Posts tagged brain injury
Articles and news from the latest research reports.
New Theory of Synapse Formation in the Brain
The human brain keeps changing throughout a person’s lifetime. New connections are continually created while synapses that are no longer in use degenerate. To date, little is known about the mechanisms behind these processes. Jülich neuroinformatician Dr. Markus Butz has now been able to ascribe the formation of new neural networks in the visual cortex to a simple homeostatic rule that is also the basis of many other self-regulating processes in nature. With this explanation, he and his colleague Dr. Arjen van Ooyen from Amsterdam also provide a new theory on the plasticity of the brain – and a novel approach to understanding learning processes and treating brain injuries and diseases.
The brains of adult humans are by no means hard wired. Scientists have repeatedly established this fact over the last few years using different imaging techniques. This so-called neuroplasticity not only plays a key role in learning processes, it also enables the brain to recover from injuries and compensate for the loss of functions. Researchers only recently found out that even in the adult brain, not only do existing synapses adapt to new circumstances, but new connections are constantly formed and reorganized. However, it was not yet known how these natural rearrangement processes are controlled in the brain. In the open-access journal PLOS Computational Biology, Butz and van Ooyen now present a simple rule that explains how these new networks of neurons are formed.
"It’s very likely that the structural plasticity of the brain is the basis for long-term memory formation," says Markus Butz, who has been working at the recently established Simulation Laboratory Neuroscience at the Jülich Supercomputing Centre for the past few months. "And it’s not just about learning. Following the amputation of extremities, brain injury, the onset of neurodegenerative diseases, and strokes, huge numbers of new synapses are formed in order to adapt the brain to the lasting changes in the patterns of incoming stimuli."
Activity regulates synapse formation
Τhese results show that the formation of new synapses is driven by the tendency of neurons to maintain a ‘pre-set’ electrical activity level. If the average electric activity falls below a certain threshold, the neurons begin to actively build new contact points. These are the basis for new synapses that deliver additional input – the neuron firing rate increases. This also works the other way round: as soon as the activity level exceeds an upper limit, the number of synaptic connections is reduced to prevent any overexcitation – the neuron firing rate falls. Similar forms of homeostasis frequently occur in nature, for example in the regulation of body temperature and blood sugar levels.
However, Markus Butz stresses that this does not work without a certain minimal excitation of the neurons: “A neuron that no longer receives any stimuli loses even more synapses and will die off after some time. We must take this restriction into account if we want the results of our simulations to agree with observations.” Using the visual cortex as an example, the neuroscientists have studied the principles according to which neurons form new connections and abandon existing synapses. In this region of the brain, about 10% of the synapses are continuously regenerated. When the retina is damaged, this percentage increases even further. Using computer simulations, the authors succeeded in reconstructing the reorganization of the neurons in a way that conforms to experimental results from the visual cortex of mice and monkeys with damaged retinas.
The visual cortex is particularly suitable for demonstrating the new growth rule, because it has a property referred to as retinotopy: This means that points projected beside each other onto the retina are also arranged beside each other when they are projected onto the visual cortex, just like on a map. If areas of the retina are damaged, the cells onto which the associated images are projected receive different inputs. “In our simulations, you can see that areas which no longer receive any input from the retina start to build crosslinks, which allow them to receive more signals from their neighbouring cells,” says Markus Butz. These crosslinks are formed slowly from the edge of the damaged area towards the centre, in a process resembling the healing of a wound, until the original activity level is more or less restored.
Synaptic and structural plasticity
"The new growth rule provides structural plasticity with a principle that is almost as simple as that of synaptic plasticity," says co-author Arjen van Ooyen, who has been working on models for the development of neural networks for decades. As early as 1949, psychology professor Donald Olding Hebb discovered that connections between neurons that are frequently activated will become stronger. Those that exchange little information will become weaker. Today, many scientists believe that this Hebbian principle plays a central role in learning and memory processes. While synaptic plasticity in involved primarily in short-term processes that take from a few milliseconds to several hours, structural plasticity extends over longer time scales, from several days to months.
Structural plasticity therefore plays a particularly important part during the (early) rehabilitation phase of patients affected by neurological diseases, which also lasts for weeks and months. The vision driving the project is that valuable ideas for the treatment of stroke patients could result from accurate predictions of synapse formation. If doctors knew how the brain structure of a patient will change and reorganize during treatment, they could determine the ideal times for phases of stimulation and rest, thus improving treatment efficiency.
