1. Mild traumatic brain injury causes long-term damage in mice

    January 3, 2018 by Ashley

    From the Wiley press release:

    A new Annals of Clinical and Translational Neurology study in mice found that mild traumatic brain injury (TBI) can precipitate not only acute damage but also a lifelong degenerative process.

    At 24 months, animals exposed to repetitive mild TBI showed clear evidence of learning and working memory impairment with a lack of spatial memory and certain motor deficits. There was also evidence of ongoing degeneration of neuron projections as well as neuroinflammation. These changes were also observed after a single mild TBI, albeit to a lesser degree than repetitive mild TBI.

    “This is the first demonstration of what is, in essence, lifelong behavioural and pathological consequences of mild TBI in a relevant pre-clinical model,” said co-author Dr. William Stewart, of the University of Glasgow, in the UK. “Read with our previous characterisations at earlier time points in survival from injury, we can now see not only that repetitive mild TBI can precipitate lifelong and evolving pathology, but that even just a single mild TBI at a young age can lead to changes over normal ageing at very late survival points.”

    “This recognition of lifelong consequences of mild TBI in this model provides a promising platform for studies into processes driving these pathologies, and also strategies for their prevention,” added lead author Dr. Benoit Mouzon, of the Roskamp Institute in Florida.


  2. Study examines relationship between traumatic brain injury and alcohol use

    November 27, 2017 by Ashley

    From the Elsevier press release:

    Head injury, which often damages brain regions overlapping with those involved in addictive behaviors, does not worsen drinking behavior in people with heavy alcohol use, according to a new study published in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. The study, led by Dr. Andrew Mayer of the Mind Research Network and University of New Mexico in Albuquerque, New Mexico, also found that combining head injury with heavy alcohol use did not further alter the structure or function of the brain.

    “Individuals who consume too much alcohol are prone to experience more accidents as a result of their intoxication,” said Dr. Mayer. Importantly, he added, heavy alcohol use and traumatic brain injury (TBI) affect similar regions of the brain. This has led researchers to think that the common combination of head injury and heavy drinking may interact to worsen the brain damage already caused by chronic alcohol exposure.

    The study compared people with a recent history of heavy alcohol use and TBI with a control group carefully matched on lifetime history of alcohol exposure. Mayer and colleagues found the opposite of what they expected — heavy drinkers with a history of a TBI did not have worse drinking behavior, such as how often and how much they drank, compared with drinkers without a history of TBI.

    The researchers also used imaging techniques to measure the structure of the brain and its activity when the participants were given a taste of their favorite drink. “On average, the brains of the two groups were similar both in terms of the amount of lost tissue, as well as how each person’s brain responded to their favorite drink,” said Dr. Mayer, suggesting that TBI does not further damage brain circuitry in heavy drinkers.

    “The observation that the participants with TBI did not have greater neurocircuitry dysfunction than those without TBI might translate into greater therapeutic optimism for the treatment of individuals with a combination of TBI plus heavy drinking histories,” said Dr. Cameron Carter, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.


  3. Injury from contact sport has harmful, though temporary effect on memory

    November 22, 2017 by Ashley

    From the McMaster University press release:

    McMaster University neuroscientists studying sports-related head injuries have found that it takes less than a full concussion to cause memory loss, possibly because even mild trauma can interrupt the production of new neurons in a region of the brain responsible for memory.

    Though such losses are temporary, the findings raise questions about the long-term effects of repeated injuries and the academic performance of student athletes.

    The researchers spent months following dozens of athletes involved in high-contact sports such as rugby and football, and believe that concussions and repetitive impact can interrupt neurogenesis — or the creation of new neurons — in the hippocampus, a vulnerable region of the brain critical to memory.

    The findings were presented today (Tuesday, November 14th) at the Society for Neuroscience’s annual conference, Neuroscience 2017, in Washington D.C.

    “Not only are newborn neurons critical for memory, but they are also involved in mood and anxiety,” explains Melissa McCradden, a neuroscience postdoctoral fellow at McMaster University who conducted the work. “We believe these results may help explain why so many athletes experience difficulties with mood and anxiety in addition to memory problems.”

