Posts Tagged neuroscience

[WEB SITE] UC study explores how low risk stress reduction treatments may benefit epilepsy patients

Patients with epilepsy face many challenges, but perhaps the most difficult of all is the unpredictability of seizure occurrence. One of the most commonly reported triggers for seizures is stress.

A recent review article in the European journal Seizure, by researchers at University of Cincinnati Epilepsy Center at the UC Gardner Neuroscience Institute, looks at the stress-seizure relationship and how adopting stress reduction techniques may provide benefit as a low risk form of treatment.

The relationship between stress and seizures has been well documented over the last 50 years. It has been noted that stress can not only increase seizure susceptibility and in rare cases a form of reflex epilepsy, but also increase the risk of the development of epilepsy, especially when stressors are severe, prolonged, or experienced early in life.

“Studies to date have looked at the relationship from many angles,” says Michael Privitera, MD, director of the UC Epilepsy Center and professor in the Department of Neurology and Rehabilitation Medicine at the UC College of Medicine. “The earliest studies from the 1980s were primarily diaries of patients who described experiencing more seizures on ‘high-stress days’ than on ‘low-stress days.'”

Privitera and Heather McKee, MD, an assistant professor in the Department of Neurology and Rehabilitation Medicine, looked at 21 studies from the 1980s to present–from patients who kept diaries of stress levels and correlation of seizure frequency, to tracking seizures after major life events, to fMRI studies that looked at responses to stressful verbal/auditory stimuli.

“Most all [of these studies] show increases in seizure frequency after high-stress events. Studies have also followed populations who have collectively experienced stressful events, such as the effects of war, trauma or natural disaster, or the death of a loved one,” says Privitera. All of which found increased seizure risk during such a time of stress.

For example, a 2002 study evaluated the occurrence of epileptic seizures during the war in Croatia in the early 1990s. Children from war-affected areas had epileptic seizures more often than children not affected by the war. Additionally, the 10-year follow up showed that patients who had their first epileptic seizure during a time of stress were more likely to have controlled epilepsy or even be off medication years later.

“Stress is a subjective and highly individualized state of mental or emotional strain. Although it’s quite clear that stress is an important and common seizure precipitant, it remains difficult to obtain objective conclusions about a direct causal factor for individual epilepsy patients,” says McKee.

Another aspect of the stress-seizure relationship is the finding by UC researchers that there were higher anxiety levels in patients with epilepsy who report stress as a seizure precipitant. The researchers suggest patients who believe stress is a seizure trigger may want to talk with their health care provider about screening for anxiety.

“Any patient reporting stress as a seizure trigger should be screened for a treatable mood disorder, especially considering that mood disorders are so common within this population,” adds McKee.

The researchers report that while some small prospective trials using general stress reduction methods have shown promise in improving outcomes in people with epilepsy, large-scale, randomized, controlled trials are needed to convince both patients and providers that stress reduction methods should be standard adjunctive treatments for people with epilepsy.

“What I think some of these studies point to is that efforts toward stress reduction techniques, though somewhat inconsistent, have shown promise in reducing seizure frequency. We need future research to establish evidence-based treatments and clarify biological mechanisms of the stress-seizure relationship,” says Privitera.

Overall, he says, recommending stress reduction methods to patients with epilepsy “could improve overall quality of life and reduce seizure frequency at little to no risk.”

Some low risk stress reduction techniques may include controlled deep breathing, relaxation or mindfulness therapy, as well as exercise, or establishing routines.

Source: UC study explores how low risk stress reduction treatments may benefit epilepsy patients

, , , , , , , , , , , ,

Leave a comment

[WEB SITE] Study investigates plasticity of motor representations in patients with brain tumors

Winner of the Brainlab Community Neurosurgery Award, Sandro Krieg, MD, presented his research, Plasticity of Motor Representations in Patients with Brain Lesions: a Navigated TMS Study, during the 2017 American Association of Neurological Surgeons (AANS) Annual Scientific Meeting.

This study investigated the spatial distributions of motor representations in terms of tumor-induced brain plasticity by analyzing navigated transcranial magnetic stimulation (nTMS) motor maps derived from 100 patients with motor eloquently located brain tumors in or adjacent to the precentral gyrus (PrG).

The research evoked 8,774 motor potentials (MEPs) that were elicited in six muscles of the upper and lower extremity by stimulating four gyri in patients with five possible tumor locations. Regarding the MEP frequency of each muscle-gyrus subdivision per patient, the expected frequency was 3.53 (8,774 divided by 100 patients, further divided by six muscles and four gyri). Accordingly, the patient ratio for each subdivision was calculated by defining the per-patient minimum data points as three.

