Posts tagged brain injury
Articles and news from the latest research reports.
![Modeling shockwaves through the brain
Since the start of the military conflicts in Iraq and Afghanistan, more than 300,000 soldiers have returned to the United States with traumatic brain injury (TBI) caused by exposure to bomb blasts — and in particular, exposure to improvised explosive devices, or IEDs. Symptoms of traumatic brain injury can range from the mild, such as lingering headaches and nausea, to more severe impairments in memory and cognition.
Since 2007, the U.S. Department of Defense has recognized the critical importance and complexity of this problem, and has made significant investments in traumatic brain injury research. Nevertheless, there remain many gaps in scientists’ understanding of the effects of blasts on the human brain; most new knowledge has come from experiments with animals.
Now MIT researchers have developed a scaling law that predicts a human’s risk of brain injury, based on previous studies of blasts’ effects on animal brains. The method may help the military develop more protective helmets, as well as aid clinicians in diagnosing traumatic brain injury — often referred to as the “invisible wounds” of battle.
“We’re really focusing on mild traumatic brain injury, where we know the least, but the problem is the largest,” says Raul Radovitzky, a professor of aeronautics and astronautics and associate director of the MIT Institute for Soldier Nanotechnologies (ISN). “It often remains undetected. And there’s wide consensus that this is clearly a big issue.”
While previous scaling laws predicted that humans’ brains would be more resilient to blasts than animals’, Radovitzky’s team found the opposite: that in fact, humans are much more vulnerable, as they have thinner skulls to protect much larger brains.
A group of ISN researchers led by Aurélie Jean, a postdoc in Radovitzky’s group, developed simulations of human, pig, and rat heads, and exposed each to blasts of different intensities. Their simulations predicted the effects of the blasts’ shockwaves as they propagated through the skulls and brains of each species. Based on the resulting differences in intracranial pressure, the team developed an equation, or scaling law, to estimate the risk of brain injury for each species.
“The great thing about doing this on the computer is that it allows you to reduce and possibly eventually eliminate animal experiments,” Radovitzky says.
The MIT team and co-author James Q. Zheng, chief scientist at the U.S. Army’s soldier protection and individual equipment program, detail their results this week in the Proceedings of the National Academy of Sciences.
Air (through the) head
A blast wave is the shockwave, or wall of compressed air, that rushes outward from the epicenter of an explosion. Aside from the physical fallout of shrapnel and other chemical elements, the blast wave alone can cause severe injuries to the lungs and brain. In the brain, a shockwave can slam through soft tissue, with potentially devastating effects.
In 2010, Radovitzky’s group, working in concert with the Defense and Veterans Brain Injury Center, a part of the U.S. military health system, developed a highly sophisticated, image-based computational model of the human head that illustrates the ways in which pressurized air moves through its soft tissues. With this model, the researchers showed how the energy from a blast wave can easily reach the brain through openings such as the eyes and sinuses — and also how covering the face with a mask can prevent such injuries. Since then, the team has developed similar models for pigs and rats, capturing the mechanical response of brain tissue to shockwaves.
In their current work, the researchers calculated the vulnerability of each species to brain injury by establishing a mathematical relationship between properties of the skull, brain, and surrounding flesh, and the propagation of incoming shockwaves. The group considered each brain structure’s volume, density, and celerity — how fast stress waves propagate through a tissue. They then simulated the brain’s response to blasts of different intensities.
“What the simulation allows you to do is take what happens outside, which is the same across species, and look at how strong was the effect of the blast inside the brain,” Jean says.
In general, they found that an animal’s skull and other fleshy structures act as a shield, blunting the effects of a blast wave: The thicker these structures are, the less vulnerable an animal is to injury. Compared with the more prominent skulls of rats and pigs, a human’s thinner skull increases the risk for traumatic brain injury.
Shifting the problem
This finding runs counter to previous theories, which held that an animal’s vulnerability to blasts depends on its overall mass, but which ignored the role of protective physical structures. According to these theories, humans, being more massive than pigs or rats, would be better protected against blast waves.
