Posts Tagged brain

[WEB SITE] Half the brain encodes both arm movements

October 8, 2018, Society for Neuroscience
Half the brain encodes both arm movements

Patients implanted with electrocorticography arrays completed a 3D center-out reaching task. Electrode locations were based upon the clinical requirements of each patient and were localized to an atlas brain for display (A). B. Patients were seated in the semi-recumbent position and completed reaching movements from the center to the corners of a 50cm physical cube based upon cues from LED lights located at each target while hand positions and ECoG signals were simultaneously recorded. Each patient was implanted with electrodes in a single cortical hemisphere and performed the task with the arm contralateral (C) and ipsilateral (D) to the electrode array in separate recording sessions. Credit: Bundy et al., JNeuros(2018)

Individual arm movements are represented by neural activity in both the left and right hemispheres of the brain, according to a study of epilepsy patients published in JNeurosci. This finding suggests the unaffected hemisphere in stroke could be harnessed to restore limb function on the same side of the body by controlling a brain-computer interface.

The right side of the brain is understood to control the left side of the body, and vice versa. Recent evidence, however, supports a connection between the same side of the brain and body during .

Eric Leuthardt, David Bundy, and colleagues explored brain activity during such ipsilateral movements during a reaching task in four  whose condition enabled invasive monitoring of their brains through implanted electrodes. Using a machine learning algorithm, the researchers demonstrate successful decoding of speed, velocity, and position information of both left and right arm movements regardless of the location of the electrodes.

In addition to advancing our understanding of how the brain controls the body, these results could inform the development of more effective rehabilitation strategies following brain injury.

Half the brain encodes both arm movements

In the study a patient implanted with electrodes only on the left side of the brain was asked to make movements to 8 targets in 3D space with both their right and left arms. Using recordings from these electrodes, the authors were able to predict the hand speed, direction, and position for both arms showing that movements of both arms are encoded on one side of the brain. Credit: David Bundy and Eric Leuthardt

 Explore further: New research on the brain’s backup motor systems could open door to novel stroke therapies

More information: Unilateral, Three-dimensional Arm Movement Kinematics are Encoded in Ipsilateral Human Cortex, JNeurosci (2018). DOI: 10.1523/JNEUROSCI.0015-18.2018

via Half the brain encodes both arm movements

, , , , , , ,

Leave a comment

[WEB SITE] Neuroscientists unravel how two different types of brain plasticity work on synapses

 

The brain’s crucial function is to allow organisms to learn and adapt to their surroundings. It does this by literally changing the connections, or synapses, between neurons, strengthening meaningful patterns of neural activity in order to store information. The existence of this process – brain plasticity – has been known for some time.

But actually, there are two different types of brain plasticity at work on synapses. One is “Hebbian plasticity”; it is the one which effectively allows for the recording of information in the synapses, named after pioneering neuroscientist Donald Hebb. The other, more recently discovered, is “homeostatic synaptic plasticity” (HSP), and, like other “homeostatic” processes in the body such as maintaining a constant body temperature, its purpose is to keep things stable. In this case, HSP ensures that the brain doesn’t build up too much activity (as is the case in epilepsy) or become too quiet (as can happen when you lose synapses in Alzheimer’s Disease).

However, little is known about how these two types of plasticity actually interact in the brain. Now, a team of neuroscientists at the Champalimaud Centre for the Unknown, in Lisbon, Portugal, has begun to unravel the fundamental processes that happen in the synapse when the two mechanisms overlap. Their results were published in the journal iScience.

“In theory, the two types of plasticity act as opposing forces”, says Anna Hobbiss, first author of the new study, which was led by Inbal Israely. “Hebbian plasticity reacts to activity at the synapses by inciting them to get stronger while HSP reacts to it by making them weaker. We wanted to understand, on a cellular and molecular level, how the synapse deals with these two forces when they are present at the same time.”