The tumor-location specific patient ratios were higher for frontal tumors in both gyri than for other tumor locations. This suggests that the finger representation reorganization in these frontal gyri, which corresponds to location of dorsal premotor areas, might be due to within-premotor reorganization rather than relocation of motor function from PrG into premotor areas one might expect from the Rolandic tumors. The research indicates that reorganization of the finger motor representations might be limited along the middle-to-dorsal dimension of the dorsal premotor areas (posterior MFG and SFG) and might not cross rostrally from the primary motor cortex (PrG) to the dorsal premotor cortex.

Source: Study investigates plasticity of motor representations in patients with brain tumors

, , , , , , , ,

Leave a comment

[WEB SITE] Cannabidiol shows promise to reduce seizures for people with difficult-to-treat epilepsy

Taking cannabidiol may cut seizures in half for some children and adults with Lennox-Gastaut syndrome (LGS), a severe form of epilepsy, according to new information released today from a large scale controlled clinical study that will be presented at the American Academy of Neurology’s 69th Annual Meeting in Boston, April 22 to 28, 2017. Cannabidiol is a molecule from the cannabis plant that does not have the psychoactive properties that create a “high.”

Nearly 40 percent of people with LGS, which starts in childhood, had at least a 50 percent reduction in drop seizures when taking a liquid form of cannabidiol compared to 15 percent taking a placebo.

When someone has a drop seizure, their muscle tone changes, causing them to collapse. Children and adults with LGS have multiple kinds of seizures, including drop seizures and tonic-clonic seizures, which involve loss of consciousness and full-body convulsions. The seizures are hard to control and usually do not respond well to medications. Intellectual development is usually impaired in people with LGS.

Although the drop seizures of LGS are often very brief, they frequently lead to injury and trips to the hospital emergency room, so any reduction in drop seizure frequency is a benefit.

“Our study found that cannabidiol shows great promise in that it may reduce seizures that are otherwise difficult to control,” said study author Anup Patel, MD, of Nationwide Children’s Hospital and The Ohio State University College of Medicine in Columbus and a member of the American Academy of Neurology.

For the randomized, double-blind, placebo-controlled study, researchers followed 225 people with an average age of 16 for 14 weeks. The participants had an average of 85 drop seizures per month, had already tried an average of six epilepsy drugs that did not work for them and were taking an average of three epilepsy drugs during the study.

Participants were given either a higher dose of 20 mg/kg daily cannabidiol, a lower dose of 10 mg/kg daily cannabidiol or placebo as an add-on to their current medications for 14 weeks.

Those taking the higher dose had a 42 percent reduction in drop seizures overall, and for 40 percent, their seizures were reduced by half or more.

Those taking the lower dose had a 37 percent reduction in drop seizures overall, and for 36 percent, seizures were reduced by half or more.

Those taking the placebo had a 17 percent reduction in drop seizures, and for 15 percent, seizures were reduced by half or more.

There were side effects for 94 percent of those taking the higher dose, 84 percent of those taking the lower dose and 72 percent of those taking placebo, but most side effects were reported as mild to moderate. The two most common were decreased appetite and sleepiness.

Those receiving cannabidiol were up to 2.6 times more likely to say their overall condition had improved than those receiving the placebo, with up to 66 percent reporting improvement compared to 44 percent of those receiving the placebo.

“Our results suggest that cannabidiol may be effective for those with Lennox-Gastaut syndrome in treating drop seizures,” said Patel. “This is important because this kind of epilepsy is incredibly difficult to treat. While there were more side effects for those taking cannabidiol, they were mostly well-tolerated. I believe that it may become an important new treatment option for these patients.”

There is currently a plan to submit a New Drug Application to the FDA later this year.

Source: Cannabidiol shows promise to reduce seizures for people with difficult-to-treat epilepsy

, , , , , , , , , , , , ,

Leave a comment

[WEB SITE] Much of what we know about the brain may be wrong: The problem with fMRI

The past decade has brought us jaw-dropping insights about the hidden workings of our brains, in part thanks to a popular brain scan technique called fMRI. But a major new study has revealed that fMRI interpretation has a serious flaw, one that could mean that much of what we’ve learned about our brains this way might need a second look.

