The Hollow Mask Illusion: Beyond Charlie Chaplin

Update - This paper dragon is an even better illustration of the effect, and you can make your own (if you have a printer). Amaze your friends! Really, you will.

Everyone's talking about the hollow mask illusion, a.k.a the hollow face illusion. Wired have a nice piece about this freaky visual phenomenon, complete with YouTube video so that you can see it for yourself. It's seriously weird. Here it is again, lifted from YouTube with KeepVid.com:

The illusion is a form of depth inversion. It involves a hollow (concave) object which appears to be non-hollow (convex). This happens whether the object is stationary or moving, but it's even more striking when it's in motion, as in the video above. When the mask of Charlie Chaplin rotates so that the inside is facing you, it suddenly appears as if it's looking out at you - but rotating in the opposite direction. This happens even though you know what's really going on.

The current surge of interest in the illusion was sparked by a recent fMRI study, Understanding why patients with schizophrenia do not perceive the hollow-mask illusion using dynamic causal modelling. But the fact that people with schizophrenia are generally immune to this illusion has been known for a long time. The illusion itself is even older - in fact, in one form or another, it goes back centuries.

But why exactly does it happen? That's an important question, because if you want to understand why schizophrenics are immune to it, you really need to know why it works on "normal people". (Notice that we normal people are the ones who are fooled while schizophrenics see reality as it is - R. D. Laing would be so pleased).

Most people seem to assume that the answer is pretty simple: it's expectation. We strongly expect things to be convex, so when we see something concave our brain tries to re-interpret it as convex. Easy! Hold on. There's a bit more to it than that.

The intricacies of the mask illusion are discussed in a paper called The hollow-face illusion: Object-specific knowledge, general assumptions or properties of the stimulus? The authors, Hill and Johnston, start out by discussing three possible explanations for the illusion.


First off, it could be that the illusion is driven by object-specific knowledge, i.e. knowledge about faces. (I've previously discussed the theory that faces are "special" - that our brains are specialized to percieve human faces.) According to this account, our brains expect that faces are convex, not hollow. This "top-down" expectation is so strong that it over-rides the "bottom-up" data of our eyes, and we see what we expect to see. Presumably, we also have specific expectations about teddy-bears and pineapples, which is why we see the hollow jelly moulds (above) as convex...

But Hill and Johnston point out that there's a second possibility - maybe our brains just expect everything to be convex. Rather than being about the specific object - a mask or face - the illusion might represent a more general expectation of convexity. There's some evidence for this, because there have been reports that the illusion works even for objects which the viewer has never seen before.

A variant of this explanation claims that the illusion is all about light. Maybe we expect that light always comes from above - because after all, it usually does. So we assume that the hollow mask is actually a convex face lit from above. This isn't a very good theory, however, especially because in the video above, the light actually comes from the side...

The final possible explanation considered by Hill & Johnston has nothing to do with expectation at all. Some people have claimed that the illusion occurs because the information reaching our eyes is ambiguous - it simply doesn't tell us whether the object is convex or concave. However, as Hill and Johnston point out, this is only true of information reaching one eye. We have two eyes, which gives us depth perception, meaning that we should be able to tell that the mask is hollow. Also, this wouldn't explain why the hollow mask never looks hollow. If it were ambiguous, it should be 50-50 whether it looks convex or concave.

They then go on to report the results of six different experiments investigating various aspects of the illusion. These are worth reading as they're a good example of the ways in which even something as subjective as visual illusions can be scientifically studied. After considering all of the resuls Hill & Johnston conclude

In summary, the hollow-face illusion appears to reflect a combination of the explanations offered. Some ambiguously interpretable bottom-up data must be present.That, coupled with a general bias towards convexity, is sufficient to generate the illusion, even when this interpretation is incompatible with other, unambiguous, bottom-up data. However, familiar orientations and patterns of shading and surface-colour information can greatly enhance this effect for both faces and other familiar objects.

In other words, the illusion probably is driven by expectation, but it also relies on their being some ambigious information in the first place. And while the expectations in question don't need to be about specific objects, like faces, it helps if they are.

Hill, H., & Johnston, A. (2007). The hollow-face illusion: Object-specific knowledge, general assumptions or properties of the stimulus? Perception, 36 (2), 199-223 DOI: 10.1068/p5523

The Hollow Mask Illusion: Beyond Charlie Chaplin

Update - This paper dragon is an even better illustration of the effect, and you can make your own (if you have a printer). Amaze your friends! Really, you will.