    For the study, researchers administered memory tests and assessed different types of athletes in two blocks over the course of two years. In the first block, they compared athletes who had suffered a concussion, uninjured athletes who played the same sport, same-sport athletes with musculoskeletal injuries, and healthy athletes who acted as a control group.

    Concussed athletes performed worse on the memory assessment called a mnemonic similarity test (MST), which evaluates a person’s ability to distinguish between images that are new, previously presented, or very similar to images previously presented.

    In the second study, rugby players were given the MST before the season started, halfway through the season, and one month after their last game. Scores for injured and uninjured athletes alike dropped midseason, compared to preseason scores, but recovered by the postseason assessment.

    Both concussed and non-concussed players showed a significant improvement in their performance on the test after a reprieve from their sport.

    For the concussed athletes, this occurred after being medically cleared to return to full practice and competition. For the rugby players, they improved after approximately a month away from the sport.

    If neurogenesis is negatively affected by concussion, researchers say, exercise could be an important tool in the recovery process, since it is known to promote the production of neurons. A growing body of new research suggests that gentle exercise which is introduced before a concussed patient is fully symptom free, is beneficial.

    “The important message here is that the brain does recover from injury after a period of reprieve,” says McCradden. “There is a tremendous potential for the brain to heal itself.”


  4. Study finds mapping brain connectivity with MRI may predict outcomes for cardiac arrest survivors

    November 3, 2017 by Ashley

    From the Johns Hopkins Medicine press release:

    A new study led by Johns Hopkins researchers found that measures of connectivity within specific cerebral networks were strongly linked to long-term functional outcomes in patients who had suffered severe brain injury following a cardiac arrest.

    A description of the findings, published in October in the journal Radiology, suggests that mapping and measuring such connectivity may result in highly accurate and reliable markers of long-term recovery trajectories in people with neurological damage caused by heart attacks, strokes, brain hemorrhage or trauma.

    “By analyzing functional MRI data we are able to see where brain network disruption is occurring, and determine how these changes relate to the likelihood of recovery from brain damage,” says Robert Stevens, M.D., associate professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine, and the paper’s senior author.

    Cardiac arrest, or the sudden loss of heart function, affects an estimated 535,000 people in the United States each year, according to the American Heart Association. The loss of blood flow, and its restoration through resuscitation, is associated with rapid and widespread damage to the brain, leading to disabling neurological and cognitive problems in survivors.

    Several modifiable factors, such as timeliness and quality of cardiac resuscitation and the strict control of body temperature to avoid fever, strongly influence the magnitude of brain damage and the prospects for recovery, says Stevens.

    He adds that current methods to predict how an individual will recover over time are limited, but advanced imaging techniques such as quantitative brain mapping using MRI data could transform practice by allowing clinicians to make better-informed decisions about care. MRI can specifically and accurately identify changes in tissue structure, blood flow and functional activation. Functional connectivity is determined by analyzing the temporal correlation of functional activation in different parts of the brain, thereby establishing the strength of connections between anatomically distinct regions. Clusters of brain regions that are highly correlated are called networks, and the degree of correlation can be measured within and between networks.

    For their study, the Hopkins researchers and their colleagues assessed the brain’s functional activation in 46 patients who were in a coma after cardiac arrest between July 2007 and October 2013. MRI was performed on all patients on average 12.6 days after cardiac arrest, and the analysis focused on four networks in the brain: dorsal attention network (DAN, which is active when a person uses energy to focus attention); default mode network (DMN, which is active when an individual is at rest); executive control network (ECN, which is active while initiating tasks and is associated with reward and inhibition); and salience network (SN, a network that determines the importance of stimuli and may direct activation of other cognitive networks). Of the participants, 32 were men, and the average age was 49.

