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Jack Sisson's TBI Blog

A hug is duct tape for the soul.

 

From Fox News:


In one study, individuals with a history of traumatic brain injury had significantly higher occurrence for psychiatric disorders and suicide attempts.

There have been a lot of questions about country singer Mindy McCready’s substance abuse and its association with her recent suicide. But the question we should be asking is: “Did Mindy McCready’s brain injury kill her?”

Many people know about Mindy’s violent relationship with the father of her oldest son, Billy McKnight. McKnight was arrested in 2005 on charges of attempted murder for beating and choking Mindy. Mindy suffered from seizures and she attributed her brain injury to the abuse by McKnight.

It seems as though every day there is another story about a man abusing his wife or girlfriend. But we rarely hear about the link between domestic violence and traumatic brain injury.

According to a 1999 study by Dr. Kathleen Monahan and Dr. Daniel O’Leary, more than 90 percent of all injuries secondary to domestic violence occur to the head, neck or face. Drs. Helene Jackson, Elizabeth Philip, et al., studied 53 women living in a domestic violence shelter in 1998 and found the women experienced five brain injuries in the prior year and almost 30 percent reported 10 injuries the prior year. In 2003, 99 battered women were studied by Dr. Eve Valera, who found 76 percent sustained at least one brain injury caused by their partner and 50 percent sustained multiple brain injuries.

There are many ways the victims of domestic violence can sustain a brain injury: a blow to the head with an object, pushed against a wall or any other solid surface, punched in the face or head, strenuous shaking of the body, falling and hitting their head, being strangled, near drowning or being shot in the face or head.

The Jackson Philip study conducted in three domestic violence shelters showed 92 percent had been hit in the head by their partners, most more than once; 83 percent had been both hit in the head and severely shaken; and 8 percent of them had been hit in the head more than 20 times in the past year. 

The more often they had been abused, the more frequent were their symptoms and 40 percent reported a loss of consciousness. In a study of 46 victims of domestic violence conducted by Dr. John Corrigan and his colleagues, 67 percent had symptoms associated with traumatic brain injury and 30 percent reported loss of consciousness after a blow to the head.

These repeated brain injuries can lead to increased problems cognitively, physically and emotionally, which just exacerbates the vicious cycle of the violent relationship. These victims typically lack the knowledge about their brain injury so they do not seek services related to their injury. Also, the professional system to help victims of domestic violence is often unaware of the correlation between this crime and traumatic brain injury. By not linking the psychodynamic issues between the assault and their brain injury, professionals are not referring these victims to appropriate rehabilitation services.

Having one traumatic brain injury increases the likelihood of another TBI. Following just a single brain injury, a person’s reaction time may be slower, judgment may be off, and may be more impulsive and inattentive to prevent future brain injuries. Because of the nature of domestic violence, victims are susceptible to repeated injuries, which increase symptoms. These symptoms may include difficulty concentrating, confusion, difficulty making decisions and solving problems (which appears as poor judgment to the public), headaches, memory problems, depression and feeling overwhelmed. 

And in a violent relationship the abuser is likely controlling the victim’s access to medical care or rehabilitation services as well not making the necessary adjustments those with brain injuries need.  According to one study, “Pattern of Re-assault in Batterer Programs,” the recidivism rate among psychologically untreated batterers is almost 61 percent.

Domestic violence is the leading cause of injury to young women ages 15 to 44.  The frequency of physical abuse within a relationship tends to increase and become more violent over time.  More than 70 percent of women who sustain injuries due to domestic disputes are injured after they separate from their partner or spouse -- and one woman is beaten by her husband or partner every 15 seconds in the United States.  About 95 percent of all victims of domestic violence are women, and approximately 50 percent of all homeless women and children in the United States fled from a domestic violence situation.

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From Reuters:


Researchers found that people who ate or drank lots of coffee, tea, oranges and red wine were just as likely to develop neurological problems over the next 14 years as those who skimped on antioxidant-rich foods.


"The literature on antioxidants and dementia has been mixed," said Elizabeth Devore, who led the new research at Brigham and Women's Hospital in Boston.

Although there's some evidence that specific vitamins have a protective effect in the brain, she said it's unclear whether that's the case for all antioxidants - which include vitamin C, vitamin E, selenium and flavonoids.

"There is the thought that overall antioxidants might be helpful, but it's also true that if you actually look at the individual antioxidants, there's not necessarily a reason to think that one would behave exactly the same way in the body as the next."

The Netherlands-based study included 5,395 people aged 55 years and older, who reported their usual consumption of 170 different foods in 1990.

Devore and her colleagues tracked those participants over the next 14 years, during which 599 were diagnosed with dementia - including 484 with Alzheimer's disease - and 601 had a first stroke.

People who consumed the most antioxidants, according to an analysis of their diets, were just as likely to end up having either of those neurological disorders as study participants who hardly got any antioxidants.

That pattern held after the researchers took into account people's ages, how much they ate in general and whether they smoked, according to the findings published Wednesday in Neurology.

There was also no link between total dietary antioxidants and white or gray matter volume in the brain, according to scans done on 462 of the participants.

Since the study looked only at foods consumed, it can't address whether antioxidant supplements may impact dementia or stroke risk, according to Devore.

Her team concludes that it's still likely certain individual antioxidants have positive effects on the brain.