Radovitzky says this reasoning stems from studies of “blast lung” — blast-induced injuries such as tearing, hemorrhaging, and swelling of the lungs, where it was found that mass matters: The larger an animal is, the more resilient it may be to lung damage. Informed by such studies, the military has since developed bulletproof vests that have dramatically decreased the number of blast-induced lung injuries in recent years.
“There have essentially been no reported cases of blast lung in the last 10 years in Iraq or Afghanistan,” Radovitzky notes. “Now we’ve shifted that problem to traumatic brain injury.”
In collaboration with Army colleagues, Radovitzky and his group are performing basic research to help the Army develop helmets that better protect soldiers. To this end, the team is extending the simulation approach they used for blast to other types of threats.
His group is also collaborating with audiologists at Massachusetts General Hospital, where victims of the Boston Marathon bombing are being treated for ruptured eardrums.
“They have an exact map of where each victim was, relative to the blast,” Radovitzky says. “In principle, we could simulate the event, find out the level of exposure of each of those victims, put it in our scaling law, and we could estimate their risk of developing a traumatic brain injury that may not be detected in an MRI.”
Joe Rosen, a professor of surgery at Dartmouth Medical School, sees the group’s scaling law as a promising window into identifying a long-sought mechanism for blast-induced traumatic brain injury.
“Eighty percent of the injuries coming off the battlefield are blast-induced, and mild TBIs may not have any evidence of injury, but they end up the rest of their lives impaired,” says Rosen, who was not involved in the research. “Maybe we can realize they’re getting doses of these blasts, and that a cumulative dose is what causes [TBI], and before that point, we can pull them off the field. I think this work will be important, because it puts a stake in the ground so we can start making some progress.”](http://33.media.tumblr.com/4ceffdeaa6a80bfe4a2e34856255de00/tumblr_ncp8j3tCQC1rog5d1o1_500.jpg)
Modeling shockwaves through the brain
Since the start of the military conflicts in Iraq and Afghanistan, more than 300,000 soldiers have returned to the United States with traumatic brain injury (TBI) caused by exposure to bomb blasts — and in particular, exposure to improvised explosive devices, or IEDs. Symptoms of traumatic brain injury can range from the mild, such as lingering headaches and nausea, to more severe impairments in memory and cognition.
Since 2007, the U.S. Department of Defense has recognized the critical importance and complexity of this problem, and has made significant investments in traumatic brain injury research. Nevertheless, there remain many gaps in scientists’ understanding of the effects of blasts on the human brain; most new knowledge has come from experiments with animals.
Now MIT researchers have developed a scaling law that predicts a human’s risk of brain injury, based on previous studies of blasts’ effects on animal brains. The method may help the military develop more protective helmets, as well as aid clinicians in diagnosing traumatic brain injury — often referred to as the “invisible wounds” of battle.
“We’re really focusing on mild traumatic brain injury, where we know the least, but the problem is the largest,” says Raul Radovitzky, a professor of aeronautics and astronautics and associate director of the MIT Institute for Soldier Nanotechnologies (ISN). “It often remains undetected. And there’s wide consensus that this is clearly a big issue.”
While previous scaling laws predicted that humans’ brains would be more resilient to blasts than animals’, Radovitzky’s team found the opposite: that in fact, humans are much more vulnerable, as they have thinner skulls to protect much larger brains.
A group of ISN researchers led by Aurélie Jean, a postdoc in Radovitzky’s group, developed simulations of human, pig, and rat heads, and exposed each to blasts of different intensities. Their simulations predicted the effects of the blasts’ shockwaves as they propagated through the skulls and brains of each species. Based on the resulting differences in intracranial pressure, the team developed an equation, or scaling law, to estimate the risk of brain injury for each species.
“The great thing about doing this on the computer is that it allows you to reduce and possibly eventually eliminate animal experiments,” Radovitzky says.
The MIT team and co-author James Q. Zheng, chief scientist at the U.S. Army’s soldier protection and individual equipment program, detail their results this week in the Proceedings of the National Academy of Sciences.
Air (through the) head
A blast wave is the shockwave, or wall of compressed air, that rushes outward from the epicenter of an explosion. Aside from the physical fallout of shrapnel and other chemical elements, the blast wave alone can cause severe injuries to the lungs and brain. In the brain, a shockwave can slam through soft tissue, with potentially devastating effects.