On TV and in movies, we’ve all seen doctors stick an X-ray up on the lightbox and play out a dramatic scene: “What’s that dark spot, doctor?” “Hm…”

In reality, though, a modern medical scan contains so much data, no single pair of doctor’s eyes could possibly interpret it. The brain scan known as fMRI, for functional magnetic resonance imaging, produces a massive data set that can only be understood by custom data analysis software. Armed with this analysis, neuroscientists have used the fMRI scan to produce a series of paradigm-shifting discoveries about our brains.

Now, an unsettling new report, which is causing waves in the neuroscience community, suggests that fMRI’s custom software can be deeply flawed — calling into question many of the most exciting findings in recent neuroscience.

The problem researchers have uncovered is simple: the computer programs designed to sift through the images produced by fMRI scans have a tendency to suggest differences in brain activity where none exist. For instance, humans who are resting, not thinking about anything in particular, not doing anything interesting, can deliver spurious results of differences in brain activity. It’s even been shown to indicate brain activity in a dead salmon, whose stilled brain lit up an MRI as if it were somehow still dreaming of a spawning run.

The report throws into question the results of some portion of the more than 40,000 studies that have been conducted using fMRI, studies that plumb the brainy depths of everything from free will to fear. And scientists are not quite sure how to recover.

“It’s impossible to know how many fMRI studies are wrong, since we do not have access to the original data,” says computer scientist Anders Eklund of Linkoping University in Sweden, who conducted the analysis.

How it should have worked: Start by signing up subjects. Scan their brains while they rest inside an MRI machine. Then scan their brains again when exposed to pictures of spiders, say. Those subjects who are afraid of spiders will have blood rush to those regions of the brain involved in thinking and feeling fear, because such thoughts or feelings are suspected to require more oxygen. With the help of a computer program, the MRI machine then registers differences in hemoglobin, the iron-rich molecule that makes blood red and carries oxygen from place to place. (That’s the functional in fMRI.) The scan then looks at whether those hemoglobin molecules are still carrying oxygen to a given place in the brain, or not, based on how the molecules respond to the powerful magnetic fields. Scan enough brains and see how the fearful differ from the fearless, and perhaps you can identify the brain regions or structures associated with thinking or feeling fear.

That’s the theory, anyway. In order to detect such differences in brain activity, it would be best to scan a large number of brains, but the difficulty and expense often make this impossible. A single MRI scan can cost around $2,600, according to a 2014 NerdWallet analysis. Further, the differences in the blood flow are often tiny. And then there’s the fact that computer programs have to sift the through images of the 1,200 or so cubic centimeters of gelatinous tissue that make up each individual brain and compare them to others, a big data analysis challenge.

Eklund’s report shows that the assumptions behind the main computer programs used to sift such big fMRI data have flaws, as turned up by nearly 3 million random evaluations of the resting brain scans of 499 volunteers from Cambridge, Massachusetts; Beijing; and Oulu, Finland. One program turned out to have a 15-year-old coding error (which has now been fixed) that caused it to detect too much brain activity. This highlights the challenge of researchers working with computer code that they are not capable of checking themselves, a challenge not confined just to neuroscience.

An FMRI scan during working memory tasks.

The brain is even more complicated than we thought.Worse, Eklund and his colleagues found that all the programs assume that brains at rest have the same response to the jet-engine roar of the MRI machine itself as well as whatever random thoughts and feelings occur in the brain. Those assumptions appear to be wrong. The brain at rest is “actually a bit more complex,” Eklund says.

More specifically, the white matter of the brain appears to be underrepresented in fMRI analyses while another specific part of the brain — the posterior cingulate, a region in the middle of the brain that connects to many other parts — shows up as a “hot spot” of activity. As a result, the programs are more likely to single it out as showing extra activity even when there is no difference. “The reason for this is still unknown,” Eklund says.

Overall, the programs had a false positive rate — detecting a difference where none actually existed — of as much as 70 percent.

Unknown unknowns: This does not mean all fMRI studies are wrong. Co-author and statistician Thomas Nichols of the University of Warwick calculates that some 3,500 studies may be affected by such false positives, and such false positives can never be eliminated entirely. But a survey of 241 recent fMRI papers found 96 that could have even worse false-positive rates than those found in this analysis.

“The paper makes an important criticism,” says Nancy Kanwisher, a neuroscientist at MIT (TED Talk: A neural portrait of the human mind), though she points out that it does not undermine those fMRI studies that do not rely on these computer programs.

Nonetheless, it is worrying. “I think the fallout has yet to be fully evaluated. It appears to apply to quite a few studies, certainly the studies done in a generic way that is the bread-and-butter of fMRI,” says Douglas Greve, a neuroimaging specialist at Massachusetts General Hospital. What’s needed is more scrutiny, Greve suggests.