"There have been a number of studies that have shown that higher intake of dietary vitamin E is associated with lower risk of dementia," Devore told Reuters Health. The same goes for vitamin C and stroke risk, she added.

That suggests people should continue eating plenty of fruits and vegetables, including berries, and seek out specific antioxidants, she said.

"For dementia specifically and stroke specifically, if you're worried about those… you should try to take in vitamin E for dementia and vitamin C for stroke."

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Wow, this is a major step forward for prisons....in Scotland, that is. Yes, Scotland is showing an admirably progressive stance in calling for all prisoners to be tested for signs of brain injury. Again, this is something Jack has been trying to get the United States to do for years. Let's hope Scotland is successful in getting this implemented. One more argument for our side as we continue to struggle here in America.


From Scotsman.com:

PRISONERS in Scotland’s jails should undergo tests for signs of brain injury and be prescribed mood-altering drugs to help bring down re-offending rates, according to experts.

Studies have shown that up to half of the prison population have suffered brain trauma caused by accidents and assaults that could be a factor in persistent offending.
Now the Howard League Scotland, a penal reform charity, is urging the Scottish Prison Service to introduce screening programmes to pick up injuries that could be treated using drugs. Research has found that criminals with attention deficit hyperactivity disorder (ADHD) – which can be caused by brain injury – who took drugs such as Ritalin were between 32 and 41 per cent less likely to re-offend.
Trials of screening systems are already taking place south of the Border, including at HMP Leeds, and will be rolled out to include young offenders found to have traumatic brain injury.
The Howard League believes Scotland should also become a test base, as while crime has fallen to a 37-year low, re-offending rates have remained high, with 42 per cent of offenders committing another crime within two years.
A spokeswoman for the Howard League Scotland added: “There is a need to better understand the complexity of issues that contribute to offending behaviour. Research suggests a higher incidence of traumatic brain injury (TBI) amongst the prison population than in the population at large, and this clearly has implications for those working across the criminal justice system.
“Howard League Scotland has written to the chief executive of the Scottish Prison Service to highlight these findings and to emphasise the importance of early identification of those with a history of TBI.
“This holds the key to enabling effective rehabilitation and, within a custodial setting, ensuring that those affected are offered the most appropriate treatment.”
According to researchers, although brain injuries can affect judgment, memory and behaviour and lead to a pattern of offending, this “hidden disability” can go unrecognised and untreated.
Professor Huw Williams, a neuropsychology expert from Exeter University who has carried out brain injury research in prison populations, said: “Given the prevalence of brain injuries in the prison population, it is very important that judges and sheriffs do know if it has been a factor in a person’s behaviour.

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From PsychCentral:


At 3 a.m., wearing pajamas and socks, an 89-year-old man with Lewy Body Dementia was found by a security guard four floors below his apartment. His walker was later found abandoned on the second floor. Agitated and confused, he insisted repeatedly that he was looking for his “other” apartment. “I know we have two, exactly alike, one that we sleep in at night,” he said. “But I can’t find the other one.”

A 65-year-old woman diagnosed with early-onset Alzheimer’s Disease had what had become a typical spat with her spouse of 40 years. He argued, furious and insulted, “I’m your husband! Don’t you know me?!” “You look exactly like him,” she said quietly, “but I know that you’re not him.” Nothing could convince her otherwise, though the man told her many things only her husband would know. “You are one of the two imposters that come around here, not my husband,” she insisted.

Are these the plots of psycho-thriller movies? Scary stories told around a campfire? Disturbing dreams? No – they are two examples of a neuropsychological condition called Capgras Delusion or Capgras Syndrome, also known as the “Imposter Syndrome” (Hirstein and Ramachandran, 1997).

Capgras Syndrome, named for Joseph Capgras, the French psychiatrist who first described it, also can be seen occasionally in people who are psychotic (typically schizophrenic), or where there has been some type of brain injury or disease (Hirstein and Ramachandran, 1997). Regardless of its source, it can be equally perplexing and upsetting for the person experiencing it as it is for those around him or her to encounter it.

Within psychiatry and psychology, Capgras is considered extremely rare (Ellis and Lewis, 2001, Hirstein and Ramachandran, 1997). There is evidence, however, that it is not as rare as most clinicians believe. It is “uncommon,” but often overlooked (Dohn and Crews, 1986). From my own experience as the director of care for a home care agency, I concur: I see it often enough within my population of people with Alzheimer’s and other related dementias (ADRD) that it is likely not extremely rare.

While Capgras may not be typical, it certainly deserves to be better known both by the general public and among helping professionals. For those of us who love or work with such patients, we need to know how to manage the challenging behaviors that arise from it. Assessment of such patients’ potential danger to others needs to be performed (Silva, Leong, Weinstock, and Boyer, 1989). Awareness of the presence of Capgras also will help caregivers and families know how to better manage their own behavior around and feelings about its symptoms, particularly for the sake of those who are deemed “imposters.”

What Causes Capgras Syndrome?

It’s not known for certain what causes Capgras, but researchers have evolved several credible theories. One is from neurologist V.S. Ramachandran (Ramachandran, 2007). Ramachandran believes that a malfunction between the brain’s visual cortex and the emotional feeling of “familiarity” causes the sufferer to think he or she is seeing a perfect duplicate, not the real thing. The eyes are reporting correctly, but emotions of familiarity aren’t present. The conclusion: here’s an exact imposter.