    One year after the patients’ cardiac arrests, the researchers assessed survivors with the Cerebral Performance Category (CPC) Scale, a commonly used measure of neurological function following cardiac arrest. The test uses a scale from 1 to 5, with 1 indicating minimal to no disability and 5 indicating brain death. Eleven of the 46 patients who had favorable outcomes (a score of 1 or 2) showed higher connectivity within the DMN network, as well as greater anti-correlation (when one is active the other is not) between the SN and ECN and the SN and DMN, when compared with patients who had an unfavorable outcome (CPC greater than 2). Remarkably, the functional connectivity markers predicted outcomes more accurately when compared with structural measures of, for example, tissue damage, used in conventional MRI scans.

    “These findings highlight a potential realm of precision medicine using brain network biomarkers that are discriminative and predictive of outcomes,” says Haris Sair, M.D., interim director of neuroradiology at the Johns Hopkins University School of Medicine and the study’s lead author. “In the future, connectivity biomarkers may help guide new therapies for targeted treatment to improve brain function.”


  5. Study suggests football position and length of play affect brain impact

    November 1, 2017 by Ashley

    From the Radiological Society of North America press release:

    Researchers have found that damage to white matter in the brains of former college and professional football players due to recurrent head impacts can be related to playing position and career duration, according to a new study published online in the journal Radiology.

    Most previous research on head impacts in football has focused on cognitively impaired former football players. This is the first neuroimaging study to compare former football players with no evidence of cognitive impairment to analyze the effects of different playing histories and concussion exposure.

    “Our study, by including both former collegiate and professional players, gives us the ability to examine career duration and playing position along with concussion history,” said study author Kevin Guskiewicz, Ph.D., research director for the Center for the Study of Retired Athletes at the University of North Carolina at Chapel Hill (UNC-Chapel Hill). “By doing so, we found that these factors are all important when considering the long-term effects of playing football.”

    The research team recruited 64 former collegiate and professional football players, aged 52 to 65. Half of the former athletes played only college football, and half continued on to the professional league. Half of the former players reported three or more prior concussions, while the other half reported one or no prior concussions. The researchers recruited an equal number of speed and non-speed playing positions. The non-speed positions consisted of offensive or defensive linemen.

    Two MRI techniques — diffusion tensor imaging (DTI) and functional MRI (fMRI) — were used to examine 61 of the former players. MRI data from the other three players were excluded due to excessive movement or inability to complete the MRI exam. DTI was used to analyze white matter structural integrity, while fMRI was used to assess brain function while the players performed a memory task.

    “While DTI and fMRI have been used previously in the field of concussion research, we are among the first to combine the two techniques,” said co-author Michael Clark, medical student at UNC-Chapel Hill. “We were interested in how white matter and the ability to recruit brain resources to complete a memory task might be affected by head impact exposure in terms of career length and the position played. By using two different and complementary types of MRI, we were able to see the relationship between structure and function, both of which are affected by head impact exposure.”

    The results showed a significant interaction between career duration and concussion history. Former college players with three or more concussions had lower integrity in a broadly distributed area of white matter compared to those with one concussion or less. However, the opposite was true for former professional players.

    The researchers speculate that players with a long career duration, exposure to recurrent concussive events, and who are cognitively normal in their late 50s may not be reflective of the highly exposed former professional football player population as a whole.

    “We’re not exactly sure why this is the case for the former pros,” Clark said. “It may have to do with the sample of athletes we recruited into the study. But the findings could suggest that a career with additional exposure to football is not necessarily worse than a shorter duration of exposure.”

    The non-speed players with a history of recurrent concussion had reduced integrity in the frontal white matter and lower measure of activation during the fMRI task than those with one concussion or less. This was not the case for the speed players.

    The interactions observed between concussion histories and playing positions suggest there may be important differences in the mechanisms of injury between speed and non-speed players. The magnitude, location and frequency of head impacts in football differ by position. Offensive backs experience impacts at greater acceleration. Linemen, however, tend to experience a greater overall frequency of impacts, and have the greatest proportion of impacts to the front of the helmet. The high proportion of frontal impacts experienced by non-speed players may result in more localized damage to frontal white matter tracts as compared to the more variable impact locations experienced by speed position players.

    “These findings suggest the playing position of an athlete may change the effects of concussions on the brain,” Dr. Guskiewicz said. “The mechanisms of concussions in non-speed players are fundamentally different from those of speed position players, suggesting that perhaps position-specific helmets are warranted.”

    The researchers added that more work is needed to better understand the results and to determine the underlying mechanisms regarding how subconcussive and concussive impacts affect brain health later in life.


  6. When the brain’s wiring breaks

    October 15, 2017 by Ashley

    From the University of North Carolina Health Care press release:

    Among all the bad things that can happen to the brain when it is severely jolted — in a car accident, for example — one of the most common and worrisome is axon damage. Axons are the long stalks that grow out of the bodies of neurons and carry signals to other neurons. They are part of the brain’s “wiring,” and they sometimes grow to amazing lengths — from the brain all the way down to the spinal cord. But axons are thin and fragile. When the brain receives a strong blow, axons are often stressed past their structural limits. They either break or swiftly degenerate.

    That much we know. But scientists haven’t understood what happens next. What happens to the neuron when its axon goes south?

    “Getting at the precise mechanisms of what happens after axon damage has been really challenging,” says Anne Marion Taylor, PhD, an assistant professor in the UNC/NC State Joint Department of Biomedical Engineering. “But we think we’ve finally figured out a key part of what happens and why.”

    In a Nature Communications paper, Taylor and colleagues have revealed new molecular details of axotomy — when neurons are damaged or completely severed.

    Shrinking dendritic spines, rising excitability

    Scientists do know that a severed axon will cause a neuron to quickly lose some of its incoming connections from other neurons. These connections occur at short, root-like tendrils called dendrites, which sprout from the neuron’s cell body, or soma. Dendrites themselves grow tiny protrusions called spines to create actual connections, or synapses, with incoming axons. It’s these dendritic spines that shrink in number following axotomy.

    As it loses input connections, the wounded neuron also becomes more excitable: the neuron becomes more likely to fire signals down its truncated axon when stimulated to do so by other neurons. Neurons normally have a mix of inputs. Some are excitatory, pushing the neuron to fire; others are inhibitory, restraining the neuron from firing. Neurons with axons that have been truncated show a disruption of the normal excitatory/inhibitory balance in favor of excitability.

    This enhanced excitability in the weeks and months following injury is thought to be largely an adaptive, beneficial response — a switch to a neuronal “seeking mode” like that seen in developing brains. This beneficial switch increases the chance that the neuron with the truncated axon can hook up with a new partner and continue to be a productive member of neural society.

    “Neurologists know this,” said Taylor, a member of the UNC Neuroscience Center. “It’s why they promote physical therapy and retraining for people who suffer head injury. During this extended period of excitability, PT and retraining can help guide injured neurons along beneficial pathways.”

    But the injury-induced excitability in a neuron may cause problems too. A neuron can die from overexcitement (neuroscientists call this excitotoxicity). Neuronal hyperactivity after injury also may lead to intractable pain, muscle spasms, or agitation in the patient. In the days immediately after injury, doctors often treat brain-injury patients with drugs such as gabapentin designed specifically to suppress neuronal hyper-excitability.

    What scientists haven’t understood very well are the biological details, the hows and whys of dendrite spine loss and hyper-excitability. Those details have been elusive because of the spaghetti-like complexity of the brain, which makes it extremely difficult for a scientist to isolate a neuron and its axon for manipulation and analysis, either in a lab dish or a lab animal.

    Several years ago, as a biomedical engineering graduate student at the University of California-Irvine, Taylor invented a device to help solve this problem. It’s a microfluidic chamber with tiny grooves that trap individual axons from cultured neurons as they grow longer.

    “The axons aren’t able to turn around, so they just keep growing straight until they reach a separate compartment,” Taylor says. “We can cut an axon in its compartment and then look at responses in the associated soma or dendrites without affecting axons in other compartments.”

