Posts Tagged brain

[TED TALK] How To Rewire Your Brain: Neuroscientist Dr. Joe Dispenza Explains The Incredible Science Behind Neuroplasticity – YouTube

Dr Joe Dispenza, D.C., studied biochemistry at Rutgers University in New Brunswick, N.J. He has a Bachelor of Science degree with an emphasis in Neuroscience and also received his Doctor of Chiropractic Degree at Life University in Atlanta, Georgia, graduating magna cum laude.

Over the last 10 years, Dr. Dispenza has lectured in over 17 different countries on six continents educating people about the role and function of the human brain.

His approach, taught in a very simple method, creates a bridge between true human potential and the latest scientific theories of neuroplasticity. He explains how thinking in new ways, as well as changing beliefs, can literally rewire one’s brain. The premise of his work is founded in his total conviction that every person on this planet has within them, the latent potential of greatness and true unlimited abilities.

His new book, Evolve Your Brain: The Science of Changing Your Mind connects the subjects of thought and consciousness with the brain, the mind, and the body. The book explores “the biology of change.” That is, when we truly change our mind, there is a physical evidence of change in the brain.

As an author of several scientific articles on the close relationship between the brain and the body, Dr. Dispenza ties information together to explain the roles these functions play in physical health and disease.

In his research into spontaneous remissions, Dr. Dispenza has found similarities in people who have experienced so-called miraculous healings, showing that they have actually changed their mind, which then changed their health.

One of the scientists, researchers, and teachers featured in the award winning film, “What the BLEEP Do We Know!?” Dr. Dispenza is often remembered for his comments on how a person can create their day, which he discussed in the film. He also has guest appearances in the theatrical directors cut, “What the BLEEP Down the Rabbit Hole.. as well as the extended Quantum Edition DVD set.

To find out more information on Joe Dispenza goto http://www.drjoedispenza.com/

via Dr Joe Dispenza- TED Talks with Dr Joe Dispenza – YouTube

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[WEB SITE] Researchers develop new prediction method for epileptic seizures

Epileptic seizures strike with little warning and nearly one third of people living with epilepsy are resistant to treatment that controls these attacks. More than 65 million people worldwide are living with epilepsy.

Now researchers at the University of Sydney have used advanced artificial intelligence and machine learning to develop a generalized method to predict when seizures will strike that will not require surgical implants.

Dr Omid Kavehei from the Faculty of Engineering and IT and the University of Sydney Nano Institute said: “We are on track to develop an affordable, portable and non-surgical device that will give reliable prediction of seizures for people living with treatment-resistant epilepsy.”

In a paper published this month in Neural Networks, Dr Kavehei and his team have proposed a generalized, patient-specific, seizure-prediction method that can alert epilepsy sufferers within 30 minutes of the likelihood of a seizure.

Dr Kavehei said there had been remarkable advances in artificial intelligence as well as micro- and nano-electronics that have allowed the development of such systems.

“Just four years ago, you couldn’t process sophisticated AI through small electronic chips. Now it is completely accessible. In five years, the possibilities will be enormous,” Dr Kavehei said.

The study uses three data sets from Europe and the United States. Using that data, the team has developed a predictive algorithm with sensitivity of up to 81.4 percent and false prediction rate as low as 0.06 an hour.

“While this still leaves some uncertainty, we expect that as our access to seizure data increases, our sensitivity rates will improve,” Dr Kavehei said.

Carol Ireland, chief executive of Epilepsy Action Australia, said: “Living with constant uncertainty significantly contributes to increased anxiety in people with epilepsy and their families, never knowing when the next seizure may occur.

“Even people with well controlled epilepsy have expressed their constant concern, not knowing if or when they will experience a seizure at work, school, traveling or out with friends.

“Any progress toward reliable seizure prediction will significantly impact the quality of life and freedom of choice for people living with epilepsy.”

Dr Kavehei and lead author of the study, Nhan Duy Truong, used deep machine learning and data-mining techniques to develop a dynamic analytical tool that can read a patient’s electroencephalogram, or EEG, data from a wearable cap or other portable device to gather EEG data.