In so doing, the authors have surprisingly shown that, contrary to what might be expected, HSP facilitates Hebbian plasticity, and thus influences memory formation and learning. This means that these two types of plasticity “may actually not be such distinct processes, but instead work together at the same synapses”, says Israely.

The team’s goal was to determine the changes in size of minute structures called dendritic spines, which are the “receiving end” of the synapse. The size of these spines changes to reflect the strength of the synaptic connection.

For this, they studied cells from the mouse hippocampus, a part of the brain which is crucial for learning. In their experiments, they blocked activity in the cells by introducing a potent neurotoxin called tetrodotoxin, thus simulating the loss of input to a certain part of the brain (“think about a person suddenly becoming blind, which leads to loss of input from the eyes to the brain”, says Hobbiss).

Forty eight hours later, they mimicked a small recovery of activity at only one synapse by releasing a few molecules of a neurotransmitter called glutamate on single spines of single neurons. This was possible thanks to a very high resolution, state-of-the-art laser technology, called two-photon microscopy, which allowed the scientists to very precisely visualize and target individual dendritic spines.

As this process evolved, the team closely watched what was happening to the spines – and they saw various anatomical changes. First, the silencing of all neural activity made the spines grow in size. “The spines are like little microphones, which, when there is silence, ramp up the ‘volume’ to try and catch even the faintest noise”, Hobbiss explains.

The scientists then activated individual spines with pulses of glutamate and watched them for two hours. One of the things they thought could happen was that the size of the spines would not grow further, since they had already turned up their ‘volume’ as far is it would go. But the opposite happened: the spines grew even more, with the smaller spines showing the biggest growth.

Finally, the authors also saw growth in neighboring spines, even though the experiment only targeted one spine. “We found that after a lack of activity, other spines in the vicinity also grew, further enhancing the cell’s sensitivity to restored neural transmission”, says Hobbiss. “The cells become more sensitive, more susceptible to encode information. It is as though the ‘gain’ has been turned up”, she adds.

“The fact that neighboring spines grew together with an active spine signifies that homeostatic plasticity changes one of the hallmark features of information storage, which is that plasticity is limited to the site of information entry”, Israely explains. “So, in this sense, the different plasticity mechanisms which are at work in the neuron can cooperate to change which and how many inputs respond to a stimulus. I think this is an exciting finding of our study.”

Taken together, these results show that homeostatic plasticity can actually rev up Hebbian plasticity, the type required for storing information. “Our work adds a piece to the puzzle of how the brain performs one of its fundamental tasks: being able to encode information while still keeping a stable level of activity”, concludes Hobbiss.

The misregulation of homeostatic plasticity – the stabilizing one – has started to be implicated in human health, specifically neurodevelopmental disorders such as Fragile X syndrome and Rett syndrome as well as neurodegenerative ones such as Alzheimer’s Disease. “Perhaps this balance is what allows us to be able to learn new information while retaining stability of that knowledge over a lifetime”, says Israely.

 

via Neuroscientists unravel how two different types of brain plasticity work on synapses

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

Leave a comment

[Factsheet] Understanding TBI: Part 2 – Brain injury impact on individuals functioning – Model Systems Knowledge Translation Center (MSKTC)

Father teaching child with blocks

Written by Thomas Novack, PhD and Tamara Bushnik, PhD in collaboration with the MSKTC

 

A traumatic brain injury interferes with the way the brain normally works. When nerve cells in the brain are damaged, they can no longer send information to each other in the normal way. This causes changes in the person’s behavior and abilities. The injury may cause different problems, depending upon which parts of the brain were damaged most.

There are three general types of problems that can happen after TBI: physical, cognitive and emotional/ behavioral problems. It is impossible to tell early on which specific problems a person will have after a TBI. Problems typically improve as the person recovers, but this may take weeks or months. With some severe injuries changes can take many years.