In 2010, Radovitzky’s group, working in concert with the Defense and Veterans Brain Injury Center, a part of the U.S. military health system, developed a highly sophisticated, image-based computational model of the human head that illustrates the ways in which pressurized air moves through its soft tissues. With this model, the researchers showed how the energy from a blast wave can easily reach the brain through openings such as the eyes and sinuses — and also how covering the face with a mask can prevent such injuries. Since then, the team has developed similar models for pigs and rats, capturing the mechanical response of brain tissue to shockwaves.
In their current work, the researchers calculated the vulnerability of each species to brain injury by establishing a mathematical relationship between properties of the skull, brain, and surrounding flesh, and the propagation of incoming shockwaves. The group considered each brain structure’s volume, density, and celerity — how fast stress waves propagate through a tissue. They then simulated the brain’s response to blasts of different intensities.
“What the simulation allows you to do is take what happens outside, which is the same across species, and look at how strong was the effect of the blast inside the brain,” Jean says.
In general, they found that an animal’s skull and other fleshy structures act as a shield, blunting the effects of a blast wave: The thicker these structures are, the less vulnerable an animal is to injury. Compared with the more prominent skulls of rats and pigs, a human’s thinner skull increases the risk for traumatic brain injury.
Shifting the problem
This finding runs counter to previous theories, which held that an animal’s vulnerability to blasts depends on its overall mass, but which ignored the role of protective physical structures. According to these theories, humans, being more massive than pigs or rats, would be better protected against blast waves.
Radovitzky says this reasoning stems from studies of “blast lung” — blast-induced injuries such as tearing, hemorrhaging, and swelling of the lungs, where it was found that mass matters: The larger an animal is, the more resilient it may be to lung damage. Informed by such studies, the military has since developed bulletproof vests that have dramatically decreased the number of blast-induced lung injuries in recent years.
“There have essentially been no reported cases of blast lung in the last 10 years in Iraq or Afghanistan,” Radovitzky notes. “Now we’ve shifted that problem to traumatic brain injury.”
In collaboration with Army colleagues, Radovitzky and his group are performing basic research to help the Army develop helmets that better protect soldiers. To this end, the team is extending the simulation approach they used for blast to other types of threats.
His group is also collaborating with audiologists at Massachusetts General Hospital, where victims of the Boston Marathon bombing are being treated for ruptured eardrums.
“They have an exact map of where each victim was, relative to the blast,” Radovitzky says. “In principle, we could simulate the event, find out the level of exposure of each of those victims, put it in our scaling law, and we could estimate their risk of developing a traumatic brain injury that may not be detected in an MRI.”
Joe Rosen, a professor of surgery at Dartmouth Medical School, sees the group’s scaling law as a promising window into identifying a long-sought mechanism for blast-induced traumatic brain injury.
“Eighty percent of the injuries coming off the battlefield are blast-induced, and mild TBIs may not have any evidence of injury, but they end up the rest of their lives impaired,” says Rosen, who was not involved in the research. “Maybe we can realize they’re getting doses of these blasts, and that a cumulative dose is what causes [TBI], and before that point, we can pull them off the field. I think this work will be important, because it puts a stake in the ground so we can start making some progress.”
Cooling of Dialysis Fluids Protects Against Brain Damage
While dialysis can cause blood pressure changes that damage the brain, cooling dialysis fluids can protect against such effects. The findings come from a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). The cooling intervention can be delivered without additional cost and is simple to perform.
While dialysis is an essential treatment for many patients with kidney disease, it can cause damage to multiple organs, including the brain and heart, due to the sudden removal of bodily fluids.
To characterize dialysis-induced brain injury and to see whether cooled dialysis fluids (called dialysate) might help reduce such injury, Christopher McIntyre, DM, and his colleagues randomized 73 new dialysis patients to dialyze with body temperature dialysate or dialysate cooled to 0.5◦C below body temperature for 1 year.
The study demonstrated that dialysis drives progressive white matter brain injury due to blood pressure instability; however, patients who dialyzed at 0.5◦C below body temperature were completely protected against such white matter changes.