Everyone's talking about the hollow mask illusion, a.k.a the hollow face illusion. Wired have a nice piece about this freaky visual phenomenon, complete with YouTube video so that you can see it for yourself. It's seriously weird. Here it is again, lifted from YouTube with KeepVid.com:

The illusion is a form of depth inversion. It involves a hollow (concave) object which appears to be non-hollow (convex). This happens whether the object is stationary or moving, but it's even more striking when it's in motion, as in the video above. When the mask of Charlie Chaplin rotates so that the inside is facing you, it suddenly appears as if it's looking out at you - but rotating in the opposite direction. This happens even though you know what's really going on.

The current surge of interest in the illusion was sparked by a recent fMRI study, Understanding why patients with schizophrenia do not perceive the hollow-mask illusion using dynamic causal modelling. But the fact that people with schizophrenia are generally immune to this illusion has been known for a long time. The illusion itself is even older - in fact, in one form or another, it goes back centuries.

But why exactly does it happen? That's an important question, because if you want to understand why schizophrenics are immune to it, you really need to know why it works on "normal people". (Notice that we normal people are the ones who are fooled while schizophrenics see reality as it is - R. D. Laing would be so pleased).

Most people seem to assume that the answer is pretty simple: it's expectation. We strongly expect things to be convex, so when we see something concave our brain tries to re-interpret it as convex. Easy! Hold on. There's a bit more to it than that.

The intricacies of the mask illusion are discussed in a paper called The hollow-face illusion: Object-specific knowledge, general assumptions or properties of the stimulus? The authors, Hill and Johnston, start out by discussing three possible explanations for the illusion.


First off, it could be that the illusion is driven by object-specific knowledge, i.e. knowledge about faces. (I've previously discussed the theory that faces are "special" - that our brains are specialized to percieve human faces.) According to this account, our brains expect that faces are convex, not hollow. This "top-down" expectation is so strong that it over-rides the "bottom-up" data of our eyes, and we see what we expect to see. Presumably, we also have specific expectations about teddy-bears and pineapples, which is why we see the hollow jelly moulds (above) as convex...

But Hill and Johnston point out that there's a second possibility - maybe our brains just expect everything to be convex. Rather than being about the specific object - a mask or face - the illusion might represent a more general expectation of convexity. There's some evidence for this, because there have been reports that the illusion works even for objects which the viewer has never seen before.

A variant of this explanation claims that the illusion is all about light. Maybe we expect that light always comes from above - because after all, it usually does. So we assume that the hollow mask is actually a convex face lit from above. This isn't a very good theory, however, especially because in the video above, the light actually comes from the side...

The final possible explanation considered by Hill & Johnston has nothing to do with expectation at all. Some people have claimed that the illusion occurs because the information reaching our eyes is ambiguous - it simply doesn't tell us whether the object is convex or concave. However, as Hill and Johnston point out, this is only true of information reaching one eye. We have two eyes, which gives us depth perception, meaning that we should be able to tell that the mask is hollow. Also, this wouldn't explain why the hollow mask never looks hollow. If it were ambiguous, it should be 50-50 whether it looks convex or concave.

They then go on to report the results of six different experiments investigating various aspects of the illusion. These are worth reading as they're a good example of the ways in which even something as subjective as visual illusions can be scientifically studied. After considering all of the resuls Hill & Johnston conclude

In summary, the hollow-face illusion appears to reflect a combination of the explanations offered. Some ambiguously interpretable bottom-up data must be present.That, coupled with a general bias towards convexity, is sufficient to generate the illusion, even when this interpretation is incompatible with other, unambiguous, bottom-up data. However, familiar orientations and patterns of shading and surface-colour information can greatly enhance this effect for both faces and other familiar objects.

In other words, the illusion probably is driven by expectation, but it also relies on their being some ambigious information in the first place. And while the expectations in question don't need to be about specific objects, like faces, it helps if they are.

Hill, H., & Johnston, A. (2007). The hollow-face illusion: Object-specific knowledge, general assumptions or properties of the stimulus? Perception, 36 (2), 199-223 DOI: 10.1068/p5523

Annotated Links

Sydney Spiesel writes about the myriad claimed treatments for autism in Slate. He's skeptical

If there is any illness for which 100 treatments are available, you can be sure that none of them works.

True. But he doesn't do a great job of addressing why parents swear by such ineffective treatments. His answer is the "Hawthorne Effect". I think there's rather more to it than that. For one thing, Spiesel does not consider the possibility that a treatment might have no effect at all - not even a non-specific "placebo effect" - and still become popular.

But that happens. A PLoS ONE paper, From Traditional Medicine to Witchcraft, tries to explain why. Although it features some maths and lots of graphs, the argument is summed up in a sentence

Superstitious treatments and maladaptive practices can spread because their very ineffectiveness results in sick individuals demonstrating the practice for longer than efficacious treatments, leading to more salient demonstration and more converts

In other words, the less well a treatment works, the longer it gets used, and therefore, the more likely it is for other people to see it being used and adopt it. Of course this only holds under when people are completely unable to tell whether treatments used by others work or not. This may be a valid assumption.


Psychology Today interviews rebellious British psychiatrist David Healy about his new book, Mania, which I really need to read. Healy notes that bipolar disorder became a fashionable diagnosis starting in the mid 1990s. A while back I plotted a graph showing how often bipolar disorder was mentioned in the British media. It became much more popular after about 2000 - which sort of makes sense.

Healy's one of the few people who manages to be deeply skeptical of much about modern psychiatric diagnosis and treatment while avoiding Tom Cruiseist anti-psychiatry. His last book was a homage to ECT, ferchrisakes. A lot of people felt actively betrayed by that. But if you still doubt Healy's intellect, his use in the interview of a Buffy metaphor to explain the history of "mood stabilizing drugs" should set you straight. Genius.

Annotated Links

Sydney Spiesel writes about the myriad claimed treatments for autism in Slate. He's skeptical

If there is any illness for which 100 treatments are available, you can be sure that none of them works.

True. But he doesn't do a great job of addressing why parents swear by such ineffective treatments. His answer is the "Hawthorne Effect". I think there's rather more to it than that. For one thing, Spiesel does not consider the possibility that a treatment might have no effect at all - not even a non-specific "placebo effect" - and still become popular.

But that happens. A PLoS ONE paper, From Traditional Medicine to Witchcraft, tries to explain why. Although it features some maths and lots of graphs, the argument is summed up in a sentence

Superstitious treatments and maladaptive practices can spread because their very ineffectiveness results in sick individuals demonstrating the practice for longer than efficacious treatments, leading to more salient demonstration and more converts

In other words, the less well a treatment works, the longer it gets used, and therefore, the more likely it is for other people to see it being used and adopt it. Of course this only holds under when people are completely unable to tell whether treatments used by others work or not. This may be a valid assumption.


Psychology Today interviews rebellious British psychiatrist David Healy about his new book, Mania, which I really need to read. Healy notes that bipolar disorder became a fashionable diagnosis starting in the mid 1990s. A while back I plotted a graph showing how often bipolar disorder was mentioned in the British media. It became much more popular after about 2000 - which sort of makes sense.

Healy's one of the few people who manages to be deeply skeptical of much about modern psychiatric diagnosis and treatment while avoiding Tom Cruiseist anti-psychiatry. His last book was a homage to ECT, ferchrisakes. A lot of people felt actively betrayed by that. But if you still doubt Healy's intellect, his use in the interview of a Buffy metaphor to explain the history of "mood stabilizing drugs" should set you straight. Genius.

Depression, Neurogenesis and Herpes

Previously, I've discussed the neurogenesis theory of depression in two rather skeptical posts. Not that I'm on some kind of anti-neurogenesis theory crusade, but a study just published adds to the evidence that all's not well with that hypothesis.

The paper is Singer et. al.'s Conditional ablation and recovery of forebrain neurogenesis in the mouse. Via some cunning genetic engineering, the authors created mice with a gene for a protein called herpes simplex virus thymidine kinase. As the name suggests, this is a protein normally found in, er, herpes. Ganciclovir is a drug which can be used to treat herpes and related viral infections. And, as you might expect, cells engineered to express the herpes protein die when exposed to ganciclovir.

The authors engineered mice which expressed herpes simplex virus thymidine kinase, but only in neural progenitor cells. These are the cells which eventually become new neurones in the adult brain. They found that injections of gancyclovir devasasted the production of new neurones in the engineered mice. (It had no effect on normal mice, of course, because their brain cells weren't half mouse, half herpes). That's not all that surprising.

However, they also found that gancyclovir treatment had no effect on the ability of 28 days treatment imipramine, an antidepressant, to affect the mice's behaviour. (The measure of antidepressant action was the Tail Suspension Test). That's a result, because a lot of people are interested in the theory that antidepressants work by boosting neurogenesis in the hippocampus. If that were true, blocking neurogenesis should also block the effects of antidepressants.