Structure and function of the brain

The brain is the control center for all human activity, including vital processes (breathing and moving) as well as thinking, judgment, and emotional reactions. Understanding how different parts of the brain work helps us understand how injury affects a person’s abilities and behaviors.

Left vs. Right Brain

  • The brain is divided into two halves (hemispheres). The left half controls movement and sensation in the right side of the body, and the right half controls movement and sensation in the left side. Thus, damage to the right side of the brain may cause movement problems or weakness on the body’s left side.
  • For most people, the left half of the brain is responsible for verbal and logical functions including language (listening, reading, speaking, and writing), thought and memory involving words.
  • The right half is responsible for nonverbal and intuitive functions such as putting bits of information together to make up an entire picture, recognizing oral and visual patterns and designs (music and art), and expressing and understanding emotions.

Brain Areas & Associated Functions

The brain is made up of six parts that can be injured in a head injury. The effect of a brain injury is partially determined by the location of the injury. Sometimes only a single area is affected, but in most cases of TBI multiple areas have been injured. When all areas of the brain are affected, the injury can be very severe.

Image of Brain with Lobe Information

Six parts Functions
Brain Stem
  • Breathing
  • Heart Rate
  • Swallowing
  • Reflexes for seeing and hearing
  • Controls sweating, blood pressure, digestion, temperature
  • Affects level of alertness
  • Ability to sleep
  • Sense of balance
Cerebellum
  • Coordination of voluntary movement
  • Balance and equilibrium
  • Some memory for reflex motor acts
Frontal Lobe
  • How we know what we are doing within our environment
  • How we initiate activity in response to our environment
  • Judgments we make about what occurs in our daily activities
  • Controls our emotional response
  • Controls our expressive language
  • Assigns meaning to the words we choose
  • Involves word associations
  • Memory for habits and motor activities
  • Flexibility of thought, planning and organizing
  • Understanding abstract concepts
  • Reasoning and problem solving
Parietal Lobe
  • Visual attention
  • Touch perception
  • Goal directed voluntary movements
  • Manipulation of objects
  • Integration of different senses
Occipital Lobes
  • Vision
Temporal Lobes
  • Hearing ability
  • Memory aquisition
  • Some visual perceptions such as face recognition and object identification
  • Categorization of objects
  • Understanding or processing verbal information
  • Emotion

Physical Problems

Most people with TBI are able to walk and use their hands within 6-12 months after injury. In most cases, the physical difficulties do not prevent a return to independent living, including work and driving.

In the long term the TBI may reduce coordination or produce weakness and problems with balance. For example, a person with TBI may have difficulty playing sports as well as they did before the injury. They also may not be able to maintain activity for very long due to fatigue.

Cognitive (Thinking) Problems

  • Individuals with a moderate-to-severe brain injury often have problems in basic cognitive (thinking) skills such as paying attention, concentrating, and remembering new information and events.
  • They may think slowly, speak slowly and solve problems slowly.
  • They may become confused easily when normal routines are changed or when things become too noisy or hectic around them.
  • They may stick to a task too long, being unable to switch to different task when having difficulties.
  • On the other hand, they may jump at the first solution they see without thinking it through.
  • They may have speech and language problems, such as trouble finding the right word or understanding others.
  • After brain injury, a person may have trouble with all the complex cognitive activities necessary to be independent and competent in our complex world. The brain processes large amounts of complex information all the time that allows us to function independently in our daily lives. This activity is called executive function because it means being the executive or being in charge of one’s own life.

Emotional/Behavioral Problems

Behavioral and emotional difficulties are common and can be the result of several causes:

  • First, the changes can come directly from damage to brain tissue. This is especially true for injuries to the frontal lobe, which controls emotion and behavior.
  • Second, cognitive problems may lead to emotional changes or make them worse. For example, a person who cannot pay attention well enough to follow a conversation may become very frustrated and upset in those situations.
  • Third, it is understandable for people with TBI to have strong emotional reactions to the major life changes that are caused by the injury. For example, loss of job and income, changes in family roles, and needing supervision for the first time in one’s adult life can cause frustration and depression.