Another argument for open data. Eklund and his colleagues were only able to discover this methodological flaw thanks to the open sharing of group brain scan data by the 1,000 Functional Connectomes Project. Unfortunately, such sharing of brain scan data is more the exception than the norm, which hinders other researchers attempting to re-create the experiment and replicate the results. Such replication is a cornerstone of the scientific method, ensuring that findings are robust. Eklund, for one, therefore encourages neuroimagers to “share their fMRI data, so that other researchers can replicate their findings and re-analyze the data several years later.” Only then can scientists be sure that the undiscovered activity of the human brain is truly revealed … and that dead salmon are not still dreaming.

ABOUT THE AUTHOR

David Biello is an award-winning journalist writing most often about the environment and energy. His book “The Unnatural World” publishes November 2016. It’s about whether the planet has entered a new geologic age as a result of people’s impacts and, if so, what we should do about this Anthropocene. He also hosts documentaries, such as “Beyond the Light Switch” and the forthcoming “The Ethanol Effect” for PBS. He is the science curator for TED.

Source: The problem with fMRI |

 

, , , , , , ,

Leave a comment

[WEB SITE] Your left hand knows what your right hand is doing

The saying goes that “your left hand doesn’t know what your right hand is doing,” but actually, your left hand is paying more attention than you’d think. Researchers at Tel-Aviv University found that when people practiced finger movements with their right hand while watching their left hand on 3D virtual reality headsets, they could use their left hand more efficiently after the exercise. The work, appearing in Cell Reports, provides a new strategy to improve physical therapy for people with limited strength in their hands.

“We are tricking the brain,” says lead author Roy Mukamel, a professor of psychology at Tel Aviv University in Israel. “This entire experiment ended up being a nice demonstration about how to combine software engineering and neuroscience.”

After completing baseline tests to assess the initial motor skills of each hand, 53 participants strapped on virtual reality headsets, which showed simulated versions of their hands. During the first experiment, the participants completed a series of finger movements with their right hand while the screen showed their virtual left hand moving instead. Next, the participants put a motorized glove on their left hand, which moved their fingers to match the motions of the right hand. While this occurred, the headsets again showed their virtual left hand moving instead of their right.

After analyzing the results, the researchers discovered that the left hand’s performance significantly improved (i.e., had more precise movements in a faster amount of time) when the screen showed the left hand. But the most notable improvements occurred when the virtual reality screen showed the left hand moving while the motorized glove moved the right hand in reality.

The researchers also used fMRI to track which brain structures were activated during the experiments in 18 of the participants. The scientists noted that one section of the brain, called the superior parietal lobe, was activated in each person during training. They also discovered that the level of activity in this brain region was correlated to the level of improved performance in the left hand–the more activity, the better the left hand performed.

“Technologically these experiments were a big challenge,” says Mukamel. “We manipulated what people see and combined it with the passive movement of the hand to show that our hands can learn when they’re not moving under voluntary control.”

The researchers are optimistic that this research can be applied to patients in physical therapy programs who have lost the strength or control of their hands. “We need to show a way to obtain high-performance gains relative to other traditional types of therapies,” says Mukamel. “If we can train one hand without voluntarily moving it and still show significant improvements in the motor skills of that hand, then that’s the ideal.”

This work was supported through the Sagol School of Neuroscience and School of Psychological Sciences at Tel-Aviv University in Israel.

Article: Neural Network Underlying Intermanual Skill Transfer in Humans, Ossmy and Mukamel, Cell Reports, 10.1016/j.celrep.2016.11.009, published 13 December 2016.

Source: Your left hand knows what your right hand is doing – Medical News Today

, , , , , , , ,

Leave a comment

[WEB SITE] ADD Program receives $19.5 million NIH contract to test drugs for treating epilepsy

The University of Utah College of Pharmacy’s Anticonvulsant Drug Development (ADD) Program has been awarded a five-year $19.5 million contract renewal with the National Institutes of Health (NIH) to test drugs to treat epilepsy, and the major focus of the project is to address needs that affect millions of people worldwide -identify novel investigational compounds to prevent the development of epilepsy or to treat refractory, or drug-resistant, epilepsy.

The ADD program began in 1975 and since then has tested the vast majority of drugs used to control seizures in patients with epilepsy, helping millions of people worldwide. Unfortunately, almost one-third of the estimated 50 million people with the disorder has refractory, or unresponsive, epilepsy that isn’t adequately controlled by medications currently available. The contract renewal, awarded through the National Institute of Neurological Disorders and Stroke (NINDS) to the U Department of Pharmacology and Toxicology, represents a shift in the mission to identify new therapies, according to ADD Director Karen S. Wilcox, Ph.D., professor and chair of pharmacology and toxicology and principal investigator of the contract.

