More than a century ago, scientists discovered something usual about how people with schizophrenia move their eyes. The men, psychologist and inventor Raymond Dodge and psychiatrist Allen Diefendorf, were trying out one of Dodge’s inventions: an early incarnation of the modern eye tracker. When they used it on psychiatric patients, they found that most of their subjects with schizophrenia had a funny way of following a moving object with their eyes.
When a healthy person watches a smoothly moving object (say, an airplane crossing the sky), she tracks the plane with a smooth, continuous eye movement to match its displacement. This action is called smooth pursuit. But smooth pursuit isn’t smooth for most patients with schizophrenia. Their eyes often fall behind and they make a series of quick, tiny jerks to catch up or even dart ahead of their target. For the better part of a century, this movement pattern would remain a mystery. But in recent decades, scientific discoveries have led to a better understanding of smooth pursuit eye movements – both in health and in disease.
Scientists now know that smooth pursuit involves a lot more than simply moving your eyes. To illustrate, let’s say a sexy jogger catches your eye on the street. When you first see the runner, your eyes are stationary and his or her image is moving across your retinas at some relatively constant rate. Your visual system (in particular, your visual motion-processing area MT) must first determine this rate. Then your eyes can move to catch up with the target and match its speed. If you do this well, the jogger’s image will no longer be moving relative to your retinas. From your visual system’s perspective, the jogger is running in place and his or her surroundings are moving instead. From both visual cues and signals about your eye movements, your brain can predict where the jogger is headed and keep moving your eyes at just the right speed to keep pace.
Although the smooth pursuit abnormalities in schizophrenia may sound like a movement problem, they appear to reflect a problem with perception. Sensitive visual tests show that motion perception is disrupted in many patients. They can’t tell the difference between the speeds of two objects or integrate complex motion information as well as healthy controls. A functional MRI study helped explain why. The study found that people with schizophrenia activated their motion-processing area MT less than controls while doing motion-processing tasks. The next logical question – why MT doesn’t work as well for patients – remains unanswered for now.
In my last two posts I wrote about how delusions can develop in healthy people who don’t suffer from psychosis. The same is true of not-so-smooth pursuit. In particular, healthy relatives of patients with schizophrenia tend to have jerkier pursuit movements than subjects without a family history of the illness. They are also impaired at some of the same motion-processing tests that stymie patients. This pattern, along with the results of twin studies, suggests that smooth pursuit dysfunction is inherited. Following up on this idea, two studies have compared subjects’ genotypes with the inheritance patterns of smooth pursuit problems within families. While they couldn’t identify exactly which gene was involved (a limitation of the technique), they both tracked the culprit gene to the same genetic neighborhood on the sixth chromosome.
Despite this progress, the tale of smooth pursuit in schizophrenia is more complex than it appears. For one, there’s evidence that smooth pursuit problems differ for patients with different forms of the disorder. Patients with negative symptoms (like social withdrawal or no outward signs of emotion) may have problems with the first step of smooth pursuit: judging the target’s speed and moving their eyes to catch up. Meanwhile, those with more positive symptoms (like delusions or hallucinations) may have more trouble with the second step: predicting the future movement of the target and keeping pace with their eyes.
It’s also unclear exactly how common these problems are among patients; depending on the study, as many as 95% or as few as 12% of patients may have disrupted smooth pursuit. The studies that found the highest rates of smooth pursuit dysfunction in patients also found rates as high as 19% for the problems among healthy controls. These differences may boil down to the details of how the eye movements were measured in the different experiments. Still, the studies all agreed that people with schizophrenia are far more likely to have smooth pursuit problems than healthy controls. What the studies don’t agree on is how specific these problems are to schizophrenia compared with other psychiatric illnesses. Some studies have found smooth pursuit abnormalities in patients with bipolar disorder and major depression as well as in their close relatives; other studies have not.
Despite these messy issues, a group of scientists at the University of Aberdeen in Scotland recently tried to tell whether subjects had schizophrenia based on their eye movements alone. In addition to smooth pursuit, they used two other measures: the subject’s ability to fix her gaze on a stable target and how she looked at pictures of complex scenes. Most patients have trouble holding their eyes still in the presence of distractors and, when shown a meaningful picture, they tend to look at fewer objects or features in the scene.
Taking the results from all three measures into account, the group could distinguish between a new set of patients with schizophrenia and new healthy controls with an accuracy of 87.8%. While this rate is high, keep in mind that the scientists removed real-world messiness by selecting controls without other psychiatric illnesses or close relatives with psychosis. This makes their demonstration a lot less impressive – and a lot less useful in the real world. I don’t think this method will ever become a viable alternative to diagnosing schizophrenia based on their clinical symptoms, but the approach may hold promise in a similar vein: identifying young people who are at risk for developing the illness. Finding these individuals and helping them sooner could truly mean the difference between life and death.