    A loss of inhibition

    Taylor and her colleagues used the device in the new study to analyze what happens when an axon is severed. They found that events within the neuron itself drive the resulting dendrite spine loss and hyper-excitability. Signals originating at the site of injury move rapidly back along the remaining portion of the axon to the neuronal soma and nucleus, triggering a new pattern of gene activity. Taylor’s team managed to block the neuron’s gene activity to prevent the dendritic spine loss and hyper-excitability.

    Taylor and colleagues analyzed how gene activity changed before and after axotomy. Multiple genes were altered following axotomy. The activity for one of these genes, encoding a protein called netrin-1, turned out to be sharply reduced. A separate analysis showed a similar drop in netrin-1 in affected neurons in rats whose axons from the brain to the spinal cord had been cut. Together, these results hinted that netrin-1’s absence might be a major factor driving neuronal changes after axotomy.

    When Taylor and colleagues added netrin-1 to axotomized neurons to restore the protein to normal levels — even two full days after severing the axon — they found that the treatment quickly reversed all of the dendritic spine loss and most of the hyper-excitability.

    “The treated neurons more closely resembled uninjured controls,” Taylor says. “This was a striking finding and we were surprised to find that netrin-1 normalized both the number of synapses and excitability, even when applied days after injury.”

    She added, “We’re a long way off, but we really do hope to translate this netrin-1 finding into a new therapy. Ideally, it would do what gabapentin and related head-injury drugs aim to do, only better and more precisely.”


  7. Memory decline after head injury may be prevented by slowing brain cell growth

    September 27, 2017 by Ashley

    From the Rutgers University press release:

    The excessive burst of new brain cells after a traumatic head injury that scientists have traditionally believed helped in recovery could instead lead to epileptic seizures and long-term cognitive decline, according to a new Rutgers New Jersey Medical School study.

    In the September issue of Stem Cell Reports, Viji Santhakumar, associate professor in the department of Pharmacology, Physiology and Neuroscience, and her colleagues, challenge the prevailing assumption by scientists in the field that excessive neurogenesis (the birth of new brain cells) after injury is advantageous.

    “There is an initial increase in birth of new neurons after a brain injury but within weeks, there is a dramatic decrease in the normal rate at which neurons are born, depleting brain cells that under normal circumstances should be there to replace damaged cells and repair the brain’s network,” said Santhakumar. “The excess new neurons lead to epileptic seizures and could contribute to cognitive decline.”

    In the United States an estimated 1.7milllion people sustain a TBI each year, making the condition a major cause of death and disability. Symptoms can include impaired thinking or memory, personality changes and depression and vision and hearing problems as well as epilepsy. About 80 percent of those who develop epilepsy after a brain injury have seizures within the first two years after the damage occurs.

    Santhakumar said while researchers who study epilepsy have started to look more closely at how preventing excessive neurogenesis after brain injury could prevent seizures, neuroscientists have traditionally viewed the process as helpful to overall brain recovery.

    Studying laboratory rats, Rutgers scientists found, however, that within a month after experimental brain injury, the number of new brain cells declined dramatically, below the numbers of new neurons that would have been detected if an injury had not occurred.

    When scientists were able to prevent the excessive neurogenesis which occurs within days of the injury with a drug similar to one under trial for chemotherapy treatments, the rate of birth of new brain cells went back to normal levels and risk for seizures was reduced.

    “That’s why we believe that limiting this process might be beneficial to stopping seizures after brain injury,” she said.

    While the regenerative capability of brain cells, in the hippocampus — the part of the brain responsible for learning and memory — slows down as part of the aging process, the Rutgers scientists determined that the process that occurred after a head injury was related to injury and not age.

    “It is normal for the birth of new neurons to decline as we age,” said Santhakumar. “But what we found in our study was that after a head injury the decline seems to be more rapid.”


  8. Popular bottle-breaking trick is giving insight to brain injuries

    September 25, 2017 by Ashley

    From the Brigham Young University press release:

    As many YouTube videos show, striking the top of a liquid-filled bottle can shatter the bottom. Now researchers are hoping to use new knowledge of that party trick to help fill a gap in something much more serious: brain research.

    A study by engineering professors from Brigham Young University, Utah State University and the Tokyo University of Agriculture and Technology details exactly what happens when a liquid at rest — like the water in a bottle — is suddenly put into motion. Using high-speed photography, the team shows how the swift acceleration causes small bubbles to form in the liquid and then rapidly collapse, releasing a destructive shockwave.

    The proper term for the phenomenon is called cavitation, a process well known to engineers for causing damage in pipes and marine propellers. The new study, published in the Proceedings of the National Academy of Sciences, details an alternative formula that more accurately predicts when cavitation will happen.

    While the finding has immediate implications for many industrial processes interrupted by cavitation-induced damage, there’s also growing evidence linking cavitation to brain trauma.

    “The brain is surrounded by fluid, and when you have impact, it’s possible you are experiencing cavitation within that fluid,” said study co-author Scott Thomson, associate professor of mechanical engineering at BYU.

    Fluid dynamics experts know how to predict when cavitation will occur in a fluid already in motion, but their formula doesn’t work so well when a resting fluid is rapidly accelerated. The new study fixes that problem by finalizing a new equation that considers a fluid’s depth and acceleration.

    For the brain, knowing this alternative cavitation formula could be used to better predict brain injuries caused by high-velocity impact. “And once we’re able to predict when that will happen, we can better design safety devices to help prevent serious brain damage,” Thomson said.

    Those safety devices could be for athletic applications, such as football helmets, or even military applications.

    “If a blast wave is above a certain magnitude, there may not be much we can do to prevent brain injury for a soldier,” said study author Tadd Truscott, associate professor of mechanical engineering at Utah State University. “But maybe a helmet can be developed to detect when that trauma has happened so a soldier can be removed from the front line and be saved from repeat exposure to blasts.”


  9. Study suggests playing smartphone health app aids concussion recovery in teens

    September 1, 2017 by Ashley

    From the Ohio State University Wexner Medical Center press release:

    Generally, after suffering a concussion, patients are encouraged to avoid reading, watching TV and using mobile devices to help their brains heal. But new research shows that teen-agers who used a mobile health app once a day in conjunction with medical care improved concussion symptoms and optimism more than with standard medical treatment alone.

    Researchers from The Ohio State University Wexner Medical Center and Cincinnati Children’s Hospital Medical Center collaborated on the study with Jane McGonigal of the Institute for the Future, who developed the mobile health app called SuperBetter after she suffered a concussion.

    Results of the study are published online in the journal Brain Injury.

    The 19 teens who participated in the study received standard of care for concussion symptoms that persisted beyond 3 weeks after the head injury, and the experimental group also used the SuperBetter app as a gamified symptoms journal.

    “We found that mobile apps incorporating social game mechanics and a heroic narrative can complement medical care to improve health among teenagers with unresolved concussion symptoms, said first author Lise Worthen-Chaudhari, a physical rehabilitation specialist who studies movement at Ohio State’s Wexner Medical Center’s Neurological Institute.

    The American Academy of Neurology recommends limiting cognitive and physical effort and prohibiting sports involvement until a concussed individual is asymptomatic without using medication. However, this level of physical, cognitive and social inactivity represents a lifestyle change with its own risk factors, including social isolation, depression and increased incidence of suicidal ideology, the researchers noted.

    In addition, cognitive rest often involves limiting screen stimulation associated with popular modes of interpersonal interaction, such as text messaging and social networking on digital platforms, including Facebook, Twitter, Instagram and multiplayer video gaming, thereby blocking common avenues for social connection.

    “Teens who’ve had a concussion are told not to use media or screens, and we wanted to test if it was possible for them to use screens just a little bit each day, and get the bang for the buck with that,” Worthen-Chaudhari said. “The app rewrites things you might be frustrated about as a personal, heroic narrative. So you might start out feeling ‘I’m frustrated. I can’t get rid of this headache,’ and then the app helps reframe that frustration to ‘I battled the headache bad guy today. And I feel good about that hard work’.”