“We’re proud that over the past 41 years, the ADD program has played a key role in identifying and characterizing many of the drugs now available to treat patients with epilepsy and to control their seizures,” Wilcox says. “Now, we’re looking for drugs that can modify or prevent the disease, particularly in those patients either with refractory epilepsy or at risk for developing epilepsy following a brain injury.”

Epilepsy is a group of neurological disorders characterized by a tendency for repeated seizures over time. It occurs when permanent changes in the brain result in abnormal or excessive neuronal activity in the brain. An estimated 2.9 million people in the United States and 50 million people worldwide have active epilepsy, according the Centers for Disease Control and World Health Organization. There is no cure for epilepsy and the mainstay of treatment is anti-seizure medications.

ADD is a long-standing program dedicated to testing drugs to treat epilepsy. It has received continuous funding from NINDS’ Epilepsy Therapy Screening Program (ETSP) (formerly known as the Anticonvulsant Screening Program) since its founding in 1974. In collaboration, the ETSP and the ADD Program have evaluated more than 32,000 compounds. ADD received the contract in a competitive bidding process. The renewal of the contractual relationship between the NINDS and the University of Utah reflects the ongoing commitment of the NIH and the ETSP to finding and developing novel therapies for epilepsy and represents a unique partnership between government, industry, and academia.

“The NIH-NINDS ETSP is pleased to continue the productive relationship with the University of Utah,” says Dr. John Kehne, a Program Director at NINDS and head of the ETSP. “These and other efforts supported by the NINDS will help to discover new pharmacotherapies to address the unmet medical needs of people living with epilepsy.”

In addition to its focus on evaluating potential candidate drugs for the treatment of therapy-resistant epilepsy, the mission of the ADD Program includes efforts to identify novel therapies for different types of epilepsy. The program also serves as a base for innovative basic research that sheds new light on the pathophysiology of epilepsy and provides a unique training environment for students, research fellows, and visiting scientists. Currently, the ADD program employ18 researchers, technicians, and staff. Cameron S. Metcalf, Ph.D is associate director and a co-Investigator of the contract and Peter J. West, Ph.D., and Misty D. Smith, Ph.D, research assistant professors of pharmacology and toxicology, are also co-investigators on the contract renewal.

Although there currently is no cure for epilepsy, Wilcox, who previously served as a co-Investigator of ADD before taking over as PI in 2016, believes that can be changed.

“The brain has remarkable plasticity throughout a person’s life,” she says. “If we learn enough about neuroscience and the details of how the brain works, it’s very possible to find a cure.”

Source: University of Utah Health Sciences

Source: ADD Program receives $19.5 million NIH contract to test drugs for treating epilepsy

, , , , , , , , , , , ,

Leave a comment

[WEB SITE] Brain plasticity after injury: an interview with Dr Swathi Kiran

What is brain plasticity and why is it important following a brain injury?

Brain plasticity is the phenomenon by which the brain can rewire and reorganize itself in response to changing stimulus input. Brain plasticity is at play when one is learning new information (at school) or learning a new language and occurs throughout one’s life.

Brain plasticity is particularly important after a brain injury, as the neurons in the brain are damaged after a brain injury, and depending on the type of brain injury, plasticity may either include repair of damaged brain regions or reorganization/rewiring of different parts of the brain.

MRI brain injury

How much is known about the level of injury the brain can recover from? Over what time period does the brain adapt to an injury?

A lot is known about brain plasticity immediately after an injury. Like any other injury to the body, after an initial negative reaction to the injury, the brain goes through a massive healing process, where the brain tries to repair itself after the injury. Research tells us exactly what kinds of repair processes occur hours, days and weeks after the injury.

What is not well understood is how recovery continues to occur in the long term. So, there is a lot research showing that the brain is plastic, and undergoes recovery even months after the brain damage, but what promotes such recovery and what hinders such recovery is not well understood.

It is well understood that some rehabilitative training promotes brain injury and most of the current research is focused on this topic.

What techniques are used to study brain plasticity?

Human brain plasticity has mostly been studied using non-invasive imaging methods, because these techniques allow us to measure the gray matter (neurons), white matter (axons) at a somewhat coarse level. MRI and fMRI techniques provide snapshots and video of the brain in function, and that allows us to capture changes in the brain that are interpreted as plasticity.