Ramachandran also reports that a brain injury patient with Capgras was able to correctly identify his mother when he heard her on the phone, but not when he saw her. He hypothesizes that sounds may be correctly connected to the feelings of familiarity in some cases (Ramachandran, 2007).

There are several features particular to Capgras:
  1. The patient has a brain injury or disease.
  2. He or she recognizes that a person or place is exactly like the “real” one, but insists it is not.
  3. The imposter always is a person or place with which the patient is familiar, not a stranger, vague acquaintance, or a new place.
  4. The problem does not fruitfully yield to psychological analysis or interpretation; it is a biological disorder.
Prosopagnosia, a better-known form of facial misidentification, differs from Capgras in that it causes a total inability to recognize previously familiar faces (Ellis and Lewis, 2001). Capgras includes easy recognition of the face, but disagreement about the person’s true identity.

Are Capgras Sufferers Potentially Dangerous?

There are some reported cases where those suffering from Capgras delusion have become dangerous to others, with violent behavior resulting in injury and even death. There is very little research on this subject and not much information with which to reliably predict violence — which is striking given that great hostility and resentment are typical of how sufferers of Capgras view “imposters.”

In a paper by Silva, Leong, Weinstock, and Boyer (1989), they stated that at that time there was little published on the subject of danger and Capgras. A further search in the literature for this article found no papers published later than that date. 

Continue reading at PsychCentral

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Thousands of nerve fibers in it help us eat, drink and swallow. Without them, we would not taste. The tongue helps us speak. Quietly, its surface defends our bodies from germs.
Yet for everything the tongue can do, perhaps one of its most exciting roles is to serve as a direct "gateway" to the brain through thousands of nerve endings.
Now researchers at the U.S. Army Medical Research and Materiel Command in collaboration with the University of Wisconsin-Madison and NeuroHabilitation Corporation are leveraging the power of those tiny nerves. They are aiming to restore lost physical and mental function for service members and civilians who suffered traumatic brain injury or stroke, or who have Parkinson's or multiple sclerosis.
 
The treatment involves sending specially-patterned nerve impulses to a patient's brain through an electrode-covered oral device called a "PoNS," a battery-operated appliance placed on the tongue. The 20-30 minute stimulation therapy, called cranial nerve non-invasive neuromodulation, or CN-NiNM, is accompanied with a custom set of physical, occupational, and cognitive exercises, based on the patient's deficits. The idea is to improve the brain's organizational ability and allow the patient to regain neural control.

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From Evansville Courier & Press:

It has been more than 60 years since the Harlow studies demonstrated the key role of touch in the normal development of baby rhesus monkeys. Since then, there has been a steady parade of studies supporting the important role of touch in the development of people of all ages. Touch has both psychological and physiological impact and we need touch to develop normally throughout the life cycle.

While other important senses such as vision and hearing usually decline as a normal part of the aging process, touch remains a viable and important sense. Just as the importance of touch increases, many seniors become more seriously touch deprived. In fact, they experience less touch than any other age group.

Touch appears to be such a simple behavior; why then are so many seniors touch deprived? Ours is a culture that is ambivalent toward seniors. On one hand, growing old is considered to be a significant achievement. On the other hand, judging from our popular culture, looking old is not desirable. We go to great lengths to keep from appearing old. This attitude that old is not attractive is probably one of the major reasons for touch deprivation in seniors.

Not all seniors desire to be touched, and we need to be sensitive to this preference. While touch reassures and conveys concern and love, it enters into the senior's private space. In particular, touch between men is, well, a touchy situation. Touch may be a symbol of status or power and that defeats the positive emotional impact of touch. Often letting seniors be the initiators of touch can be the most important clue to their needs and desires.

Being careful with touch is also appropriate for other reasons. Many of these deprived seniors are in their late 70s and 80s. By this time, skin-related changes affect the relationship between touch and seniors. Much of the fatty tissue that pads the skin is gone. Our skin has become thin and transparent and is much more vulnerable to injury. We need to be more careful that touch does not break or bruise the skin. Even though a hand massage may be therapeutic, massages need to be more carefully implemented since arthritis is often an issue.

Seniors who live alone in their homes or in assisted living facilities and nursing homes are most likely to be touch deprived. These folks live in situations that do not naturally invite hugs. Relatives and friends, whose touch is most likely to be welcomed, can consider making hugs and touches on the arms, shoulders or hands part of their visits, but they should be gentle.

The folks who care for our seniors in institutional settings have a major role in implementing touch. Not only do they supplement touch by family and friends, they may actually replace it. Often institutionalized seniors have no relatives or friends to see them on a regular basis. Staff members are in a key position to implement touch on a daily basis. Unlike other medical procedures, touch costs nothing and requires little effort, yet the payoff is enormous.

Finally, therapeutic pets are an important source of touch. There is nothing like a gentle dog to bring a smile to the face of a resident. Therapy dogs should be much more widely used in institutions because their touch, or lick as the case may be, provides what seniors really need, unconditional affection.

Link to Evansville Courier & Press.

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From PsychCentral:


A recent study has found that U.S. soldiers returning from Iraq and Afghanistan with mild traumatic brain injury (TBI) have measurable abnormalities in the white matter of their brains — described by scientists as “potholes.”

According to psychiatrists with University of Iowa Health Care, TBI — including concussions — is one of the most common types of neurological disorder, affecting approximately 1.3 million Americans annually. It has received more attention recently because of its impact on two groups of patients: professional athletes, especially football players; and soldiers returning from war with blast-related TBI.