    Concussion symptoms can include a variety of complaints, including headaches, confusion, depression, sleep disturbance, fatigue, irritability, agitation, anxiety, dizziness, difficulty concentrating or thinking clearly, sensitivity to light and noise, and impaired cognitive function.

    Within the SuperBetter app, symptoms were represented as bad guys such as headaches, dizziness or feeling confused, and medical recommendations were represented as power ups, including sleep, sunglasses or an academic concussion management plan. Participants invited allies to join their personal network in the app and they could view their in-app activity and could send resilience points, achievements, comments and personalized emails in response to activity.

    “Since 2005, the rate of reported concussions in high school athletes has doubled, and youth are especially at risk,” said study collaborator Dr. Kelsey Logan, director of the division of sports medicine at Cincinnati Children’s. “Pairing the social, mobile app SuperBetter with traditional medical care appears to improve outcomes and optimism for youth with unresolved concussion symptoms. More study is needed to investigate ways that leveraging interactive media may complement medical care and promote health outcomes among youth with concussion and the general population.”


  10. Brain injury in kids might lead to alcohol abuse

    August 28, 2017 by Ashley

    From the Frontiers press release:

    Researchers at Ohio State University have surveyed previous studies to investigate the relationship between traumatic brain injuries and alcohol abuse. They found evidence that traumatic brain injuries in children and adolescents could be a risk-factor for alcohol abuse in later life.

    When we think of the link between alcohol and traumatic brain injuries, we probably think of a person’s increased risk of injury while drunk. Alcohol intoxication is indeed a significant risk factor for traumatic brain injuries, and one study has reported that alcohol use is involved in as many as 50% of emergency department admissions for traumatic brain injuries in the US.

    Intriguingly, an animal study conducted by Zachary Weil, a researcher at Ohio State University, made him suspect that the converse might also be true, particularly in young people. “We recently reported that mice that experience a traumatic brain injury as juveniles drink significantly more alcohol as adults,” says Weil. “When we started to look at the human literature it became clear that alcohol and traumatic brain injuries were very connected. There were some hints that brain injuries might actually make someone more susceptible to alcohol abuse.”

    Weil was inspired to look more closely at the past literature, and what he and his team found was recently published in Frontiers in Behavioral Neuroscience. The researchers found that it was difficult to tell if their hypothesis was true in adults. “So many adults that have brain injuries are already heavy drinkers and therefore it’s really hard to tell for sure if a brain injury has affected their drinking,” explains Weil.

    However, for people who suffer a traumatic brain injury in childhood or adolescence, there was a clearer link to alcohol abuse problems in later life. For example, children under 5 years of age who suffer a traumatic brain injury are over 3.6 times more likely to exhibit substance abuse as teenagers, compared with uninjured children.

    So, why would a traumatic brain injury potentially lead to alcohol abuse? The team found evidence in the literature that brain injury can negatively affect factors that are associated with reducing alcohol abuse. For example, forming stable romantic relationships, getting involved in extracurricular activities and maintaining full-time employment are all associated with a reduced risk of substance abuse, but all are less likely in brain injury survivors.

    Traumatic brain injuries can also make people more impulsive and less aware of the consequences of their actions, and there is also evidence that brain injury survivors may use alcohol to help deal with the negative consequences of their injury.

    Beyond its psychological effects, traumatic brain injury can cause significant inflammation in the brain. Alcohol also generates neuroinflammation, and evidence from animal studies suggests that this inflammation might drive further drinking.

    Finally, traumatic brain injuries can damage specific neurochemical systems in the brain that are vulnerable during childhood development, such as the dopaminergic system. A dysfunctional dopaminergic system is a risk factor for substance abuse, suggesting another potential link between childhood brain injury and alcohol abuse in adulthood.

    So, how can we address the problem? “This is an important issue because drinking after brain injury is associated with health problems and poorer outcomes. Specifically targeting substance abuse problems in the brain-injured population could do a lot of good,” says Weil.

    The researchers caution that the link between brain injuries and alcohol abuse has not yet been completely established and more work is needed. “This has not been completely confirmed in humans, but there is a lot of suggestive evidence,” explains Weil.