Also, more recently, there are invasive stimulation methods such as transcranial direct current stimulation or transcranial magnetic stimulation which allow providing electric current or magnetic current to different parts of the brain and such stimulation causes certain changes in the brain.

How has our understanding advanced over recent years?

One of the biggest shifts in our understanding of brain plasticity is that it is a lifelong phenomenon. We used to previously think that the brain is plastic only during childhood and once you reach adulthood, the brain is hardwired, and no new changes can be made to it.

However, we now know that even the adult brain can be modified and reorganized depending on what new information it is learning. This understanding has a profound impact on recovery from brain injury because it means that with repeated training/instruction, even the damaged brain is plastic and can recover.

What role do you see personalized medicine playing in brain therapy in the future?

One reason why rehabilitation after brain injury is so complex is because no two individuals are alike. Each individual’s education and life experiences have shaped their brain (due to plasticity!) in unique ways, so after a brain injury, we cannot expect that recovery in two individuals will be occur the same way.

Personalized medicine allows the ability to tailor treatment for each individual taking into account their strengths and weaknesses and providing exactly the right kind of therapy for that person. Therefore, one size treatment does not fit all, and individualized treatments prescribed to the exact amount of dosage will become a reality.

Senior couple tablet

What is ‘automedicine’ and do you think this could become a reality?

I am not sure we understand what automedicine can and cannot do just yet, so it’s a little early to comment on the reality. Using data to improve our algorithms to precisely deliver the right amount of rehabilitation/therapy will likely be a reality very soon, but it is not clear that it will eliminate the need for doctors or rehabilitation professionals.

What do you think the future holds for people recovering from strokes and brain injuries and what’s Constant Therapy’s vision?

The future for people recovering from strokes and brain injuries is more optimistic than it has ever been for three important reasons. First, as I pointed above, there is tremendous amount of research showing that the brain is plastic throughout life, and this plasticity can be harnessed after brain injury also.

Second, recent advances in technology allow patients to receive therapy at their homes at their convenience, empowering them to take control of their therapy instead of being passive consumers.

Finally, the data that is collected from individuals who continuously receive therapy provides a rich trove of information about how patients can improve after rehabilitation, what works and what does not work.

Constant Therapy’s vision incorporates all these points and its goal to provide effective, efficient and reasonable rehabilitation to patients recovering from strokes and brain injury.

Where can readers find more information?

About Dr Swathi Kiran

DR SWATHI KIRANSwathi Kiran is Professor in the Department of Speech and Hearing Sciences at Boston University and Assistant in Neurology/Neuroscience at Massachusetts General Hospital. Prior to Boston University, she was at University of Texas at Austin. She received her Ph.D from Northwestern University.

Her research interests focus around lexical semantic treatment for individuals with aphasia, bilingual aphasia and neuroimaging of brain plasticity following a stroke.

She has over 70 publications and her work has appeared in high impact journals across a variety of disciplines including cognitive neuroscience, neuroimaging, rehabilitation, speech language pathology and bilingualism.

She is a fellow of the American Speech Language and Hearing Association and serves on various journal editorial boards and grant review panels including at National Institutes of Health.

Her work has been continually funded by the National Institutes of Health/NIDCD and American Speech Language Hearing Foundation awards including the New Investigator grant, the New Century Scholar’s Grant and the Clinical Research grant. She is the co-founder and scientific advisor for Constant Therapy, a software platform for rehabilitation tools after brain injury.

Source: Brain plasticity after injury: an interview with Dr Swathi Kiran

, , , , , , , , , ,

Leave a comment

[WEB SITE] Scientists Take Big Step Toward Being Able To Repair Brain Injuries – Huffington Post

SOFIA GRADE
Embryonic neurons (shown in red) transplanted into the adult mouse brain connect with host neurons (shown in black), rebuilding neural circuits previously lost due to an injury.

Scientists have long been working toward a day when a traumatic injury or stroke doesn’t cause brain cells to be permanently lost.

Executing this extremely difficult task would involve figuring out how to transplant new neurons into brain tissue. But neurons form precise connections with each other, and are guided by physiological signals that are active during early brain development ― meaning that you can’t sow a fistful of new neurons into mature brain tissue and expect them to grow the way they should.

But scientists are making progress.

Embryonic neurons transplanted into the damaged brain of mice formed proper connections with their neighbors and restored function, researchers wrote in a study published Wednesday in the journal Nature.

By the fourth week, the transplanted young cells became the type of cells normally seen in that area of the brain. They were functional and responded to visual signals from the eyes. Moreover, the cells didn’t develop aberrant connections, something that could lead to epileptic seizures.