It is estimated that 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan have experienced TBI.

“In the military population we studied, patients with TBI have more alterations, sometimes called ‘potholes,’ in the white matter of their brains than patients without a history of TBI,” said senior study author Ricardo Jorge, M.D., UI professor of psychiatry.

“The more severe the injury, the more white matter abnormalities occur. There is also a correlation between increased numbers of potholes and increased severity of cognitive alterations in executive functions — the ability to make a plan or a decision, for example.”

The researchers note that, despite its prevalence, diagnosing mild TBI is difficult. They often have to rely on a patient’s recollection of a possible past head injury.

In addition, symptoms of mild TBI tend to be wide-ranging and non-specific, including problems with vision, hearing, balance, emotions, and thinking, researchers said, noting there are few tools available to identify the condition or monitor the brain’s recovery or deterioration.

Jorge and his research team used an MRI-based brain-scanning technique called diffusion tensor imaging (DTI) to study the brains of 72 veterans with mild TBI and 21 veterans without mild TBI.

DTI measures the diffusion of water along the thin fibers known as axons that form connections between brain cells. When axons are intact, water flow follows the axon boundaries and has a well-defined direction, researchers explained.

When the axon is damaged, water diffuses in many directions, a situation referred to as low fractional anisotropy. ”Decreased directionality of the water diffusion is a measure of lower integrity in the white matter,” Jorge said.

Analysis of the DTI data allowed the researchers to detect areas of lower integrity in the patients’ white matter even though these potholes are scattered randomly throughout the brain and occur in different places in different patients.

Veterans with mild TBI had significantly more potholes than veterans without TBI, the researchers report. The difference was not influenced by age, time since trauma, a history of mild TBI unrelated to deployment, or coexisting psychological problems like depression, anxiety, or post-traumatic stress disorder (PTSD).

The number of potholes did, however, correlate with poorer performance on cognitive tests measuring decision-making and planning skills, the researchers noted.

The team also examined the brains of civilians with non-combat-related mild TBI who were assessed early after the injury. The researchers found that these patients have even more white matter potholes than the military group.

Although the results suggest that DTI measurements might hold promise as a tool for detecting and tracking mild TBI, Jorge cautioned that the current study is not large or specific enough to confirm that DTI-detected potholes are a biomarker for TBI brain damage.

“To establish if this DTI approach is a useful technique for diagnosing mild TBI, we need to replicate these findings in a larger study and with patients who have mild TBI from other causes,” he said.

The study was published online in the American Journal of Psychiatry.

Source: University of Iowa Health Care


Link to PsychCentral.

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From The Monitor:

About two dozen local people are helping researchers find a way to prevent dementia.

The University of Texas Health Science Center is looking for more people to help them find answers to this question.

The Regional Academic Health Center in Harlingen is one of about 30 sites in the country where the study is being conducted, Dr. Sara Espinoza, the local principal investigator, said.

The study is called Aspirin in Reducing Events in the Elderly. The study’s principal investigator is Dr. Richard Grimm, medical director of the Berman Center for Outcomes and Clinical Research in Minneapolis.

“We know that aspirin prevents heart disease and stroke in middle-aged people,” said Espinoza, an associate professor of medicine at the UT Health Science Center in San Antonio. “There is some evidence that aspirin may prevent dementia or cognitive impairment.”

Past studies suggest that aspirin, as an anti-inflammatory drug, could be a protective for dementia, she said.

The study includes persons 65 and older who are in good health. Some will be given aspirin; others will take a placebo. They will then be monitored annually for five years. Harlingen residents participating in the study are tested and examined at the RAHC’s Clinical Research Unit.

Espinoza said the study has far-reaching effects because conditions such as dementia, including Alzheimer’s disease, could be caused by inflammation.

Diabetes is considered an inflammatory condition, and that can lead to disability. Therefore, the study is also being conducted to see if aspirin can reduce the possibility of people becoming disabled to the point where they are unable to care for themselves.

The study is also being conducted at sites in Australia, begun about two years ago. Espinoza said the study’s operators intend to enroll people in the program until December, but the deadline could be extended.

The South Texas site, which includes the RAHC as an extension of the University of Texas Health Science Center in San Antonio, has about 219 subjects enrolled, Espinoza said, with 25 to 30 enrolled in Harlingen.

She would like to see more local residents enrolled in the program.

“We can enroll as many who want to be enrolled,” she said. “We have no limit on how many are enrolled.”
Link to The Monitor.

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From Fox News:

Certain forms of dementia may be caused by a gene mutation that makes proteins in the brain clump together, a new study finds.

The most common cause of frontotemporal dementia and a motor neuron disease called amyotrophic lateral sclerosis (ALS, or 
Lou Gehrig's disease) is a genetic mutation that creates extra copies of a DNA sequence, but the actual mechanism of the diseases is unknown. A team of researchers has now found that proteins, molecules that normally help cells function, are being produced from the mutated gene and appear to be causing the clumping seen in both those diseases.

The findings, described online Feb. 7 in the journal Science, could explain how these diseases arise and might even be treated.

About 10 percent of FTLD (frontotemporal lobar degeneration) and ALS patients have a mutation in the C9orf72 gene, which contains a short repeated DNA sequence. Healthy people have about 25 repeats of this sequence, but there are hundreds of repeats in these patients. Their brains exhibit telltale clumps of proteins in the hippocampus and cerebellum regions.