Brain injury can bring on disturbing new behaviors or change a person’s personality. This is very distressing to both the person with the TBI and the family. These behaviors may include:

  • Restlessness
  • Acting more dependent on others
  • Emotional or mood swings
  • Lack of motivation
  • Irritability
  • Aggression
  • Lethargy
  • Acting inappropriately in different situations
  • Lack of self-awareness. Injured individuals may be unaware that they have changed or have problems. This can be due to the brain damage itself or to a denial of what’s really going on in order to avoid fully facing the seriousness of their condition.

Fortunately, with rehabilitation training, therapy and other supports, the person can learn to manage these emotional and behavioral problems.

Disclaimer

This information is not meant to replace the advice from a medical professional. You should consult your health care provider regarding specific medical concerns or treatment.

Source

Our health information content is based on research evidence whenever available and represents the consensus of expert opinion of the TBI Model Systems directors.

Our health information content is based on research evidence and/or professional consensus and has been reviewed and approved by an editorial team of experts from the TBI Model Systems.

Authorship

Understanding TBI was developed by Thomas Novack, PhD and Tamara Bushnik, PhD in collaboration with the Model System Knowledge Translation Center. Portions of this document were adapted from materials developed by the University of Alabama TBIMS, Baylor Institute for Rehabilitation, New York TBIMS, Mayo Clinic TBIMS, Moss TBIMS, and from Picking up the pieces after TBI: A guide for Family Members, by Angelle M. Sander, PhD, Baylor College of Medicine (2002).

via Understanding TBI: Part 2 – Brain injury impact on individuals functioning | Model Systems Knowledge Translation Center (MSKTC)

, , , , , , ,

Leave a comment

[VIDEO] This video of a freshly removed human brain is fascinating to watch

Even though you use your brain to do a lot of thinking, you probably don’t think about your brain that often. It’s an incredibly complex, incredibly precious organ. It’s also incredibly squishy, as you can see in an amazing teaching video that demonstrates a freshly removed brain straight from autopsy.

As the neuroanatomist handles the vulnerable blob with the utmost care, it’s awe-inspiring to realise that each one of us has a squishy brain just like it – and it contains all our memories and thoughts.

As neuroanatomist Suzanne Strensaas says in the video, most of us tend to think that the brain is like a rubber ball. However, if you’re a trauma surgeon or a neurosurgeon, you realize that the brain is really very, very soft and much more vulnerable than the impression you get from textbooks.

As she’s holding the 1.4 kg (3 lbs) brain in both palms, it’s absolutely crazy to realise that right there is the entire set of life experiences of what was once a living, feeling human being.

“We are fortunate enough to show you what a normal, unfixed, recently deceased patient’s brain would look like,” says Stensaas.

As she explains, the cancer patient whose autopsy this brain is from, died from cell transplant complications. And seeing how Stensaas handles the specimen, we feel honoured to be able to learn so much thanks to the patient who donated their body to science.

Even though she continues to rotate it, presumably to avoid holding it in one place for too long, she manages to leave a slight indentation of her finger on top of one of the hemispheres.

And it turns out that even when a brain is preserved in a fixation solution, it can’t be left sitting at the bottom of the tank as that will make it squat and out of shape – hence scientists loop a cord through one of the arteries to suspend the brain in the liquid (who knew!).

via This video of a freshly removed human brain is fascinating to watch

, ,

Leave a comment

[VIDEO] Your Brain on Depression: Neuroscience, Animated – YouTube

Depression is a multifaceted and insidious disorder, nearly as complex as the brain itself. As research continues to suggest, the onset of depression can be attributed to an interplay of the many elements that make us human—namely, our genetics, the structure and chemistry of our brains, and our lived experience. Second only, perhaps, to the confounding mechanics of anesthesia, depression is the ultimate mind-body problem; understanding how it works could unlock the mysteries of human consciousness.