Wearable technology could be attached to an affordable device based on the readily available Raspberry Pi technology that could give a patient a 30-minute warning and percentage likelihood of a seizure.

An alarm would be triggered between 30 and five minutes before a seizure onset, giving patients time to find a safe place, reduce stress or initiate an intervention strategy to prevent or control the seizure.

Dr Kavehei said an advantage of their system is that is unlikely to require regulatory approval, and could easily work with existing implanted systems or medical treatments.

The algorithm that Dr Kavehei and team have developed can generate optimized features for each patient. They do this using what is known as a ‘convolutional neural network’, that is highly attuned to noticing changes in brain activity based on EEG readings.

Other technologies being developed typically require surgical implants or rely on high levels of feature engineering for each patient. Such engineering requires an expert to develop optimized features for each prediction task.

An advantage of Dr Kavehei’s methodology is that the system learns as brain patterns change, requiring minimum feature engineering. This allows for faster and more frequent updates of the information, giving patients maximum benefit from the seizure prediction algorithm.

The next step for the team is to apply the neural networks across much larger data sets of seizure information, improving sensitivity. They are also planning to develop a physical prototype to test the system clinically with partners at the University of Sydney’s Westmead medical campus.

 

via Researchers develop new prediction method for epileptic seizures

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[Abstract+References] Brain Plasticity and Modern Neurorehabilitation Technologies

Abstract

In recent decades, interest in studies on basic and applied aspects of how the nervous system functions has been growing rapidly around the world. The recovery of lost functions rests on processes of neuroplasticity, which is determined by the ability of the brain to transform its structures in response to injury. The effects of both routine and state-of-the-art neurorehabilitation technologies are ensured by synaptic plasticity— long-term potentiation and long-term depression, which influence learning and the preservation of new knowledge and skills obtained during rehabilitation. The introduction of new methods of neuroimaging, neurophysiology, and mathematical statistics have powerfully stimulated the development of the neuroplasticity doctrine. It has become clear that the main role in the recovery of injured functions is played by the reorganization of cortical nets and not by tissue reparation as such. The Research Center of Neurology has accumulated significant experience in the use of innovative treatment methods based on modern neurorehabilitation principles. Some of them are used for acute stroke; among other things, their effectiveness and safety have been shown with regard to patients in intensive care units (cyclic robotic mechanotherapy) and patients with severe motor deficit and an associated somatic pathology (stimulation of plantar support zones). Opportunities to assess neuroplasticity under various rehabilitation methods using fMRI and navigated transcranial magnetic stimulation (TMS) are revealed. The center also studies the fundamentals of consciousness using original neuroimaging and neurophysiological protocols for the sake of its recovery. The center is actively introducing its data into the practice of domestic clinics specializing in recovery medicine and neurorehabilitation.

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via Braind Modern Neurorehabilitation Technologies | SpringerLink

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[BLOG POST] Where does the controversial finding that adult human brains don’t grow new neurons leave ongoing research?

Scientists have known for about two decades that some neurons – the fundamental cells in the brain that transmit signals – are generated throughout life. But now a controversial new study from the University of California, San Francisco, casts doubt on whether many neurons are added to the human brain after birth.

As a translational neuroscientist, this work immediately piqued my interest. It has direct implications for the research my lab does: We transplant young neurons into damaged brain areas in mice in an attempt to treat epileptic seizures and the damage they’ve caused. Like many labs, part of our work is based on a foundational belief that the hippocampus is a brain region where new neurons are born throughout life.

If the new study is right, and human brains for the most part don’t add new neurons after infancy, researchers like me need to reconsider the validity of the animal models we use to understand various brain conditions – in my case temporal lobe epilepsy. And I suspect other labs that focus on conditions including drug addiction, depression and post-traumatic stress disorder are thinking about what the UCSF study means for their investigations, too.

In the brain of a baby who died soon after birth, there are many new neurons (green in this image) in the hippocampus. Sorrells et alCC BY-ND

When and where are new neurons born?

