1. Traumatic brain injury associated with dementia in working-age adults

    July 26, 2017 by Ashley

    From the University of Helsinki press release:

    According to a study encompassing the entire Finnish population, traumatic brain injury associated with an increased risk for dementia in working-age adults. Yet, no such relationship was found between traumatic brain injury and later onset of Parkinson’s disease or ALS.

    The researchers believe that these results may play a significant role for the rehabilitation and long-term monitoring of traumatic brain injury patients.

    Traumatic brain injuries (TBI) are among the top causes of death and disability, particularly among the young and middle aged. Approximately one in three that suffer from moderate-to-severe TBI die, and approximately half of the survivors will suffer from life-long disabilities.

    Degenerative brain diseases include memory disorders such as Alzheimer’s disease as well as Parkinson’s disease and amyotrophic lateral sclerosis (ALS). While the connection between TBI and degenerative brain diseases has been known, no comprehensive research data exist on the impact of TBI on degenerative brain diseases among adults of working age.

    Researchers from the University of Helsinki and the Helsinki University Hospital have now examined the relationship between TBI and degenerative brain diseases in a study encompassing the entire Finnish population. The study combined several nationwide registers to monitor more than 40,000 working-age adults, who survived the initial TBI, for ten years. Importantly, the persons´ level of education and socioeconomic status were accounted for.

    “It seems that the risk for developing dementia after TBI is the highest among middle-aged men. The more severe the TBI, the higher the risk for subsequent dementia. While previous studies have identified good education and high socioeconomic status as protective factors against dementia, we did not discover a similar effect among TBI survivors,” explains Rahul Raj, docent of experimental neurosurgery and one of the primary authors of the study.

    A significant discovery is that the risk of dementia among TBI survivors who have seemingly recovered well remains high for years after the injury. Raj points out that TBI patients may occasionally be incorrectly diagnosed with dementia due to the damage caused by the TBI itself, but such possible errors were considered in the study.

    “According to our results, it might be so that the TBI triggers a process that later leads to dementia.”

    “These results are significant for the rehabilitation and monitoring of TBI patients. Such a reliable study of the long-term impact of TBI has previously been impossible,” says Professor Jaakko Kaprio, a member of the research group.

    The WHO has predicted that TBI will become a leading cause of death and long-term illness during the next ten years. Already one per cent of the population in the United States suffers from a long-term disability caused by TBI. In western countries, the ageing of the population and age-related accidents increase the amount of TBIs, while in Asia, TBIs caused by traffic accidents are on the rise.

    Dementia is commonly seen as a problem of the elderly. However, the Finnish study shows that TBI may cause dementia to develop before old age, and that dementia caused by injuries are much more common than was thought.

    “It is a tragedy when an adult of working age develops dementia after recovering from a brain injury, not just for the patient and their families, but it also negatively impacts the whole society. In the future, it will be increasingly important to prevent TBIs and to develop rehabilitation and long-term monitoring for TBI patients,” says Docent Raj.


  2. No link seen between traumatic brain injury and cognitive decline

    July 24, 2017 by Ashley

    From the Boston University Medical Center press release:

    Although much research has examined traumatic brain injury (TBI) as a possible risk factor for later life dementia from neurodegenerative diseases such as Alzheimer’s disease (AD), little is known regarding how TBI influences the rate of age-related cognitive change. A new study now shows that history of TBI (with loss of consciousness) does not appear to affect the rate of cognitive change over time for participants with normal cognition or even those with AD dementia.

    These findings appear in the Journal of Alzheimer’s Disease.

    More than 10 million individuals worldwide are affected annually by TBI, however the true prevalence is likely even greater given that a majority of TBIs are mild in severity and may not be recognized or reported. TBI is a major public health and socioeconomic concern resulting in $11.5 billion in direct medical costs and $64.8 billion in indirect costs to the U.S. health system in 2010 alone.

    According to the researchers the relationship between TBI and long-term cognitive trajectories remains poorly understood due to limitations of previous studies, including small sample sizes, short follow-up periods, biased samples, high attrition rates, limited or no reports of exposure to repetitive head impacts (such as those received through contact sports), and very brief cognitive test batteries.

    In an effort to examine this possible connection, researchers compared performance on cognitive tests over time for 706 participants (432 with normal cognition; 274 AD dementia) from the National Alzheimer’s Coordinating Center database. Normal and AD dementia participants with a history of TBI with loss of consciousness were matched to an equal number of demographically and clinically similar participants without a TBI history. The researchers also examined the possible role of genetics in the relationship between TBI and cognitive decline by studying a gene known to increase risk for AD dementia, the APOE ?4 gene.

    “Although we expected the rates of cognitive change to differ significantly between those with a history of TBI compared to those with no history of TBI, we found no significant difference between the groups, regardless of their APOE genotype,” explained corresponding author Robert Stern, PhD, Director of the Clinical Core of the Boston University Alzheimer’s Disease Center (BU ADC) and professor of neurology, neurosurgery and anatomy and neurobiology at Boston University School of Medicine.

    The study’s first author Yorghos Tripodis, PhD, Associate Director of the Data Management and Biostatistics Core of the BU ADC and associate professor of Biostatistics at Boston University School of Public Health, cautioned, “Our findings should still be interpreted cautiously due to the crude and limited assessment of TBI history available through the NACC database.” The researchers recommended that future studies should collect information on the number of past TBIs (including mild TBIs, as well as exposure to sub-concussive trauma through contact sports and other activities) along with time since TBI, which may play a significant role in cognitive change.


  3. Strategic brain training positively affects neural connectivity for individuals with TBI

    June 5, 2017 by Ashley

    From the Center for BrainHealth press release:

    A recent study from the Center for BrainHealth at The University of Texas at Dallas shows that a certain type of instructor-led brain training protocol can stimulate structural changes in the brain and neural connections even years after a traumatic brain injury (TBI).

    The findings, published in Brain and Behavior, further suggest that changes in cortical thickness and neural network connectivity may prove an effective way to quantitatively measure treatment efficacy, an ability that has not existed until now. Building upon previous research, the study challenges the widely held belief that recovery from a TBI is limited to two years after an injury.

    “A TBI disrupts brain structure. These brain changes can interfere with brain network communication and the cognitive functions those networks support,” said Dr. Kihwan Han, research scientist at the Center for BrainHealth and lead author of the study.

    “For people with chronic TBI, they may have trouble with daily tasks such as creating shopping lists and resolving conflicts with others for many years after the injury. These findings provide hope for people who thought, ‘This is as good as my recovery is going to get’ and for the medical community who have yet to find a way to objectively measure a patient’s recovery,” he said.

    The study included 60 adults with TBI symptoms lasting an average of eight years. Participants were randomly placed into one of two cognitive training groups: strategy-based training or knowledge-based training. Over an eight-week period, the strategy-based training group learned strategies to improve attention and reasoning. The knowledge-based training group learned information about the structure and function of the brain as well as the effects of sleep and exercise on brain performance.

    Magnetic resonance imaging measured cortical thickness and resting-state functional connectivity (rsFC) before training, after training and three months post-training. Previous studies have shown that cortical thickness and rsFC can be potential markers for training-induced brain changes.

    Individuals in the strategy-based reasoning training showed a greater change in cortical thickness and connectivity compared to individuals who received the knowledge-based training. Changes in cortical thickness and functional connectivity also correlated to an individual’s ability to switch between tasks quickly and consistently to achieve a specific goal.

    “People who showed the greatest change in cortical thickness and connectivity, showed the greatest performance increases in our cognitive tasks. Perhaps future studies could investigate the added benefit of brain stimulation treatments in combination with cognitive training for individuals with chronic TBI who experience problems with attention, memory or executive functions,” Han said.

    The work was supported by the Department of Defense, the Meadows Foundation and the Friends of BrainHealth Distinguished New Scientist Award.


  4. How the injured brain tells the body it’s hurt

    May 30, 2017 by Ashley

    From the Johns Hopkins Medicine press release:

    Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans.

    Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells’ purpose is to defend and protect the body, ironically the brain’s “call to arms” may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain.

    In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain.

    “This work describes an entirely new way that the brain talks with the body,” says Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. “Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body’s own excessive immune response.”

    Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years.

    The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell’s metabolism by breaking down fatty molecules into smaller components that cells use for every day functions.

    To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working.

    Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2’s involvement but still didn’t tell them about the signal sent from the brain to activate the body’s immune response. According to Haughey, after many failed experiments to determine the brain’s messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of “exosomes” — miniature vesicles released from cells.

    “That conversation was the ‘Ah-ha’ moment when it all began to make sense,” says Haughey.

    He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell’s surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA.

    To test that exosomes were the source of this brain to body communication, Haughey’s research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains.

    The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain.

    When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury.

    Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs — short bits of RNA that don’t code for genes — at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation.

    “Given the therapeutic potential of the nSMase target, we’re now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use,” says Haughey.


  5. Brain injury causes impulse control problems in rats

    May 24, 2017 by Ashley

    From the University of British Columbia press release:

    New research from the University of British Columbia confirms for the first time that even mild brain injury can result in impulse control problems in rats.

    The study, published in the Journal of Neurotrauma, also found that the impulsivity problems may be linked to levels of an inflammatory molecule in the brain, and suggest that targeting the molecule could be helpful for treatment.

    “Few studies have looked at whether traumatic brain injuries cause impulse control problems,” said the study’s lead author, Cole Vonder Haar, a former postdoctoral research fellow in the UBC department of psychology who is now an assistant professor at West Virginia University. “This is partly because people who experience a brain injury are sometimes risk-takers, making it difficult to know if impulsivity preceded the brain injury or was caused by it. But our study confirms for the first time that even a mild brain injury can cause impulse control problems.”

    For the study, researchers gave rats with brain injuries a reward test to measure impulsivity.

    Rats that were unable to wait for the delivery of a large reward, and instead preferred an immediate, but small reward, were considered more impulsive.

    The researchers found that impulsivity in the rats increased regardless of the severity of the brain injury. The impulsivity also persisted eight weeks after injury in animals with a mild injury, even after memory and motor function returned.

    “These findings have implications for how brain injury patients are treated and their progress is measured,” said Vonder Haar. “If physicians are only looking at memory or motor function, they wouldn’t notice that the patient is still being affected by the injury in terms of impulsivity.”

    After analyzing samples of frontal cortex brain tissue, the researchers also found a substantial increase in levels of an inflammatory molecule, known as interleukin-12, that correlated with levels of impulsivity. Interleukins are groups of proteins and molecules responsible for regulating the body’s immune system.

    The study builds on the researchers’ previous findings about the link between interleukin-12 and impulsivity.

    Catharine Winstanley, the study’s senior author and associate professor in the UBC department of psychology, said the findings are important because impulsivity is linked to addiction vulnerability.

    “Addiction can be a big problem for patients with traumatic brain injuries,” she said. “If we can target levels of interleukin-12, however, that could potentially provide a new treatment target to address impulsivity in these patients.”


  6. Brain’s power to adapt offers short-term gains, long-term strains

    May 9, 2017 by Ashley

    From the Penn State press release:

    Like air-traffic controllers scrambling to reconnect flights when a major hub goes down, the brain has a remarkable ability to rewire itself after suffering an injury. However, maintaining these new connections between brain regions can strain the brain’s resources, which can lead to serious problems later, including Alzheimer’s Disease, according to researchers.

    After a head injury, the brain can show enhanced connectivity by using alternative routes between two previously connected regions of the brain that need to communicate, as well as make stronger connections, said Frank G. Hillary, associate professor of psychology, Penn State. These new connections between damaged areas are often referred to as hyperconnections, he added.

    Hyperconnectivity has been called a compensatory reaction to brain injury and it’s a little counterintuitive because it implies that the brain can increase its functional response when you take away physical resources,” said Hillary. “If the axon — the physical connection — between brain areas is removed, the brain can retain that connection functionally by using alternative routes. So what we’re seeing is there are all sorts of ways in which the brain can adapt and one way is to heighten the response, but the question is what does that do for you in the short term and what are the potential secondary consequences in the long term.”

    Because neural networks are typically designed to communicate as efficiently as possible, disruptions may mean that new networks are less efficient and use more energy, said Hillary, who worked with Jordan H. Grafman, director, brain injury research at Shirley Ryan Abilitylab and professor of physical medicine and rehabilitation, neurology and psychiatry and behavioral sciences at the Northwestern University in Chicago.

    It’s costly metabolically and it’s costly with respect to how quickly you think,” said Hillary. “One of the primary cognitive deficits in all neurological disorders — multiple sclerosis, traumatic brain injury, schizophrenia — is impairments in how quickly you can think, called processing speed. In neurological disorders, processing speed diminishes and it can be related to a decrease in brain efficiency.”

    Over time, these chronic inefficiencies may cascade into serious brain disorders, according to the researchers, who report their findings in the current issue of Trends in Cognitive Science.

    “If we know which patients would be susceptible to pathological hyperconnectivity following a traumatic brain injury, we might be able to develop new interventions to alter the course of that process,” said Grafman. Prior research has suggested a connection between brain injury and Alzheimer’s Disease, according to the researchers.

    “We know that brain injury is a risk factor for Alzheimer’s Disease later in life and the long-term effect of hyperconnections may be a link to how it happens,” said Hillary, who also is a faculty member at Penn State College of Medicine.

    Just as inefficient motors tend to pollute more, inefficient neural connections may build up harmful deposits that can further impair the brain. Although other factors, such as genetics, are likely involved, the researchers noted that higher deposits of amyloid beta — a marker of Alzheimer’s Disease — are often located at sites where there is the highest connectivity.

    “Where there’s a lot of activity going on, it increases metabolic byproducts and if you don’t clear them, they collect,” said Hillary. “Heavy activation, heavy connectivity can put pressure on network hubs and that’s why those hubs are some of the first to go in Alzheimer’s.”

    While more research is needed and possible treatment targets for Alzheimer’s or other neurological conditions remain uncertain, Hillary said the findings underscore the need to take precautions against brain injury.

    “What I always tell my students is be good to your brain,” said Hillary. “You only get one brain and while it can adapt to some injuries over your life, there is probably a cost for those adjustments.”


  7. Study suggests traumatic brain injuries affect women differently

    April 8, 2017 by Ashley

    From the Endocrine Society press release:

    Traumatic brain injuries affect the body’s stress axis differently in female and male mice, according to research presented at the Endocrine Society’s 99th annual meeting, ENDO 2017, in Orlando, Fla. The results could help explain why women who experience blast injuries face a greater risk of developing mental health problems than men.

    About 1.5 million people are diagnosed with traumatic brain injury (TBI) each year. Blast injuries are particularly common in the military population. Between 15 percent and 30 percent of soldiers who experience a TBI are later diagnosed with neuropsychiatric disorders such as depression, anxiety or post-traumatic stress disorder (PTSD). Even though men are more likely to experience a TBI, women have an elevated risk of developing mental health disorders due to the injury.

    The study examined how blast injuries disrupt the stress axis, specifically the hypothalamic-pituitary-adrenal (HPA) axis, a signaling pathway involved in the body’s stress response. The hormones produced by the glands in the stress axis affect parts of the brain involved in regulating fear and anxiety.

    “The study suggests that mild blast traumatic brain injuries dysregulate the neuroendocrine stress axis differently in women and men,” said Ashley Russell, the first author and a Neuroscience Ph.D. candidate at the Uniformed Services University of the Health Sciences (USU) in Bethesda, Md. “The research provides a missing link between a mild blast injury and the subsequent development of neuropsychiatric disorders such as anxiety and PTSD.”

    Researchers exposed both male and female mice to a mild blast injury of 15 psi using the ORA Advanced Blast Simulator at USU. When compared to mice that did not receive blast injury, injured mice produced altered levels of corticosterone, a hormone released when the stress axis is activated. This difference in the stress response was observed both short- and long-term post blast injury. Blast-injured female mice showed greater dysregulation of corticosterone levels than male mice with TBI.

    The scientists also sought to examine how a stressor may alter activation of corticotropin releasing factor (CRF) neurons in various brain regions involved in fear and anxiety regulation. In response to a stressor, female mice had heightened activation of CRF neurons in the stress integration center of the brain compared to male mice, an effect attributed to circulating estrogen levels.

    Understanding precisely how TBI can interfere with the body’s stress response may open the door to developing better interventions to treat both TBI and the resulting mental health conditions, Russell said.

    “Traumatic brain injury causes short- and long-term neuroendocrine dysregulation that may result in anxiety- and stress-related disorders,” she said. “Unfortunately, there are no therapeutic interventions to mitigate this response. More research is needed in this area to determine why these effects occur and how to treat them.”


  8. Potential drugs and targets for brain repair

    April 3, 2017 by Ashley

    From the PLOS press release:

    Researchers have discovered drugs that activate signaling pathways leading to specific adult brain cell types from stem cells in the mouse brain, according to a study publishing on 28 March in the open access journal PLOS Biology by Kasum Azim of the University of Zurich and colleagues from INSERM/university of Lyon and University of Portsmouth. The results may open new avenues for drug development aimed at treatment of degenerative brain disorders.

    New neurons, and support cells called oligodendrocytes, arise during development throughout adulthood from neural stem cells in the subventricular zone, a region of the forebrain adjacent to the ventricles. The transcriptional changes associated with the development of each cell type in the newborn mouse have been catalogued in publicly accessible databases. Similarly, the transcriptional changes produced by thousands of chemicals approved for clinical use have also been catalogued. In the new study, the authors used these databases (which included their own previously generated data) to find overlaps between transcriptional changes associated with cell differentiation and drug treatments, on the premise that these might identify potential therapies to reverse neurodegenerative diseases.

    Toward that end, they characterized differences in signaling pathways in “microdomains” of the subventricular zone where neurons or oligodendrocytes get their start in life. They found several potentially important differences between neuron-specific and oligodendrocyte-specific microdomains, and used these findings to identify similar changes in gene expression in the small molecule drug database.

    That led them to a set of small molecule drugs whose transcriptional signatures were similar to those of either neuronal or oligodendrocytic development. They showed that one such molecule, called LY-294002 specifically enhanced normal oligodendrogenesis from neural stem cells in newborn mice. In adult mice, different molecules (AR-A014418 and CHIR99021) counteracted the gradual loss of neurogenic capacity and lineage diversity of the adult subventricular zone. Finally, this later molecule promoted robust regeneration of oligodendrocytes and a smaller increase in neurons in a model of perinatal hypoxic brain injury.

    These results may be valuable in several ways. First, because the small molecule drug data point to important cellular pathways, they provide new insights into the mechanisms of neural development and repair, which can be exploited to develop new strategies for treatment. Second, they identify several new drugs, each already approved for clinical use, whose therapeutic potential for brain injury repair can now be explored. Finally, they provide a proof-of-principle for a novel approach to identify other potentially valuable new drugs that can directly affect neural regeneration, and that may be developed for treating brain diseases.

    “Controlling the fate of neural stem cells is a key therapeutic strategy in regenerative medicine,” said Azim and coworkers. “The strategy outlined in this study may allow us to quickly identify multiple drug candidates and get them into the drug development pipeline, where their potential as treatments can then be further assessed.”


  9. Biomechanical analysis of head injury in pediatric patients

    March 30, 2017 by Ashley

    From the Journal of Neurosurgery Publishing Group press release:

    The biomechanics of head injury in youths (5 to 18 years of age) have been poorly understood. A new study reported in the Journal of Neurosurgery: Pediatrics set out to determine what biomechanical characteristics predispose youths with concussions to experience transient or persistent postconcussion symptoms.

    Background. A form of traumatic brain injury, concussion is usually caused by a blow to the head or some other event that causes the brain to suddenly shift position within the skull. Various symptoms are associated with concussion: headache, dizziness, confusion, visual problems, concentration difficulties, irritability, depression, and more. Some young patients experience concussion-related symptoms for only a short time, but for others, symptoms linger. When symptoms resolve within a few weeks after the incident, they are known as transient post-concussion symptoms (TPCSs); when three or more concussion-related symptoms last more than four weeks after the incident, they are called persistent post-concussion symptoms (PPCSs).

    The Study. To determine the biomechanics of head impacts leading to transient or persistent post-concussion symptoms in youths, a Canadian group of concussion researchers recruited patients 5 to 18 years of age, who had been treated for concussion at any of nine emergency departments within the Pediatric Emergency Research Canada (PERC) network. A questionnaire about the incident was completed by patients or their parents/guardians; the questions elicited information about the type of head impact, what surface impacted the head, and what area of the head was impacted, as well as a detailed description of the event. Based on the information provided by the questionnaires, the researchers were able to reconstruct individual head-impact events in their laboratory. Completed questionnaires from 233 pediatric patients (182 with TPCSs and 51 with PPCSs) had sufficient information to recreate the head-impact event.

    The reconstructions of concussion scenarios were restricted to head impacts resulting from a vertical, gravity-related fall — onto the floor, grass, or ice, for example. Falls may have occurred in the home or during a sports event, from a height or standing position. Youths may have worn helmets or been bareheaded at the time of impact. All of this information was taken into account in the reconstruction.

    To simulate head impacts in youths with transient or persistent symptoms, the researchers used a headform, approximately the size of the patient’s head, and a monorail drop rig that dropped the headform onto an anvil at an impact velocity estimated for each head-impact incident. The surface of the anvil impacted by the headform was covered by material corresponding to the surface struck by the patient’s head: concrete, hardwood, grass, ice, etc. The angle of the headform when dropped was adjusted so that the area of impact on the headform corresponded to the site of impact on the patient’s head. If the patient had been wearing a helmet and/or mask at the time of injury, a similar helmet or mask was used in the simulation.

    In addition to physical models of head impact, the researchers used computational and finite element models to determine force, energy, peak linear and rotational acceleration, and maximal principal strain in brain tissue, and to measure cumulative strain damage associated with falls in the young patients. The researchers then compared values for these variables between patients with TPCSs and those with PPCSs. They found no statistically significant differences between the two patient groups for any of these variables.

    The researchers also examined whether one or more of the biomechanical variables could predict the occurrence of persistent symptoms (PPCSs). Again they found no statistically significant evidence that any of the biomechanical variables examined led to PPCSs, although “a trend shown for some variables indicated larger magnitudes of response were associated with PPCSs.”

    An important finding in these pediatric patients was “higher brain tissue strain responses for lower energy and impact velocities than those measured in adults, suggesting that youths are at higher risk of concussive injury at lower event severities.”

    Using the same techniques in head-injured adults, the researchers previously were able to identify statistically significant differences between patient groups. They offer several suggestions as to why this was not the case with youths and suggest other means by which one may be able to differentiate TPCSs from PPCSs, such as structural magnetic resonance imaging, diffusion tensor imaging, and arterial spin labeling. They also pose the possibility that PPCSs may be related more to the amount of brain tissue altered by the injury than to symptomology. Future biomechanical studies of pediatric brain injury, the investigators suggest, should include quantitative measures of the injury linked to clinical outcomes, patient predisposition, and history of concussion.

    Although this study was unable to definitively identify biomechanical variables that differentiate between TPCSs and PPCSs in youths, the researchers believe it is the first biomechanical analysis of a large number of pediatric concussion cases. Thus the data collected can be used in later investigations of youth concussions, both as a reference for future studies and as validation of the physical and computation models that were used.

    Details of the study are reported in the article, “Pediatric concussion: biomechanical differences between outcomes of transient and persistent (> 4 weeks) postconcussion symptoms,” by Andrew Post, Ph.D., and colleagues (published online today in the Journal of Neurosurgery: Pediatrics).

    When asked about the importance of this paper, Dr. Post stated, “This work is the first to examine the biomechanics of brain injury for youth using these types of methods. It has provided the first look into the mechanics of injury and provides a detailed dataset from which to improve our understanding of brain trauma in pediatric populations.”


  10. Children prenatally exposed to alcohol more likely to have academic difficulties

    March 28, 2017 by Ashley

    From the Research Society on Alcoholism:

    Despite greater awareness of the dangers of prenatal exposure to alcohol, the rates of Fetal Alcohol Spectrum Disorders remain alarmingly high. This study evaluated academic achievement among children known to be prenatally exposed to maternal heavy alcohol consumption as compared to their peers without such exposure, and explored the brain regions that may underlie academic performance.

    Researchers assessed two groups of children, eight to 16 years of age: 67 children with heavy prenatal alcohol exposure (44 boys, 23 girls) and 61 children who were not prenatally exposed to alcohol (33 boys, 28 girls). Scores on standardized tests of academic areas such as reading, spelling, and math were analyzed. In addition, a subsample of 42 children (29 boys, 13 girls) had brain imaging, which allowed the authors to examine the relations between the cortical structure (thickness and surface area) of their brains and academic performance.

    The alcohol-exposed children performed significantly worse than their peers in all academic areas, with particular weaknesses found in math performance. Brain imaging revealed several brain surface area clusters linked to math and spelling performance. The children without prenatal alcohol exposure demonstrated the expected developmental pattern of better scores associated with smaller brain surface areas, which may be related to a typical developmental process known as pruning. However, alcohol-exposed children did not show this pattern, possibly due to atypical or delayed brain development, which has been observed in other research studies. These results support previous findings of lower academic performance among children prenatally exposed to alcohol compared to their peers, which appear to be associated with differences in brain development, and highlight the need for additional attention and support for these children.