Emma Allen, a visual artist, and Dr. Daisy Thompson-Lake, a clinical neuroscientist, are fascinated by the physical processes that underlie mental health conditions. Together, they created Adam, a stop-motion animation composed of nearly 1,500 photographs. The short film illuminates the neuroscience of depression while also conveying its emotive experience.

“It was challenging translating the complicated science into an emotional visual story with scenes that would flow smoothly into each other,” Allen told The Atlantic.

“One of the most complex issues we had to deal with,” added Thompson-Lake, “is that there no single neuroscientific explanation for depression…While scientists agree that there are biological and chemical changes within the brain, the actual brain chemistry is very unique to the individual—although, of course, we can see patterns when studying large numbers of patients.” As a result, Allen and Thompson-Lake attempted a visual interpretation of depression that does not rely too heavily on any one explanation.

The film’s first sequence depicts the brain’s vast network of neuronal connections. Neurons communicate via synapses, across which electrical and chemical signals are exchanged. In a depressed patient’s brain, some of these processes are inefficient or dysfunctional, as the animation illustrates. Next, we see a positron emission tomography (PET) scan of a depressed brain, demarcated by darkened areas. Finally, the animation shows activity in the hippocampus and the frontal lobe. Abnormalities in the activity of both of these areas of the brain have been implicated in depression by recent research.

For Allen, one of the main objectives in creating Adam was to help dispel the notion that depression is a character flaw. “A common misconception is that the person is at fault for feeling this way, and that to ask for help is a weakness or embarrassing,” Allen said. “But depression has a physical component that needs treating.”

“The shame surrounding mental health still exists,” Allen continued. “In fact, in the case of Kate Spade, it was reported that she was concerned about the stigma her brand might face if this were made public.”

And who, exactly, is Adam? “Daisy lost a friend to suicide,” said Allen, “so the film is named in his memory.”

“Adam” was directed by animator Emma Allen and neuroscientist Daisy Thompson-Lake. It is part of The Atlantic Selects, an online showcase of short films from independent creators, curated by The Atlantic.

 

, , , ,

Leave a comment

[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

, , ,

Leave a comment

[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

, , , , , , ,

Leave a comment

[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.