No doubt, the adult human brain is able to learn throughout life and to change and adapt – a capability brain scientists call neuroplasticity, the brain’s ability to reorganize itself by rewiring connections. Yet, a central dogma in the field of neuroscience for nearly 100 years had been that a child is born with all the neurons she will ever have because the adult brain cannot regenerate neurons.

Just over half a century ago, researchers devised a way to study proliferation of cells in the mature brain, based on techniques to incorporate a radioactive label into new cells as they divide. This approach led to the startling discovery in the 1960s that rodent brains actually could generate new neurons.

Neurogenesis – the production of new neurons – was previously thought to only occur during embryonic life, a time of extremely rapid brain growth and expansion, and the rodent findings were met with considerable skepticism. Then researchers discovered that new neurons are also born throughout life in the songbird brain, a species scientists use as a model for studying vocal learning. It started to look like neurogenesis plays a key role in learning and neuroplasticity – at least in some brain regions in a few animal species.

Even so, neuroscientists were skeptical that many nerve cells could be renewed in the adult brain; evidence was scant that dividing cells in mammalian brains produced new neurons, as opposed to other cell types. It wasn’t until researchers extracted neural stem cells from adult mouse brains and grew them in cell culture that scientists showed these precursor cells could divide and differentiate into new neurons. Now it is generally well accepted that neurogenesis takes place in two areas of the adult rodent brain: the olfactory bulbs, which process smell information, and the hippocampus, a region characterized by neuroplasticity that is required for forming new declarative memories.

Adult neural stem cells cluster together in what scientists call niches – hotbeds for cultivating the birth and growth of new neurons, recognizable by their distinctive architecture. Despite the mounting evidence for regional growth of new neurons, these studies underscored the point that the adult brain harbors only a few stem cell niches and their capacity to produce neurons is limited to just a few types of cells.

With this knowledge, and new tools for labeling proliferating cells and identifying maturing neurons, scientists began to look for postnatal neurogenesis in primate and human brains.

What’s happening in adult human brains?

Many neuroscientists believe that by understanding the process of adult neurogenesis we’ll gain insights into the causes of some human neurological disorders. Then the next logical step would be trying to develop new treatments harnessing neurogenesis for conditions such as Alzheimer’s disease or trauma-induced epilepsy. And stimulating resident stem cells in the brain to generate new neurons is an exciting prospect for treating neurodegenerative diseases.

Because neurogenesis and learning in rodents increases with voluntary exercise and decreases with age and early life stress, some workers in the field became convinced that older people might be able to enhance their memory as they age by maintaining a program of regular aerobic exercise.

However, obtaining rigorous proof for adult neurogenesis in the human and primate brain has been technically challenging – both due to the limited experimental approaches and the larger sizes of the brains, compared to reptiles, songbirds and rodents.

Researchers injected a compound found in DNA, nicknamed BrdU to identify brand new neurons in human adult hippocampus – but the labeled cells were extremely rare. Other groups demonstrated that adult human brain tissue obtained during neurosurgery contained stem cell niches that housed progenitor cells that could generate new neurons in the lab, showing that these cells had an inborn neurogenic capacity, even in adults.

But even when scientists saw evidence for new neurons in the brain, they tended to be scarce. Some neurogenesis experts were skeptical that evidence based on incorporating BrdU into DNA was a reliable method for proving that new cells were actually being born through cell division, rather than just serving as a marker for other normal cell functions.

Further questions about how long human brains retain the capacity for neurogenesis arose in 2011, with a study that compared numbers of newborn neurons migrating in the olfactory bulbs of infants versus older individuals up to 84 years of age. Strikingly, in the first six months of life, the baby brains contained lots of chains of young neurons migrating into the frontal lobes, regions that guide executive function, long-range planning and social interactions. These areas of the human cortex are hugely increased in size and complexity compared to rodents and other species. But between 6 to 18 months of age, the migrating chains dwindled to a thin stream. Then, a very different pattern emerged: Where the migrating chains of neurons had been in the infant brain, a cell-free gap appeared, suggesting that neural stem cells become depleted during the first six months of life.

Questions still lingered about the human hippocampus and adult neurogenesis as a source for its neuroplasticity. One group came up with a clever approach based on radiocarbon dating. They measured how much atmospheric ¹⁴C – a radioactive isotope derived from nuclear bomb tests – was incorporated into people’s DNA. This method suggested that as many as 700 new cells are added to the adult human hippocampus every day. But these findings were contradicted by a 2016 study that found that the neurogenic cells in the adult hippocampus could only produce non-neuronal brain cells called microglia.

Rethinking neurogenesis research

Now the largest and most comprehensive study conducted to date presents even stronger evidence that robust neurogenesis doesn’t continue throughout adulthood in the human hippocampus – or if it does persist, it is extremely rare. This work is controversial and not universally accepted. Critics have been quick to cast doubt on the results, but the finding isn’t totally out of the blue.

So where does this leave the field of neuroscience? If the UCSF scientists are correct, what does that mean for ongoing research in labs around the world?

Because lots of studies of neurological diseases are done in mice and rats, many scientists are invested in the possibility that adult neurogenesis persists in the human brain, just as it does in rodents. If it doesn’t, how valid is it to think that the mechanisms of learning and neuroplasticity in our model animals are comparable to those in the human brain? How relevant are our models of neurological disorders for understanding how changes in the hippocampus contribute to disorders such as the type of epilepsy I study?

In my lab, we transplant embryonic mouse or human neurons into the adult hippocampus in mice, after damage caused by epileptic seizures. We aim to repair this damage and suppress seizures by seeding the mouse hippocampus with neural stem cells that will mature and form new connections. In temporal lobe epilepsy, studies in adult rodents suggest that naturally occurring hippocampal neurogenesis is problematic. It seems that the newborn hippocampal neurons become highly excitable and contribute to seizures. We’re trying to inhibit these newborn hyperexcitable neurons with the transplants. But if humans don’t generate new hippocampal neurons, then maybe we’re developing a treatment in mice for a problem that has a different mechanism in people.

Perhaps our species has evolved separate mechanisms for neuroplasticity, distinct from those used by species such as rats and mice. One possibility is that there are other sites in the human brain where neurogenesis occurs – its a big structure and more exploration will be necessary. If it turns out to be true that the human brain has a diminished capacity for neurogenesis after birth, the finding will have important implications for how neuroscientists like me think about tackling brain disorders.

Perhaps most importantly, this work underscores how crucial it is to learn how to increase the longevity of the neurons we do have, born early in life, and how we might replace or repair neurons that become damaged.

via Where does the controversial finding that adult human brains don’t grow new neurons leave ongoing research?

 

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[WEB PAGE] Excitatory magnetic brain stimulation reduces emotional arousal to fearful faces, study shows

February 6, 2018

A new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging looks at the modulation of emotion in the brain

A new study published in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging reports that processing of negative emotion can be strengthened or weakened by tuning the excitability of the right frontal part of the brain.

Using magnetic stimulation outside the brain, a technique called repetitive transcranial magnetic stimulation (rTMS), researchers at University of Münster, Germany, show that, despite the use of inhibitory stimulation currently used to treat depression, excitatory stimulation better reduced a person’s response to fearful images.

The findings provide the first support for an idea that clinicians use to guide treatment in depression, but has never been verified in a lab. “This study confirms that modulating the frontal region of the brain, in the right hemisphere, directly effects the regulation of processing of emotional information in the brain in a ‘top-down’ manner,” said Cameron Carter, M.D., Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, referring to the function of this region as a control center for the emotion-generating structures of the brain. “These results highlight and expand the scope of the potential therapeutic applications of rTMS,” said Dr. Carter.

In depression, processing of emotion is disrupted in the frontal region of both the left and right brain hemispheres (known as the dorsolateral prefrontal cortices, dlPFC). The disruptions are thought to be at the root of increased negative emotion and diminished positive emotion in the disorder. Reducing excitability of the right dlPFC using inhibitory magnetic stimulation has been shown to have antidepressant effects, even though it’s based on an idea-that this might reduce processing of negative emotion in depression-that has yet to be fully tested in humans.

Co-first authors Swantje Notzon, M.D., and Christian Steinberg, Ph.D, and colleagues divided 41 healthy participants into two groups to compare the effects of a single-session of excitatory or inhibitory magnetic stimulation of the right dlPFC. They performed rTMS while the participants viewed images of fearful faces to evoke negative emotion, or neutral faces for a comparison.

Excitatory and inhibitory rTMS had opposite effects-excitatory reduced visual sensory processing of fearful faces, whereas inhibitory increased visual sensory processing. Similarly, excitatory rTMS reduced participants’ reaction times to respond to fearful faces and reduced feelings of emotional arousal to fearful faces, which were both increased by inhibitory rTMS.

Although the study was limited to healthy participants, senior author Markus Junghöfer, Ph.D., notes that “…these results should encourage more research on the mechanisms of excitatory and inhibitory magnetic stimulation of the right dlPFC in the treatment of depression.”

 

via Excitatory magnetic brain stimulation reduces emotional arousal to fearful faces, study shows

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[ARTICLE] Robotic Arm with Brain – Computer Interfacing – Full Text PDF

Abstract

Brain Computer Interfaces (BCI), is a modern technology which is currently revolutionizing the field of signal processing. BCI helped in the evolution of a new world where man and computer had never been so close. Advancements in cognitive neuro-sciences facilitated us with better brain imaging techniques and thus interfaces between machines and the human brain became a reality. Electroencephalography (EEG), which is the measurement and recording of electric signals using sensors arrayed across the scalp can be used for applications like prosthetic devices, applications in warfare, gaming, virtual reality and robotics upon signal conditioning and processing.

This paper is entirely based on Brain-Computer Interface with an objective of actuating a robotic arm with the help of device commands derived from EEG signals. This system unlike any other existing technology is purely non-invasive in nature, cost effective and is one of its kinds that can serve various requirements such as prosthesis. This paper suggests a low cost system implementation that can even serve as a reliable substitute for the existing technologies of prosthesis like BIONICS. […]

via Robotic Arm with Brain – Computer Interfacing – ScienceDirect

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[WEB SITE] Monthly cycles of brain activity linked to seizures in patients with epilepsy

January 8, 2018
UC San Francisco neurologists have discovered monthly cycles of brain activity linked to seizures in patients with epilepsy. The finding, published online January 8 in Nature Communications, suggests it may soon be possible for clinicians to identify when patients are at highest risk for seizures, allowing patients to plan around these brief but potentially dangerous events.

“One of the most disabling aspects of having epilepsy is the seeming randomness of seizures,” said study senior author Vikram Rao, MD, PhD, an assistant professor of neurology at UCSF and member of the UCSF Weill Institute for Neurosciences. “If your neurologist can’t tell you if your next seizure is a minute from now or a year from now, you live your life in a state of constant uncertainty, like walking on eggshells. The exciting thing here is that we may soon be able to empower patients by letting them know when they are at high risk and when they can worry less.”

Epilepsy is a chronic disease characterized by recurrent seizures — brief storms of electrical activity in the brain that can cause convulsions, hallucinations, or loss of consciousness. Epilepsy researchers around the world have been working for decades to identify patterns of electrical activity in the brain that signal an oncoming seizure, but with limited success. In part, Rao says, this is because technology has limited the field to recording brain activity for days to weeks at most, and in artificial inpatient settings.

At UCSF Rao has pioneered the use of an implanted brain stimulation device that can quickly halt seizures by precisely stimulating a patient’s brain as a seizure begins. This device, called the NeuroPace RNS® System, has also made it possible for Rao’s team to record seizure-related brain activity for many months or even years in patients as they go about their normal lives. Using this data, the researchers have begun to show that seizures are less random than they appear. They have identified patterns of electrical discharges in the brain that they term “brain irritability” that are associated with higher likelihood of having a seizure.