While proteins in other forms of dementia are known, patients with this mutation have clumps of other, unknown proteins, said study co-author Dieter Edbauer, a neuroscientist at Ludwig Maximilian University of Munich, in Germany. The mutated gene lacks the label that normally tells cells to start making a protein, and is located in a stretch of the DNA that isn't normally active.

Protein mystery

Edbauer and his colleagues hypothesized that if the gene were somehow activated, it would cause three different proteins to be made, and these proteins would aggregate in cells and cause disease.

To test their hypothesis, the researchers took both diseased and healthy brain tissue from deceased patients and filtered it through a fine mesh. Clumps of brain tissue from the patients got stuck in the mesh. By making antibodies (proteins produced by the body to target and fight off foreign invaders) that recognized the three specific proteins, the scientists were able to determine that these were the proteins in the clumps.

"This study helps to resolve a major question about how C9orf72 mutations cause FTD and ALS," said neurologist Adam Boxer of the University of California, San Francisco, who was not involved in the study.

"It suggests that these mutations can lead to creation of a new toxic protein that aggregates and accumulates in cells, similar to other neurodegenerative diseases such as Huntington's and Alzheimer's, which are also associated with toxic protein aggregates," Boxer told LiveScience.

Others agree that the findings, if replicated, will be important. "It would be good to confirm their results using an independent method," said neuropathologist Ian Mackenzie of Vancouver General Hospital and the University of British Columbia, in Canada.

Understanding the diseases

There are several possible explanations for how the proteins are being made. One is that the ribosome, the cellular machinery that reads genetic instructions to make proteins, is misreading the mutated gene. Another possibility is that the repeated sequence is forming a hairpin shape that attracts the ribosome and tells it to make proteins.

It's unclear whether the clumps are causing the diseases or are simply markers. If the protein clumps are in fact responsible, scientists might be able to treat the disease by getting rid of those proteins, Edbauer said.

FTD and ALS are characterized by personality changes, language abnormalities and movement disorders, which often appear before the age of 65. There is currently no cure.

Link to Fox News.

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From PressConnects.com:


Concussions or mild traumatic brain injuries inflicted on thousands of U.S. troops who fought in Iraq and Afghanistan may be linked to post-traumatic stress disorder and suicide, according to new research.

Mild TBI, often caused by exposure to makeshift bomb explosions, can be difficult to identify and have lasting effects, according to two studies published in the latest issue of The Journal of Head Trauma Rehabilitation.

“What these papers say to me is that there is something to TBI, and particularly military TBI, producing specific abnormalities in the brain that lead to more vulnerability to PTSD and to suicide,” says Dan Perl, a neuropathologist and lead investigator at the Pentagon’s brain repository research center.


Suicides in the military increased to record levels last year: There were 349 potential cases in 2012, a 13percent increase over the previous record of 310 suicides in 2009, according to Pentagon data.

Mild brain damage from a blast has been called the signature wound of the Iraq and Afghanistan wars because improvised explosive devices, or IEDs, have been so commonly used against U.S. troops.

Scientists warned that it was crucial to identify mild TBI and allow time for troops to recover because back-to-back head injuries could cause permanent damage. Military doctors have worked hard in recent years to identify the wound and pull servicemembers from combat. The most recent military data show that in early 2011, an average of 16 mild TBIs per day were diagnosed.

Diagnosis was based on momentary loss of consciousness, dizziness, headaches or difficulty concentrating after a soldier is caught in the blast wave of an IED.

But in a study of 52 combat veterans funded by the Department of Veterans Affairs at the University of Rochester School Medicine, scientists using a new, more sensitive MRI scan found brain lesions in servicemembers who were exposed to a blast, but who had not reported any of the classic symptoms.

In addition, the damage was linked with cases of severe PTSD, underscoring a theory that these lesions can render a person more susceptible to developing that mental illness.

“Is there some kind of vulnerability (to PTSD) that is imparted on the brain by repeated bomb blasts?” says Jeffrey Bazarian, lead author. “In addition, are the current tests that rely purely on symptoms to diagnose concussion from blast adequate?”

Other research by the National Center for Veterans Studies found that troops in combat who suffered less severe cases of mild TBI actually had a higher risk of suicidal thoughts than those whose brain injury symptoms, such as loss of consciousness, were more severe.

“Other studies have also reported that psych symptoms such as insomnia and depression may be worse for less severe TBIs. But this is the first to show the same holds true for suicide risk,” says Craig Bryan, assistant director for the national center and the paper’s lead author.

Link to PressConnects.com.

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From CBS News:

Maintaining physical fitness through middle age could go a long way in staving off dementia, new research suggests.

The study, published Feb. 4 in the Annals of Internal Medicine, found middle-aged adults who were in shape were significantly less likely to develop dementia or Alzheimer's disease by the time they reached 65 compared to their unfit counterparts.

The new research adds evidence for an effective way to avoid a disease that currently cannot be prevented, slowed or cured. About 5.3 million Americans are affected by Alzheimer's disease, according to federal estimates, and by the 2050, that number is expected to at least double. Alzheimer's is the sixth-leading U.S. cause of death, killing almost 84,000 Americans each year.

