Canadian student has “out of body experiences” whenever she wants
After attending a lecture on “out of body experiences,” a 24-year-old student from the University of Ottawa approached her professor saying, “I thought everybody could do that.” She can apparently do this at will — making her the first person with this condition to be studied.
The resulting paper, which now appears in Frontiers in Human Neuroscience, describes the condition as something of an illusion, where a person’s ability to track their body’s position in space and time has somehow become externalized. In this extraordinary case, the university student claims she can do this whenever she wants — to induce the feeling that she can experience her body moving outside the boundaries of her physical body, while remaining aware of her unmoving physical body.
So, if you’re a neuroscientist studying this particular person, what do you do? You put her in a brain scanner, of course. Writing in ABC News, Gillian Mohney explains more:

[Claude] Messier and his co-author interviewed the student and had her undergo an MRI to see if her brain activity might shed light on her unusual ability.
Messier said the girl first noticed her ability when she was a child and had a hard time going to sleep during naps. To pass the time she would “float” above her body.
"I feel myself moving, or, more accurately, can make myself feel as if I am moving. I know perfectly well that I am not actually moving," the student told the researchers. "In fact, I am hyper-sensitive to my body at that point, because I am concentrating so hard on the sensation of moving…For example, if I ‘spin’ for long enough, I get dizzy."
Messier said at some point the student’s brain showed similar activity to that of a high-level athlete who can vividly imagine themselves winning a competition. One difference, however, was that her brain activity was focused on one side, and the athletes usually show activity on both brain hemispheres.
Messier said more study was needed, but he said that this discovery could mean many more people have this ability but find it “unremarkable.” The discovery could be similar to how synesthesia, a mix of multiple senses, was discovered in a wider population.
Alternately, the ability could be something that everyone is able to do as an infant or child, but lose as they get older.

Wild stuff. Typically, this condition happens as the result of an injury, psychological illness, lesions on the brain, or from a drug that induces the illusion. The researchers speculate that this ability might be present in infancy but that it’s lost without regular practice. They also hypothesize that it’s more prevalent in young people… and that it’s a skill that might be developed.

Canadian student has “out of body experiences” whenever she wants

After attending a lecture on “out of body experiences,” a 24-year-old student from the University of Ottawa approached her professor saying, “I thought everybody could do that.” She can apparently do this at will — making her the first person with this condition to be studied.

The resulting paper, which now appears in Frontiers in Human Neuroscience, describes the condition as something of an illusion, where a person’s ability to track their body’s position in space and time has somehow become externalized. In this extraordinary case, the university student claims she can do this whenever she wants — to induce the feeling that she can experience her body moving outside the boundaries of her physical body, while remaining aware of her unmoving physical body.

So, if you’re a neuroscientist studying this particular person, what do you do? You put her in a brain scanner, of course. Writing in ABC News, Gillian Mohney explains more:

[Claude] Messier and his co-author interviewed the student and had her undergo an MRI to see if her brain activity might shed light on her unusual ability.

Messier said the girl first noticed her ability when she was a child and had a hard time going to sleep during naps. To pass the time she would “float” above her body.

"I feel myself moving, or, more accurately, can make myself feel as if I am moving. I know perfectly well that I am not actually moving," the student told the researchers. "In fact, I am hyper-sensitive to my body at that point, because I am concentrating so hard on the sensation of moving…For example, if I ‘spin’ for long enough, I get dizzy."

Messier said at some point the student’s brain showed similar activity to that of a high-level athlete who can vividly imagine themselves winning a competition. One difference, however, was that her brain activity was focused on one side, and the athletes usually show activity on both brain hemispheres.

Messier said more study was needed, but he said that this discovery could mean many more people have this ability but find it “unremarkable.” The discovery could be similar to how synesthesia, a mix of multiple senses, was discovered in a wider population.

Alternately, the ability could be something that everyone is able to do as an infant or child, but lose as they get older.

Wild stuff. Typically, this condition happens as the result of an injury, psychological illness, lesions on the brain, or from a drug that induces the illusion. The researchers speculate that this ability might be present in infancy but that it’s lost without regular practice. They also hypothesize that it’s more prevalent in young people… and that it’s a skill that might be developed.

Know the brain, and its axons, by the clothes they wear

It is widely know that the grey matter of the brain is grey because it is dense with cell bodies and capillaries. The white matter is almost entirely composed of lipid-based myelin, but there is also a little room in the grey matter for a few select axons to be at least partially myelinated. A group of well known researchers, mostly from Harvard and MIT, decided to look for possible patterns in the myelin found in cortical grey matter. Their Science published findings suggest that this dynamic balance struck up by each axon, somewhere between zero and full myelination, does not tip to the benefit of action potential speed alone. Instead, it follows a more subtle give and take between different kinds cells.

In looking down the length of an axon, longitudinally that is, each segment of myelin is separated by a node. The thickness of the myelin coat varies significantly from node to node. Presumably then, so does the speed and reliability of the spike propagated in that segment. The researchers suggest however, that it is more the phase and offset of these nodes that matters. The distance to first node in particular is important because it is here that the spike shape is first initiaillized. As Doug Fields points out in a perspective that accompanies the paper, spike shape (usually inconsequential in computational models) has important functional implications including the amount of transmitter released, the refractory period and the spike frequency.

Within the cortical grey, it is now known that the bare initial segment of the axon isirresistible to other cells. Their synaptic overtures are regularly accepted and also reciprocated by the axon’s own transmitter release from bare, noncanonical release sites. The researchers found that the length of the myelin-free axon initial segment had a graded distribution with the more superficially located pyramidal cells in the mouse cortex having longer “open” axon. In layer II/III bare stretches up to o 55 µm were evident.

The technology that makes it possible to reconstruct serial sections of brain is perhaps the most advanced—and certainly the most industrialized—in neuroscience. It is precisely the same technique used in the recent Brainbow II studies, which incidentally have also yielded some the most celebrated images in science. But I must say, reader, if you are not blown away by the above mentioned details on myelination, you are not alone. That you are still here indicates that you expect something more.

So forgive me, rightfully esteemed authors, if I suggest you have an opportunity here perhaps not yet missed, but rapidly growing stale. Ken, Sebastian, Jeff—Doug, where is the missing myelin mechanics? In the name of all that is Holy, myelination requires a breaking of symmetry, namely it has to wrap in one direction. We have asked previously, in detail, how this constraint is applied in whole brain and nerve, going down an axon, going to immediately adjacent axons, and also to the multiple arms of any one oligodendrocyte.

As myelin undergoes phase transitions in development, does its 3D tubular mesh align like slow motion lipid spin glasses? Is direction imposed individually at each turn, or in bulk transition, perhaps reflective of temperature dependent crystal or magnetic domain formation? More speculatively, can firing axons, simultaneously pulsing mechanically in the radial direction, rectify their continuous cellular substructure into miniscule torques which aid and abet myelination? How does bulk myelination vary across the bilaterally symetric halves of the brain, across the callosum, and down the altogether unique myelin of the nerves units of the body? Now that we clearly have the technology, lets answer these questions and begin to piece this brain together ground up.

The power of the screw and the drill, known to any machinist, is not lost here. The authors own recent incredible work attests to that. They reference their previous discovery of helical substructure in stacked endoplasmic reticulum sheets connected through unique membrane motiffs. Might neurons themselves be chiral, or at least their axons or apical dendrite have a preferred hand? If it is now possible to image effervescent cell organelles, centriolar-defined coordinate systems, the windings of microtubule arrays even down to the tiny symmetry-breaking protein hooks which preferentially adorn them in axons vs dendrtites, certainly we can now construct geometry on larger scales of the brain.

Even Recreational Marijuana May Be Linked To Brain Changes

Adding to earlier evidence that marijuana may be linked to lasting neurological changes, a new study in the Journal of Neuroscience today finds that even casual pot smoking may have an effect on the size and structure of certain brain regions. The new research reports that for each additional joint a person smokes per week, the greater the odds of structural changes to areas involved in motivation, reward, and emotion. Though it seems like the country has embraced pot as a relatively harmless option in recent years, the authors of the study say that their findings suggest otherwise, especially for young people whose brains are still developing.

“This study raises a strong challenge to the idea that casual marijuana use isn’t associated with bad consequences,” said study author Hans Breiter, psychiatry and behavioral sciences professor at Northwestern University Feinberg School of Medicine and psychiatrist at Northwestern Memorial Hospital. “Some of these people only used marijuana to get high once or twice a week. People think a little recreational use shouldn’t cause a problem, if someone is doing OK with work or school. Our data directly says this is not the case.”

In the new study, the team looked at the brains of people 18-25 years old, some of whom smoked pot recreationally and some who did not. None of the participants showed any signs of being addicted to the drug.

Using different brain imaging techniques, the researchers were able to measure the volume, shape, and grey matter density of two key structures: the nucleus accumbens and the amygdala. The nucleus accumbens is involved in the reward circuit, including pleasure-seeking and motivation, and it’s strongly linked to addiction. The amygdala is involved in emotion, particularly in fear, anxiety, and the stress response, and in drug craving.

The team found that both brain structures varied in multiple ways, according to the number of joints per week the participants smoked – in other words, the more joints smoked, the more brain changes were evident. The nucleus accumbens was especially likely to show alterations in shape and density, and to be larger, as a function of joints per week.

“These are core, fundamental structures of the brain,” said study author Anne Blood, director of the Mood and Motor Control Laboratory at Massachusetts General Hospital and psychiatry professor at Harvard Medical School. “They form the basis for how you assess positive and negative features about things in the environment and make decisions about them.”

What’s interesting about the study is that it suggests that even sometimes-smokers show changes in the brain. What’s not clear is whether there were differences in the pot smokers’ behavior or cognitive function. But the authors suggest that the brain changes seen here may be a sort of precursor to addiction: Earlier studies in animals have shown that the active ingredient in pot, tetrahydrocannabinol (THC), may affect neural connectivity, which could be an early sign of a bourgeoning addiction.

“It may be that we’re seeing a type of drug learning in the brain,” said author Jodi Gilman, at Massachusetts General Center for Addiction Medicine. “We think when people are in the process of becoming addicted, their brains form these new connections.”

Although a majority of people in the country support legalization of marijuana, not everyone is so convinced. Last year, Breiter’s team showed that everyday pot smoking in teenagers was, even two years after stopping, linked to brain abnormalities and to poorer working memory. “With the findings of these two papers,” Breiter said, “I’ve developed a severe worry about whether we should be allowing anybody under age 30 to use pot unless they have a terminal illness and need it for pain.”

Capgras and Fregoli Delusions

When people hear the words “psychiatric disorder,” they often think of depression, bipolar disorder, or schizophrenia. However, there are other psychiatric disorders that are not well-known, but are fascinating nonetheless. 

Have you ever thought that a close friend or family member, perhaps even your significant other, had been replaced by an imposter, a pretender? On the other end of the spectrum, perhaps you’ve thought that everybody around you was actually the same person assuming different disguises and playing different roles. If so, you may have an obscure psychological disorder.

Capgras Delusion

People suffering from this disorder believe that some of the people around them are imposters. They believe that familiar people and even pets have been replaced by imposters. They recognize the face of their family members or beloved pets, but they believe the real person has been replaced by an imposter. It is unknown exactly what causes Capgras Delusion, but it has been seen in people who suffer from other psychiatric disorders or have experienced a head trauma. It has been suggested that sufferers of Capgras Delusion have lost the connection between the area of the brain that recognize faces and the area that supplies an emotional response to the faces seen. Though the person recognizes the face as that of their wife, sister, or dog, they no longer have the emotional response usually connected to that face. Because of the lack of emotion, they may believe that the person cannot be who they think they are because if they were, the sufferer would have an emotional response to them. One sufferer of Capgras Delusion is profiled here on YouTube. Treatment for Capgras Delusion includes individual therapy that involves reframing and reality testing as well as antipsychotics and other drugs.

Fregoli Syndrome

This is similar to Capgras Delusion, but involves the sufferer believing that those around them are actually other people in disguise. When they see their wife, for example, they believe she is actually their doctor or some other person they know. This is named after Leopoldo Fregoli, who was an Italian actor known for his ability to quickly change appearance during stage performances. It was first described in 1927 in a paper in which the authors discussed a 27-year-old woman who was living in London. She believed she was being followed and persecuted by two actors she saw at the theatre often. She felt these people were taking the form of others she knew or had previously met. In a more recent case, the sufferer was a 21-year-old man who was schizophrenic. He believed that his daily facial cream attracted female students. He met a young woman on Facebook and wanted to have a relationship with her, but she was not interested. The man then developed the belief that when he was contacted by other women on Facebook, they were not who they appeared to be, but rather they were the first young woman in disguise. The man believed that this young woman was applying the same cream to her face to transform her appearance. Causes of Fregoli Syndrome are not entirely known, but it has been found in people taking the drug Levodopa. This is used to treat Parkinson’s Disease and dopamine responsive dystonia. Traumatic brain injuries are another possible cause. Treatment usually includes antipsychotic drugs. In some cases, antidepressants and anticonvulsants are prescribed.

Causes:

Traumatic brain injury

Injury to the right frontal and left temporo-parietal areas can cause Fregoli syndrome. Research by Feinberg, et al. has shown that significant deficits in executive and memory functions follow shortly after damage in the right frontal or left temporoparietal areas. Tests performed on patients that have suffered from a brain injury revealed that basic attention ability and visuomotor processing speed are typically normal. However, these patients made many errors when they were called to participate in detailed attention tasks. Selective attention tests involving auditory targets were also performed, and brain-injured patients had many errors; this meant that they were deficient in their response regulation and inhibition.

Fusiform gyrus

Current research has shown that lesions in the right temporal lobe and the fusiform gyrus may contribute to DMSs. MRIs of patients exemplifying Fregoli symptoms have shown parahippocampal and hippocampal damage in the anterior fusiform gyrus, as well as the middle and inferior of the right temporal gyri. The inferior and medial of the right temporal gyri are the storage locations for long-term memory in retrieving information on visual recognition, specifically of faces; thus, damage to these intricate connections could be one of the leading factors in face misidentification disorders.

Recently, a face-specific area in the fusiform gyrus has been discovered and is close to the anterior fusiform gyrus. MRI studies performed by Hudson, et al. have shown lesions in the anterior fusiform gyrus, which is close to the face specific area (ventral fusiform cortex), may also be associated with Fregoli syndrome and other DMSs. Such damage may cause disruption in long-term visual memory and lead to improper associations of human faces.

On another note, our brains interpret visual scenes in two pathways: one is via the Parietal lobe-occipital dorsal pathway (visual spatial material is analyzed here), and the other is via the temporal-occipital ventral pathway (recognizes objects and faces). Thus, lesions in either structures or disruption of delicate connections may produce DMSs.

Abnormal P300

Delusional misidentification syndrome is thought to occur due to a dissociation between identification and recognition processes. The integration of information for further processing is referred to as working memory (WM). The P300 (P stands for positive voltage potential and the 300 for the 300-millisecond poststimulus) is an index of WM and is used during a WM test in DMS patients. In comparison to normal patients, DMS patients generally exhibit an attenuated amplitude of P300 at many abductions. These patients also exhibit prolonged latencies of P300 at all abductions. These implications suggest that DMSs are accompanied by abnormal WM, specifically affecting the prefrontal cortex (both outside and inside).

Sources: 1 2 3 4

How memories stick together
Scientists at the Salk Institute have created a new model of memory that explains how neurons retain select memories a few hours after an event.
This new framework provides a more complete picture of how memory works, which can inform research into disorders liked Parkinson’s, Alzheimer’s, post-traumatic stress and learning disabilities.
"Previous models of memory were based on fast activity patterns," says Terrence Sejnowski, holder of Salk’s Francis Crick Chair and a Howard Hughes Medical Institute Investigator. “Our new model of memory makes it possible to integrate experiences over hours rather than moments.”
Over the past few decades, neuroscientists have revealed much about how long-term memories are stored. For significant events—for example, being bit by a dog—a number of proteins are quickly made in activated brain cells to create the new memories. Some of these proteins linger for a few hours at specific places on specific neurons before breaking down.
This series of biochemical events allow us to remember important details about that event—such as, in the case of the dog bite, which dog, where it was located and so on.
One problem scientists have had with modeling memory storage is explaining why only selective details and not everything in that 1-2 hour window is strongly remembered. By incorporating data from previous literature, Sejnowski and first author Cian O’Donnell, a Salk postdoctoral researcher, developed a model that bridges findings from both molecular and systems observations of memory to explain how this 1-2 hour memory window works. The work is detailed in the latest issue of Neuron.
Using computational modeling, O’Donnell and Sejnowski show that, despite the proteins being available to a number of neurons in a given circuit, memories are retained when subsequent events activate the same neurons as the original event. The scientists found that the spatial positioning of proteins at both specific neurons and at specific areas around these neurons predicts which memories are recorded. This spatial patterning framework successfully predicts memory retention as a mathematical function of time and location overlap.
"One thing this study does is link what’s happing in memory formation at the cellular level to the systems level," says O’Donnell. "That the time window is important was already established; we worked out how the content could also determine whether memories were remembered or not. We prove that a set of ideas are consistent and sufficient to explain something in the real world."
The new model also provides a potential framework for understanding how generalizations from memories are processed during dreams.
While much is still unknown about sleep, research suggests that important memories from the day are often cycled through the brain, shuttled from temporary storage in the hippocampus to more long-term storage in the cortex. Researchers observed most of this memory formation in non-dreaming sleep. Little is known about if and how memory packaging or consolidation is done during dreams. However, O’Donnell and Sejnowski’s model suggests that some memory retention does happen during dreams.
"During sleep there’s a reorganizing of memory—you strengthen some memories and lose ones you don’t need anymore," says O’Donnell. "In addition, people learn abstractions as they sleep, but there was no idea how generalization processes happen at a neural level."
By applying their theoretical findings on overlap activity within the 1-2 hour window, they came up with a theoretical model for how the memory abstraction process might work during sleep.
Image: The hippocampus is a region of the brain largely responsible for memory formation. Courtesy of the Salk Institute for Biological Studies.

How memories stick together

Scientists at the Salk Institute have created a new model of memory that explains how neurons retain select memories a few hours after an event.

This new framework provides a more complete picture of how memory works, which can inform research into disorders liked Parkinson’s, Alzheimer’s, post-traumatic stress and learning disabilities.

"Previous models of memory were based on fast activity patterns," says Terrence Sejnowski, holder of Salk’s Francis Crick Chair and a Howard Hughes Medical Institute Investigator. “Our new model of memory makes it possible to integrate experiences over hours rather than moments.”

Over the past few decades, neuroscientists have revealed much about how long-term memories are stored. For significant events—for example, being bit by a dog—a number of proteins are quickly made in activated brain cells to create the new memories. Some of these proteins linger for a few hours at specific places on specific neurons before breaking down.

This series of biochemical events allow us to remember important details about that event—such as, in the case of the dog bite, which dog, where it was located and so on.

One problem scientists have had with modeling memory storage is explaining why only selective details and not everything in that 1-2 hour window is strongly remembered. By incorporating data from previous literature, Sejnowski and first author Cian O’Donnell, a Salk postdoctoral researcher, developed a model that bridges findings from both molecular and systems observations of memory to explain how this 1-2 hour memory window works. The work is detailed in the latest issue of Neuron.

Using computational modeling, O’Donnell and Sejnowski show that, despite the proteins being available to a number of neurons in a given circuit, memories are retained when subsequent events activate the same neurons as the original event. The scientists found that the spatial positioning of proteins at both specific neurons and at specific areas around these neurons predicts which memories are recorded. This spatial patterning framework successfully predicts memory retention as a mathematical function of time and location overlap.

"One thing this study does is link what’s happing in memory formation at the cellular level to the systems level," says O’Donnell. "That the time window is important was already established; we worked out how the content could also determine whether memories were remembered or not. We prove that a set of ideas are consistent and sufficient to explain something in the real world."

The new model also provides a potential framework for understanding how generalizations from memories are processed during dreams.

While much is still unknown about sleep, research suggests that important memories from the day are often cycled through the brain, shuttled from temporary storage in the hippocampus to more long-term storage in the cortex. Researchers observed most of this memory formation in non-dreaming sleep. Little is known about if and how memory packaging or consolidation is done during dreams. However, O’Donnell and Sejnowski’s model suggests that some memory retention does happen during dreams.

"During sleep there’s a reorganizing of memory—you strengthen some memories and lose ones you don’t need anymore," says O’Donnell. "In addition, people learn abstractions as they sleep, but there was no idea how generalization processes happen at a neural level."

By applying their theoretical findings on overlap activity within the 1-2 hour window, they came up with a theoretical model for how the memory abstraction process might work during sleep.

Image: The hippocampus is a region of the brain largely responsible for memory formation. Courtesy of the Salk Institute for Biological Studies.

science-junkie:

How To: Improve your Memory

Nearly everyone wants a better memory. To just be able to remember the last item on a shopping list, or where they put their car keys. But most importantly, remember all the information for exams. This video has tips and tricks to improving your memory in all kinds of ways.

Source:

1. http://en.wikipedia.org/wiki/Memory
2. http://www.helpguide.org/life/improving_memory.htm
3. http://www.spring.org.uk/2013/10/10-surprising-and-mostly-easy-ways-to-improve-your-memory.php

Language and Your Brain

For centuries, researchers have studied the brain to find exactly where mechanisms for producing and interpreting language reside. Theories abound on how humans acquire new languages and how our developing brains learn to process languages.

By Voxy.

(Source: neuromorphogenesis)

Did You Hear That? Specific Brain Activity Linked With Imagined Hearing
Being able to distinguish what is real and what is not may seem pretty basic, but the inability to perform this task could be a marker of many psychiatric disorders. This task, known to researchers as “reality monitoring,” is at the core of a study from scientists at Yale University.
Previous research has demonstrated that there are specific brain areas related to whether a person correctly identifies a visual stimulus as something that actually happened or was “self-generated.” Researchers Eriko Sugimori, Marcia Johnson, and colleagues at Yale University hypothesized that this relationship may not be specific to just the visual system, and that specific brain activity may also distinguish heard and imagined words.
To find out, the researchers had participants undergo an auditory task in a functional magnetic resonance imaging (fMRI) scanner.
The participants were shown a cue on a computer screen telling them whether they would hear a word, imagine a word spoken by a recorded male voice, or see a shape. After this cue, they were presented with the given word or shape and then instructed to rate from 1-3 on how well they heard or imagined the word, or rate whether the shape was more square or circular.
Approximately five minutes after the scan, the participants completed a test in which they were shown a word on screen and asked to indicate whether they had heard the word, imagined the word, or if the word had not been presented.
The researchers analyzed the fMRI data and found that increased activity in the left middle frontal gyrus (MFG) during encoding for imagined words was associated with correctly identifying them as “imagined” later. And an area of the left inferior frontal gyrus (IFG) showed greater activity during encoding for words that were later reported as “heard” versus “imagined,” regardless of the actual source of the word.
Intriguingly, the fMRI data also showed that activation in the superior temporal gyrus (STG) for mistakenly “heard” items was greater for participants who were more prone to auditory hallucinations (as measured by the Auditory Hallucination Experience Scale).
Temporal regions of the brain, like the STG, are often involved in processing auditory information, and the researchers hypothesized that errors in reality monitoring might occur when STG activity is increased during auditory imagination – that is, increased activity in the STG may provide a false signal that a word was heard when it was only imagined.
“It may be that people prone to auditory hallucinations are good auditory imagers — that is, they relatively effortlessly or spontaneously produce vivid auditory imaginations that rival those of actually heard words,” Sugimori and colleagues write.
The researchers believe these findings may be important for identifying neural correlates of behavior in certain psychiatric populations, including individuals diagnosed with schizophrenia, for whom hallucinations are symptoms associated with the illness.

Did You Hear That? Specific Brain Activity Linked With Imagined Hearing

Being able to distinguish what is real and what is not may seem pretty basic, but the inability to perform this task could be a marker of many psychiatric disorders. This task, known to researchers as “reality monitoring,” is at the core of a study from scientists at Yale University.

Previous research has demonstrated that there are specific brain areas related to whether a person correctly identifies a visual stimulus as something that actually happened or was “self-generated.” Researchers Eriko Sugimori, Marcia Johnson, and colleagues at Yale University hypothesized that this relationship may not be specific to just the visual system, and that specific brain activity may also distinguish heard and imagined words.

To find out, the researchers had participants undergo an auditory task in a functional magnetic resonance imaging (fMRI) scanner.

The participants were shown a cue on a computer screen telling them whether they would hear a word, imagine a word spoken by a recorded male voice, or see a shape. After this cue, they were presented with the given word or shape and then instructed to rate from 1-3 on how well they heard or imagined the word, or rate whether the shape was more square or circular.

Approximately five minutes after the scan, the participants completed a test in which they were shown a word on screen and asked to indicate whether they had heard the word, imagined the word, or if the word had not been presented.

The researchers analyzed the fMRI data and found that increased activity in the left middle frontal gyrus (MFG) during encoding for imagined words was associated with correctly identifying them as “imagined” later. And an area of the left inferior frontal gyrus (IFG) showed greater activity during encoding for words that were later reported as “heard” versus “imagined,” regardless of the actual source of the word.

Intriguingly, the fMRI data also showed that activation in the superior temporal gyrus (STG) for mistakenly “heard” items was greater for participants who were more prone to auditory hallucinations (as measured by the Auditory Hallucination Experience Scale).

Temporal regions of the brain, like the STG, are often involved in processing auditory information, and the researchers hypothesized that errors in reality monitoring might occur when STG activity is increased during auditory imagination – that is, increased activity in the STG may provide a false signal that a word was heard when it was only imagined.

“It may be that people prone to auditory hallucinations are good auditory imagers — that is, they relatively effortlessly or spontaneously produce vivid auditory imaginations that rival those of actually heard words,” Sugimori and colleagues write.

The researchers believe these findings may be important for identifying neural correlates of behavior in certain psychiatric populations, including individuals diagnosed with schizophrenia, for whom hallucinations are symptoms associated with the illness.

Memory Accuracy and Strength Can Be Manipulated During Sleep

The sense of smell might seem intuitive, almost something you take for granted. But researchers from NYU Langone Medical Center have found that memory of specific odors depends on the ability of the brain to learn, process and recall accurately and effectively during slow-wave sleep — a deep sleep characterized by slow brain waves.

The sense of smell is one of the first things to fail in neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, and schizophrenia. Indeed, down the road, if more can be learned from better understanding of how the brain processes odors, researchers believe it could lead to novel therapies that target specific neurons in the brain, perhaps enhancing memory consolidation and memory accuracy.

Reporting in the Journal of Neuroscience online April 9, researchers in the lab of Donald A. Wilson, PhD, a professor in the departments of Child and Adolescent Psychiatry and Neuroscience and Physiology at NYU Langone, and a research scientist at the NYU-affiliated Nathan Kline Institute for Psychiatric Research, showed in experiments with rats that odor memory was strengthened when odors sensed the previous day were replayed during sleep. Memories deepened more when odor reinforcement occurred during sleep than when rats were awake.

When the memory of a specific odor learned when the rats were awake was replayed during slow-wave sleep, they achieved a stronger memory for that odor the next day, compared to rats that received no replay, or only received replay when they were awake.

However, when the research team exposed the rats to replay during sleep of an odor pattern that they had not previously learned, the rats had false memories to many different odors. When the research team pharmacologically prevented neurons from communicating to each other during slow-wave sleep, the accuracy of memory of the odor was also impaired.

The rats were initially trained to recognize odors through conditioning. Using electrodes in the olfactory bulb, a part of the brain responsible for perceiving smells, the researchers stimulated different smell perceptions, according to precise patterns of electrical stimulation. Then, by replaying the patterns electrically, they were able to test the effects of slow-wave sleep manipulation.

Replay of learned electrical odors during slow-wave sleep enhanced the memory for those odors. When the learned smells were replayed while the rats were awake, the strength of the memory decreased. Finally, when a false pattern that the rat never learned was incorporated, the rats could not discriminate the smell accurately from the learned odor.

“Our findings confirm the importance of brain activity during sleep for both memory strength and accuracy,” says Dr. Wilson, the study’s senior author. “What we think is happening is that during slow-wave sleep, neurons in the brain communicate with each other, and in doing so, strengthen their connections, permitting storage of specific information.”

(Source: communications.med.nyu.edu)

frontal-cortex:

Gallery of Paleontology and Comparative Anatomy in Paris

frontal-cortex:

Gallery of Paleontology and Comparative Anatomy in Paris

Wizard of Odds or Even Steven?  The science of gambling fallacies

Imagine yourself, a picture of sartorial elegance and sipping champagne from a crystal flute, in Le Grande Casino at Monte Carlo. It is a Monday night – in fact, the date is August 18, 1913 – and you are enjoying the tables surrounded by other, all of whom are similarly well-dressed, well-heeled and well-oiled. 

You hear, from the roulette table, a growing commotion and you wander over to see what is going on. At the table you discover that the wheel has spun, 20 times in a row, black (a pattern a little less likely than tossing 20 heads in a row with a coin).

You watch with interest the next spin of the wheel. It too lands on black, as does the next spin – and the next, and the next.

With 24 spins in a row landing on black you place your chips on the table. Where would you put your money? On the black, anticipating the next spin of the wheel will land a 25th black? Or on red, reasoning that the chances of the next spin landing on black are almost zero?

If you said black, you’d have won (the wheel eventually spun 26 blacks in a row).

If you said “red” you’ve have exhibited a behaviour known as the “gambler’s fallacy”, a phenomenon which, according to a paper published today in the Proceedings of the National Academy of Sciences (PNAS), can be narrowed down to a specific part of the brain – the insular cortex.

Odds and ends

The outcome of each spin of a roulette wheel is independent of the spin before it. The ball landing on red on one spin does not affect the probability of red on the next spin, or of black. Coin tosses are the same.

In the case of French or European Roulette, de rigueur at Le Grande, the chance of spinning black, on any given spin, is 18/37. That means the chances of spinning 26 blacks in a row are 1 in 136,823,184, exactly the same chances of spinning 26 reds in a row, or any other 26 black/red combination.

However, because we have evolved in a world in which most sequential events are causally related, we have evolved processes that help us recognise those relationships. As such, most of us have difficulty in interpreting sequences of independent events as independent.

That difficulty gives rise to the gambler’s fallacy: even if we know two or more events are independent it becomes difficult to ignore what just happened when trying to decide the probability of what will happen next. Instead, we develop false beliefs, or misperceptions about causal relations.

Indeed, the same processes are at work when we begin to engage in superstitious behaviours.

Introduction to the insula

The authors of today’s PNAS paper have now unpacked some of the puzzle around how such misperceptions arise.

Comparing healthy participants to those with focal brain lesions, they showed that patients with damage to a brain structure called the insular cortex (also known as the insula) do not suffer from false beliefs, or cognitive distortions, driven by long event sequences or near misses.

That is, their data suggest the insula plays a role in our developing beliefs about causal relations even when two events are, objectively, independent events.

The insula is an old brain structure associated with so-called homoeostatic body processes (such as taste, visceral sensations and autonomic responses like blood pressure and heart beat).

In mammals, particularly the great apes, there is evidence that the insula plays a role in the development of empathy and emotional self-awareness.

More recently, similarities between the insula in humans, some whales and dolphins and both African and Asian elephants have been reported.

All those species work with their fellows to achieve collective goals. That ability to cooperate and collaborate requires emotional control now for a potential reward later.

Both those features of the insula, autonomic processing and awareness of a person’s own state, might begin to explain the role of the insula in sustaining gambling behaviours.

Gambling is exciting and a visceral activity that stimulates the autonomic nervous system as well as the dopaminergic or cortical reward systems. The paper’s authors postulate that a disruption of those processes, by damage to the insula, disrupts the mechanism that reinforces gambling activity.

If they are right, they speculate, therapies that modulate insula functioning might eventually be shown also to moderate problem gambling. Perhaps they will also affect superstitious behaviours.

If so, count me out: my money would have been on 13 … black!

neuromorphogenesis:

The Psychology of Music

- by University of Florida. 

psydoctor8:

Famed amnesia case,  K.C. died last week. Having lost both hippocampuses after a motorcycle accident, he was somehow able to hold on to some memories, though “devoid of all context and emotion”… and his identity.  

That’s actually a common theme in the neuroscience of accidents. It’s easy to see the victims of brain damage as reduced or diminished, and they are in some ways. But much of what they feel from moment to moment is exactly what you or I feel, and there’s almost nothing short of death that can make you forget who you are. Amid all the fascinating injuries in neuroscience history, you’ll come across a lot of tales of woe and heartbreak. But there’s an amazing amount of resiliency in the brain, too. [via]

psydoctor8:

Famed amnesia case,  K.C. died last week. Having lost both hippocampuses after a motorcycle accident, he was somehow able to hold on to some memories, though “devoid of all context and emotion”… and his identity.  

That’s actually a common theme in the neuroscience of accidents. It’s easy to see the victims of brain damage as reduced or diminished, and they are in some ways. But much of what they feel from moment to moment is exactly what you or I feel, and there’s almost nothing short of death that can make you forget who you are. Amid all the fascinating injuries in neuroscience history, you’ll come across a lot of tales of woe and heartbreak. But there’s an amazing amount of resiliency in the brain, too. [via]

Fact or fiction? Common myths about autism explained

April is Autism Awareness Month. Is your knowledge of autism spectrum disorder (ASD) up-to-date?

Dr. Jeffrey Skowron, Regional Clinical Director for Autism Intervention Specialists in Worcester says there are many myths around autism, but they largely fall into two camps: treatment and causes.

Myth: Vaccines cause autism

This is one of the biggest myths about autism. This idea, based on research that has since been debunked and retracted by medical journals, took off after celebrity Jenny McCarthy claimed her son had autism because of vaccines.

“There’s no credible scientific evidence that autism is related to vaccines in any way,” said Dr. Skowron.

So why does the myth continue to have momentum? Dr. Skowron says that around the time parents start to see signs of autism in their children is around the time when they receive multiple vaccines.

“They will say that their child is having issues with certain aspects of their development, and they ask why is he or she acting this way. It’s just a coincidence that the two events—vaccinations and developing social skills—happen at this time. But frankly it’s hard for parents to diagnose social skills in a six-month-old because they really aren’t having social interactions yet.”

Myth: Autism is a disease

Autism is not a disease, it’s a collection of behaviors or symptoms, which makes it a syndrome.

“We aren’t sure of the underlying pathology or physical issues related to it. Although there is more evidence,” said Dr. Skowron. “There are several different presentations of the behavior we call autism. Most likely it’s a disorder of the brain.”

Because children display the signs of autism shortly after birth, researchers believe there’s a large genetic component which Dr. Skowron says the prevalence of autism with siblings and twins supports. There is a 90 percent likelihood that if one twin has autism, the other will too according to the National Institute for Neurological Disorders and Stroke. Between siblings, there is a five percent chance that they will both be diagnosed with autism.

Myth: More people have autism than ever

A recent report from the Centers for Disease Control and Prevention finds that 1 in 68 children are diagnosed with autism. A decade ago, the rate was 1 in 150.

But while Dr. Skowron admits that it’s hard to say why those rates are higher, he says it’s not simply an increased prevalence of autism. “It’s a myth to say that more people have autism,” he said.

“It could be that we’re just finding it more often. Families are looking for the signs more, and they have better access to pediatricians, clinicians, and psychologists that are better able to diagnose them,” he said. “What you should really be saying is that more people are diagnosed with autism today than ever before.”

Myth: Treatments turn kids into robots

Some say that behavioral therapy, the recommended treatment for autism, is highly impersonal, which Dr. Skowron said “is simply not true.”

“People say it turns kids into robots,” said Dr. Skowron, who has been working in applied behavioral analysis for 20 years. “It seems very personal to me. Based on the needs of the kids you form a strong bond with the person. The families play a big role in the treatment, and they can have a great affect on the treatment of the child.”

Doctors typically prescribe antipsychotic medications to treat severe symptoms of autism, which can include anxiety, depression, or obsessive-compulsive disorder.

“The best and most effective treatment for autism is applied behavior analysis,” said Dr. Skowron. “There is scientific evidence showing the effectiveness of treating autism this way. Any other methods just don’t have the same body of research toward them.”

Myth: There’s a cure for autism

There is no cure for autism spectrum disorder, according to the National Institute for Neurological Disorders and Stroke, although there is research going toward this effort. While treatment can be very effective, the social deficits and symptoms are there throughout the person’s life.

“They can learn to compensate with in very effective ways to the point that other people might not even know,” said Dr. Skowron. “But whatever physical problems are in the brain of that person, those will remain throughout the person’s life. So people have to learn ways around that.”

Because of the varying degrees of autism, while some may require a supportive environment, people with autism can successfully live independently.

Myth: People with autism can’t love

Because those who are autistic can have an impaired ability to make friends or carry on a conversation, a common myth is that people with autism can’t love or show emotions such as empathy.

“They may have deficits in social interaction skills and in conveying those emotions to other people, but those emotions are there,” said Dr. Skowron. “There are some people that say if your child is diagnosed with autism, so they can never have a relationship—well that’s just not true. People with autism can have relationships, spouses, girlfriends, and boyfriends. There’s a variety and spectrum of abilities and deficits associated with autism, and people can display these to varying degrees.”

People with autism can go on to have jobs, relationships, and families with effective intervention therapies.

Myth: Foods can cause autism

Autism spectrum disorder (ASD) is largely a genetic disorder, and although researchers say environment does play a role in early development, there is not substantial medical evidence finding a relationship between autism and food. Despite this, some families try nutritional therapies like gluten-free diets to treat autism.

Children with autism who improve their behavior as a result of eliminating certain foods from their diets likely have a food allergy, said Dr. Skowron.

“For instance, if a child has a lactose allergy, then drinking milk will make them feel bad and it will probably interfere with their treatment or education, but it’s not because of the milk exacerbating the condition of autism, it’s because drinking the milk makes them feel bad because they’re allergic. Some parents think that a gluten-free diet helps their child with autism, and it may make the child feel better, but it’s not because the wheat or gluten causes autism, it’s because the child has a wheat allergy.”

Doctors recommend that any families following one of the controversial nutritional therapies should be sure to consult a nutritionist and closely follow the child’s nutritional status.

Get the facts:

“Things like treatment involving diet or avoiding vaccinations, avoiding certain foods, those just don’t have credible scientific evidence,” said Dr. Skowron. The true key to treating autism? He says start behavioral therapy intensively when the child is very young.

“If it’s started early, and we’re talking when they’re toddlers, we can see even in the most extreme cases there are huge differences by the time the child is a teenager depending on their function needs.”

To find resources for your family and friends, or to learn more about autism, find more information at:

The Autism Resource Center

Autism Speaks

National Institute of Neurological Disorders and Stroke (NINDS)

Mass ABA

Image1: A boy plays with seeds during therapy at the therapy and development center for autistic kids in the Asociacion Guatemalteca por el Autismo, or Guatemalan Association for Autism, building in Guatemala City March 13, 2014.The center is the only one in the country that specifically conducts programs for autistic children, according to the association.

Image2: Alexander Prentice, 5, of Burton, Mich., smiles as he searches for items at the bottom of a sand bin in the reinforcement room, which allows technicians to work with children on building on skill sets at Genesee Health System’s new Children’s Autism Center on Jan. 16, 2014 in Flint.

The Psychology of Music

- by University of Florida.