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The new study, based on recordings from the brains of 37 patients fitted with NeuroPace implants, confirmed previous clinical and research observations of daily cycles in patients’ seizure risk, explaining why many patients tend to experience seizures at the same time of day. But the study also revealed that brain irritability rises and falls in much longer cycles lasting weeks or even months, and that seizures are more likely to occur during the rising phase of these longer cycles, just before the peak. The lengths of these long cycles differ from person to person but are highly stable over many years in individual patients, the researchers found.

The researchers show in the paper that when the highest-risk parts of a patient’s daily and long-term cycles of brain irritability overlap, seizures are nearly seven times more likely to occur than when the two cycles are mismatched.

Rao’s team is now using this data to develop a new approach to forecasting patients’ seizure risk, which could allow patients to avoid potentially dangerous activities such as swimming or driving when their seizure risk is highest, and to potentially take steps (such as additional medication doses) to reduce their seizure risk, similar to how people with asthma know to take extra care to bring their inhalers when pollen levels are high.

“I like to compare it to a weather forecast,” Rao said. “In the past, the field has focused on predicting the exact moment a seizure will occur, which is like predicting when lightning will strike. That’s pretty hard. It may be more useful to be able tell people there is a 5 percent chance of a thunderstorm this week, but a 90 percent chance next week. That kind of information lets you prepare.”

Source:
https://www.ucsf.edu/

via Monthly cycles of brain activity linked to seizures in patients with epilepsy

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[ARTICLE] The Functional Recovery and the Associated Cortical Reorganization Following Constraint-Induced Movement Therapies (CIMTs) in Stroke. – Full Text PDF

Abstract

Constraint-Induced Movement Therapies (CIMTs) including the original Constraint- Induced Movement Therapy (CIMT) and the Modified Constraint-Induced Movement Therapy (mCIMT) gained considerable popularity as a treatment approach for upper extremity rehabilitation among patients with mild-to-moderate stroke.

However, a major barrier in rehabilitation generally and in CIMTs specifically; is the limited objectivity of some commonly used outcome measures and lack sensitivity to define “True” recovery vs. compensation. Thereby, they may not sufficiently detect of long term consequences and the associated neurological recovery. An essential approach to overcome such barrier is to better understand functional motor recovery, associated neural changes and how they may relate to recovery of the pre-morbid movement pattern.

Such Understanding for these relationships would add more in-depth insights on the
functional relevance of plastic brain changes in stroke following CIMTs to optimize the field of neuro-rehabilitation. This review synthesizes findings from studies to on the use of the CIMTs including CIMT and mCIMT as efficient practice in the management of upper limb dysfunction following a stroke. The analysis will include (1) the functional recovery and (2) the cortical reorganization following the use of mCIMT and CIMT on patients in the chronic stage following stroke.

Introduction

Stroke is considered the fifth leading cause of death in the United
States [1]. To date, stroke affects at least 6.4 million persons in the United
States [2]. Projections show that by 2030, an additional 3.4 million
people above 18 years will have had a stroke which is approximately a
20.5% increase in prevalence from 2012 statistics [1]. Stroke is a leading
cause of serious long-term disability in the United States [1].

Arm paresis is one of the most common impairments after stroke
[3,4]. After six months, about two-thirds of patients continue to suffer
from arm sensorimotor impairment that impacts the individual’s
activities of daily living [5]. Motor deficits consist of weakness of
specific muscles [6], abnormal muscle tone [7-9], abnormal postural
adjustments [10], abnormal movement synergies [11], lack of mobility
between structures at the shoulder girdle [10] and incorrect timing
of components within a movement pattern [12]. As a result of such
impairment, patients may progressively avoid using the affected arm in
favor of the unaffected arm for successful ADL, resulting in a learned
non-use phenomenon [13].[…]

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[WEB SITE] Findings reveal how seizures can have lasting detrimental effects on memory

October 16, 2017

Although it’s been clear that seizures are linked to memory loss and other cognitive deficits in patients with Alzheimer’s disease, how this happens has been puzzling. In a study published in the journal Nature Medicine, a team of researchers reveals a mechanism that can explain how even relatively infrequent seizures can lead to long-lasting cognitive deficits in animal models. A better understanding of this new mechanism may lead to future strategies to reduce cognitive deficits in Alzheimer’s disease and other conditions associated with seizures, such as epilepsy.

“It’s been hard to reconcile how infrequent seizures can lead to persistent changes in memory in patients with Alzheimer’s disease,” said corresponding author Dr. Jeannie Chin, assistant professor of neuroscience at Baylor College of Medicine. “To solve this puzzle, we worked with a mouse model of Alzheimer’s disease focusing on the genetic changes that seizures might trigger in the memory center of the brain, the hippocampus, that could lead to loss of memory or other cognitive deficits.”

The researchers measured the levels of a number of proteins involved in memory and learning and found that levels of the protein deltaFosB strikingly increase in the hippocampus of Alzheimer’s disease mice that had seizures. DeltaFosB already is well known for its association with other neurological conditions linked to persistent brain activity of specific brain regions, such as addiction. In this study, the researchers found that after a seizure, the deltaFosB protein remains in the hippocampus for an unusually long time; its half-life – the time it takes for the amount of protein to decrease by half – is eight days. Most proteins have a half-life that is between hours and a day or two.

“Interestingly, because deltaFosB is a transcription factor, meaning that its job is to regulate the expression of other proteins, these findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory,” Chin said. “In fact, we found that when the levels of deltaFosB increase, those of other proteins, such as calbindin, decrease. Calbindin also has been known for a long time to be involved in Alzheimer’s disease and epilepsy, but its mechanism of regulation was not known. We then hypothesized that deltaFosB might be regulating the production of calbindin.”

Further investigations supported the researchers’ hypothesis. The scientists showed that deltaFosB can bind to the gene calbindin suppressing the expression of the protein. When they either prevented deltaFosB activity or experimentally increased calbindin expression in the mice, calbindin levels were restored and the mice improved their memory. And when researchers experimentally increased deltaFosB levels in normal mice, calbindin expression was suppressed and the animals’ memory deteriorated, demonstrating that deltaFosB and calbindin are key regulators of memory.

Connecting pieces of the puzzle

“Our findings have helped us answer the question of how even infrequent seizures can have such lasting detrimental effects on memory,” Chin said. “We found that seizures can increase the levels of deltaFosB in the hippocampus, which results in a decrease in the levels of calbindin, a regulator of memory processes. DeltaFosB has a relatively long half-life, therefore even when seizures are infrequent, deltaFosB remains in the hippocampus for weeks acting like a brake, reducing the production of calbindin and other proteins, and disrupting the consequent brain activity involved in memory. The regulation of gene expression far outlasts the actual seizure event that triggered it.”

The scientists found the same changes in deltaFosB and calbindin levels in the hippocampus of Alzheimer’s disease patients and in the temporal lobe of epilepsy patients. However, they underscore that it is too soon to know whether regulating deltaFosB or calbindin could improve or prevent memory problems or other cognitive deficits in people with Alzheimer’s disease. However, “now that we know that the levels of deltaFosB and calbindin are effective markers of brain activity in the hippocampus and memory function, we propose that these markers could potentially help assess clinical therapies for Alzheimer’s and other diseases with seizures,” Chin said.

Source: Findings reveal how seizures can have lasting detrimental effects on memory

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[BLOG POST] Strength training improves the nervous system’s ability to drive muscles

Imagine that the New Year has just begun. You’ve made a resolution to improve your physical fitness. In particular, you want to improve your muscle strength. You’ve heard that people with stronger muscles live longer and have less difficulty standing, walking, and using the toilet when they get older (Rantanen et al. 1999; Ruiz et al. 2008). So, you join a fitness centre and hire a personal trainer. The trainer assesses your maximal strength, and then guides you through a 4-week program that involves lifting weights which are about 80% of your maximum.

Sure enough, after the program, you become stronger (probably around 20% stronger) (Carroll et al. 2011). You think this is great – and it is! You are so excited, you decide to stand in front of your mirror, flex your biceps, and take a selfie (your plan is to post the picture to Facebook to show your friends how much bigger your muscles got). However, after examining the picture, you realise your muscles did not get bigger. Or perhaps they did get a little bigger, but not enough to explain your substantial improvement in strength. You are somewhat disappointed in this, but then you remember your goal was to get stronger, not necessarily bigger, so you post the picture, anyway.