"Alzheimer disease and other types of dementia (all-cause dementia) are important public health problems, particularly in light of the aging population," write the researchers, led by Dr. Laura DeFina, medical director of research at The Cooper Institute in Dallas. "Because of the effect of dementia on quality of life and functional status, identifying preventable causes of dementia is critical."

Researchers looked at more than 19,000 middle-aged individuals who were given a treadmill exercise test as part of a preventive visit to a doctor's office that occurred at a Texas clinic between 1971 and 2009. They eventually compared these results to available Medicare data on the individuals' health claims to determine whether or not they developed dementia.

Based on the amount of time those individuals could run on a treadmill, participants were divided into groups "most" and "least" fit. The researchers discovered more than 1,600 cases of dementia among the group, and a closer look revealed those who were most fit at an earlier age were about 40 percent less likely to develop dementia compared to those with the lowest fitness levels.


The study was observational, meaning it did not prove cause-and effect, nor did researchers determine a level of fitness required to avoid dementia and Alzheimer's. However, they speculated that better fitness could reduce risks of diabetes and hypertension, which are established risk factors for dementia.

The authors hope the findings may influence adults to hit the gym and increase their fitness levels.

"Physical activity changes in midlife may lead to improved fitness levels, resulting in less all-cause dementia with aging," they wrote.

Hearing loss may be linked to dementia
Beta blockers may stave off dementia, study suggests
Upcoming Alzheimer's studies may change how disease is treated
The study also had limitations in that other factors may also have influenced the findings, since it did not measure other protective behaviors like healthy eating, which may have been common among the most physically fit participants.

However, this is far from the first article to suggest fitness is a risk factor for dementia and Alzheimer's.

A recent MRI study in the Oct. 23 issue of Neurology found adults who engaged in physical activity reduced risk for "brain shrinkage," a precursor to Alzheimer's.

An August 21 study in Neurology found obese middle-aged adults were more likely to experience declines in memory and cognitive skills compared to normal-weight adults.

In an accompanying editorial published in the same journal issue, Dr. Mary Sano, professor of psychiatry and director of Alzheimer's disease research at Mount Sinai School of Medicine in New York City, wrote that this study adds to the "tidal wave of evidence" that physical fitness could bring about benefits across many different areas of health, including prevention of dementia.

"Unfortunately, adherence to exercise regimens is notoriously difficult," she wrote. Sano argues that people are most likely to exercise in the face of health issues, and a healthy person may ignore such warnings from doctors.

"Nevertheless, Alzheimer disease is the second most feared disease among U.S. adults, behind only cancer," according to Sano. "This fear may provide both the context for physicians to introduce the topic of physical activity and the motivation for patients to heed advice to increase physical activity."

Link to CBS News.

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From The Verge:

A SAFER HELMET HAS BECOME FOOTBALL’S HOLY GRAIL

If you were one of the viewers who helped make last night’s Super Bowl among the most-watched television events in history, you may not have spent much time worrying about the players’ safety. But if so, the NFL wanted to make sure you knew it shares your concern. As part of a long-running effort, the league ran several ads on the topic, the longest of which recapped a century of safety advances. As SB Nation’s Jon Boisexplained, the spot alludes to rule changes from the elimination of "flying wedge" blocking formations to the prohibition on horse-collar tackles. Unsurprisingly, though, the commercial emphasized the evolution of the football helmet, from a thin piece of leather to today’s advanced plastic shells, complete with face guard. And while the NFL and its partners continue to improve safety — from rule changes to high-tech devices like injury-detecting cameras — the helmet has taken center stage.

That’s because in recent years the questions around player safety have changed. Concern about broken bodies has begun to center on that most complicated part of the human anatomy: the brain. Since at least 2009 the league has wrestled with the problem of Chronic Traumatic Encephalopathy (CTE), a degenerative brain disease. Research suggests a link between CTE and the sort of brain injury a football player might suffer hundreds or even thousands of times in his career — that includes concussions that lay a player out as well as "sub-concussions," minor traumas that easily go undiagnosed. CTE-afflicted individuals suffer from dementia and depression; several former players have committed suicide and been posthumously diagnosed with CTE, including 12-time Pro Bowl linebacker Junior Seau, who last March shot himself in the chest. (The NFL's 30-second commercial, titled "Protecting the game," features three players among the 4,000 involved in concussion-related lawsuits against the league.)

In the wake of such high-profile tragedies, the NFL — along with football fans, players, and coaches everywhere — has had to face the realization that what used to be called "bell ringers" are in fact serious brain injuries. Football, in other words, now has to understand the brain. Football has to get smarter.

That means first understanding CTE, and then taking steps to prevent it. The condition first came to light in 2002. The body of Mike Webster, a former Steeler who’d died of a heart attack, showed a brain clogged with tau proteins, a condition associated with Alzheimer’s disease. Before his death Webster had suffered depression and a downward spiral. "Iron Mike" had gone from being a Hall of Famer, maybe one of football’s greatest centers, to penniless and sleeping in his car. He was just 50 when he died.

Bennet Omalu, the pathologist who diagnosed CTE in Webster, soon found the condition in other athletes. Other researchers followed; CTE appeared not just in long-retired professional players, but in high-school players as well. Unfortunately, the only way to diagnose CTE was posthumously, when the subject’s brain could be sectioned and examined.

That changed only recently, when UCLA researchers using proprietary brain-imaging techniques identified tau proteins in five still-living ex-NFL players. The tau buildup fit the pattern for CTE; all the players had suffered at least one concussion during their careers, reinforcing the link between brain trauma and CTE.