Photo credit: Travis Nep Smith on Flickr, used via Creative Commons License
Benson PJ, Beedie SA, Shephard E, Giegling I, Rujescu D, & St Clair D (2012). Simple viewing tests can detect eye movement abnormalities that distinguish schizophrenia cases from controls with exceptional accuracy. Biological psychiatry, 72 (9), 716-24 PMID: 22621999
I don’t work with schizophrenics so the information you presented was new to me. However, there has also been some really fascinating research on visual tracking among people with Autism – http://ed.ted.com/lessons/a-new-way-to-diagnose-autism-ami-klin
Thanks for the link! I’ve heard a little about eye movements in autism but not nearly enough. Will check out the talk and learn more. Thank for commenting and for the info.
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Reblogged this on Free psychology.
Thanks for sharing!
You’re welcome! 🙂
So ‘Schizophrenics’ are shifty eyed? More modern phrenology!
Not at all. First of all, no one said anything about being “shifty-eyed.” And as to phrenology, its flaw was that it lacked any experimental rigor. Gall based his claims on anecdotes, sometimes assigning a certain attribute to a certain region of the brain based on one individual. There have been many decades of experimental research to verify this eye-tracking pattern in patients. It’s based on data, not anecdotes.
Reading your article, I felt I was looking Biopsychiatry in the eye more than ‘Schizophrenia’, Rebecca. I could write a book in reply, and more than a few have, so to speak, so I just expressed my scepticism instead. My inverted commas around ‘Schizophrenia’ are deliberate, I doubt its very existence as a useful label for anything a person can be or have or do. Biopsychiatry means the sort of biomechanical psychology currently back in vogue. Phrenology was an earlier form of it.
Science has learned a lot since phrenology was in vogue, but less about brains than some like to boast and very little indeed about minds. And anecdotes and data are far from mutually exclusive.
Since I am one of the many who do not believe there is an ‘illness’ called’ Schizophrenia’ I strongly reject any attempt to screen for it, particularly in young people who are only ‘at risk of developing the disease’. Finding them could indeed mean the difference between life and death. Psychiatric drugs and ECT can and do kill people.
Thanks, Rebecca, John
At first glance I can see how this research could be interpreted as pseudoscience, but the evidence for it is actually quite overwhelming.
Phrenology was proposed during a time when theories did not require concrete data to support them. Thankfully, by the mid 1800s the scientific community began emphasizing the importance of data to support hypotheses and phrenology was abandoned (no study could demonstrate measurements of brain volume with the attributes they were ascribed to).
With schizophrenia eye movement studies, as wild as it seems, the data strongly supports the association between impaired smooth pursuit and schizophrenia. Truly a very surprising, fascinating (and verified) discovery!
Thanks for reading and commenting! That’s why I wrote about this topic, because it’s well-known in the psychiatry community but it would seem surprising and wild to the rest of the world. I think that’s what’s so wonderful about science – it never fails to surprise us.
Reblogged this on lynndllcurtis and commented:
Another look at schizophrenia
This article was very informing. Schizoprenia is caused when the neurotransmitter dopamine has excessive amounts in the brain causing a person to experience hallucinations and delusions. Scientists have created antipsychotic drugs to block dopamine receptors as well as reduce the amount of dopamine running in the brain. Although these drugs work to stop the schizprenia symptoms, they can have some serious side effects to those taking it. Dopamine is produced and used in many parts of the brain, so when the drug is taken, it does not just reduce the dopamine in the area needed. It reduces dopamine production in the brain as a whole. So with a long term use of the drug, it can cause the production of symptoms similar to those of Parkinsons disease, which is caused by the lack of production of dopamine. People with Parkinson’s disease can take a drug to reduce the symptoms. The drug increases production of dopamine. So in order to avoid the symptoms you have to find a way for the brain to have the perfect amount of dopamine. Not to little and not to much.
We had discussion over Schizophrenia in our Psychology class. Schizophrenia causes a person to experience hallucinations and delusions. These two are the positive symptoms. A delusion is a false belief the persists despite compelling contradictory evidence.And the delusional person often becomes preoccupied with his erroneous beliefs and rejects any evidence that contradicts them. So when it comes to “Looking Schizophrenia in the eye ” , I think the reason behind blinking their eyes several times than the “non-Schizophrenia” affected person could be the delusion. Somehow their delusion denies certain realities they see and that could probably result into such behaviors.