New approach for numerous applications
"It was previously assumed that structural plasticity also follows the principle of Hebbian plasticity. The findings suggest that structural plasticity is governed by the homeostatic principle instead, which was not taken into consideration before," says Prof. Abigail Morrison, head of the Simulation Laboratory Neuroscience at Jülich. Her team is already integrating the new rule into the freely accessible simulation software NEST, which is used by numerous scientists worldwide.
These findings are also of relevance for the Human Brain Project. Neuroscientists, medical scientists, computer scientists, physicists, and mathematicians in Europe are working hand in hand to simulate the entire human brain on high-performance computers of the next generation in order to better understand how it functions. “Due to the complex synaptic circuitry in the human brain, it’s not plausible that its fault tolerance and flexibility are achieved based on static connection rules. Models are therefore required for a self-organization process,” says Prof. Markus Diesmann from Jülich’s Institute of Neuroscience and Medicine, who is involved in the project. He heads Computational and Systems Neuroscience (INM-6), a subinstitute working at the interface between neuroscientific research and simulation technology.
Stem cells help repair traumatic brain injury by building a “biobridge”
University of South Florida researchers have suggested a new view of how stem cells may help repair the brain following trauma. In a series of preclinical experiments, they report that transplanted cells appear to build a “biobridge” that links an uninjured brain site where new neural stem cells are born with the damaged region of the brain.
Their findings were recently reported online in the peer-reviewed journal PLOS ONE.
“The transplanted stem cells serve as migratory cues for the brain’s own neurogenic cells, guiding the exodus of these newly formed host cells from their neurogenic niche towards the injured brain tissue,” said principal investigator Cesar Borlongan, PhD, professor and director of the USF Center for Aging and Brain Repair.
Based in part on the data reported by the USF researchers in this preclinical study, the U.S. Food and Drug Administration recently approved a limited clinical trial to transplant SanBio Inc’s SB632 cells (an adult stem cell therapy) in patients with traumatic brain injury.
Stem cells are undifferentiated, or blank, cells with the potential to give rise to many different cell types that carry out different functions. While the stem cells in adult bone marrow or umbilical cord blood tend to develop into the cells that make up the organ system from which they originated, these multipotent stem cells can be manipulated to take on the characteristics of neural cells.
To date, there have been two widely-held views on how stem cells may work to provide potential treatments for brain damage caused by injury or neurodegenerative disorders. One school of thought is that stem cells implanted into the brain directly replace dead or dying cells. The other, more recent view is that transplanted stem cells secrete growth factors that indirectly rescue the injured tissue.
The USF study presents evidence for a third concept of stem-cell mediated brain repair.
The researchers randomly assigned rats with traumatic brain injury and confirmed neurological impairment to one of two groups. One group received transplants of bone marrow-derived stem cells (SB632 cells) into the region of the brain affected by traumatic injury. The other (control group) received a sham procedure in which solution alone was infused into the brain with no implantation of stem cells.
At one and three months post-TBI, the rats receiving stem cell transplants showed significantly better motor and neurological function and reduced brain tissue damage compared to rats receiving no stem cells. These robust improvements were observed even though survival of the transplanted cells was modest and diminished over time.
The researchers then conducted a series of experiments to examine the host brain tissue.
At three months post-traumatic brain injury, the brains of transplanted rats showed massive cell proliferation and differentiation of stem cells into neuron-like cells in the area of injury, the researchers found. This was accompanied by a solid stream of stem cells migrating from the brain’s uninjured subventricular zone — a region where many new stem cells are formed – to the brain’s site of injury.
In contrast, the rats receiving solution alone showed limited proliferation and neural-commitment of stem cells, with only scattered migration to the site of brain injury and virtually no expression of newly formed cells in the subventricular zone. Without the addition of transplanted stem cells, the brain’s self-repair process appeared insufficient to mount a defense against the cascade of traumatic brain injury-induced cell death.
The researchers conclude that the transplanted stem cells create a neurovascular matrix that bridges the long-distance gap between the region in the brain where host neural stem cells arise and the site of injury. This pathway, or “biobridge,” ferries the newly emerging host cells to the specific place in the brain in need of repair, helping promote functional recovery from traumatic brain injury.