“This study demonstrates that paying attention to improving the tolerability of dialysis treatment—in this case by the simple and safe intervention of reducing the temperature of dialysate—does not just make patients feel better, but also can completely protect the brain from progressive damage,” said Dr. McIntyre.
(Source: newswise.com)
Network measures predict neuropsychological outcome after brain injury
Cognitive neuroscience research has shown that certain brain regions are associated with specific cognitive abilities, such as language, naming, and decision-making.
How and where these specific abilities are integrated in the brain to support complex cognition is still under investigation. However, researchers at the University of Iowa and Washington University in St. Louis, Missouri, believe that several hub regions may be especially important for the brain to function as an integrated network.
In research published online Sept. 15 in the Early Edition of the Proceedings of the National Academy of Sciences, scientists studied neurological patients with focal brain damage, and found that damage to six hub locations—identified in a model developed at Washington University using resting state fMRI, functional connectivity analyses, and graph theory—produced much greater cognitive impairment than damage to other locations.
Doctors have long observed that despite having similar locations or extent of brain injury, patients often present with wide-ranging degrees of impairment and exhibit different recovery trajectories. A better understanding of brain networks and hubs may improve the understanding of outcomes of brain injuries (for example, stroke, resection, or trauma) and help inform prognosis and rehabilitation efforts.
“We were able to identify a set of brain hubs and show that damage to those locations unexpectedly causes widespread cognitive impairments,” says David Warren, cognitive neuroscientist at the University of Iowa and lead study author. “We hope that this framework will help neurologists with diagnosis and prognosis, and neurosurgeons with surgical planning.”
Two contrasting views of brain hubs exist. One view focuses on the sheer number of connections between brain regions, with those regions showing the most connections considered hubs.
Warren and his colleagues contend that the number of connections a given region makes may not reflect the importance of a region to network function because it can be strongly influenced by network size. Instead, their framework defines hubs as brain regions that show correlated activity with multiple brain systems (rather than regions). The authors predicted that because hubs should be critical for brain function and complex cognition, damage to true hubs should produce widespread cognitive impairment.
This study evaluated long-term cognitive and behavioral data in 30 patients in the Iowa Neurological Patient Registry—19 with focal damage to one of the authors’ six target hub locations and 11 with damage to two control locations that fit the alternative hub definition.
On average, patients with lesions to target hubs had significant impairment in nine major cognitive domains—orientation/attention, perception, memory, language skills, motor performance, concept formation/reasoning, executive functions, emotional functions, and adaptive functions. In contrast, the group with lesions to control hubs was significantly impaired in just three of the nine domains (executive functions, emotional functions, and adaptive functions).
Additionally, the target group had significantly greater cognitive deficits than the control group in seven of nine domains (all except perception and emotional functions), again showing the widespread cognitive effects of target hub lesions.
“With a grant from the McDonnell Foundation, we’re planning to follow up by exploring the effects of damage to additional brain hubs, examining how damage to hubs alters brain activation, and studying neurosurgery patients prospectively before and after their surgeries,” says senior study author Daniel Tranel, professor of neurology in the UI Carver College of Medicine and psychology in the College of Liberal Arts and Sciences. “We think that this work could have a tremendous influence on clinical practice.”
(Source: now.uiowa.edu)
Compound protects brain cells after traumatic brain injury
A new class of compounds has now been shown to protect brain cells from the type of damage caused by blast-mediated traumatic brain injury (TBI). Mice that were treated with these compounds 24-36 hours after experiencing TBI from a blast injury were protected from the harmful effects of TBI, including problems with learning, memory, and movement.
Traumatic brain injury caused by blast injury has emerged as a common health problem among U.S. servicemen and women, with an estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan having experienced TBI. The condition is associated with many neurological complications, including cognitive and motor decline, as well as acquisition of psychiatric symptoms like anxiety and depression, and brain tissue abnormalities that resemble Alzheimer’s disease.