Magnetic stimulation of the brain can be used to test how well a person can voluntarily drive their muscles.

Interestingly, the observations you made are completely consistent with the scientific literature. Within the first weeks of strength training, muscle strength can improve without a change in the size or architecture of the muscle (e.g., Blazevich et al. 2007). Consequently, researchers have speculated that initial improvements in muscle strength from strength training are due primarily to changes in the central nervous system. One hypothesis has been that strength training helps the nervous system learn how to better “drive” or communicate with muscles. This ability is termed voluntary activation, and it can be tested by stimulating the motor area of an individual’s brain while they perform a maximal contraction (Todd et al. 2003). If the stimulation produces extra muscle force, it means that the individual’s nervous system was not maximally activating their muscles. Currently, there is no consensus as to whether voluntary activation can actually be improved by strength training.

Therefore, we conducted a randomised, controlled trial in which one group of participants completed four weeks of strength training, while a control group did not complete the training (Nuzzo et al. in press). For the group who performed the training, each exercise session consisted of four sets of strong contractions of the elbow flexor muscles (i.e., the muscles that bend the elbow, such as the biceps). Before and after the four week intervention, both groups were tested for muscle strength, voluntary activation, and several other measures. The participants were healthy, university-aged, and they had limited or no experience with strength training.

WHAT DID WE FIND?

Prior to the intervention, the strength training and control groups had similar levels of muscle strength and activation of the elbow flexor muscles. After the intervention, the group who performed the strength training improved their strength by 13%. They also improved their voluntary activation from 88.7% to 93.4%. The control group did not improve muscle strength or voluntary activation.

SIGNIFICANCE AND IMPLICATIONS

The results from our study show that four weeks of strength training improves the brain’s ability to “drive” the elbow flexor muscles to produce their maximal force. This helps to explain how muscles can become stronger, without a change in muscle size or architecture. Moreover, the results suggest that clinicians should consider strength training as a treatment for patients with motor impairments (e.g., stroke), as these individuals are likely to have poor voluntary activation (Bowden et al. 2014).

PUBLICATION

Nuzzo JL, Barry BK, Jones MD, Gandevia SC, Taylor JL. Effects of four weeks of strength training on the corticomotoneuronal pathway. Med Sci Sports Exerc,  doi: 10.1249/MSS.0000000000001367.

KEY REFERENCES

Blazevich AJ, Gill ND, Deans N, Zhou S. Lack of human muscle architectural adaptation after short-term strength training. Muscle Nerve 35: 78-86.

Bowden JL, Taylor JL, McNulty PA. Voluntary activation is reduced in both the more- and less-affected upper limbs after unilateral stroke.Front Neurol 5: 239, 2014.

Carroll TJ, Selvanayagam VS, Riek S, Semmler RG. Neural adaptations to strength training: moving beyond transcranial magnetic stimulation and reflex studies. Acta Physiol 202: 119-140, 2011.

Rantanen T, Guralnik JM, Foley D, Masaki K, Leveille S, Curb JD, White L. Midline hand grip strength as a predictor of old age disability.JAMA 281: 558-560, 1999.

Ruiz JR, Sui X, Lobelo F, Morrow Jr. JR, Jackson AW, Sjöström M, Blair SN. Association between muscular strength and mortality in men: prospective cohort study. BMJ 337: a439, 2008.

Todd G, Taylor JL, Gandevia SC. Measurement of voluntary activation of fresh and fatigued human muscles using transcranial magnetic stimulation. J Physiol 555: 661-671, 2003.

AUTHOR BIO

Jim Nuzzo is a Postdoctoral Fellow at Neuroscience Research Australia (NeuRA). His research investigates how strength training alters the neural connections between the brain and muscles. Click here to read Jim’s other blogs.

Source: Strength training improves the nervous system’s ability to drive muscles – Motor Impairment

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