Neuroscience

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Decoding Dreams
“[I was] somewhere, in a place like a studio to make a TV program or something,” a groggy study participant recounted (in Japanese). “A male person ran with short steps from the left side to the right side. Then, he tumbled.” The participant had recently been awoken by Masako Tamaki, a postdoc in the lab of neuroscientist Yukiyasu Kamitani of the ATR Computational Neuroscience Laboratories in Kyoto, Japan. He was lying in a functional magnetic resonance imaging (fMRI) scanner, doing his best to recall what he had been dreaming about. “He stumbled over something, and stood up while laughing, and said something,” the participant continued. “He said something to persons on the left side.”
At first blush, the story doesn’t seem particularly informative. But the study subject saw a man, not a woman. And he was inside some sort of workplace. That fragmented information is enough for Kamitani and his team, who recorded dream appearances of 20 key objects, such as “male” or “room,” and used a machine-learning algorithm to correlate those concepts with the fMRI images to find patterns that could be used to predict what people were dreaming about without having to wake them. Such information could help inform the study of why people dream, an elusive question in neurobiology, Kamitani says. “Knowing what is represented during sleep would help to understand the function of dreaming.”
Analyzing more than 200 dream reports—some 30–45 hours of interviews with each of three participants—Kamitani and his colleagues built a “dream-trained decoder” based on fMRI imagery of the V1, V2, and V3 areas of the visual cortex. “We find some rule, or mapping, or pattern between what the person is seeing and what activity is happening in the brain,” Kamitani explains. And it worked, according to Kamitani, who presented the results at the Society for Neuroscience meeting in New Orleans in October 2012, predicting whether or not the 20 objects occurred in dreams with 75–80 percent accuracy.
But while Kamitani’s dream-decoding study is interesting, says neurobiologist David Kahn of Harvard Medical School, the algorithms used are quite primitive, only providing a handful of clues about the dream’s content. “We still have a long way to go before we can actually re-create the story that is the dream,” he says. “This is almost science fiction, because we’re way, way far from it … [but] this is an added tool.”
“Decoding is very primitive,” Kamitani agrees, “but I think there are a lot of potentials.” One way to get a more complete picture of the dream is to increase the complexity of the decoder, he notes. In this first study, for example, the researchers focused on nouns representing visual objects, but going forward, Kamitani says he hopes to include other concepts, like verbs. “By analyzing that aspect we may be able to add some action aspects in the dream.”
Furthermore, researchers might not have to fully interpret the dream themselves to benefit from the new decoder. Instead, the clues gleaned from the fMRI images could simply be used to jog participants’ memories. “We know that dreams—even the most vivid dreams we remember, [like] nightmares or lucid dreams—are really fragile memories,” says Antonio Zadra, an experimental psychologist at the University of Montreal. “Unless you wrote it down or told it to someone in the morning, usually even before lunch, that memory will start fading. And by night, you might just have the essence.”
Unfortunately, that failing memory was the only resource for researchers studying dreams. Now, with a little bit of supplemental information, they may be able to help participants recall dreams more precisely. “The subjective reports are never complete,” Kamitani says. “By giving the subject what we reconstructed, they may remember something more.”
At an even more basic level, the decoder could help scientists understand what’s happening in the brain during dreaming. “To create this whole virtual world out of nothing—with no visual input or auditory input—is quite fascinating and undoubtedly very complex,” Zadra says. “This research will certainly help us better understand what brain areas are doing what, to even allow for this to happen.”
In Kamitani’s study, for example, the researchers found that areas of higher-level visual processing, which respond to more abstract features, were more useful for interpreting dream content than lower-level processing areas. This makes sense, given that those lower areas of the visual cortex are more closely connected to the direct input from the retina. But, Kamitani notes, this could simply have to do with the way the study was designed. “We didn’t train the decoder with low-level visual features,” such as shape or contrast, he says. “We just used the semantic category information.”
Indeed, given the richness of the dreaming experience, such visual qualities may well be encoded during sleep. “Your brain creates a whole virtual world for you when you are dreaming, complete with characters, settings, interactions, dialogues,” says Zadra. “But you’re actually in your bed asleep; there is no visual input. So your brain is literally creating this virtual world from A to Z.”

Decoding Dreams

“[I was] somewhere, in a place like a studio to make a TV program or something,” a groggy study participant recounted (in Japanese). “A male person ran with short steps from the left side to the right side. Then, he tumbled.” The participant had recently been awoken by Masako Tamaki, a postdoc in the lab of neuroscientist Yukiyasu Kamitani of the ATR Computational Neuroscience Laboratories in Kyoto, Japan. He was lying in a functional magnetic resonance imaging (fMRI) scanner, doing his best to recall what he had been dreaming about. “He stumbled over something, and stood up while laughing, and said something,” the participant continued. “He said something to persons on the left side.”

At first blush, the story doesn’t seem particularly informative. But the study subject saw a man, not a woman. And he was inside some sort of workplace. That fragmented information is enough for Kamitani and his team, who recorded dream appearances of 20 key objects, such as “male” or “room,” and used a machine-learning algorithm to correlate those concepts with the fMRI images to find patterns that could be used to predict what people were dreaming about without having to wake them. Such information could help inform the study of why people dream, an elusive question in neurobiology, Kamitani says. “Knowing what is represented during sleep would help to understand the function of dreaming.”

Analyzing more than 200 dream reports—some 30–45 hours of interviews with each of three participants—Kamitani and his colleagues built a “dream-trained decoder” based on fMRI imagery of the V1, V2, and V3 areas of the visual cortex. “We find some rule, or mapping, or pattern between what the person is seeing and what activity is happening in the brain,” Kamitani explains. And it worked, according to Kamitani, who presented the results at the Society for Neuroscience meeting in New Orleans in October 2012, predicting whether or not the 20 objects occurred in dreams with 75–80 percent accuracy.

But while Kamitani’s dream-decoding study is interesting, says neurobiologist David Kahn of Harvard Medical School, the algorithms used are quite primitive, only providing a handful of clues about the dream’s content. “We still have a long way to go before we can actually re-create the story that is the dream,” he says. “This is almost science fiction, because we’re way, way far from it … [but] this is an added tool.”

“Decoding is very primitive,” Kamitani agrees, “but I think there are a lot of potentials.” One way to get a more complete picture of the dream is to increase the complexity of the decoder, he notes. In this first study, for example, the researchers focused on nouns representing visual objects, but going forward, Kamitani says he hopes to include other concepts, like verbs. “By analyzing that aspect we may be able to add some action aspects in the dream.”

Furthermore, researchers might not have to fully interpret the dream themselves to benefit from the new decoder. Instead, the clues gleaned from the fMRI images could simply be used to jog participants’ memories. “We know that dreams—even the most vivid dreams we remember, [like] nightmares or lucid dreams—are really fragile memories,” says Antonio Zadra, an experimental psychologist at the University of Montreal. “Unless you wrote it down or told it to someone in the morning, usually even before lunch, that memory will start fading. And by night, you might just have the essence.”

Unfortunately, that failing memory was the only resource for researchers studying dreams. Now, with a little bit of supplemental information, they may be able to help participants recall dreams more precisely. “The subjective reports are never complete,” Kamitani says. “By giving the subject what we reconstructed, they may remember something more.”

At an even more basic level, the decoder could help scientists understand what’s happening in the brain during dreaming. “To create this whole virtual world out of nothing—with no visual input or auditory input—is quite fascinating and undoubtedly very complex,” Zadra says. “This research will certainly help us better understand what brain areas are doing what, to even allow for this to happen.”

In Kamitani’s study, for example, the researchers found that areas of higher-level visual processing, which respond to more abstract features, were more useful for interpreting dream content than lower-level processing areas. This makes sense, given that those lower areas of the visual cortex are more closely connected to the direct input from the retina. But, Kamitani notes, this could simply have to do with the way the study was designed. “We didn’t train the decoder with low-level visual features,” such as shape or contrast, he says. “We just used the semantic category information.”

Indeed, given the richness of the dreaming experience, such visual qualities may well be encoded during sleep. “Your brain creates a whole virtual world for you when you are dreaming, complete with characters, settings, interactions, dialogues,” says Zadra. “But you’re actually in your bed asleep; there is no visual input. So your brain is literally creating this virtual world from A to Z.”

