recall and tell stories about their relationships with other people..." A series of 14 one minute narratives was collected from each subject using the Relationships Anecdotes Paradigm (RAP) method, a structured interview designed to elicit descriptions of meaningful life events with another person. The participants then rated each episode on a 5-point Likert scale for positive and negative emotions.

The investigators rated the narratives in another fashion to extract common themes. The core conflictual relationship theme (CCRT) method (Luborsky & Crits-Christoph, 1998) is a psychotherapy instrument used to measure patterns within interpersonal relationships:
From a content analysis of the relationship narratives, it is possible to identify three kinds of relationship components: (a) wishes (wishes, intentions, goals of the individual or self); (b) responses from the other to the self; and (c) responses of the self to the other...

The main CCRT relationship patterns are defined as the most repetitive relationship themes across an individual’s relationship narratives, usually those ranking first and second in frequency across the narratives. These main CCRTs have been a focus for the conduct of both psychotherapy and psychotherapy research (Luborsky & Crits-Christoph, 1998).
Then a neuroimaging study was conducted with 11 of the participants (5 were ultimately tossed out for various reasons). It's notable that all subjects were free of psychiatric disorders, and none were in therapy. So the direct application of the results to psychotherapy practice is questionable. That said, what were the experimental procedures? For the narratives,
The two most repetitive wishes (W), responses from others (RO), and responses of self (RS) were identified for each participant’s set of 14 narratives. These repetitive themes are hereafter referred to as the main CCRTs. Weighted scores were then assigned to each narrative based on the frequency with which the participant’s main CCRT themes appeared in her or his 14 narratives. For example, if a participant’s main RO was "hurt me" and it appeared in seven of 14 narratives, then each narrative containing the RO "hurt me" received a weighted score of 7....
The weighted scores for the other elements were tallied up, and 3 narratives each were selected for the high and the low CCRT/emotion conditions [NOTE: these two factors could not be distinguished from each other]. In addition, narratives from one of the excluded participants served as the control, non-autobiographical relationship episodes:
...The control episodes were selected to be similar to the personal condition in narrative structure, emotion, and CCRT content and yet have no autobiographical relevance to the participant.
The three types of stimuli were presented in a block design: six 30-s blocks of personal narratives and six 30-s blocks of control narratives (half high, half low CCRT/emotion), with resting baseline thrown in for good measure. A sample CCRT narrative is shown below (click on image for a larger view).

Figure I (Loughead et al. (2010). Sample CCRT relationship episode.

The fMRI results came as no surprise to anyone: personal autobiographical memories activate the brain to a greater extent than someone else's memories. Wow!
The network of frontal and parietal regions observed for the main effect of narrative type, which includes the anterior cingulate, precuneus/posterior cingulate, inferior frontal gyrus, inferior parietal lobule, and middle frontal gyri, is consistent with the existent neuroimaging literature on recall of autobiographical memories (Buckner & Carroll, 2007...).

Figure II (Loughead et al. (2010). Brain images showing group main effect for narrative type (personal, control). Statistical parametric maps are displayed in radiological convention (left is right) standardized into Talairach space. ACC, anterior cingulate; Inf Front, inferior frontal gyrus; Mid Front, middle frontal gyrus; Inf Parietal; inferior parietal lobule. No voxels were above threshold for CCRT/emotion (high, low) main effect or the interaction.

And there was absolutely no difference in brain activity elicited by the low CCRT and high CCRT conditions. So much for the CCRT method, at least in this non-psychiatric population. However, exploratory analyses showed correlations between BOLD signal and CCRT score in the left hippocampus, parahippocampal gyrus, and middle occipital gyrus. Not in the amygdala, however. The lack of main effect or interaction for the main variable of interest did not prevent the authors from speculating wildly:
Our exploratory analysis suggests that narratives characterized by increasing amounts of the most repetitive (i.e., main CCRT patterns) are special from a neurobiological perspective... When narratives are high in CCRT content, this is somewhat akin to exposing, or reflecting back, the main CCRT themes to a patient (i.e., providing a transference interpretation). Thus, an area of further study suggested by these results is how exposure to the main CCRT themes (or transference interpretation) could modulate brain activation in the medial temporal and occipital lobes in treatment populations.
Never mind that no psychotherapist was involved at all, since none of the participants were In Treatment. And what wild speculation would be complete without... MIRROR NEURONS!
Memories, the self, and emotion have long been of interest to psychotherapy, and theory of mind/mentalization and the mirror neuron system have been proposed as specific mechanisms of psychotherapy process (Fonagy & Bateman 2006...). These results demonstrate that the essential psychotherapy activity of recall of autobiographical relationship episodes engages neural substrates for systems that have been identified by research as central for psychotherapy process.


Buckner RL, Carroll DC. (2007). Self-projection and the brain. Trends in Cognitive Sciences 11:49-57.

Fonagy P, Bateman AW. (2006). Mechanisms of change in mentalization-based treatment of BPD. Journal of Clinical Psychology 62:411-430.

Loughead, J., Luborsky, L., Weingarten, C., Krause, E., German, R., Kirk, D., & Gur, R. (2010). Brain activation during autobiographical relationship episode narratives: A core conflictual relationship theme approach. Psychotherapy Research, 1-16 DOI: 10.1080/10503300903470735

Luborsky L, Crits-Christoph P. (1998). Understanding transference: The core conflictual relationship theme method (2nd ed.). Washington, DC: American Psychological Association.

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