Which brings us back to helmets. Protecting the head means protecting the brain, the intuition goes, so a race has begun to build a better helmet. But it’s not an easy problem to solve. Football is a contact sport, with players who are almost by definition physical anomalies: they are stronger and faster than average human beings, and they’re stronger and faster than they were even a decade ago. (Former Vikings quarterback Fran Tarkenton wrote a recent op-ed for the Wall Street Journal, noting that when he was a player forty years ago, few lineman weighed more than 250 pounds; today they’re routinely more than 300 pounds. Tarkenton offered this as evidence the league isn’t quite as vigilant about performance-enhancing substances as it would like to claim.) When large men traveling at high speeds hit one another, it doesn’t take a physics major to predict the results.

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From The Times Picayune:

Ex-NFL quarterback John Fourcade keeps a framed photo of a 1990 game. He’s wearing aSaints uniform and eyeblack. It’s the first quarter under the dome in Minnesota, with 56,000 fannies in the seats. Fourcade’s is on the turf.

The camera caught him head-on, helmet off, eyes glazed. Three team staffers kneel around him. He seems to stare into nothingness.

“I’m in another land. Dazed and confused.” Fourcade said, glancing at the print in his Marrero bedroom. “I went back in a few plays later and played the rest of the game.”

Soon after, he threw a perfect pass, he says – to a Vikings linebacker.

“He caught it and ran down the sideline. I said, ‘Okey dokey.’ I didn’t bother chasing him.”

These days, Fourcade wakes up every day in pain that he attributes to hits like the one he took that day.

Stiff headaches squat above his eyeballs, he says. Fourcade beats them back with Vicodin, Tylenol, whatever’s handy. He “squinches” at bright lights, has trouble focusing at night. His vision blurs.

At 52, he creaks, he said, from a pair of cracked vertebrae. He’s had three operations on each knee, and three on each shoulder. One on a hand, another on an elbow.

Fourcade started all of 11 games as a pro. All told, he played in a few dozen NFL games. As a quarterback, he rarely got touched in practice, never facing the barrage of sub-concussive helmet shots that researchers now say can foster brain damage.

Still, Fourcade counts at least three concussions. The response, he said, was always the same: Smelling salts, “Where are you?” “How many fingers?” Back on the field.

Whether the head shots caused his problems is unknown, and possibly unknowable. But Fourcade has a hunch. He’s among more than 4,000 former NFL players enmeshed in a bitter legal battle with the league over damages and future monitoring and treatment.

“Yeah, I’m worried. I’ve been having headaches for years. I had Lasix (surgery). It hasn’t done anything,” Fourcade said of his vision problems, adding that he’s uninsured. “You come to a point, how much pain can a man take now? I’d like to be able to go see a doctor when I need it.”

The controversy over concussions and brain injury has taken center stage in the lead-up to Super Bowl 2013 in New Orleans -- a city with its own beef against the NFL. The local consensus: the league jettisoned the Saints’ season with excessive Bountygatepunishments out of self-interest, hoping to project a proactive stance on violence in the sport.

The league, meanwhile, has been busy this week touting its heavy support for new scientific research, player safety measures and an education campaign intended to reach sports youth, aiming to burnish its commitment to the issue.
But at the same time, the league is fighting to have the players’ suit tossed out before it really begins, and before details of the allegations – that the league shirked its duty to protect players and rebuked compelling research while promoting violent hits – emerge in a federal courtroom.

Nearly 300 players who at some point wore a Saints uniform are involved as plaintiffs against the league.

They range from the heralded to the hardly noticed. From Hall of Fame linebacker Rickey Jackson, who played in 227 games for the Saints and 49ers, to Cephus Weatherspoon, a wide receiver who is credited with playing a single game.

Many are linemen, the helmet-to-helmet infantrymen of the NFL who, according to some studies, suffer the greatest brain damage.

Among them, too, is Conrad Dobler, who played offensive guard in the 1970s and was named “pro football’s dirtiest player” by Sports Illustrated because of his penchant for spitting on players, punching them and kicking them in the head.

Some, like Klaus Wilmsmeyer, punted the ball.

Also on board are the families of several ex-players, such as heralded linebacker Junior Seau, who died and were later deemed to have suffered severe brain injuries,

Seau played 20 seasons in the NFL, then in May, at 43, committed suicide by shooting himself in the chest – possibly so his brain could be preserved for research. Brain specialists later diagnosed him with chronic traumatic encephalopathy, or CTE.

The neurodegenerative disease, associated with repeated head trauma, has now been discovered in the brains of several former NFL players, many of them suicides.

Seau’s death, along with the growing roster of ex-players who have joined the litigation, have only added steam to questions about the high-impact future of the game itself, from Pop Warner to the pros.

The ex-Saints involved in the lawsuit are a motley crew.

Tom Dempsey, who kicked a still-NFL record 63-yard field goal for the Saints during the 1969 season, now suffers from dementia that he suspects came from crashing into human wedges on kickoff returns.

Dempsey, 66, now struggles with his ABC’s, with memory loss, and with anger. He says he could use the money to help with treatments such as a hyperbaric regimen aimed at sending more oxygen to his brain. He wouldn’t mind some lagniappe either.

“I would like to make some money on it,” Dempsey also says, at home in Jefferson, where he now spends most of his days. “I think I earned it.”