Soldiers with blast injuries suffer pituitary hormone problems
Researchers studying British soldiers who fought in Afghanistan have highlighted hormonal problems that commonly result from blast injuries.
Soldiers with injuries affecting the pituitary gland may suffer psychological and metabolic symptoms which impede their recovery.
The researchers, from Imperial College London and the Royal Centre for Defence Medicine, say identifying these sufferers will enable them to receive appropriate hormone replacement therapy.
The research was funded by the Medical Research Council is published in the journal Annals of Neurology.
The study looked at 19 British soldiers with moderate to severe brain injury caused by blasts from improvised explosive devices (IEDs) while on duty in Afghanistan, and a group of 39 individuals with moderate to severe traumatic brain injuries caused by road traffic accidents, falls and assaults.
It found that a much higher proportion of soldiers with blast injuries had pituitary hormone problems (32 per cent) than in the non-blast control group (2.6 per cent).
One in five of the soldiers ended up receiving hormone treatment with growth hormone, testosterone and/or hydrocortisone – a replacement for the stress hormone cortisol.
The study also showed that the soldiers who had pituitary dysfunction following blast injury had more severe damage to white matter connections within the brain, and more severe cognitive problems, such as being slow in processing information, than those who did not have hormone problems.
The recent conflicts in Iraq and Afghanistan have seen rapid advances in personal protective equipment and in the medical management of severe trauma. These gains have meant that increasing numbers of soldiers are surviving previously fatal and complex injuries.
Injuries caused by IEDs are so numerous that they have been called the ‘signature injury’ of these conflicts. Between December 2009 and March 2012, 183 UK soldiers survived a moderate to severe blast traumatic brain injury in Afghanistan. The number of such injuries among US troops is much higher. The complex physical forces involved in a blast have led to much speculation about how the blast wave itself causes brain injury.
Dr Tony Goldstone, from the MRC Clinical Sciences Centre at Imperial College London, who led the study, said: “This study was set up to see if there were facets unique to the kind of trauma caused to the brain by IEDs. We found that there was a high prevalence of hormonal problems in soldiers with these kinds of injuries.
“This study involved a relatively small number of soldiers, and so assessment of additional patients will be needed to confirm such a prevalence rate. However the results do emphasise the importance of actively screening for pituitary problems in all soldiers and others who have had moderate to severe brain injury from exposure to blast. This will enable identification of those who may benefit from hormonal treatments to aid their rehabilitation, recovery and quality of life.”
The patients were treated in the multi-disciplinary traumatic brain injury clinic at the Imperial Centre for Endocrinology at Imperial College Healthcare NHS Trust and scanned at the Computational, Cognitive and Clinical Neuroimaging Laboratory at Imperial College London by Professor David Sharp and Major David Baxter.
Air Marshal Paul Evans, Surgeon General said: “I fully support the research that has been undertaken by Imperial College London and the Ministry of Defence. As Surgeon General, I am committed to ensuring Service personnel benefit from the latest advances in medical research and we continue to conduct research into traumatic brain injury with colleagues at Imperial College London as well as our US and other NATO partners. A Defence Medical Services working group identifies priority areas for TBI research and MOD policy continues to be reviewed in light of emerging best practice. Working in partnership will ensure our personnel benefit as well as enable best practice to be shared between the MOD and NHS.”
Professor David Lomas, Chair of the MRC’s Population and Systems Medicine Board, which funded the research, said: “Trauma is a serious health problem that has a major impact on people in both a civilian and military setting. By linking academic and military research programmes through studies such as this we will build a greater understanding of acute trauma that will inform future approaches to trauma management, to ensure that people suffering major injury receive the most advanced specialist care.”
New approach helps those with traumatic brain injury
Greg Noack was 24 when he moved from Ontario to Victoria, B.C. He had just graduated from college and was looking forward to a fresh start.
One early morning in 1996, as he was returning home from his graveyard shift at the hotel, Noack was attacked from behind by a group of men.
He doesn’t remember being struck on the head. He does remember waking from a 15-day coma to learn he had suffered a traumatic brain injury (TBI).
Noack, through the care of his health-care team, relearned how to walk, write, and feel particular emotions.
“I was enamoured by what my therapists were able to do for me,” said Noack. “I was lucky that I got back most of my function.”
Three years post-injury, Noack enrolled in Sault College’s Occupational Therapist Assistant/Physical Therapist Assistant Program and graduated with honours.
Shortly after, Noack was hired by the Toronto Rehab Acquired Brain Injury Rehab team as an occupational therapist assistant and later became a rehab therapist.
Most recently, he was seconded to Dr. Robin Green’s traumatic brain injury research team.
Dr. Green, Senior Scientist and Neuropsychologist, Toronto Rehab and Canada Research Chair in Traumatic Brain Injury, and her Toronto Rehab team have been studying impediments to brain injury recovery as well as treatments to offset the impediments.
Dr. Green’s work suggests that moderate-severe TBI may be a progressive neurological disorder –a whole new way of perceiving the condition.
“What may be occurring after a serious brain injury,” said Dr. Green, “is that damaged tissue is leaving healthy areas of the brain disconnected and under stimulated. Over time, healthy areas may deteriorate.”
Importantly, they discovered that in people with chronic moderate-severe TBI, environmental enrichment – increased physical, social and cognitive stimulation - can offset this deterioration.
Her research paper, entitled “Environmental enrichment may protect against hippocampal atrophy in the chronic stages of traumatic brain injury,” was published September 24 in Frontiers in Human Neuroscience.
In their study of 25 patients with moderate-severe TBI, her team found a positive reaction to environmental enrichment.
Those who reported greater amounts of environmental enrichment – for example, reading, problem solving exercises, puzzles, physical activity, socializing – at 5 months after their injury showed less shrinkage of the hippocampus (associated with memory functioning) from 5 to 28 months post-injury.
“People with moderate-severe TBI are commonly unable to return to the same level of engagement in their work, school or social lives as before the injury,” said Dr. Green. “However, those with greater environmental enrichment may be keeping vulnerable areas stimulated. Environmental enrichment is also known to increase production of neurons in the hippocampus and to promote their integration into existing brain networks.”
Based on the findings from their study, Green’s team is now engaged in research designed to proactively offset deterioration, which includes the delivery of environmental enrichment to patients. Noack is instrumental in delivering enriched therapy for TBI patients who are enrolled in one of Dr. Green’s research studies.
“One thing I loved about this study is that it facilitated greater customization of a patient’s care,” said Noack. “I could see how my patients benefited from the increased amount of stimulation through extended therapy.”
“Although the brains of patients are showing negative changes, patients are still showing recovery of their functioning in spite of it,” said Dr. Green. “If we are able to offset the negative brain changes through the treatments we are developing, we may be able to very significantly improve patients’ recovery and the quality of their aging with a brain injury.”
(Source: uhn.ca)
The Concussed Brain at Work: fMRI Study Documents Brain Activation During Concussion Recovery
For the first time, researchers have documented irregular brain activity within the first 24 hours of a concussive injury, as well as an increased level of brain activity weeks later—suggesting that the brain may compensate for the injury during the recovery time.
The findings are published in the September issue of the Journal of the International Neuropsychological Society
Thomas Hammeke, PhD, professor of psychiatry and behavioral medicine at the Medical College of Wisconsin, is the lead author. Collaborators at the Cleveland Clinic; St. Mary’s Hospital in Enid, Okl.; the University of North Carolina; Franklin College in Franklin, Ind., and the Marshfield Clinic in Marshfield, Wis., co-authored the paper.
To study the natural recovery from sports concussion, 12 concussed high school football athletes and 12 uninjured teammates were evaluated at 13 hours and again at seven weeks following concussive injury.
The concussed athletes showed the expected postconcussive symptoms, including decreased reaction time and lowered cognitive abilities. Imaging via fMRI (functional magnetic resonance imaging) showed decreased activity in select regions of the right hemisphere of the brain, which suggests the poor cognitive performance of concussion patients is related to that underactivation of attentional brain circuits.
Seven weeks post-injury, the concussed athletes showed improvement of cognitive abilities and normal reaction time. However, imaging at that time showed the post-concussed athletes had more activation in the brain’s attentional circuits than did the control athletes.
“This hyperactivation may represent a compensatory brain response that mediates recovery,” said Dr. Hammeke. “This is the first study to demonstrate that reversal in activation patterns, and that reversal matches the progression of symptoms from the time of the injury through clinical recovery.”
“Deciding when a concussed player should return to the playing field is currently an inexact science,” said Dr. Stephen Rao, director of the Schey Center for Cognitive Neuroimaging at the Cleveland Clinic and a senior author. “Measuring changes in brain activity during the acute recovery period can provide a scientific basis for making this critical decision.”
Each year, an estimated 3.8 million people sustain a traumatic brain injury (TBI). TBI is a contributing factor to a third of all injury-related deaths in the United States. More than three-quarters of the TBI’s that occur are concussions or other forms of mild TBI, many of which may go undiagnosed.
(Image: Corbis)
Injuries From Teen Fighting Deal a Blow to IQ
New study explores connection between physical fights, cognitive decline
A new Florida State University study has found that adolescent boys who are hurt in just two physical fights suffer a loss in IQ that is roughly equivalent to missing an entire year of school. Girls experience a similar loss of IQ after only a single fighting-related injury.
The findings are significant because decreases in IQ are associated with lower educational achievement and occupational performance, mental disorders, behavioral problems and even longevity, the researchers said.
“It’s no surprise that being severely physically injured results in negative repercussions, but the extent to which such injuries affect intelligence was quite surprising,” said Joseph A. Schwartz, a doctoral student who conducted the study with Professor Kevin Beaver in FSU’s College of Criminology and Criminal Justice.
Their findings are outlined in the paper, “Serious Fighting-Related Injuries Produce a Significant Reduction in Intelligence,” which was published in the Journal of Adolescent Health. The study is among the first to look at the long-term effects of fighting during adolescence, a critical period of neurological development.
About 4 percent of high school students are injured as a result of a physical fight each year, the researchers said.
Schwartz and Beaver used data from the National Longitudinal Study of Adolescent Health collected between 1994 and 2002 to examine whether serious fighting-related injuries resulted in significant decreases in IQ over a 5- to 6-year time span. The longitudinal study began with a nationally representative sample of 20,000 middle and high school students who were tracked into adulthood through subsequent waves of data collection. At each wave of data collection, respondents were asked about a wide variety of topics, including personality traits, social relationships and the frequency of specific behaviors.
Perhaps not surprisingly, boys experienced a higher number of injuries from fighting than girls; however, the consequences for girls were more severe, a fact the researchers attributed to physiological differences that give males an increased ability to withstand physical trauma.
The researchers found that each fighting-related injury resulted in a loss of 1.62 IQ points for boys, while girls lost an average of 3.02 IQ points, even after controlling for changes in socio-economic status, age and race for both genders. Previous studies have indicated that missing a single year of school is associated with a loss of 2 to 4 IQ points.
The impact on IQ may be even greater when considering only head injuries, the researchers said. The data they studied took into account all fighting-related physical injuries.
The findings highlight the importance of schools and communities developing policies aimed at limiting injuries suffered during adolescence whether through fighting, bullying or contact sports, Schwartz said.
“We tend to focus on factors that may result in increases in intelligence over time, but examining the factors that result in decreases may be just as important,” he said. “The first step in correcting a problem is understanding its underlying causes. By knowing that fighting-related injuries result in a significant decrease in intelligence, we can begin to develop programs and protocols aimed at effective intervention.”
Speedier scans reveal new distinctions in resting and active brain
A boost in the speed of brain scans is unveiling new insights into how brain regions work with each other in cooperative groups called networks.
Scientists at Washington University School of Medicine in St. Louis and the Institute of Technology and Advanced Biomedical Imaging at the University of Chieti, Italy, used the quicker scans to track brain activity in volunteers at rest and while they watched a movie.
“Brain activity occurs in waves that repeat as slowly as once every 10 seconds or as rapidly as once every 50 milliseconds,” said senior researcher Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology. “This is our first look at these networks where we could sample activity every 50 milliseconds, as well as track slower activity fluctuations that are more similar to those observed with functional magnetic resonance imaging (fMRI). This analysis performed at rest and while watching a movie provides some interesting and novel insights into how these networks are configured in resting and active brains.”
Understanding how brain networks function is important for better diagnosis and treatment of brain injuries, according to Corbetta.
The study appears online in Neuron.
Researchers know of several resting-state brain networks, which are groups of different brain regions whose activity levels rise and fall in sync when the brain is at rest. Scientists used fMRI to locate and characterize these networks, but the relative slowness of this approach limited their observations to activity that changes every 10 seconds or so. A surprising result from fMRI was that the spatial pattern of activity (or topography) of these brain networks is similar at rest and during tasks.
In contrast, a faster technology called magnetoencephalography (MEG) can detect activity at the millisecond level, letting scientists examine waves of activity in frequencies from slow (0.1-4 cycles per second) to fast (greater than 50 cycles per second).
“Interestingly, even when we looked at much higher temporal resolution, brain networks appear to fluctuate on a relatively slow time scale,” said first author Viviana Betti, PhD, a postdoctoral researcher at Chieti. “However, when the subjects went from resting to watching a movie, the networks appeared to shift the frequency channels in which they operate, suggesting that the brain uses different frequencies for rest and task, much like a radio.”
In the study, the scientists asked one group of volunteers to either rest or watch the movie during brain scans. A second group was asked to watch the movie and look for event boundaries, moments when the plot or characters or other elements of the story changed. They pushed a button when they noticed these changes.
As in previous studies, most subjects recognized similar event boundaries in the movie. The MEG scans showed that the communication between regions in the visual cortex was altered near the movie boundaries, especially in networks in the visual cortex.
“This gives us a hint of how cognitive activity dynamically changes the resting-state networks,” Corbetta said. “Activity locks and unlocks in these networks depending on how the task unfolds. Future studies will need to track resting-state networks in different tasks to see how correlated activity is dynamically coordinated across the brain.”
(Source: news.wustl.edu)
Second known case of patient developing synesthesia after brain injury
About nine months after suffering a stroke, the patient noticed that words written in a certain shade of blue evoked a strong feeling of disgust. Yellow was only slightly better. Raspberries, which he never used to eat very often, now tasted like blue – and blue tasted like raspberries.
High-pitched brass instruments—specifically the brass theme from James Bond movies—elicited feelings of ecstasy and light blue flashes in his peripheral vision and caused large parts of his brain to light up on an MRI. Music played by a euphonium, a tenor-pitched brass instrument, shut down those sensations.
The patient said he was initially frightened by the mixed messages his brain was sending him and the conflicting senses he was experiencing. He was so worried that something was seriously wrong with him that he raised it with a nurse only as he was leaving an appointment at St. Michael’s Hospital in downtown Toronto.
Physicians and researchers immediately recognized he had synesthesia, a neurological condition in which people experience more than one sense at the same time. They may “see” words or numbers as colours, hear sounds in response to smells or feel something in response to sight.
Most synesthetes are born with the condition, and include some of the world’s most famous authors and artists, including author Vladimir Nabakov, composer Franz Liszt, painter Vasily Kandinsky and singer-songwriter Billy Joel.
The Toronto patient is only the second known person to have acquired synesthesia as a result of a brain injury, in this case a stroke. His case was described in the August issue of the journal Neurology by Dr. Tom Schweizer, a neuroscientist and director of the Neuroscience Research Program at St. Michael’s Li Ka Shing Knowledge Institute.
Dr. Schweizer examined the patient’s brain activity in a functional MRI and compared it to six men of similar age (45) and education (18 years) as each listened to the James Bond Theme and a euphonium solo.
When the James Bond Theme was played, large areas of the patient’s brain lit up including the thalamus (the brain’s information switchboard), the hippocampus (which deals with memory and spatial navigation) and the auditory cortex (which processes sound).
"The areas of the brain that lit up when he heard the James Bond Theme are completely different from the areas we would expect to see light up when people listen to music," Dr. Schweizer said. "Huge areas on both sides of the brain were activated that were not activated when he listened to other music or other auditory stimuli and were not activated in the control group."
The patient and members of the control group also viewed 10-second blocks of words presented in black (which elicits no emotional response in the patient), yellow (mild disgust response) and blue (intense disgust response).
Reading blue letters produced extensive activity in the parts of the patient’s brain responsible for sensory information and processing emotional stimuli and similar but less intense responses for yellow letters. Control groups showed no heightened brain activity in response to the different coloured letters.
Dr. Schweizer said the fact that the patient had very targeted and specific responses to certain stimuli – and that these responses were not experienced by the control group – suggests that his synesthesia was caused as his brain tried to repair itself after his stroke and got cross-wired.
The patient’s stroke occurred in the thalamus, the brain’s central relay station. That’s the same part of the brain affected by the only other reported case of acquired synesthesia.
(Source: eurekalert.org)
Key target responsible for triggering detrimental effects in brain trauma identified
Researchers studying a type of cell found in the trillions in our brain have made an important discovery as to how it responds to brain injury and disease such as stroke. A University of Bristol team has identified proteins which trigger the processes that underlie how astrocyte cells respond to neurological trauma.
The star-shaped astrocytes, which outnumber neurons in humans, are a type of glial cell that comprise one of two main categories of cell found in the brain along with neurons. The cells, which have branched extensions that reach synapses (the connections between neurons) blood vessels, and neighbouring astrocytes, play a pivotal role in almost all aspects of brain function by supplying physical and nutritional support for neurons. They also contribute to the communication between neurons and the response to injury.
However, the cells are also known to trigger both beneficial and detrimental effects in response to neurological trauma. When the brain is subjected to injury or disease, the cells react in a number of ways, including a change in shape. In severe cases, the altered cells form a scar, which is thought to have beneficial, as well as detrimental effects by allowing prompt repair of the blood-brain barrier, and limiting cell death, but also impairing the regeneration of nerve fibres and the effective incorporation of neuronal grafts - where additional neuronal cells are added to the injured site.
The cells change shape via the regulation of a structural component of the cell called the actin cytoskeleton, which is made up of filaments that shrink and grow to physically manoeuvre parts of the cell. In the lab, the team cultured astrocytes in a dish and were able to make them change shape by chemically or genetically manipulating proteins that control actin, and also by mimicking the environment that the cells would be exposed to during a stroke.
By doing so the team found that very dramatic changes in cell shape were caused by controlling the actin cytoskeleton in the in vitro stroke model. The team also identified additional protein molecules that control this process, suggesting that a complex mechanism is involved.
Dr Jonathan Hanley from the University’s School of Biochemistry said: “Our findings are crucial to our understanding of how the brain responds to many disorders that affect millions of people every year. Until now, the details of the actin-based mechanisms that control astrocyte morphology were unknown, so we anticipate that our work will lead to future discoveries about this important process.”
(Source: eurekalert.org)
When Head Meets Soccer Ball, How Does Your Brain Fare?
Soccer players who frequently head-butt the ball—a commonly used tactic for passing or scoring in a game—may be risking brain injury, memory loss, and impaired cognitive ability, according to a study published in the journal Radiology.
Brain injury and the lasting effects of concussion in sport have become a major health issue in recent years, especially in such hard-hitting sports as American football. Although the thump of a soccer ball on a forehead seems fairly innocuous, compared with a crashing tackle on the three-yard line, a soccer player may “head” the ball hundreds or even thousands of times during the course of the season. The cumulative effect of many “sub-concussive” blows to the brain has been unknown and unstudied until now.
"We chose to study soccer because it is the world’s most popular sport," says the report’s lead author Michael Lipton, associate director of the Gruss Magnetic Resonance Research Center at the Albert Einstein College of Medicine in New York. "It is widely played by millions of people of all ages, including children, and there is concern that heading the ball, an essential part of the game, might cause damage to the brain."
Lipton and his colleagues examined 37 amateur players, all adults, who had played soccer for an average of 22 years each and had played regularly over the previous year. They filled out questionnaires about their playing style and how frequently they headed the ball on the field and in training drills. Then they were given memory tests and highly sophisticated brain scans, using a type of MRI called diffusion-tensor imaging that looks at microscopic changes in the white matter in the brain. White matter is the tissue that conveys messages from one region of the brain to another.
The researchers found that players had to head the ball a certain number of times in a season before white matter abnormalities started to appear on imaging. The threshold varied from player to player but was generally in the range of 900 to 1,500 headers in a season. Beyond this threshold, the brain abnormalities quickly became more apparent. Those who headed the ball more than 1,800 times in a season scored measurably worse on memory tests than those who had headed the ball less frequently. The difference in scores was in the range of 10 to 20 percent.
"To put this into perspective I should make it clear that all of these players’ functions were still within norms," said Lipton. "These are all basically functional young professionals and students."
So, should soccer players—and parents of young soccer players—be worried?
"All we have at this point is some evidence that shows an association between heading and what looks like brain injury. However, we do not yet have the type of data that permits us to prove a causal role for heading or to generalize our findings to other specific individuals. In the meantime, controlling the amount of heading that people do may provide an approach for preventing brain injury as a consequence of heading."
"I should emphasize that we very much see soccer as an excellent source of beneficial physical activity. This should not be curtailed. Our message is to understand the role of heading in the game and look at how we can enhance the safety of soccer play and facilitate its expansion."