"The lack of neuroprotective treatments for traumatic brain injury is a serious problem in our society," says Andrew Pieper, senior study author and associate professor of psychiatry, neurology, and radiation oncology at the University of Iowa Carver College of Medicine. “Everyone involved in this work is motivated to find a way to offer hope for patients, which today include both military personnel and civilians, by establishing a basis for a new treatment to combat the deleterious neuropsychiatric outcomes after blast injury.”
It is known that TBI, as well as certain neurodegenerative diseases, damages axons—the tendril-like fibers that sprout from brains cells (neurons) and form the connections called synapses. In TBI, axon damage is followed by death of the neuron. The new study, published Sept. 11 in the journal Cell Reports, shows that a group of compounds, called the P7C3 series, blocks axon damage and preserves normal brain function following TBI.
Pieper led the team of scientists that discovered the P7C3 compound several years ago at UT Southwestern Medical Center. Subsequent studies showed that the root compound and its active analogs protect newborn neurons from cell death and also protect mature neurons in animal models of neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS).
The researchers have also previously shown efficacy of P7C3 molecules in brain injury due to concussion, and plan to investigate whether these compounds might be applicable in stroke as well, given that there appear to be common factors mediating neuronal cell death in these conditions.
By tweaking the structure of the original P7C3 compound, Pieper and his colleagues Joseph Ready and Steven McKnight, at UT Southwestern Medical Center, have further improved its potency and drug-like properties. In the latest study, Pieper’s team at the UI Carver College of Medicine, including co-first authors graduate student Terry Yin, senior technician Jeremy Britt, and graduate student Hector De Jesus-Cortes, tested the neuroprotective effects of the newest version, (-)-P7C3-S243, which can be given orally, in mice with blast-induced TBI.
In the study, blast-induced TBI caused learning, memory, and movement problems in the mice, which resemble the problems experienced by people affected by TBI. The researchers found that (-)-P7C3-S243 prevented acute memory and learning impairment caused by TBI. The compound also prevented TBI-associated balance and coordination problems in mice exposed to blast-injury. By examining the brain tissue at a cellular level, the team also found that the protection afforded to brain functions after injury was matched by preservation of normal neuronal axon structure and synaptic neurotransmission.
Importantly, the compound still produced its protective effects even when treatment was delayed until 24 to 36 hours after the blast injury.
"Seeing protection even when the compound was given this long after injury was important because it represents a liberal window of time within which almost all patients would be expected to be able to access treatment after injury," Pieper says.
The team also found that learning, memory, and coordination problems caused by the TBI persisted in untreated mice at least eight months after the single injury occurred, suggesting that the compound actually prevented these problems rather simply speeding up a normal recovery process.
In a separate study led by Pieper’s colleagues McKnight and Ready at UT Southwestern, and also published on Sept. 11 in the journal Cell, the team has identified the biological mechanism by which P7C3 compounds act in the brain. The compounds activate the molecular pathway that preserves neuronal levels of an energy molecule known as nicotinamide adenine dinucleotide (NAD).
"Based on the well-established role of NAD in axonal degeneration, the ability of (-)-P7C3-S243 to protect mice after blast-mediated traumatic brain injury is likely related to preservation of NAD levels," Pieper explains. "Now that we understand the mechanism of action of the P7C3 class of compounds, we can see why they should have therapeutic utility in an unusually broad spectrum of neurodegenerative conditions, without impeding any of a number of other normal forms of cell death.
"Our ultimate goal is to facilitate development of a new class of neuroprotective drugs with wide applicability to treating patients with TBI and other currently untreatable forms of neurodegeneration," he adds.
Xenon gas protects the brain after head injury
Head injury is the leading cause of death and disability in people aged under 45 in developed countries, mostly resulting from falls and road accidents. The primary injury caused by the initial mechanical force is followed by a secondary injury which develops in the hours and days afterwards. This secondary injury is largely responsible for patients’ mental and physical disabilities, but there are currently no drug treatments that can be given after the accident to stop it from occurring.
Scientists at Imperial College London found that xenon, given within hours of the initial injury, limits brain damage and improves neurological outcomes in mice, both in the short term and long term. The findings, published in the journal Critical Care Medicine, could lead to clinical trials of xenon as a treatment for head injury in humans.