Filed under Neuroscience 2012 dream-trained decoder dreaming neuroscience sleep brain science

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Scientists explore the illusion of memory
A memory might seem like a permanent, precious essence carved deep into the circuits of the brain. But it is not. Instead, scientists are discovering that a memory changes every time you think about it.
"Every time you recall a memory, it becomes sensitive to disruption. Often that is used to incorporate new information into it." That’s the blunt assessment from one of the world’s leading experts on memory, Dr. Eric Kandel from Columbia University.
And that means our memories are not abstract snapshots stored forever in a bulging file in our mind, but rather, they’re a collection of brain cells — neurons that undergo chemical changes every time they’re engaged.
So when we think about something from the past, the memory is called up like a computer file, reviewed and revised in subtle ways, and then sent back to the brain’s archives, now modified slightly, updated, and changed.
As scientists increasingly understand the biological process of memory, they are also learning how to interrupt it, and that means they might one day be able to ease the pain of past trauma, or alter destructive habits and addictions, as though shaking an Etch A Sketch, erasing the scribbles on the mind, and starting fresh.
In his McGill University lab, researcher Karim Nader routinely erases the memory of his laboratory rats. But first he has to give them a memory and he does that by putting them in an isolation cubicle, playing a tone, and then delivering a small electrical shock to their feet.
Read more

Scientists explore the illusion of memory

A memory might seem like a permanent, precious essence carved deep into the circuits of the brain. But it is not. Instead, scientists are discovering that a memory changes every time you think about it.

"Every time you recall a memory, it becomes sensitive to disruption. Often that is used to incorporate new information into it." That’s the blunt assessment from one of the world’s leading experts on memory, Dr. Eric Kandel from Columbia University.

And that means our memories are not abstract snapshots stored forever in a bulging file in our mind, but rather, they’re a collection of brain cells — neurons that undergo chemical changes every time they’re engaged.

So when we think about something from the past, the memory is called up like a computer file, reviewed and revised in subtle ways, and then sent back to the brain’s archives, now modified slightly, updated, and changed.

As scientists increasingly understand the biological process of memory, they are also learning how to interrupt it, and that means they might one day be able to ease the pain of past trauma, or alter destructive habits and addictions, as though shaking an Etch A Sketch, erasing the scribbles on the mind, and starting fresh.

In his McGill University lab, researcher Karim Nader routinely erases the memory of his laboratory rats. But first he has to give them a memory and he does that by putting them in an isolation cubicle, playing a tone, and then delivering a small electrical shock to their feet.

Read more

Filed under brain memory memory disruption PTSD OCD neuroscience psychology science

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Pesticides and Parkinson’s: UCLA researchers uncover further proof of a link
For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson’s disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California’s Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.
Now, UCLA researchers have discovered a link between Parkinson’s and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.
Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson’s disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.
Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson’s. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.
The investigators believe their findings concerning benomyl may be generalized to all Parkinson’s patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.
The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Pesticides and Parkinson’s: UCLA researchers uncover further proof of a link

For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson’s disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California’s Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Now, UCLA researchers have discovered a link between Parkinson’s and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson’s disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson’s. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson’s patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Filed under parkinson's disease pesticides benomyl brain neuron environment science

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Rainfall, brain infection linked in sub-Saharan Africa
The amount of rainfall affects the number of infant infections leading to hydrocephalus in Uganda, according to a team of researchers who are the first to demonstrate that these brain infections are linked to climate.
Hydrocephalus — literally “water on the brain” — is characterized by the buildup of the fluid that is normally within and surrounding the brain, leading to brain swelling. The swelling will cause brain damage or death if not treated. Even if treated, there is only a one-third chance of a child maintaining a normal life after post-infectious hydrocephalus develops, and that chance is dependent on whether the child has received the best treatment possible.
"The most common need for a child to require neurosurgery around the world is hydrocephalus," said Steven J. Schiff, the Brush Chair Professor of Engineering, director of the Penn State Center for Neural Engineering and a team member.
In sub-Saharan Africa, upward of 100,000 cases of post-infectious hydrocephalus a year are estimated to occur. The majority of these cases occur after a newborn has suffered from neonatal sepsis, a blood infection that occurs within the first four weeks of life, the researchers reported in a recent issue of the Journal of Neurosurgery: Pediatrics.
Benjamin C. Warf, associate professor of neurosurgery, Harvard Medical School, Boston Children’s Hospital, noticed that about three or four months after an infant in East Africa had an infection like neonatal sepsis, the child would often return to the clinic with a rapidly growing head — hydrocephalus. Schiff joined Warf to help figure out what caused this disease so frequently.
Schiff and colleagues tracked 696 hydrocephalus cases in Ugandan infants between the years 2000 and 2005. The researchers obtained localized rainfall data for the same time frame through NOAA (National Oceanic and Atmospheric Administration) weather satellites using the African Rainfall Estimation Algorithm developed at the U.S. NOAA Climate Prediction Center.
Uganda has two peak rainfall seasons, in spring and fall. By comparing the data from NOAA and the hydrocephalus cases, the researchers found that instances of the disorder rose significantly at four different times throughout the year — before and after the peak of each rainy season, when the amount of rainfall was at intermediate levels. In Uganda an intermediate rainfall is about 6 inches of rain per month.
Schiff and colleagues previously noted that different bacteria appear associated with post-infectious hydrocephalus at different seasons of the year. While the researchers have not yet characterized the full spectrum of bacteria causing hydrocephalus in so many infants, they note that environmental conditions affect conditions supporting bacterial growth, and that the amount of rain can quench bacterial infections. The moisture level clearly affects the number of cases of hydrocephalus in this region of East Africa.
"Hydrocephalus is the first major neurosurgical condition linked to climate," said Schiff, who is also professor of neurosurgery, engineering science and mechanics, and physics, and a faculty member of the Huck Institutes of the Life Sciences. "This means that a substantial component of these cases are almost certainly driven from the environmental conditions, and that means they are potentially preventable if we understand the routes and mechanisms of infection better."

Rainfall, brain infection linked in sub-Saharan Africa

The amount of rainfall affects the number of infant infections leading to hydrocephalus in Uganda, according to a team of researchers who are the first to demonstrate that these brain infections are linked to climate.

Hydrocephalus — literally “water on the brain” — is characterized by the buildup of the fluid that is normally within and surrounding the brain, leading to brain swelling. The swelling will cause brain damage or death if not treated. Even if treated, there is only a one-third chance of a child maintaining a normal life after post-infectious hydrocephalus develops, and that chance is dependent on whether the child has received the best treatment possible.

"The most common need for a child to require neurosurgery around the world is hydrocephalus," said Steven J. Schiff, the Brush Chair Professor of Engineering, director of the Penn State Center for Neural Engineering and a team member.

In sub-Saharan Africa, upward of 100,000 cases of post-infectious hydrocephalus a year are estimated to occur. The majority of these cases occur after a newborn has suffered from neonatal sepsis, a blood infection that occurs within the first four weeks of life, the researchers reported in a recent issue of the Journal of Neurosurgery: Pediatrics.

Benjamin C. Warf, associate professor of neurosurgery, Harvard Medical School, Boston Children’s Hospital, noticed that about three or four months after an infant in East Africa had an infection like neonatal sepsis, the child would often return to the clinic with a rapidly growing head — hydrocephalus. Schiff joined Warf to help figure out what caused this disease so frequently.

Schiff and colleagues tracked 696 hydrocephalus cases in Ugandan infants between the years 2000 and 2005. The researchers obtained localized rainfall data for the same time frame through NOAA (National Oceanic and Atmospheric Administration) weather satellites using the African Rainfall Estimation Algorithm developed at the U.S. NOAA Climate Prediction Center.

Uganda has two peak rainfall seasons, in spring and fall. By comparing the data from NOAA and the hydrocephalus cases, the researchers found that instances of the disorder rose significantly at four different times throughout the year — before and after the peak of each rainy season, when the amount of rainfall was at intermediate levels. In Uganda an intermediate rainfall is about 6 inches of rain per month.

Schiff and colleagues previously noted that different bacteria appear associated with post-infectious hydrocephalus at different seasons of the year. While the researchers have not yet characterized the full spectrum of bacteria causing hydrocephalus in so many infants, they note that environmental conditions affect conditions supporting bacterial growth, and that the amount of rain can quench bacterial infections. The moisture level clearly affects the number of cases of hydrocephalus in this region of East Africa.

"Hydrocephalus is the first major neurosurgical condition linked to climate," said Schiff, who is also professor of neurosurgery, engineering science and mechanics, and physics, and a faculty member of the Huck Institutes of the Life Sciences. "This means that a substantial component of these cases are almost certainly driven from the environmental conditions, and that means they are potentially preventable if we understand the routes and mechanisms of infection better."

Filed under brain brain damage hydrocephalus neonatal sepsis rainfall medicine science

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Your Brain on Big Bird: Sesame Street Helps to Reveal Patterns of Neural Development
Using brain scans of children and adults watching Sesame Street, cognitive scientists are learning how children’s brains change as they develop intellectual abilities like reading and math.
The novel use of brain imaging during everyday activities like watching TV, say the scientists, opens the door to studying other thought processes in naturalistic settings and may one day help to diagnose and treat learning disabilities.
Scientists are just beginning to use brain imaging to understand how humans process thought during real-life experiences. For example, researchers have compared scans of adults watching an entertaining movie to see if neural responses are similar across different individuals. “But this is the first study to use the method as a tool for understanding development,” says lead author Jessica Cantlon, an assistant professor in brain and cognitive sciences at the University of Rochester.
Eventually, that understanding may help pinpoint the cause when a child experiences difficulties mastering school work. “Psychologists have behavioral tests for trying to get the bottom of learning impairments, but these new imaging studies provide a totally independent source of information about children’s learning based on what’s happening in the brain,” says Cantlon.
The neuroimaging findings are detailed in a new study published Jan. 3 by the Public Library of Science’s open-access journal PLoS Biology, by Cantlon and her former research assistant Rosa Li, now a graduate student at Duke University.

Your Brain on Big Bird: Sesame Street Helps to Reveal Patterns of Neural Development

Using brain scans of children and adults watching Sesame Street, cognitive scientists are learning how children’s brains change as they develop intellectual abilities like reading and math.

The novel use of brain imaging during everyday activities like watching TV, say the scientists, opens the door to studying other thought processes in naturalistic settings and may one day help to diagnose and treat learning disabilities.

Scientists are just beginning to use brain imaging to understand how humans process thought during real-life experiences. For example, researchers have compared scans of adults watching an entertaining movie to see if neural responses are similar across different individuals. “But this is the first study to use the method as a tool for understanding development,” says lead author Jessica Cantlon, an assistant professor in brain and cognitive sciences at the University of Rochester.

Eventually, that understanding may help pinpoint the cause when a child experiences difficulties mastering school work. “Psychologists have behavioral tests for trying to get the bottom of learning impairments, but these new imaging studies provide a totally independent source of information about children’s learning based on what’s happening in the brain,” says Cantlon.

The neuroimaging findings are detailed in a new study published Jan. 3 by the Public Library of Science’s open-access journal PLoS Biology, by Cantlon and her former research assistant Rosa Li, now a graduate student at Duke University.

Filed under brain brain scans neural response learning disability MRI neuroscience science

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Research opens up possibility of therapies to restore blood-brain barrier

Research led by Queen Mary, University of London, has opened up the possibility that drug therapies may one day be able to restore the integrity of the blood-brain barrier, potentially slowing or even reversing the progression of diseases like multiple sclerosis (MS). The study, funded by the Wellcome Trust, is published in Proceedings of the National Academy of Sciences.

image

The blood-brain barrier (BBB) is a layer of cells, including endothelial cells, which line the blood vessels in the brain and spinal cord. These cells act as a barrier, stopping certain molecules, including immune cells and viruses, passing from the blood stream into the central nervous system (brain and spinal cord).

In a number of neurodegenerative brain diseases, including MS, the BBB is compromised, allowing inappropriate cells to pass into the brain with devastating consequences.

In this study the researchers identified a specific protein – known as Annexin A1 (ANXA1) – as being integral in maintaining the BBB in the brain. The authors initially found that mice bred to lack this protein showed a decrease in integrity of the BBB compared to controls.

Taking this finding, they then investigated the potential role of ANXA1 in conditions which involve progressive breakdown of the BBB, including MS and Parkinson’s disease, by examining post-mortem human brain tissue samples. ANXA1 was present in the cells of samples from individuals who did not have a neurological disease and also in samples from patients who had died with Parkinson’s disease. However, it was not detectable in the endothelial cells in samples from patients who had died with MS.

Crucially, the researchers found that treating in vitro brain endothelial cells with human recombinant ANXA1 restored the key cellular features needed to reinstate the integrity of the BBB. The same was seen with the ANXA1 knockout mice, where administering the protein reversed the permeability of the BBB within 24 hours.

Dr Egle Solito, from Barts and The London School of Medicine and Dentistry, part of Queen Mary, who co-ordinated the study said: “Our findings suggest this protein plays a key role in maintaining a functioning BBB and, more importantly, has the potential to rescue defects in the BBB. We now need to carry on our research to see how much this molecule may be exploited for therapeutic uses in conditions such as MS, or as a biomarker to help in early diagnosis.”

(Source: qmul.ac.uk)

Filed under brain cells CNS blood–brain barrier neurological diseases science

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Electric stimulation of brain releases powerful, opiate-like painkiller
Researchers used electricity on certain regions in the brain of a patient with chronic, severe facial pain to release an opiate-like substance that’s considered one of the body’s most powerful painkillers.
The findings expand on previous work done at the University of Michigan, Harvard University and the City University of New York where researchers delivered electricity through sensors on the skulls of chronic migraine patients, and found a decrease in the intensity and pain of their headache attacks. However, the researchers then couldn’t completely explain how or why.
The current findings help explain what happens in the brain that decreases pain during the brief sessions of electricity, says Alexandre DaSilva, the senior researcher in the study from the University of Michigan School of Dentistry. Other study authors include DaSilva’s PhD student, Marcos DosSantos, and also Dr. Jon-Kar Zubieta from the Molecular and Behavioral Neuroscience Institute.
In their current study, DaSilva and colleagues intravenously administered a radiotracer that reached important brain areas in a patient with trigeminal neuropathic pain (TNP), a type of chronic, severe facial pain. They applied the electrodes and electrically stimulated the skull right above the motor cortex of the patient for 20 minutes during a PET scan (positron emission tomography). The stimulation is called transcranial direct current stimulation (tDCS).
The radiotracer was specifically designed to measure, indirectly, the local brain release of mu-opioid, a natural substance that alters pain perception. In order for opiate to function, it needs to bind to the mu-opioid receptor (the study assessed levels of this receptor).
"This is arguably the main resource in the brain to reduce pain," DaSilva said. "We’re stimulating the release of our (body’s) own resources to provide analgesia. Instead of giving more pharmaceutical opiates, we are directly targeting and activating the same areas in the brain on which they work. (Therefore), we can increase the power of this pain-killing effect and even decrease the use of opiates in general, and consequently avoid their side effects, including addiction."
Most pharmaceutical opiates, especially morphine, target the mu-opioid receptors in the brain, DaSilva says.
The dose of electricity is very small, he says. Consider that electroconvulsive therapy (ECT), which is used to treat depression and other psychiatric conditions, uses amperage in the brain ranging from 200 to 1600 milliamperes (mA). The tDCS protocol used in DaSilva’s study delivered 2 mA, considerably lower than ECT.
Just one session immediately improved the patient’s threshold for cold pain by 36 percent, but not the patient’s clinical, TNP/facial pain. This suggests that repetitive electrical stimulation over several sessions are required to have a lasting effect on clinical pain as shown in their previous migraine study, DaSilva says.
The manuscript appears in the journal Frontiers in Psychiatry. The group just completed another study with more subjects, and the initial results seem to confirm the findings above, but further analysis is necessary.
Next, researchers will investigate long-term effects of electric stimulation on the brain and find specific targets in the brain that may be more effective depending on the pain condition and patients’ status. For example, the frontal areas may be more helpful for chronic pain patients with depression symptoms.

Electric stimulation of brain releases powerful, opiate-like painkiller

Researchers used electricity on certain regions in the brain of a patient with chronic, severe facial pain to release an opiate-like substance that’s considered one of the body’s most powerful painkillers.

The findings expand on previous work done at the University of Michigan, Harvard University and the City University of New York where researchers delivered electricity through sensors on the skulls of chronic migraine patients, and found a decrease in the intensity and pain of their headache attacks. However, the researchers then couldn’t completely explain how or why.

The current findings help explain what happens in the brain that decreases pain during the brief sessions of electricity, says Alexandre DaSilva, the senior researcher in the study from the University of Michigan School of Dentistry. Other study authors include DaSilva’s PhD student, Marcos DosSantos, and also Dr. Jon-Kar Zubieta from the Molecular and Behavioral Neuroscience Institute.

In their current study, DaSilva and colleagues intravenously administered a radiotracer that reached important brain areas in a patient with trigeminal neuropathic pain (TNP), a type of chronic, severe facial pain. They applied the electrodes and electrically stimulated the skull right above the motor cortex of the patient for 20 minutes during a PET scan (positron emission tomography). The stimulation is called transcranial direct current stimulation (tDCS).

The radiotracer was specifically designed to measure, indirectly, the local brain release of mu-opioid, a natural substance that alters pain perception. In order for opiate to function, it needs to bind to the mu-opioid receptor (the study assessed levels of this receptor).

"This is arguably the main resource in the brain to reduce pain," DaSilva said. "We’re stimulating the release of our (body’s) own resources to provide analgesia. Instead of giving more pharmaceutical opiates, we are directly targeting and activating the same areas in the brain on which they work. (Therefore), we can increase the power of this pain-killing effect and even decrease the use of opiates in general, and consequently avoid their side effects, including addiction."

Most pharmaceutical opiates, especially morphine, target the mu-opioid receptors in the brain, DaSilva says.

The dose of electricity is very small, he says. Consider that electroconvulsive therapy (ECT), which is used to treat depression and other psychiatric conditions, uses amperage in the brain ranging from 200 to 1600 milliamperes (mA). The tDCS protocol used in DaSilva’s study delivered 2 mA, considerably lower than ECT.

Just one session immediately improved the patient’s threshold for cold pain by 36 percent, but not the patient’s clinical, TNP/facial pain. This suggests that repetitive electrical stimulation over several sessions are required to have a lasting effect on clinical pain as shown in their previous migraine study, DaSilva says.

The manuscript appears in the journal Frontiers in Psychiatry. The group just completed another study with more subjects, and the initial results seem to confirm the findings above, but further analysis is necessary.

Next, researchers will investigate long-term effects of electric stimulation on the brain and find specific targets in the brain that may be more effective depending on the pain condition and patients’ status. For example, the frontal areas may be more helpful for chronic pain patients with depression symptoms.

Filed under brain pain facial pain migraine electricity painkiller neuroscience science

78 notes

Risk Genes for Alzheimer’s and Mental Illness Linked to Brain Changes at Birth
Some brain changes that are found in adults with common gene variants linked to disorders such as Alzheimer’s disease, schizophrenia, and autism can also be seen in the brain scans of newborns.
“These results suggest that prenatal brain development may be a very important influence on psychiatric risk later in life,” said Rebecca C. Knickmeyer, PhD, lead author of the study and assistant professor of psychiatry in the University of North Carolina School of Medicine. The study was published by the journal Cerebral Cortex on Jan. 3, 2013.
The study included 272 infants who received MRI scans at UNC Hospitals shortly after birth. The DNA of each was tested for 10 common variations in 7 genes that have been linked to brain structure in adults. These genes have also been implicated in conditions such as schizophrenia, bipolar disorder, autism, Alzheimer’s disease, anxiety disorders and depression.
For some polymorphisms – such as a variation in the APOE gene which is associated with Alzheimer’s disease – the brain changes in infants looked very similar to brain changes found in adults with the same variants, Knickmeyer said. “This could stimulate an exciting new line of research focused on preventing onset of illness through very early intervention in at-risk individuals.”
But this was not true for every polymorphism included in the study, said John H. Gilmore, MD, senior author of the study and Thad & Alice Eure Distinguished Professor and Vice Chair for Research and Scientific Affairs in the UNC Department of Psychiatry.
For example, the study included two variants in the DISC1 gene. For one of these variants, known as rs821616, the infant brains looked very similar to the brains of adults with this variant. But there was no such similarity between infant brains and adult brains for the other variant, rs6675281.
“This suggests that the brain changes associated with this gene variant aren’t present at birth but develop later in life, perhaps during puberty,” Gilmore said.
“It’s fascinating that different variants in the same gene have such unique effects in terms of when they affect brain development,” said Knickmeyer.

Risk Genes for Alzheimer’s and Mental Illness Linked to Brain Changes at Birth

Some brain changes that are found in adults with common gene variants linked to disorders such as Alzheimer’s disease, schizophrenia, and autism can also be seen in the brain scans of newborns.

“These results suggest that prenatal brain development may be a very important influence on psychiatric risk later in life,” said Rebecca C. Knickmeyer, PhD, lead author of the study and assistant professor of psychiatry in the University of North Carolina School of Medicine. The study was published by the journal Cerebral Cortex on Jan. 3, 2013.

The study included 272 infants who received MRI scans at UNC Hospitals shortly after birth. The DNA of each was tested for 10 common variations in 7 genes that have been linked to brain structure in adults. These genes have also been implicated in conditions such as schizophrenia, bipolar disorder, autism, Alzheimer’s disease, anxiety disorders and depression.

For some polymorphisms – such as a variation in the APOE gene which is associated with Alzheimer’s disease – the brain changes in infants looked very similar to brain changes found in adults with the same variants, Knickmeyer said. “This could stimulate an exciting new line of research focused on preventing onset of illness through very early intervention in at-risk individuals.”

But this was not true for every polymorphism included in the study, said John H. Gilmore, MD, senior author of the study and Thad & Alice Eure Distinguished Professor and Vice Chair for Research and Scientific Affairs in the UNC Department of Psychiatry.

For example, the study included two variants in the DISC1 gene. For one of these variants, known as rs821616, the infant brains looked very similar to the brains of adults with this variant. But there was no such similarity between infant brains and adult brains for the other variant, rs6675281.

“This suggests that the brain changes associated with this gene variant aren’t present at birth but develop later in life, perhaps during puberty,” Gilmore said.

“It’s fascinating that different variants in the same gene have such unique effects in terms of when they affect brain development,” said Knickmeyer.

Filed under brain brain development anxiety disorders autism schizophrenia genes neuroscience science

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Second impact syndrome: A devastating injury to the young brain
Physicians at Indiana University School of Medicine and the Northwest Radiology Network (Indianapolis, Indiana) report the case of a 17-year-old high school football player with second impact syndrome (SIS). A rare and devastating traumatic brain injury, SIS occurs when a person, most often a teenager, sustains a second head injury before recovery from an earlier head injury is complete. To the best of the authors’ knowledge, this is the first reported case in which imaging studies were performed after both injuries, adding new knowledge of the event. Findings in this case are reported and discussed in “Second impact syndrome in football: new imaging and insights into a rare and devastating condition. Case report,” by Elizabeth Weinstein, M.D., and colleagues, published today online, ahead of print, in the Journal of Neurosurgery: Pediatrics.

Second impact syndrome: A devastating injury to the young brain

Physicians at Indiana University School of Medicine and the Northwest Radiology Network (Indianapolis, Indiana) report the case of a 17-year-old high school football player with second impact syndrome (SIS). A rare and devastating traumatic brain injury, SIS occurs when a person, most often a teenager, sustains a second head injury before recovery from an earlier head injury is complete. To the best of the authors’ knowledge, this is the first reported case in which imaging studies were performed after both injuries, adding new knowledge of the event. Findings in this case are reported and discussed in “Second impact syndrome in football: new imaging and insights into a rare and devastating condition. Case report,” by Elizabeth Weinstein, M.D., and colleagues, published today online, ahead of print, in the Journal of Neurosurgery: Pediatrics.

Filed under brain TBI second impact syndrome head injuries case study neuroscience science

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How Neuroscientists Observe Brains Watching Movies

Unless you have been deaf and blind to the world over the past decade, you know that functional magnetic resonance brain imaging (fMRI) can look inside the skull of volunteers lying still inside the claustrophobic, coffinlike confines of a loud, banging magnetic scanner. The technique relies on a fortuitous property of the blood supply to reveal regional activity. Active synapses and neurons consume power and therefore need more oxygen, which is delivered by the hemoglobin molecules inside the circulating red blood cells. When these molecules give off their oxygen to the surrounding tissue, they not only change color—from arterial red to venous blue—but also turn slightly magnetic.

image

(Image: Todd Davidson/Stock Illustration Source)

Activity in neural tissue causes an increase in the volume and flow of fresh blood. This change in the blood supply, called the hemodynamic signal, is tracked by sending radio waves into the skull and carefully listening to their return echoes. FMRI does not directly measure synaptic and neuronal activity, which occurs over the course of milliseconds; instead it uses a relatively sluggish proxy—changes in the blood supply—that rises and falls in seconds. The spatial resolution of fMRI is currently limited to a volume element (voxel) the size of a pea, encompassing about one million nerve cells.

Neuroscientists routinely exploit fMRI to infer what volunteers are seeing, imagining or intending to do. It is really a primitive form of mind reading. Now a team has taken that reading to a new, startling level.

A number of groups have deduced the identity of pictures viewed by volunteers while lying in the magnet scanner from the slew of map­like representations found in primary, secondary and higher-order visual cortical regions underneath the bump on the back of the head.

Jack L. Gallant of the University of California, Berkeley, is the acknowledged master of these techniques, which proceed in two stages. First, a volunteer looks at a couple of thousand images while lying in a magnet. The response of a few hundred voxels in the visual cortex to each image is carefully registered. These data are then used to train an algorithm to predict the magnitude of the fMRI response for each voxel. Second, this procedure is inverted. That is, for a given magnitude of hemodynamic response, a probabilistic technique called Bayesian decoding infers the most likely image that gave rise to the observed response in that particular volunteer (human brains differ substantially, so it is difficult to use one brain to predict the responses of another).

The best of these techniques exploit preexisting, or prior, knowledge about pictures that could have been seen before. The number of mathematically possible images is vast, but the types of actual scenes that are encountered in a world populated by people, animals, trees, buildings and other objects encompass a tiny fraction of all possible images. Appropriately enough, the images that we usually encounter are called natural images. Using a database of six million natural images, Gallant’s group showed in 2009 how brain responses of volunteers to photographs they had not previously encountered could be reconstructed.

(Source: scientificamerican.com)

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Filed under fMRI neuronal activity nerve cells brain Bayesian decoding neuroscience science

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