“What we did there is proof of concept,” said neuroscientist Magdalena Götz of Ludwig-Maximilians University and the Institute of Stem Cell Research at the Helmholtz Center in Munich, Germany.

“We took the best type of neurons, chosen at a specific time, and then we put them in the lesioned brain,” she said. “That was to find out how well can it work.”

The finding is an important step forward for someday repairing brain injury by using replacement neurons, other researchers said. Still, there are many challenges left.

“I’m excited about this study,” said Sunil Gandhi of University of California, Irvine, who wasn’t involved with the research. “This is evidence that the brain can accept the addition of new neurons, which normally doesn’t happen. That’s very exciting for its potential for cell-based repair for brain.”

SOFIA GRADE
Transplanted cells formed long-range connections with thalamic cells (shown in black).

But with complicated human biology comes complicated questions. What if the new cells become cancerous? What if the trauma of brain surgery causes more harm than the good a transplant might bring?

“In the case of stroke, there are therapeutic avenues that involve behavioral rehabilitation that can help to some degree,” Gandhi said. “It is true that the options are limited and frustrating. But the alternative is that we may end up going too fast and have unwanted harmful side effects.”

Neuroscientist Zhiping Pang, of Rutgers Robert Wood Johnson Medical School, agreed.

“This is absolutely an interesting and exciting paper,” he said. “Nevertheless, translating this to human stroke patients, safety will be a concern. A lot more work needs to be done, like the current study, before we can realize this exciting cell-replacement strategy in restoring proper brain functions of a stroke patient.”

The new study is promising, Götz said, but acknowledged that things are a lot messier outside the lab. Injuries to the brain are not clean-cut. They can occur in various sites, involve different types of neurons, and are accompanied by inflammation and other meddling signals. But Götz is hopeful that these problems can be solved.

“We are doing this now in more realistic models, in models of traumatic and ischemic brain injury and all I can say is that it looks pretty good,” she said.

Another challenge is to account for glial cells in the brain, which form scar tissue when an injury happens. That’s why Götz and her team are exploring the potential for turning these glial cells into new neurons that can replace the lost ones.

That approach could also solve the problem of supply, as using cells from fetuses is not a practical option for human patients.

Some forms of neuron transplantation have been done before. People with Parkinson’s disease suffer from a death of dopamine-producing cells deep in the brain, and it’s possible to transplant into their brains new neurons that secrete dopamine and help with certain symptoms. These neurons, however, don’t need to become a part of the existing circuitry. They don’t even need to be human cells ― the first transplant of this kind was done using brain cells from pigs.

Other groups have turned to induced pluripotent stem cells, or adults cells ― from a patient’s skin, for example ― that can be reprogrammed to an embryonic state and then directed to grow into a desired type of neuron.

“What’s going to be important now is to demonstrate that neurons that are grown from pluripotent stem cells can be coaxed to wiring up into the brain,” Gandhi said.

Source: Scientists Take Big Step Toward Being Able To Repair Brain Injuries | Huffington Post

, , , , , ,

Leave a comment

[BLOG] Neuro Landscape – A brain injury blog by Dr. Mark J. Ashley, CEO, Centre for Neuro Skills

ABOUT

Dr. Mark J. Ashley is founder and president/CEO of Centre for Neuro Skills (CNS), which operates postacute brain injury rehabilitation programs at facilities in Bakersfield, Dallas, Los Angeles, and San Francisco. Dr. Ashley founded CNS in 1980. He serves on the Board of Directors of the Brain Injury Association of America (BIAA) as the emeritus chair. He also serves on the Board of Directors of the Brain Injury Association of California and is the current chair. Dr. Ashley worked to establish BIAA’s Brain Injury Business Practices College and the Business and Professional Council.

Dr. Ashley is the immediate past chair of the Corporate Advisory Committee of the American Academy for Certification of Brain Injury Specialists. He serves as the vice chairman of the Access to Treatment Committee of the Business and Professional Council, and the Federal Legislative Advisory Committee for BIAA. He is an adjunct professor at the Rehabilitation Institute of the College of Education at Southern Illinois University, and served on the California Traumatic Brain Injury Advisory Council.

He is a member of the Advisory Committee for the Department of Rehabilitation Sciences, Cyprus University of Technology, and a member of the Advisory Board for the Applied Neuroscience and Neurobehavioral Research Center, University of Cyprus. He participated in preparation of Traumatic Brain Injury Medical Treatment Guidelines for the State of Colorado Department of Labor and Employment and serves on several grant review committees.