References

  1. 1.
    C. H. Rankin, T. Abrams, R. J. Barry, et al., “Habituation revisited: An updated and revised description of the behavioral characteristics of habituation,” Neurobiol. Learn. Mem. 92 (2), 135–138 (2009).CrossRefGoogle Scholar
  2. 2.
    I. Jin, E. R. Kandel, and R. D. Hawkins, “Whereas short-term facilitation is presynaptic, intermediateterm facilitation involves both presynaptic and postsynaptic protein kinases and protein synthesis,” Learn. Mem. Cold Spring Harb. 18, 96–102 (2011).CrossRefGoogle Scholar
  3. 3.
    C. Lüscher, R. A. Nicoll, R. C. Malenka, and D. Muller, “Synaptic plasticity and dynamic modulation of the postsynaptic membrane,” Nat. Neurosci., No. 3, 545–550 (2000).CrossRefGoogle Scholar
  4. 4.
    M. Lenz, A. Vlachos, and N. Maggio, “Ischemic longterm-potentiation (iLTP): Perspectives to set the threshold of neural plasticity toward therapy,” Neural Regen. Res., No. 10, 1537–1539 (2015).CrossRefGoogle Scholar
  5. 5.
    N. Hardingham, J. Dachtler, and K. Fox, “The role of nitric oxide in pre-synaptic plasticity and homeostasis,” Front Cell Neurosci., No. 7, 1–19 (2013).CrossRefGoogle Scholar
  6. 6.
    S. D. Bury and T. A. Jones, “Unilateral sensorimotor cortex lesions in adult rats facilitate motor skill learning with the ‘unaffected’ forelimb and training-induced dendritic structural plasticity in the motor cortex,” J. Neurosci. Off. J. Soc. Neurosci. 22, 8597–8606 (2002).CrossRefGoogle Scholar
  7. 7.
    R. J. Nudo, “Postinfarct cortical plasticity and behavioral recovery,” Stroke 38, 840–845 (2007).CrossRefGoogle Scholar
  8. 8.
    A. Arvidsson, T. Collin, D. Kirik, et al., “Neuronal replacement from endogenous precursors in the adult brain after stroke,” Nat. Med. 8, 963–970 (2002).CrossRefGoogle Scholar
  9. 9.
    Y. Bach and P. Rita, “Central nervous system lesions: Sprouting and unmasking in rehabilitation,” Arch. Phys. Med. Rehabil. 62, 413–417 (1981).Google Scholar
  10. 10.
    W. T. Greenough, H. M. Hwang, and C. Gorman, “Evidence for active synapse formation or altered postsynaptic metabolism in visual cortex of rats reared in complex environments,” Proc. Natl. Acad. Sci. U. S. A. 82, 4549–4552 (1985).CrossRefGoogle Scholar
  11. 11.
    J. Liepert, H. Bauder, H. R. Wolfgang, et al., “Treatment-induced cortical reorganization after stroke in humans,” Stroke J. Cereb. Circ. 31, 1210–1216 (2000).CrossRefGoogle Scholar
  12. 12.
    Y. Sagi, I. Tavor, S. Hofstetter, et al., “Learning in the fast lane: New insights into neuroplasticity,” Neuron 73, 1195–1203 (2012).CrossRefGoogle Scholar
  13. 13.
    E. Auriel, B. L. Edlow, Y. D. Reijmer, et al., “Microinfarct disruption of white matter structure: A longitudinal diffusion tensor analysis,” Neurology 83, 182–188 (2014).CrossRefGoogle Scholar
  14. 14.
    L. A. Chernikova, M. A. Piradov, N. A. Suponeva, et al., “High-tech methods of neurorehabilitation in nervous system diseases,” in Neurology of the 21st Century: Diagnostic, Treatment, and Research Technologies: Manual for Doctors, Ed. by M. A. Piradov, S. N. Illarioshkin, and M. M. Tanashyan (ATMO, Moscow, 2015) [in Russian].Google Scholar
  15. 15.
    L. G. Tarasova, L. A. Chernikova, and A. S. Chubukov, “Hand motion recovery in poststroke hemiparesis patients by the method of intensive training of the paretic upper limb,” Lech. Fizkul’t. Sport. Med., No. 8, 34–39 (2008).Google Scholar
  16. 16.
    P. R. Prokazova, M. A. Piradov, Yu. V. Ryabinkina, et al., “Robotic mechanotherapy using the Motomed Letto 2 simulator in complex early stroke rehabilitation in the resuscitation and intensive care unit,” Annaly Klinich. Eksp. Nevrolog., No. 2, 11–15 (2013).Google Scholar
  17. 17.
    A. A. Belkin, I. A. Avdyunina, N. A. Varako, et al., “Intensive care rehabilitation: Clinical recommendations,” Vestn. Vosstanov. Med., No. 2, 139–143 (2017).Google Scholar
  18. 18.
    K. Ustinova, N. Epstein, L. Chernikova, et al., “Effect of robotic locomotor training in an individual with Parkinson’s disease: A case report,” Disab. Rehab.: Assist. Technol. 6 (1), 77–85 (2011).Google Scholar
  19. 19.
    S. N. Morozova, E. A. Zmeykina, R. N. Konovalov, et al., “Changes in functional connectivity of motor zones in the course of treatment with a Regent multimodal complex exoskeleton in neurorehabilitation of poststroke patients.” Hum. Physiol., No. 1, 54–60 (2016).Google Scholar
  20. 20.
    E. I. Kremneva, L. A. Chernikova, R. N. Konovalov, et al., “Assessing supraspinal control of locomotion in norm and in pathology using a passive motor fMRT paradigm,” Annaly Klinich. Eksp. Nevrol., No. 1, 31–37 (2012).Google Scholar
  21. 21.
    L. A. Chernikova, E. I. Kremneva, A. V. Chervyakov, et al., “New approaches in the study of the neuroplasticity process in patients with central nervous system lesions,” Hum. Physiol., No. 3, 272–277 (2013).CrossRefGoogle Scholar
  22. 22.
    O. V. Glebova, M. Yu. Maksimova, and L. A. Chernikova, “Mechanical stimulation of plantar support zones during acute moderate and severe stroke,” Vestn. Vosstanov. Med., No. 1, 71–75 (2014).Google Scholar
  23. 23.
    I. V. Saenko, S. N. Morozova, E. A. Zmeikina, et al., “Change in functional connectivity of motor zones using the Regent multimodal exoskeleton complex in stroke patients,” Fiziol. Chel., No. 1, 64–72 (2016).Google Scholar
  24. 24.
    M. A. Piradov, S. N. Illarioshkin, A. O. Gushcha, et al., “State-of-the-art neuromodulation technologies,” in Neurology of the 21st Century: Diagnostic, Treatment, and Research Technologies: Manual for Doctors, Ed. by M. A. Piradov, S. N. Illarioshkin, and M. M. Tanashyan (ATMO, Moscow, 2015), pp. 46–98 [in Russian].Google Scholar
  25. 25.
    N. A. Suponeva, I. S. Bakulin, A. G. Poidasheva, and M. A. Piradov, “Safety of transcranial magnetic stimulation: A review of international recommendations and new data,” Nervno-Myshech. Bol., No. 2, 21–36 (2017).Google Scholar
  26. 26.
    M. A. Piradov, M. V. Krotenkova, R. N. Konovalov, et al., “Neuroimaging technologies,” in Neurology of the 21st Century: Diagnostoc, Treatment, and Research Technologies: Manual for Doctors, Ed. by M. A. Piradov, S. N. Illarioshkin, and M. M. Tanashyan (ATMO, Moscow, 2015), pp. 11–82 [in Russian].Google Scholar
  27. 27.
    L. A. Legostaeva, E. A. Zmeikina, A. G. Poidasheva, et al., “Navigated transcranial magnetic stimulation under fMRT resting control during rehabilitation of patients with chronic consciousness disorders: Blind intervention study,” in VI Baltic Congress on Child Neurology: A Collection of Abstracts, (St. Petersburg, 2016), pp. 221–222 [in Russian].Google Scholar
  28. 28.
    O. A. Mokienko, R. K. Lyukmanov, L. A. Chernikova, et al., “Brain–computer interface: The first experience of clinical use in Russia,” Hum. Physiol., No. 1, 24–31 (2016).CrossRefGoogle Scholar
  29. 29.
    O. A. Mokienko, A. V. Chervyakov, S. Kulikova, et al., “Increased motor cortex excitability during motor imagery in brain–computer interface trained subjects,” Front. Comput. Neurosci. 7, 168 (2013).CrossRefGoogle Scholar
  30. 30.
    A. G. Poidasheva, G. A. Aziatskaya, A. Yu. Chernyavskii, et al., “Dynamics of cortical motor representation of the common digital extensor when teaching motor imaging using the brain–computer interface: A controlled study,” Zh. Vyssh. Nerv. Deyat. im. I.P. Pavlova, No. 4, 473–484 (2017).Google Scholar

via Braind Modern Neurorehabilitation Technologies | SpringerLink

, , , , , , , , ,

Leave a comment

[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?

 

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

Leave a comment

[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

, , , , , , , , ,

Leave a comment

%d bloggers like this: