Category: Brain Injury

Using tiny spheres filled with an anesthetic derived from a shellfish toxin, researchers at Boston Children's Hospital and the Massachusetts Institute of Technology have developed a way to delay the rise of neuropathic pain, a chronic form of pain that arises from flawed signals transmitted by damaged nerves.

The method could potentially allow doctors to stop the cascade of events by which tissue or nerve injuries evolve into neuropathic pain, which affects 3.75 million children and adults in the United States alone.

The researchers, led by Daniel Kohane, MD, PhD, of Boston Children's Department of Anesthesia and Robert Langer, ScD, of MIT, reported the results of animal studies online the week of October 8 in the Proceedings of the National Academy of Sciences.

Neuropathic pain can be long lasting and debilitating. Caused by shingles, nerve trauma, cancer and other conditions, it arises because damaged nerves send unusual signals to the spinal cord and the brain. The constant signaling effectively reprograms the central nervous system to react to any stimulus to the affected area, or even no stimulus at all, by triggering unpleasant sensations ranging from tingling and numbness to shooting, burning pain.

"Currently neuropathic pain is treated with systemic medications, but there has been significant interest in using powerful local anesthetics to block aberrant nerve discharges from the site of injury to prevent the onset of neuropathic pain," said Kohane. "Others have tried with varying degrees of success to do this in animal models using a variety of methods, but if applied clinically, those methods would require surgical intervention or could be toxic to tissues. We want to avoid both of those concerns."

The team's method combines saxitoxin, a powerful local anesthetic, and dexamethasone, which prolongs saxitoxin's effects. The two are packaged in liposomes — lipid spheres about 5.5 micrometers wide, or a bit smaller than a red blood cell — for nontoxic delivery to the site of nerve or tissue damage.

To assess whether the anesthetic-loaded liposomes (called SDLs for saxitoxin dexamethasone liposomes) might work as a potential treatment for neuropathic pain, Kohane and Langer — along with Sahadev Shankarappa, MBBS, MPH, PhD (a fellow in the Kohane lab) and others — attempted to use them to block the development of signs of neuropathy in an animal model of sciatic nerve injury. They found that a single injection of SDLs had a very mild effect, delaying the onset of neuropathic pain by about two days compared to no treatment. Three injections of SDLs at the site of injury over the course of 12 days, however, delayed the onset of pain by about a month.

The signal blockade mounted by the SDLs also appeared to prevent reprogramming of the central nervous system. The team noted that astrocytes in the spine, which help maintain the pain signaling in neuropathic patients, showed no signs of pain-related activation five and 60 days after injury in animals treated with SDLs.

"Ultimately we'd like to develop a way to reversibly block nerve signaling for a month with a single injection without causing additional nerve damage," Kohane explained. "For the moment, we're trying to refine our methods so that we can get individual injections to last longer and figure out how to generalize the method to other models of neuropathic pain.

"We also need to see whether it is safe to block nerve activity in this way for this long," he continued. "We don't want to inadvertently trade one problem for another. But we think that this approach could be fruitful for preventing and treating what is really a horrible condition."

 In recent years it has become clear that athletes who experience repeated impacts to the head may be at risk of potentially serious neurological and psychiatric problems. But a study of sports programs at three major universities, published in the October 2 Journal of Neurosurgery, finds that the way the injury commonly called concussion is usually diagnosed — largely based on athletes' subjective symptoms — varies greatly and may not be the best way to determine who is at risk for future problems. In addition, the way the term concussion is used in sports injuries may differ from how it is used in other medical contexts, potentially hindering communication about the factors most relevant to patient outcomes.

"The term 'concussion' means different things to different people, and it's not yet clear that the signs and symptoms we now use to make a diagnosis will ultimately prove to be the most important pieces of this complicated puzzle," says Ann-Christine Duhaime, MD, director of the Pediatric Brain Trauma Lab at Massachusetts General Hospital (MGH), who led the study. "Some patients who receive a diagnosis of concussion go on to have very few problems, and some who are not diagnosed because they have no immediate symptoms may have sustained a lot of force to the head with potentially serious consequences."

The current study is part of a larger investigation into the biomechanical basis of concussion and the effects of repeat impacts to the head, conducted over five years at Brown University, Dartmouth College and Virginia Tech. A total of 450 students — members of all three schools' football teams, two women's and two men's ice hockey teams — wore helmets equipped with instruments that measured the frequency, magnitude and location of head impacts experienced during practice sessions, scrimmages and games. Team trainers and physicians followed their standard procedures for assessing and diagnosing potential concussions and prescribing treatment.

During the study period more than 486,000 head impacts were recorded in participating athletes. Concussions were diagnosed in 44 participants, four of whom were diagnosed a second time for a total of 48 diagnosed concussions. A specific impact could be associated with the concussion 31 times, but no clearly associated impact was identified in the other 17 instances. The most commonly reported symptoms were mental cloudiness, headache and dizziness, and only one athlete lost consciousness. An immediate diagnosis was made only six times, and many of the athletes did not begin experiencing symptoms until several hours after the game. Although measured head impacts in those diagnosed with concussions tended to be higher, some concussion-associated impacts had considerably less measured acceleration/deceleration of the head. The authors note that the injuries reported in this study contrast with those usually seen in patients diagnosed with concussion in emergency departments, in whom a single, clearly identified head impact is typically associated with immediate changes in consciousness.

The authors add that developing strategies to prevent and manage short- and long-term consequences of head injuries requires accurate tools to determine which patients have sustained impacts that may affect the brain in significant ways, and that currently used criteria based on reported symptoms may be unreliable predictors of actual injury to the brain. They propose that replacing the single term 'concussion' with the concept of a concussion spectrum may be useful in determining the range of factors that can influence patient outcomes.

"A lot of work is needed before we can understand to what extent patients' reported symptoms — compared to such factors as the actual force imparted to the brain, previous head injuries and genetic background — influence the eventual consequences of repeated head impacts, consequences that may vary from patient to patient," says Duhaime, who is director of Pediatric Neurosurgery at MassGeneral Hospital for Children, director of Neurosurgical Trauma and Intensive Care in the MGH Department of Neurosurgery, and the Nicholas T. Zervas Professor of Neurosurgery at Harvard Medical School. "For now, however, it's sensible to err on the side of safety, realizing that more specific answers will take more time and research."

The "tiki-taka"-style of the Spanish national football team is amazing to watch: Xavi passes to Andrès Iniesta, he just rebounds the ball once and it's right at Xabi Alonso's foot. The Spanish midfielders cross the field as if they run on rails, always maintaining attention on the ball and the teammates, the opponents chasing after them without a chance.

An international team of scientists from the German Primate Center and McGill University in Canada, including Stefan Treue, head of the Cognitive Neuroscience Laboratory, has now uncovered how the human brain makes such excellence possible by dividing visual attention: The brain is capable of splitting its 'attentional spotlight' for an enhanced processing of multiple visual objects.

Results of the research are published in the journal Neuron.

When we pay attention to an object, neurons responsible for this location in our field of view are more active then when they process unattended objects. But quite often we want to pay attention to multiple objects in different spatial positions, with interspersed irrelevant objects. Different theories have been proposed to account for this ability. One is, that the attentive focus is split spatially, excluding objects between the attentional spotlights. Another possibility is, that the attentional focus is zoomed out to cover all relevant objects, but including the interspersed irrelevant ones. A third possibility would be a single focus rapidly switching between the attended objects.

Studying rhesus macaques

n order to explain how such a complex ability is achieved, the neuroscientists measured the activity of individual neurons in areas of the brain involved in vision. They studied two rhesus macaques, which were trained in a visual attention task. The monkeys had learned to pay attention to two relevant objects on a screen, with an irrelevant object between them. The experiment showed, that the macaques' neurons responded strongly to the two attended objects with only a weak response to the irrelevant stimulus in the middle. So the brain is able to spatially split visual attention and ignore the areas in between. "Our results show the enormous adaptiveness of the brain, which enables us to deal effectively with many different situations.

This multi-tasking allows us to simultaneously attend multiple objects," Stefan Treue says. Such a powerful ability of our attentive system is one precondition for humans to become perfect football-artists but also to safely navigate in everyday traffic.

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Journal Reference:

1. Robert Niebergall, Paul S. Khayat, Stefan Treue, Julio C. Martinez-Trujillo. Multifocal Attention Filters Targets from Distracters within and beyond Primate MT Neurons' Receptive Field Boundaries. Neuron, 2011; 72 (6): 1067 DOI: 10.1016/j.neuron.2011.10.013

 Companionship has the potential to reduce pain linked to nerve damage, according to a new study.

Mice that were paired with a cage-mate showed lower pain responses and fewer signs of inflammation in their nervous system after undergoing surgery that affected their nerves than did isolated mice, suggesting that the social contact had both behavioral and physiological influences.

The social contact lowered the pain response and signs of inflammation even in animals that had experienced stress prior to the nerve injury.

These mice experienced a specific kind of nerve-related pain called allodynia, which is a withdrawal response to a stimulus that normally would not elicit a response — in this case, a light touch to the paw.

"If they were alone and had stress, the animals had increased inflammation and allodynia behavior," said Adam Hinzey, a graduate student in neuroscience at Ohio State University and lead author of the study. "If the mice had a social partner, both allodynia and inflammation were reduced."

More than 20 million Americans experience the nerve pain known as peripheral neuropathy as a consequence of diabetes or other disorders as well as trauma, including spinal cord injury. Few reliable treatments are available for this persistent pain.

"A better understanding of social interaction's beneficial effects could lead to new therapies for this type of pain," Hinzey said.

Hinzey described the research during a press conference Monday (10/15) in New Orleans at Neuroscience 2012, the annual meeting of the Society for Neuroscience.

In the study, researchers paired one group of mice with a single cage-mate for one week while other mice were kept socially isolated. For three days during this week, some mice from each group were exposed to brief stress while others remain nonstressed.

Researchers then performed a nerve surgery producing sensations that mimic neuropathic pain on one group of mice and a sham procedure that didn't involve the nerves on a control group.

After determining a baseline response to a light touch to their paws, researchers tested all groups of mice behaviorally for a week after the surgery. Mice that had lived with a social partner, regardless of stress level, required a higher level of force before they showed a withdrawal response compared to isolated mice that were increasingly responsive to a lighter touch.

"Animals that were both stressed and isolated maintained a lower threshold — less force was needed to elicit a paw withdrawal response. Animals that were pair housed and not stressed withstood a significantly greater amount of force applied before they showed a paw withdrawal response," Hinzey said. "Within animals that were stressed, pairing was able to increase the threshold required to see a withdrawal response."

He and colleagues examined the animals' brain and spinal cord tissue for gene activation affecting production of two proteins that serve as markers for inflammation. These cytokines, called interleukin-1 beta (IL-1B) and interleukin-6 (IL-6), are typically elevated in response to both injury and stress.

Compared to animals that received a sham procedure, isolated mice with nerve damage had much higher levels of IL-1B gene expression in their brain and spinal cord tissue. The researchers also observed a significant decrease in gene activity related to IL-6 production in the spinal cords of nonstressed animals compared to the mice that were stressed.

"We believe that socially isolated individuals are physiologically different from socially paired individuals, and that this difference seems to be related to inflammation," said Courtney DeVries, professor of neuroscience at Ohio State and principal investigator on this work. "These data showed very nicely that the social environment is influencing not just behavior but really the physiological response to the nerve injury."

This work was supported by funds from the National Institute of Nursing Research. Additional co-authors include Brant Jarrett and Kathleen Stuller of Ohio State's Department of Neuroscience.

New studies offer vivid examples of how advances in basic brain research help reduce the trauma and suffering of innocent landmine victims, amateur and professional athletes, and members of the military.

The research was presented today at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.

From the playing field to the battlefield, neuroscientists are gaining better understanding of what happens to the brain when it suffers traumatic injury or repeated hits. While the chronic learning and memory deficits that often accompany such damage have been resistant to treatment, opportunities for effective early intervention to minimize long-term damage may be on the horizon. Scientists are also creatively applying new insights into how our brain senses odors, to better detect landmines and help both soldiers and civilians avoid becoming casualties of war.

Today's new findings show that:

• United Kingdom soldiers who sustained blast-related traumatic brain injuries were more likely to have injuries in the brain stem and cerebellum than were civilian victims of non-blast traumatic brain injuries. Damage to the "white matter" in the brains of both groups could only be detected using an advanced form of magnetic resonance imaging (David Sharp, PhD, MBBS, abstract 315.04).
• Frustrated by the lack of treatments for chronic neurological problems that frequently follow traumatic brain injury, scientists searched the brain for potential therapeutic targets and focused on inflammatory pathways. Now, they may have averted memory problems in brain-injured mice by giving them a widely available dietary supplement derived from tobacco that appears to suppress inflammation (Fiona Crawford, PhD, abstract 315.02).
• Scientists report developing a transgenic mouse with enhanced capacity to smell the explosives used in landmines, with the hopes they can be deployed to detect landmines in affected areas (Charlotte D'Hulst, PhD, abstract 815.09).

Another recent finding shows that:

• Scientists using mice to study the effect of a single encounter with a model of military blast injury found the effects of blast winds alone — which can reach 330 miles per hour — appear sufficient to induce a brain injury. They also discovered that immobilizing the head may help reduce the severity of injury (Ann McKee, MD).

"These studies are particularly outstanding for how they take some of the most complex and cutting edge science of our time and translate it into practical applications that can have an enormous, visible impact on people's lives," said Jane Roskams, PhD, of the University of British Columbia, an expert on brain repair and neural regeneration. "That one day a mere mouse might save a child from losing a limb while walking across an old mine field, or a simple dietary supplement could make life more bearable for a brain injury victim shows why the field of neuroscience is attracting so much interest these days."

This research was supported by national funding agencies such as the National Institutes of Health, as well as private and philanthropic organizations.

In many pathologies of the nervous system, there is a common event — cells called microglia are activated from surveillant watchmen into fighters. Microglia are the immune cells of the nervous system, ingesting and destroying pathogens and damaged nerve cells. Until now little was known about the molecular mechanisms of microglia activation despite this being a critical process in the body. Now new research from the Montreal Neurological Institute and Hospital — The Neuro — at McGill University provides the first evidence that mechanisms regulated by the Runx1 gene control the balance between the surveillant versus activated microglia states.

The finding, published in the Journal of Neuroscience, has significant implications for understanding and treating neurological conditions.

As surveillant watchmen, microglial cells wait for something bad to happen in the nervous system. They have a small cell body and long branches that monitor the local environment. As soon as there are signs of injury or disease, microglia are activated into fighters. The branches retract and the microglia morph into a large rounded body in order to attack and ingest pathogens: bacteria, viruses, and diseased or injured nerve cells (for example in head trauma). If microglia activation is not precisely controlled, however, it can become harmful to the body as microglia can start to attack healthy cells. For example, after epileptic seizures, the brain responds by regenerating new nerve cells. The microglia help in this process of regeneration, but they can also negatively influence the survival of the new born nerve cells if their activation persists for too long. The research team at The Neuro therefore asked important questions: How can we learn how the process of activating microglia from watchmen to fighter is controlled? What can we do to ensure that the beneficial effects of microglia activation predominate over their potentially deleterious effects?

It turns out that the process of microglia activation in the adult brain is almost a recapitulation in reverse of mechanisms that occur during nervous system development. Microglia in the developing brain are already in an early form of fighter mode and have the capacity to eliminate cell debris and redundant nerve cell connections. Pruning of the nerve cell network is a normal process during development. Soon after birth microglia are gradually deactivated from early fighters to surveillant watchmen, a state that they will maintain until there is injury or trauma in the adult brain, which causes them to revert from watchmen back to fighters.

"So the approach we took was to study the normal process of microglia deactivation during brain development on the premise that understanding this process might also help us understand adult brain microglia activation in response to injury or disease," says Dr. Stefano Stifani, lead investigator and neuroscientist at The Neuro. "Our study provides evidence for a previously unrecognized role of a particular gene, termed Runx1, in promoting the transition of microglia from an early form of activated fighter to surveillant watchmen in the postnatal mouse brain. We show that Runx1 is expressed in these early fighter microglia during the first two postnatal weeks and that if Runx1 function in these cells is inhibited they tend to persist longer and their transition into watchmen microglia is delayed. We also looked at an experimental animal model in which an artificial injury causes surveillant microglia to be activated into fighters. This showed that Runx1 expression is induced in microglia when they become activated following injury in the adult mouse nervous system, suggesting that Runx1 might be important for controlling how long fighter microglia remain activated in the adult nervous system, as it does in the developing brain."

These findings improve our understanding of microglia biology in the developing and injured adult brain. Moreover, they have potential therapeutic implications for several neurological conditions — further research could lead to the development of treatment strategies by pharmacologically targeting key modulators of microglia activation.

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Journal Reference:

1. M. Zusso, L. Methot, R. Lo, A. D. Greenhalgh, S. David, S. Stifani. Regulation of Postnatal Forebrain Amoeboid Microglial Cell Proliferation and Development by the Transcription Factor Runx1. Journal of Neuroscience, 2012; 32 (33): 11285 DOI: 10.1523/JNEUROSCI.6182-11.2012

Two studies presented at the ANESTHESIOLOGY™ 2012 annual meeting found that hereditary genes were responsible for the amount and type of pain experienced after a motor vehicle collision (MVC). Many drivers experience symptoms after an MVC, including musculoskeletal pain in the back, neck and other areas. It has been unknown why some drivers feel pain immediately after a collision or develop persistent pain after a collision, while others do not.

Previous studies suggest the etiology of pain after an MVC is not solely due to tissue damage at the time of trauma, but rather may also be strongly influenced by physiologic systems involved in the body's response to the collision. These physiologic systems influence the function of nerve cells that process pain in the brain, spinal cord and body tissues.

Researchers from the University of North Carolina collected data from 948 patients who came to one of eight emergency departments in four states for care after an MVC. Participants provided a blood sample at the time of their emergency department evaluation. The extent and severity of patient pain symptoms were assessed at the time of the emergency department visit and also six weeks after the emergency department visit (via a telephone or web-based interview). The researchers used the data for two separate studies.

The first study analyzed the role of dopamine, an important neurotransmitter in the brain. Out of the five different dopamine receptors, dopamine receptor 2 has been shown to play an important role in neurologic function. The first study assessed whether genetic variations influencing the function of the dopamine receptor 2 are associated with acute pain severity after an MVC. One specific single nucleotide polymorphism in the dopamine receptor 2, rs6276, was significantly associated with pain severity in the acute aftermath of a collision.

"The findings suggest dopamine pathways involving the dopamine receptor 2 contribute to the intensity of pain experienced immediately after an MVC," said study author Andrey V. Bortsov, M.D., Ph.D., Assistant Professor of Anesthesiology, University of North Carolina, Chapel Hill.

The second study assessed the role of the hypothalamic-pituitary adrenal (HPA) axis, a physiologic system of central importance to the body's response to stressful events. The study evaluated whether the HPA axis influences pain severity six weeks after MVC. Findings revealed the FKBP5 gene variant was associated with a 20 percent higher risk of moderate to severe neck pain six weeks after an MVC, as well as a greater extent of body pain.

"Unfortunately, patients who experience persistent pain after an MVC are often viewed with suspicion, as if they are making up their symptoms for financial gain or some other reason," said senior study author Samuel A. McLean, M.D., Assistant Professor of Anesthesiology, University of North Carolina, Chapel Hill. "Our study is the first to identify a genetic risk factor for persistent pain after an MVC, and contributes further evidence that persistent pain after a collision has a neurobiological basis. These findings also will help us begin to identify physiologic systems involved in chronic pain development after an MVC. Understanding these systems will help us to develop new interventions to prevent the transition from acute to chronic pain after a collision."

A study led by researchers at Boston University School of Medicine (BUSM) provides novel insight into the impact that Huntington's disease has on the brain. The findings, published online in Neurology, pinpoint areas of the brain most affected by the disease and opens the door to examine why some people experience milder forms of the disease than others.

Richard Myers, PhD, professor of neurology at BUSM, is the study's lead/corresponding author. This study, which is the largest to date of brains specific to Huntington's disease, is the product of nearly 30 years of collaboration between the lead investigators at BUSM and their colleagues at the McLean Brain Tissue Resource Center, Massachusetts General Hospital and Columbia University.

Huntington's disease (HD) is an inherited and fatal neurological disorder that typically is diagnosed when a person is approximately 40 years old. The gene responsible for the disease was identified in 1993, but the reason why certain neurons or brain cells die remains unknown.

The investigators examined 664 autopsy brain samples with HD that were donated to the McLean Brain Bank. They evaluated and scored more than 50 areas of the brain for the effects of HD on neurons and other brain cell types. This information was combined with a genetic study to characterize variations in the Huntington gene. They also gathered the clinical neurological information on the patients' age when HD symptoms presented and how long the patient survived with the disease.

Based on this analysis, the investigators discovered that HD primarily damages the brain in two areas. The striatum, which is located deep within the brain and is involved in motor control and involuntary movement, was the area most severely impacted by HD. The outer cortical regions, which are involved in cognitive function and thought processing, also showed damage from HD, but it was less severe than in the striatum.

The investigators identified extraordinary variation in the extent of cell death in different brain regions. For example, some individuals had extremely severe outer cortical degeneration while others appeared virtually normal. Also, the extent of involvement for these two regions was remarkably unrelated, where some people demonstrated heavy involvement in the striatum but very little involvement in the cortex, and vice versa.

"There are tremendous differences in how people with Huntington's disease are affected," Myers said. "Some people with the disease have more difficulty with motor control than with their cognitive function while others suffer more from cognitive disability than motor control issues."

When studying these differences, the investigators noted that the cell death in the striatum is heavily driven by the effects of variations in the Huntington gene itself, while effects on the cortex were minimally affected by the HD gene and are thus likely to be a consequence of other unidentified causes. Importantly, the study showed that some people with HD experienced remarkably less neuronal cell death than others.

"While there is just one genetic defect that causes Huntington's disease, the disease affects different parts of the brain in very different ways in different people," said Myers. "For the first time, we can measure these differences with a very fine level of detail and hopefully identify what is preventing brain cell death in some individuals with HD."

The investigators have initiated extensive studies into what genes and other factors are associated with the protection of neurons in HD, and they hope these protective factors will point to possible novel treatments.

A potential new treatment for traumatic brain injury (TBI), which affects thousands of soldiers, auto accident victims, athletes and others each year, has shown promise in laboratory research, scientists are reporting. TBI can occur in individuals who experience a violent blow to the head that makes the brain collide with the inside of the skull, a gunshot injury or exposure to a nearby explosion. The report on TBI, which currently cannot be treated and may result in permanent brain damage or death, appears in the journal ACS Nano.

Thomas Kent, James Tour and colleagues explain that TBI disrupts the supply of oxygen-rich blood to the brain. With the brain so oxygen-needy — accounting for only 2 percent of a person's weight, but claiming 20 percent of the body's oxygen supply — even a mild injury, such as a concussion, can have serious consequences. Reduced blood flow and resuscitation result in a build-up of free-radicals, which can kill brain cells. Despite years of far-ranging efforts, no effective treatment has emerged for TBI. That's why the scientists tried a new approach, based on nanoparticles so small that 1000 would fit across the width of a human hair.

They describe development and successful laboratory tests of nanoparticles, called PEG-HCCs. In laboratory rats, the nanoparticles acted like antioxidants, rapidly restoring blood flow to the brain following resuscitation after TBI. "This finding is of major importance for improving patient health under clinically relevant conditions during resuscitative care, and it has direct implications for the current [TBI] war-fighter victims in the Afghanistan and Middle East theaters," they say.

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Journal Reference:

1. Brittany R. Bitner, Daniela C. Marcano, Jacob M. Berlin, Roderic H. Fabian, Leela Cherian, James C. Culver, Mary E. Dickinson, Claudia S. Robertson, Robia G. Pautler, Thomas A. Kent, James M. Tour. Antioxidant Carbon Particles Improve Cerebrovascular Dysfunction Following Traumatic Brain Injury. ACS Nano, 2012; 6 (9): 8007 DOI: 10.1021/nn302615f

 It's fall football season, when fight songs and shouted play calls fill stadiums across the country. Another less rousing sound sometimes accompanies football games: the sharp crack of helmet-to-helmet collisions. Hard collisions can lead to player concussions, but the physics of how the impact of a helmet hit transfers to the brain are not well understood. A research team from the U.S. Naval Academy in Annapolis, Md., has created a simplified experimental model of the brain and skull inside a helmet during a helmet-to-helmet collision. The model illustrates how the fast vibrational motion of the hit translates into a sloshing motion of the brain inside the skull.

The researchers will present their findings at the 164th meeting of the Acoustical Society of America (ASA), held Oct. 22 — 26 in Kansas City, Missouri.

Murray Korman, a professor in the physics department at the U.S. Naval Academy, worked with his student Duncan Miller during the course of a semester to develop the experimental model. To simulate a side collision, the researchers hung one helmet from the ceiling with clothesline and swung the second helmet into the first, like a pendulum. Accelerometers mounted on the helmets recorded the vibrations before, during, and after the hit.

Figuring out simple ways to model a human head inside the helmets was a challenge, Korman notes. Human cadavers were out, and crash test mannequins were too expensive. After reading up on skull vibrations, the team settled on a wide plastic hoop, shaped like the skirt of a bell. "They say that when you get hit, you get your bell rung. No pun intended, but your skull does kind of ring like a bell," Korman says.

The researchers modeled the brain as a brass cylinder cushioned in a slot carved out of open-cell foam that mimicked fluid within the brain cavity. By choosing simple materials the researchers minimized the complexity of their set-up while retaining those elements needed to capture the essential motions of the brain and the skull. They found that their brass cylinder brain sloshed back and forth within the skull much more slowly than the rate of vibration of the initial hit. Building a model is important, Korman notes, because it can help determine how a measurable parameter, like the acceleration of a helmet during a hit, would translate into potentially damaging brain motion. "The ultimate damage comes when the brain hits the side of the skull," Korman says.

Korman says there is still a lot of work to do to improve the model. He hopes in the future to collaborate with biophysicists to incorporate more detailed knowledge of the material properties of the brain and skull. Ultimately, the model might be used to test new helmets designed to better protect the brain from hits. Korman describes futuristic helmets that might crumple on impact like plastic car bumpers, leaving the only bell ringing on the field to be done by the marching band.