/People Born Blind Are Mysteriously Protected From Schizophrenia

People Born Blind Are Mysteriously Protected From Schizophrenia


It was something Tom Pollak had heard whispers about—an odd factoid, referred to now and again, usually with bewilderment: No person who was born blind has ever been diagnosed with schizophrenia.

Over the past 60-some years, scientists around the world have been writing about this mystery. They’ve analyzed past studies, combed the wards of psychiatric hospitals, and looked through agencies that treat blind people, trying to find a case.

As time goes on, larger data sets have emerged: In 2018, a study led by a researcher named Vera Morgan at the University of Western Australia looked at nearly half a million children born between 1980 and 2001 and strengthened this negative association. Pollak, a psychiatrist and researcher at King’s College London, remembered checking in the mental health facility where he works after learning about it; he too was unable to find a single patient with congenital blindness who had schizophrenia.

These findings suggest that something about congenital blindness may protect a person from schizophrenia. This is especially surprising, since congenital blindness often results from infections, brain trauma, or genetic mutation—all factors that are independently associated with greater risk of psychotic disorders.

More strangely, vision loss at other periods of life is associated with higher risks of schizophrenia and psychotic symptoms. Even in healthy people, blocking vision for just a few days can bring about hallucinations. And the connections between vision abnormalities and schizophrenia have become more deeply established in recent years—visual abnormalities are being found before a person has any psychotic symptoms, sometimes predicting who will develop schizophrenia.

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But the whispered-about fact persists: Being born blind, and perhaps specific types of congenital blindness, shield from the very disorders vision loss can encourage later in life. A myriad of theories exist as to why—from the blind brain’s neuroplasticity to how vision plays an important role in building our model of the world (and what happens when that process goes wrong). Select researchers believe that the ties between vision and psychotic symptoms indicate there’s something new to learn here. Could it be that within this narrowly-defined phenomenon there are clues for what causes schizophrenia, how to predict who will develop it, and potentially how to treat it?

In 2004, 13 healthy people were blindfolded for 96 hours, and 10 of them reported having visual hallucinations between their first and second day in the dark.

One subject, a 29-year-old woman, saw a green face with big eyes when she was standing in front of where she knew there was a mirror—though she couldn’t see it. Another 24-year-old man, by the end of the second day, was having difficulty walking because of all the hallucinations that appeared to be in his way. He reported seeing “mounds of pebbles, or small stones…and between them was running a small stream of water.” By the end of the study, he reported seeing “ornate buildings of white-green marble” and “cartoon-like figures.”

We’ve known for a long time about the link between vision loss and hallucination. Charles Bonnet syndrome, first described in 1760, is a disorder in which people lose their vision and then start to experience hallucinations. These kinds of mental conjurings don’t necessarily come with mental illness, though people with schizophrenia have been regularly shown to also have issues with their sight.

Having unusual eye movements, problems with the retinas, unusual blink rates, and other visual aberrations makes it more likely for a person to be diagnosed with schizophrenia. One study found that those vision problems start before a person has their first psychotic episodes, not after.

Yet this association falls away among people born without sight. Pollak and Phil Corlett, an associate professor of psychiatry and psychology at Yale University, have a theory about why—which they published late last year in the journal Schizophrenia Bulletin. It’s rooted in the hypothesis that one of our brain’s most important jobs is to make predictions about the world.


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This view of the brain argues that rather than perceiving the world around us in real time, our brains create a model of what’s out there, predict and simulate what we experience, and then compare our predictions to what’s actually happening—using any errors to update or change the model in our minds. The accuracy of your past predictions are crucial for the accuracy of your overall model—it’s what you’re comparing new inputs to, and how you’re making any adjustments.

This is where vision comes in. Vision gives us a lot of information about the world around us, and is an important sense that helps link together other sensory cues, like sound and touch, Pollak said. If the way a person sees the world is off, it can make it harder to predict, correct errors, and build a model of the world that makes sense. And when people have problems with their vision, the brain has to make more predictions to explain them. On the other hand, if you couldn’t see anything, you wouldn’t build up those false representations of the world around you—which could lead to problems in thinking later on.

This might help researchers explain all those issues in vision and sensory processing early in life seen in people with schizophrenia. In a 2006 study by Elaine Walker at Emory University, she analyzed home movies of people diagnosed with schizophrenia when they were children. A lot of the children were more clumsy in the videos, like dropping a ball more frequently during catch, stumbling more often, or tilting to the left side. It suggests there’s some sort of disconnect with the way they’re sensing and interacting with the world. When children of mothers who have schizophrenia show visual dysfunction when they’re young, it can predict if they develop schizophrenia when they’re older. Children who end up with schizophrenia, both with and without a family history, have more problems with their eyes compared to children who develop non-psychotic diseases or other mental illnesses.

A person who was born blind doesn’t have the visual inputs to help shape their model of the world. They have to build it with their other senses—a model of the world that Pollak and Corlett argue could be more stable.

“The idea we’re trying to get at is, there must be something different in the representation and the stability of the internal world in congenitally blind people,” Pollak said. “And that stability, in a way, is keeping itself protective against the kind of mistakes and false inferences that you get in schizophrenia and psychotic disorders.”

The hallucinations, delusions, and bizarre behavior in people with schizophrenia are well known. But Steve Silverstein, a psychiatrist at the University of Rochester, said that he and others view those symptoms as side effects, not the cause of the disease. Actually, schizophrenia could be more rooted in cognitive deficits—disturbances in perception, attention, memory, language, or learning.

Around 2010, Silverstein read Blind Vision—a book by scientists Zaira Cattaneo and Tomaso Vecchi, on the cognitive abilities and experiences of blind people. “I was struck by how many of the compensations that the brain seems to make, or the skills that blind people develop, seem to be the exact opposite of what you find in schizophrenia,” he said.

Silverstein doesn’t disagree with Pollak and Corlett’s predictive brain theory, but thinks that the answer may be more far-reaching: that prediction is just one way a congenitally blind person’s brain has advantages over a schizophrenic brain. He thinks that being blind strengthens the brain in various ways—and in the very same ways that it is weakened when someone has schizophrenia.

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To take one example, there’s something called selective attention when it comes to listening, which is the ability to stay attentive to one source of auditory information—say, when you’re at a party and listening to one person without letting the sounds from the rest of the room distract you. In a lab setting, researchers test selective attention by playing one noise into your left ear and a different one into your right, asking you to pay attention to one and not the other.

People with schizophrenia have been shown to have problems with selective attention, Silverstein said, and meanwhile people who were born blind are better at this task than sighted people. When compared to sighted people, congenitally blind people are also better at hearing different pitches, telling pitches apart, and telling where sounds come from. People with schizophrenia are the opposite: They usually have difficulty with listening accuracy, and process speech abnormally. Not being able to properly figure out where sounds are coming from could lead to someone thinking that their own voice is coming from somewhere else, and contribute to delusional thinking.

It’s a compelling list that goes on and on: Blind people are better than sighted ones on reaction time to both sound and touch; schizophrenia patients show deficits in these areas. Blind people have better working memories, and people with schizophrenia can have impairments in memory. Congenitally blind people are also impervious to the rubber hand illusion, when a person feels like an inanimate object is part of their own body (the experiment is typically done using a rubber hand). It could mean that blind people have more stability when it comes to their bodily representation.

“I would say there are probably about 20 ways that people who are born blind are better, on average, than people in the general population,” Silverstein said. “And it’s in those same areas where people with schizophrenia tend to have more cognitive problems.” (He’s even made a chart, published in one of his papers.)

“If you’re born blind, your brain basically from an early age takes over the visual part of the brain to do other things,” Silverstein said. “And that’s thought to be the reason why some of these auditory, attentional, and body-representation skills are a little more developed in people who were born blind than other people.” Another result of blindness is that brain regions are talking to each other more, in ways they don’t in sighted people—some brain-imaging studies have seen that. People with schizophrenia, meanwhile, tend to have many fewer of these connections.

A concrete explanation for why congenital blindness protects from schizophrenia is still up for grabs—whether the protection comes from predicting the world, having a more connected brain, or relying on other senses.

There’s a lot that needs to be fleshed out. For example, there is more than one kind of congenital blindness. Cortical blindness is caused by an issue in the part of the brain that processes vision, whereas peripheral blindness is a problem in the eyes instead—but the visual part of the brain is okay. While there are still no reported cases of people with congenital cortical blindness, there might be a few people who were born blind with peripheral blindness who did develop schizophrenia. (Some of the cases are several decades old, or the person has other serious diseases, so saying for sure is tough.)

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Congenital blindness doesn’t seem to protect against any other mental illness, so it’s not a safeguard overall. Congenitally blind people have been reported to have had eating disorders and arachnophobia—a person can have those disorders without ever having seen their bodies or a spider). And if a person is born both deaf and blind, it doesn’t seem to offer protection either—that comes with higher risks for psychosis.

There’s a disease called Usher syndrome, in which people are born deaf and lose their vision early in childhood; it’s been associated with schizophrenia and psychosis. Silverstein said that it’s unclear why adding deafness to the mix removes the protection that blindness seems to offer. “One possibility is that blindness by itself presents a surmountable challenge to cope with the environment and thereby fosters compensatory sensory, perceptual, and cognitive changes that lead to a surprisingly high level of functioning,” Silverstain wrote in a 2013 paper. “Deafblindness, on the other hand, may so seriously restrict the opportunity for environmental interaction that it also stunts the development of cognitively based coping strategies.”

But in the end, it’s this extreme specificity that’s most intriguing. It could lead to a different approach to thinking about psychosis, Corlett said. The development of the visual system could be looked at more closely, along with people’s visual predictions. It could open up some basic research avenues to help gain more fundamental understanding of schizophrenia: “What’s the relationship between those really basic visual perceptual mechanisms and the onset of symptoms?” Corlett asked. We’ve made very little progress in our understanding of psychosis in particular, but also in psychiatry more broadly, in terms of how these symptoms are created in the brain. I think anything that gives us inspiration, anything that might give us a bit of leverage is really, really welcomed.”

In the U.S., work with schizophrenia patients has been heavily focused on cognitive tasks, like memory, Corlett said, but maybe cognitive training should include more focus on sensory factors and perception. Perhaps early visual training, along with cognitive training, could potentially help. And instead of a blood test, perhaps one day there could be an eye test for people to assess if they’re at high risk for psychosis.

Another thing to consider, which Silverstein has written about, is having people at risk for schizophrenia increase their reliance on their non-vision senses, to see if that enhances their functioning.

It’s not a novel approach: to go looking for where a disease doesn’t exist, in order to learn something more about it. In the 1980s and 1990s, there were people who were commonly exposed to HIV, but never developed AIDS. Studying those people led to a deeper understanding of risks, and what protective factors they may have had. It was a long-standing medical mystery that people with sickle-cell anemia were somehow protected from getting malaria. The same gene that causes abnormal red blood cells in sickle cell anemia is protective against malaria—offering a window into how malaria works in the body.

It can be difficult to study, especially for rare diseases, where you have to wait for natural cases to arise. But it can be a unique place for clues. “I often joke that it’d be interesting to study people like Keith Richards or Ozzy Osbourne: Why they haven’t been ravaged by opiate addiction in the same way or similar addiction,” Corlett said. “ What is it about these people that led them not to manifest illnesses? has been traditionally a very useful way of exploring what it means to be at risk and what it means to have pathophysiology.”

With schizophrenia and blindness, Silverstein said we’re not there yet, and probably not close. That said, he doesn’t think that we should ignore it.

“At this point, I don’t think I’d go so far as to say it’s promising,” Silverstein said. “The word I’d use is intriguing. “In some ways, this is one of the most interesting observations in a long time in schizophrenia research. Because it’s the only thing that seems to be protective against schizophrenia. I think there’s something here and this should be looked into much more.”

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