Some rather exciting experiments found that it does, most famously the much-cited Santarelli et al (2003). But a growing number of other studies, such as this one, have not confirmed this finding. This doesn't mean that Santarelli et al were wrong, but it does suggest that there's more to antidepressants than neurogenesis. The seemingly-contradictory findings of the various studies might be due to important differences in the methods used. For example, the authors of this paper say that Santarelli et al's way of blocking neurogenesis - using x-rays - may have also caused inflammation and blocked the formation of non-neural cells, such as those which go to make up blood-vessels.

Of course, it's easy enough for us to speculate along such lines - rather harder to work out what exactly is going on. With any luck, the next few years will see more progress on this important topic.

Singer, B., Jutkiewicz, E., Fuller, C., Lichtenwalner, R., Zhang, H., Velander, A., Li, X., Gnegy, M., Burant, C., & Parent, J. (2009). Conditional ablation and recovery of forebrain neurogenesis in the mouse The Journal of Comparative Neurology, 514 (6), 567-582 DOI: 10.1002/cne.22052

Depression, Neurogenesis and Herpes

Previously, I've discussed the neurogenesis theory of depression in two rather skeptical posts. Not that I'm on some kind of anti-neurogenesis theory crusade, but a study just published adds to the evidence that all's not well with that hypothesis.

The paper is Singer et. al.'s Conditional ablation and recovery of forebrain neurogenesis in the mouse. Via some cunning genetic engineering, the authors created mice with a gene for a protein called herpes simplex virus thymidine kinase. As the name suggests, this is a protein normally found in, er, herpes. Ganciclovir is a drug which can be used to treat herpes and related viral infections. And, as you might expect, cells engineered to express the herpes protein die when exposed to ganciclovir.

The authors engineered mice which expressed herpes simplex virus thymidine kinase, but only in neural progenitor cells. These are the cells which eventually become new neurones in the adult brain. They found that injections of gancyclovir devasasted the production of new neurones in the engineered mice. (It had no effect on normal mice, of course, because their brain cells weren't half mouse, half herpes). That's not all that surprising.

However, they also found that gancyclovir treatment had no effect on the ability of 28 days treatment imipramine, an antidepressant, to affect the mice's behaviour. (The measure of antidepressant action was the Tail Suspension Test). That's a result, because a lot of people are interested in the theory that antidepressants work by boosting neurogenesis in the hippocampus. If that were true, blocking neurogenesis should also block the effects of antidepressants.

Some rather exciting experiments found that it does, most famously the much-cited Santarelli et al (2003). But a growing number of other studies, such as this one, have not confirmed this finding. This doesn't mean that Santarelli et al were wrong, but it does suggest that there's more to antidepressants than neurogenesis. The seemingly-contradictory findings of the various studies might be due to important differences in the methods used. For example, the authors of this paper say that Santarelli et al's way of blocking neurogenesis - using x-rays - may have also caused inflammation and blocked the formation of non-neural cells, such as those which go to make up blood-vessels.

Of course, it's easy enough for us to speculate along such lines - rather harder to work out what exactly is going on. With any luck, the next few years will see more progress on this important topic.

Singer, B., Jutkiewicz, E., Fuller, C., Lichtenwalner, R., Zhang, H., Velander, A., Li, X., Gnegy, M., Burant, C., & Parent, J. (2009). Conditional ablation and recovery of forebrain neurogenesis in the mouse The Journal of Comparative Neurology, 514 (6), 567-582 DOI: 10.1002/cne.22052

More on that Homeopathy Analysis

As promised, I emailed the authors of that Cochrane Review of homeopathy for reducing the side effects of cancer treatment. I asked them to clarify why they had included the Pommier et al trial of Calendula ointment - a decision which attracted some criticism. Their (very prompt) response included this statement:

"...We contacted the manufacturer of the calendula ointment and they confirmed that it had been prepared in accordance with the German Homeopathic Pharmacopoeia, therefore the trial met our inclusion criteria..."

Which is a reference to the inclusion criteria as set out in their paper, i.e.:

Homeopathy (also spelt homoeopathy) was defined, for the purpose of this review, as the use of homeopathic medicines prepared in accordance with officially recognised homeopathic pharmacopoeias. Where there was doubt about the classification of the medicine, we contacted authors or the product manufactures for confirmation. Any homeopathic prescribing strategy was included (pp. 3-4).

So it looks like the debate over the inclusion of this trial boils down to a difference of opinion over the definition of "homeopathy". Critics (myself included) who questioned the inclusion of this trial did so because we hold a rather narrower concept of "homeopathy" than the authors do. Of course, there is no right or wrong definition of homeopathy - no-one holds a trademark on the term - so I think that this is where the debate is going to have to rest.

[BPSDB]