Although xenon is chemically inert, this does not mean it is biologically inactive. Xenon has been known to have general anaesthetic properties since the 1950s. Previous studies at Imperial have found that xenon can protect brain cells from mechanical injury in the lab, but this new study is the first time such an effect has been shown in live animals, a vital step before any new treatments can be tested in humans.
Mice were anaesthetised before having a controlled mechanical force applied to the brain. Some were then treated with xenon at different concentrations and at different times after injury.
Mice treated with xenon performed better in tests assessing their neurological deficits, such as movement and balance problems, in the days after injury and after one month. They also had less brain damage, even if treatment was delayed up to three hours after the injury.
Dr Robert Dickinson from the Department of Surgery and Cancer at Imperial College London, who led the study, said: “After a blow to the head, most of the damage to the brain doesn’t occur immediately but in the hours and days afterwards. At present we have no specific drugs to limit the spread of the secondary injury, but we think that is the key to successful treatment.
“This study shows that xenon can prevent brain damage and disability in mice, and crucially it’s effective when given up to at least three hours after the injury. It’s feasible that someone who hits their head in an accident could be treated in the hospital or in an ambulance in this timeframe.
“These findings provide crucial evidence to support doing clinical trials in humans.”
Brain injuries no match for sPIF treatment
Researchers at Yale School of Medicine and their colleagues have uncovered a new pathway to help treat perinatal brain injuries. This research could also lead to treatments for traumatic brain injuries and neurodegenerative disorders such as Alzheimer’s and Parkinson’s.
The findings are published in the Sept. 8 issue of Proceedings of the National Academy of Sciences.
The MicroRNA molecule let-7 is known to cause the death of neurons in the central nervous system. The research team found that a synthetic molecule derived from the embryo called PreImplantation Factor (sPIF) protects against neuronal death and brain injury by targeting let-7.
“We would never have connected the dots between PIF and let-7 without prior knowledge and experience on let-7 and H19, a developmentally regulated gene that is highly expressed in the developing embryo,” said senior author Dr. Yingqun Huang, associate professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine.
Using a rat perinatal brain injury model, Huang and the team found that sPIF rescued damaged neurons and reduced inflammation. The team performed a series of in vivo and in vitro experiments and found that sPIF helped to stop the production of let-7. “We showed that sPIF works by destabilizing the key microRNA processing protein called KH-type splicing regulatory protein,” said Huang.
Lead author Martin Mueller, who helped develop the rat perinatal brain injury model, was surprised at the consistency of the results from both the in vivo and in vitro studies. “Collectively, our findings suggest that sPIF mitigates brain damage through a novel pathway,” said Mueller. “We saw more cortical brain volume and more neurons restored in brain damaged animals receiving sPIF.”
“For the first time, we have clear indication to pursue a new line of investigation in the treatment of perinatal brain injury, and possibly traumatic brain injury,” said co-author Dr. Michael Paidas, professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine.
Paidas, who is also vice chair of obstetrics at Yale, has helped to identify PIF’s effects with co-author Eytan R. Barnea, founder of the Society for the Investigation of Early Pregnancy (SIEP) and chief scientific officer of BioIncept, LLC. Barnea discovered and characterized PIF and described key elements of its mode of action.
Based on this promising data, the FDA has awarded sPIF fast-track designation and allowed a phase 1 sPIF clinical trial to treat patients with autoimmune liver disease at the University of Miami.
Forty per cent of female prisoners enter correctional system with a traumatic brain injury
A study published today found that almost 40 per cent of Ontario female prisoners have a history of traumatic brain injury (TBI). Unlike the men participating in the study, half of these women sustained a TBI before committing their first crime.
The study, led by Dr. Angela Colantonio, senior scientist, Toronto Rehabilitation Institute, was based on a survey of men and women in Ontario correctional facilities. Published in the Journal of Correctional Health Care, it is the first Canadian study of its kind.
Typically caused by a blow to the head, TBI is a leading cause of death and disability worldwide. It kills 11,000 Canadians every year. TBI is commonly caused by falls, motor vehicle collisions,physical assault or sports injuries.
"We observed a striking gender difference. Female inmates with a TBI, compared to males, were much more likely to have suffered physical or sexual abuse as children," said Colantonio, Canadian Institutes of Health Research (CIHR) Research Chair in Gender, Work, and Health, University of Toronto. "Our research suggests the need to screen offenders and others with a history of abuse for TBI."
Dr. Colantonio highlights the need to identify inmates or others at risk of incarceration with a history of a TBI so they can receive appropriate support and treatment. This will allow the system to help prevent future offences by better assisting with the transition back into society. For example, helping individuals secure and maintain employment.
"Right now, we don’t know very much about how brain injuries affect women in the correctional system," said Colantonio. "This study indicates a need for more research, and for programs that address TBI and mental health problems among people at risk of incarceration."
Such programs should include training for correctional staff to help them recognize TBI symptoms in inmates, such as slowness to act or a failure to respond to directions. This behaviour may be misinterpreted as defiance, resulting in punishment instead of treatment.
A report last year from the Office of the Correctional Investigator showed the number of women in Canadian prisons had increased 40 per cent since 2008. The same report also found that 85 per cent of incarcerated women said they had a history of physical abuse.
"Now that we have identified this as an issue, we need to work with community organizations and correctional systems to prevent inappropriate incarceration of females with traumatic brain injury and to provide treatment so they have a better chance when they return to society," said Dr. Geoff Fernie, institute director, research, Toronto Rehabilitation Institute.
What are the risks of post-traumatic stress disorder after an accident?
Many patients continue to suffer from symptoms (headaches, pain) several months after an accident, which can pose a real handicap to their lives. The team of Emmanuel Lagarde, research director at Inserm’s Research Centre for Epidemiology and Biostatistics (Inserm/University of Bordeaux) has studied the subsequent development of 1,300 people who were admitted to A&R between 2007 and 2009 for trauma. The researchers demonstrate that it is possible to identify people who will develop post-traumatic stress disorder, which generally occurs when the individual’s life was put in danger. This will enable their care to be adjusted accordingly. Their work also reveals that post-concussion syndrome, which has wrongly been defined as the consequence of cranial trauma, is only one part of post-traumatic stress disorder.
The results of the study have been published in the journal JAMA Psychiatry.
Every year, one in ten people in France are taken to A&E with a trauma following an accident. The large majority of the victims have only mild injuries and are discharged from hospital quickly. However, a number of them continue to suffer long after their direct injuries have healed. They may, for example, have headaches, uncontrollable fear or maladies of various kinds, vision problems, balancing problems or be irritable. When the symptoms occur simultaneously in a single context, they constitute what is called a syndrome.
Following a trauma, two syndromes are described: post-concussion syndrome (PCS), which occurs after a mild cranial trauma, and post-traumatic stress disorder (PTSD), which is encountered in people who have been exposed to a stressful situation wherein their life, or that of another person, was put in danger. Post-traumatic stress disorder was initially described in soldiers who, after exposure to combat or an explosion, complain of nightmares or obsessive thoughts which they are unable to get rid of. The two syndromes have been described for several years in the successive editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association, which is a current standard reference in the area of diagnosis in mental health.
In this study, 1,300 people who were admitted to A&E at the Bordeaux Hospital Centre between 2007 and 2009 were contacted three months after their accident. Over 500 were suffering from a mild cranial trauma when they were admitted to hospital while the others had various injuries, all either mild or moderate in severity. The researchers measured the occurrence of 36 symptoms which are included in the definitions of PCS and PTSD.
‘Post-concussion syndrome (PCS) does not deserve its name because, on the one hand, the symptoms that constitute it are not specific to cranial trauma and, on the other, they do not occur simultaneously. It seems that PCS is, in reality, only one part of post-traumatic stress disorder’, explained Emmanuel Lagarde, research director at Inserm.
Post-traumatic stress disorder in the general population
The results obtained also make it possible to have a better understanding of post-traumatic stress disorder, which is still insufficiently described for non-military contexts. In the general population, this disorder occurs in 2% of injured people but this figure rises to 9% when the trauma is cranial. However, it is more frequent among women and people who have been in a road accident or have been attacked. The occurrence of PTSD is also influenced by the state of the victim’s physical and mental health before the accident. All this information can enable doctors to determine if early treatment should be provided.
This study puts the classification of post-traumatic complaints into question because it also questions the very existence of post-concussion syndrome, which should be seen as only one part of post-traumatic stress disorder. These results do not, however, question the reality of the suffering of a significant number of people affected by this disorder, for whom the symptoms continue to persist and considerably impact the quality of their lives.
‘This is why it is necessary to describe these syndromes and their origin more accurately, particularly because identifying them also has important consequences in terms of insurance, compensation and the care and rehabilitation policies of patients’, stressed Emmanuel Lagarde, who is the main author of this work.
Variations in Neuronal Networks Could Explain Traumatic Brain Injury Outcomes
A team of researchers at the Neuroscience Institute at Georgia State University has discovered that hidden differences in the properties of neural circuits can account for whether animals are behaviorally susceptible to brain injury. These results could have implications for the treatment of brain trauma.
People vary in their responses to stroke and trauma, which impedes the ability of physicians to predict patient outcomes. Damage to the brain and nervous system can lead to severe disabilities, including epilepsy and cognitive impairment.
If doctors could predict outcomes with greater accuracy, patients might benefit from more tailored treatments. Unfortunately, the complexity of the human brain hinders efforts to explain why similar brain damage can affect each person differently.
The researchers used a unique research animal, a sea slug called Tritonia diomedea, to study this question. This animal was used because unlike humans, it has a small number of neurons and its behavior is simple. Despite this simplicity, the animals varied in how neurons were connected.
Under normal conditions, this variability did not matter to the animals’ behavior, but when a major pathway in the brain was severed, some of the animals showed little behavioral deficit, while others could not produce the behavior being studied. Remarkably, the researchers could artificially rewire the neural circuit using computer-generated connections and make animals susceptible or invulnerable to the injury.
“This study is important in light of the current Obama BRAIN initiative, which seeks to map all of the connections in the human brain,” said Georgia State professor, Paul Katz, who led the research project. “it shows that even in a simple brain, small differences that have no effect under normal conditions, have major implications when the nervous system is challenged by injury or trauma.”
Results of this study were published in the most recent edition of the journal eLife. The lead author on the study, Dr. Akira Sakurai, made this discovery in the course of doing basic research. He was assisted by Ph.D. student Arianna Tamvacakis from Dr. Katz’s lab.
(Source: news.gsu.edu)
German doctors highlight the potential dangers surrounding headbanging in a Case Report published in The Lancet. Ariyan Pirayesh Islamian and colleagues from the Hannover Medical School, detail the case of a man who developed a chronic subdural haematoma (bleeding in the brain) after headbanging at a Motörhead concert.
In January 2013, a 50-year-old man came to the neurosurgical department of Hannover Medical School with a 2 week history of a constant worsening headache affecting the whole head. Although his medical history was unremarkable and he reported no previous head trauma, 4 weeks before he had been headbanging at a Motörhead concert.
A cranial CT confirmed the man had a chronic subdural haematoma on the right side of his brain. Surgeons removed the haematoma (blood clot) through a burr hole and used closed system subdural drainage for 6 days after surgery. His headache subsided and he was well on his last examination 2 months later.
Headbanging refers to the violent and rhythmic movement of the head synchronous with rock music, most commonly heavy metal. Motörhead, undoubtedly one of the greatest rock’n’roll bands on earth, helped to pioneer speed metal where fast tempo songs that have an underlying rhythm of 200bpm are aspired to.
Although generally considered harmless, headbanging-related injuries include carotid artery dissection, whiplash, mediastinal emphysema, and odontoid neck fracture. This is the first reported case showing evidence that headbanging can cause “chronic” subdural haematoma.
"Even though there are only a few documented cases of subdural haematomas, the incidence may be higher because the symptoms of this type of brain injury are often clinically silent or cause only mild headache that resolves spontaneously", explains lead author Dr Ariyan Pirayesh Islamian.**
"This case serves as evidence in support of Motörhead’s reputation as one of the most hardcore rock’n’roll acts on earth, if nothing else because of their music’s contagious speed drive and the hazardous potential for headbanging fans to suffer brain injury."