Dr. Ashley founded the Centre for Neuro Skills Clinical Research and Education Foundation (CREF), a non-profit research organization. His work has been published in numerous professional and research publications and he has written three books, “Working with Behavior Disorders: Strategies for Traumatic Brain Injury Rehabilitation” and “Traumatic Brain Injury Rehabilitation,” including this publication’s third edition.

Dr. Ashley received his Masters Degree in speech pathology and a Doctorate of Science from Southern Illinois University. The university named him Distinguished Alumni of the Year in 1995. He is an Adjunct Professor for the university’s Department of Communication Disorders and Sciences in the College of Education, specializing in brain injury and cognitive deficits. Dr. Ashley is a licensed Speech/Language Pathologist in California and Texas and is a Certified Case Manager.

He belongs to many professional associations, including the American Speech, Language, and Hearing Association, the American Congress of Rehabilitation Medicine, the American Society of Neurorehabilitation, the American Academy for the Advancement of the Science, the National Neurotrauma Society, the National Association for Independent Living, the International Association of Rehabilitation Professionals, the National Rehabilitation Association, the National Rehabilitation Administration Association, the California Speech and Hearing Association, and the Texas Speech and Hearing Association.

Source: About – Neuro Landscape

, , , , ,

Leave a comment

[WEB SITE] UCLA researchers use noninvasive ultrasound technique to jump-start the brain of coma patient

A 25-year-old man recovering from a coma has made remarkable progress following a treatment at UCLA to jump-start his brain using ultrasound. The technique uses sonic stimulation to excite the neurons in the thalamus, an egg-shaped structure that serves as the brain’s central hub for processing information.

“It’s almost as if we were jump-starting the neurons back into function,” said Martin Monti, the study’s lead author and a UCLA associate professor of psychology and neurosurgery. “Until now, the only way to achieve this was a risky surgical procedure known as deep brain stimulation, in which electrodes are implanted directly inside the thalamus,” he said. “Our approach directly targets the thalamus but is noninvasive.”

Monti said the researchers expected the positive result, but he cautioned that the procedure requires further study on additional patients before they determine whether it could be used consistently to help other people recovering from comas.

“It is possible that we were just very lucky and happened to have stimulated the patient just as he was spontaneously recovering,” Monti said.

A report on the treatment is published in the journal Brain Stimulation. This is the first time the approach has been used to treat severe brain injury.

The technique, called low-intensity focused ultrasound pulsation, was pioneered by Alexander Bystritsky, a UCLA professor of psychiatry and biobehavioral sciences in the Semel Institute for Neuroscience and Human Behavior and a co-author of the study. Bystritsky is also a founder of Brainsonix, a Sherman Oaks, California-based company that provided the device the researchers used in the study.

That device, about the size of a coffee cup saucer, creates a small sphere of acoustic energy that can be aimed at different regions of the brain to excite brain tissue. For the new study, researchers placed it by the side of the man’s head and activated it 10 times for 30 seconds each, in a 10-minute period.

Monti said the device is safe because it emits only a small amount of energy — less than a conventional Doppler ultrasound.

Before the procedure began, the man showed only minimal signs of being conscious and of understanding speech — for example, he could perform small, limited movements when asked. By the day after the treatment, his responses had improved measurably. Three days later, the patient had regained full consciousness and full language comprehension, and he could reliably communicate by nodding his head “yes” or shaking his head “no.” He even made a fist-bump gesture to say goodbye to one of his doctors.

“The changes were remarkable,” Monti said.

The technique targets the thalamus because, in people whose mental function is deeply impaired after a coma, thalamus performance is typically diminished. And medications that are commonly prescribed to people who are coming out of a coma target the thalamus only indirectly.

Under the direction of Paul Vespa, a UCLA professor of neurology and neurosurgery at the David Geffen School of Medicine at UCLA, the researchers plan to test the procedure on several more people beginning this fall at the Ronald Reagan UCLA Medical Center. Those tests will be conducted in partnership with the UCLA Brain Injury Research Center and funded in part by the Dana Foundation and the Tiny Blue Dot Foundation.

If the technology helps other people recovering from coma, Monti said, it could eventually be used to build a portable device — perhaps incorporated into a helmet — as a low-cost way to help “wake up” patients, perhaps even those who are in a vegetative or minimally conscious state. Currently, there is almost no effective treatment for such patients, he said.

Source: University of California – Los Angeles

Source: UCLA researchers use noninvasive ultrasound technique to jump-start the brain of coma patient

, , , , , , , , , ,

Leave a comment

%d bloggers like this: