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Dyslexia Doesn't Work the Way We Thought It Did

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Dyslexia is not just about reading, or even language. It’s about something more fundamental: How much can the brain adapt to what it has just observed? People with dyslexia typically have less brain plasticity than those without dyslexia, two recent studies have found.

Though the studies measured people’s brain activity in two different ways and while performing different tasks, researchers at the Hebrew University of Israel, reporting in eLife, and researchers from MIT, reporting in Neuron, both found that dyslexics’ brains did not adapt as much to repeated stimuli, including spoken words, musical notes, and faces.

Both sets of researchers found that people with dyslexia more quickly forget recent events. This type of memory is called incidental or implicit memory, and includes anything you didn't know you needed to remember when it happened. Because of how quickly their implicit memory fades, dyslexics' brains don't adapt as much after reading or hearing something repeatedly—which is perhaps why it is harder for their brains to process the words they read.

Your brain generally benefits from repetition because it relates a stimulus to what you've already experienced—like a note you have heard before or a face you’ve seen. Researchers can see this by measuring brain response with electroencephalography (EEG), a noninvasive way of measuring electrical activity in the brain by attaching electrodes to your scalp. Measured by EEG, people’s brain responses decrease when they’ve heard a repeated note. The brain gets more efficient with repetition: It knows something about the note already, so it doesn’t have to work as hard to capture all of its details. It’s a bit like when you see an animal and recognize right away that it’s a dog without having to catalogue all of the things that make it a dog. Your brain is efficient at recognizing dogs because you’ve seen them before.

SHORTER MEMORIES AND LESS ADAPTABILITY

In the Hebrew University study, led by Merav Ahissar, researchers gave subjects a musical task: The researchers played two different notes and asked which was higher. Previous research has found that people do better on this task when one of the notes is a repeat of a note they’ve heard recently. But Ahissar found that people with dyslexia did not benefit as much from the repetition. When a tone was repeated only three seconds after the "anchor" tone, they got some benefit, but not after nine seconds had elapsed. And when Ahissar’s team measured dyslexic people’s brain responses with EEG, their brain responses didn’t decrease. Their brains didn’t get any more efficient—they were less adaptable.

The MIT study, led by John Gabrieli, found similar results through a different experiment. Gabrieli used functional magnetic resonance imaging (fMRI) to measure people’s brain activity by measuring changes in blood flow in their brains. Instead of asking people to discriminate between musical notes, Gabrieli's team simply presented people with repeated things, including spoken words, written words, faces, and common objects like tables or chairs. During this task, dyslexic people's neural activity demonstrated less adaptation.

“It was a big surprise for us,” Gabrieli tells mental_floss, “because people with reading disorders don't typically have any problems with faces or objects.” Next, Gabrieli is curious to look into whether the effects of dyslexia on brain plasticity are limited to hearing and vision, or whether they also extend to other senses like touch and smell.

Together, these studies build a better understanding of how dyslexia works, and because the two studies found the same result with different methods, their results are more convincing than a single study alone. But they also raise a new question: Why is dyslexia mainly noticeable in reading if it affects other types of memories as well?

READING IS NEW—AND HARD, FROM THE BRAIN'S PERSPECTIVE

One theory is that reading is simply a difficult task. “We have a long evolutionary history in our brains for recognizing objects, recognizing faces," Gabrieli points out. That's not the case for reading. “There’s hardly a bigger challenge for brain plasticity than learning to read." More evolutionary time has allowed the brain to evolve redundant ways of accomplishing the same thing. Perhaps people with dyslexia are better at compensating for the memory gap for recognizing faces and spoken words because the brain has more alternate pathways for these processes than it does for reading.

Both Ahissar and Gabrieli are most excited that this research opens up new ways of studying—and perhaps someday treating—dyslexia. If dyslexia is a condition of reading and language only, as previously believed, “we cannot study it in animals,” Ahissar tells mental_floss. On the other hand, if it’s a condition of brain plasticity, we can—in fact, plasticity has been extensively studied in animals, and neuroscientists know a lot about it.

Someday, Gabrieli says, it may even be possible to develop drugs that would treat dyslexia by promoting brain plasticity, although researchers would have to be careful both practically and ethically.

“We can’t imagine developing a drug that would enhance language directly—that's too complicated," he notes. "But brain plasticity is something that neuroscientists are making amazing progress on.”

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Scientists Identify Cells in the Brain That Control Anxiety
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People plagued with the uncomfortable thoughts and sensations characteristic of anxiety disorders may have a small group of cells in the brain to blame, according to a new study. As NPR reports, a team of researchers has identified a class of brain cells that regulates anxiety levels in mice.

The paper, published in the journal Neuron, is based on experiments conducted on a group of lab mice. As is the case with human brains, the hippocampus in mouse brains is associated with fear and anxiety. But until now, researchers didn't know which neurons in the hippocampus were responsible for feelings of worry and impending danger.

To pinpoint the cells at work, scientists from Columbia University, the University of California, San Francisco, and other institutions placed mice in a maze with routes leading to open areas. Mice tend to feel anxious in spacious environments, so researchers monitored activity in the hippocampus when they entered these parts of the maze. What the researchers saw was a specialized group of cells lighting up when the mice entered spaces meant to provoke anxiety.

To test if anxiety was really the driving factor behind the response, they next used a technique called optogenetics to control these cells. When they lowered the cells' activity, the mice seemed to relax and wanted to explore the maze. But as they powered the cells back up, the mice grew scared and didn't venture too far from where they were.

Anxiety is an evolutionary mechanism everyone experiences from time to time, but for a growing portion of the population, anxiety levels are debilitating. Generalized anxiety disorder, social anxiety disorder, and panic disorder can stem from a combination of factors, but most experts agree that overactive brain chemistry plays a part. Previous studies have connected anxiety disorders to several parts of the brain, including the hippocampus, which governs memory as well as fear and worry.

By uncovering not just how the brain produces symptoms of anxiety but the individual cells behind them, scientists hope to get closer to a better treatment. There's more work to be done before that becomes a possibility. The anxiety cells in mice aren't necessarily a perfect indicator of which cells regulate anxiety in humans, and if a new treatment does eventually come from the discovery, it will be one of many options rather than a cure-all for every patient with the disorder.

[h/t NPR]

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Wilder Penfield: The Pioneering Brain Surgeon Who Operated on Conscious Patients
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Public Domain, Wikimedia Commons

For centuries, epilepsy was a source of mystery to scientists. Seizures were thought to be caused by everything from masturbation to demonic possession, and it wasn’t until the 1930s that a neurosurgeon showed the condition could sometimes be boiled down to specific spots in the brain. To do it, he had to open up patients’ heads and electrocute their brain tissue—while they were still conscious.

Wilder Penfield, the subject of today’s Google Doodle, was born on January 26, 1891 in Spokane, Washington. According to Vox, the Canadian-American doctor revolutionized the way we think about and treat epilepsy when he pioneered the Montreal Procedure. The operation required him to remove portions of the skulls of epilepsy sufferers to access their brains. He believed seizures were connected to small areas of brain tissue that were somehow damaged, and by removing the affected regions he could cure the epilepsy. His theory was based on the fact that people with epilepsy often experience “auras” before a seizure: vivid recollections of random scents, tastes, or thoughts.

To pinpoint the damaged brain tissue, he would have to locate the part of the brain tied to his patient’s aura. This meant that the patient would need to be awake to tell him when he struck upon the right sensation. Penfield stimulated the exposed brain tissue with an electrode, causing the patient to either feel numbness in certain limbs, experience certain smells, or recall certain memories depending on what part of the brain he touched. A local anesthetic reduced pain in the head; shocking the brain didn’t cause any pain because the organ doesn’t contain pain receptors.

During one of his surgeries, a patient famously cried, “I smell burnt toast!” That was the same scent that visited her before each seizure, and after Penfield removed the part of her brain associated with the sensation, her epilepsy went away.

Brain surgery isn’t a cure-all for every type of epilepsy, but treatments similar to the one Penfield developed are still used today. In some cases, as much as half of the brain is removed with positive results.

[h/t Vox]

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