Kyle Turley, the former offensive tackle who said he’s suffered seizures and vertigo in retirement, is on a mission to expose a league that he stridently believes looked the other way on concussions. Turley had planned to host an event focused on head injuries at LSU Health Sciences Center Thursday, but it was abruptly canceled without explanation.

Steve Baumgartner of Mandeville, a 61-year-old former lineman for the Saints and Houston Oilers in the 1970s, says he mostly joined the fight out of solidarity.

He is skeptical about claims that the NFL is guilty of neglect. Still, Baumgartner wouldn’t mind getting to the bottom of the pulsating in the back of his head. “It feels like my heartbeat is in my ears,” he says.

Pat Swilling, the former Pro Bowler and Dome Patroller, just joined the fray last week. Swilling said he took a look at his career and the growing chorus of research tying football to brain and spinal troubles, and that he’s trying to protect his rights and his family. He hasn’t suffered any ill effects yet, he says.

“I don’t think anyone knows exactly what’s going to happen to us older players as we move forward, especially the guys who played on the line of scrimmage,” said Swilling, 47. “Every down, I’m taking on a tight end or offensive lineman head-first. We’re talking about practice. How many blows to the head I’ve taken is countless. Hell, you’re talking about 15-20,000 blows to the head.”

Nobody can rightly say just how many of the former NFL players who have signed onto the lawsuit are suffering the kind of brain and nervous system disorders that have been linked to football, much less whether their injuries can be attributed to their time in the NFL.

That’s the issue at the crux of the consolidated lawsuit that now sits before a federal judge in Philadelphia: What the league knew, or was in a special position to find out; whether it skirted a duty by suppressing valid research on brain injuries; and how much of that information also was available to the NFL players’ union.

For its part, the NFL sent out a stock response to the lawsuit this week.

“Any allegation that the NFL intentionally sought to mislead players or otherwise conceal information from players concerning the risks, treatment or management of concussions is entirely without merit,” the statement read.

“The NFL has long made player safety a priority and continues to do so. In fact, the NFL was at the forefront of supporting concussion-related research and continues to support important research to help further the science and medical understanding of the management and treatment of concussions.”

Amid the increased scrutiny – including recent comments from President Obama that he would think twice about allowing a son to play football - the NFL on Thursday wheeled out a host of executives and others on Thursday in New Orleans for a news conference to discuss player health.

Players from different eras would face different challenges in proving their claims. The more distant their careers, the more difficult it may be to prove that the NFL had reason to suspect a link between concussions and long-term brain injury.



But the former players face a major hurdle first: Convincing U.S. District Judge Anita Brody that their complaints shouldn’t be governed under the NFL’s collective bargaining agreement, rather than be settled in the courts.

Just this week, the former players lodged their final legal arguments over the issue, claiming the NFL is trying to hide behind a few provisions of the labor agreements that related to the duties of teams and their doctors. On Tuesday, Brody set an April 9 hearing on the league’s motion to dismiss the case.

“It’s not a straightforward case. It’s a very complicated case that involves players from different eras, sometimes complaining of very different injuries or injuries that haven’t manifested themselves at all yet,” said Gabe Feldman, director of the Sports Law Program at Tulane University.

“What we’re dealing with right now are a lot of allegations. We know that many former players are suffering severe and often debilitating brain disease. The question is, is the NFL liable for those injuries? Those types of claims are, as a general matter, preempted by the collective bargaining agreement.”

If the case survives, Feldman said, “we have a whole host of other obstacles the players have to deal with. You have physical causation issues – proving the injuries they suffered were caused by collisions or hits they suffered while playing in the NFL, as opposed to playing college or youth football,” he said.

“It’s still very difficult. We’re talking in almost all these cases cumulative trauma,” Feldman said. “That’s just part of the battle, because no one’s going to contest the fact NFL players get injured playing football. That doesn’t mean the NFL is on the hook for those injuries.”

Feldman said it’s more likely that the NFL would settle the case if the players get beyond the April dismissal hearing, fearing the risk of a deeper public relations nightmare and high-priced individual judgments.

Many of the players have sympathetic stories; others are probably getting on a litigation train.

“Part of them are just trying to get a piece of the action,” he said. “It doesn’t cost them anything at this point. Maybe they’re buying a lottery ticket.”

In the meantime, evidence continues to mount that NFL players face a greater risk of troubling brain disease.

Last week, Baumgartner got a letter in the mail from the Department of Health and Human Services, describing a recently completed study by the National Institute for Occupational Health and Safety.

The letter targeted NFL alumni who played for at least five years between 1959 and 1988, informing them of some grim research results from a look at 3,439 former players, dead and alive.

It found that brain and nervous system disorders were more than three times higher among the group. Cases of Lou Gehrig’s disease were four times higher, as was Alzheimer’s.

Baumgartner said he’s not so worried, although he recalls taking some vicious head shots in a career that spanned seven years, including a knee to the helmet that knocked him cold.

He keeps his old helmet – its Saints colors painted over in the pale blue and white of the Houston Oilers, his next and last stop in the NFL.

The helmet, with an interior of webbed lacing and foam, is gashed and scratched on the left side. Baumgartner played on the right and took most of his helmet hits to the inside.

“I don’t have any pain, but I feel pulsing. It’s something that wakes me up all the time. I don’t sleep, I can’t hear anymore,” he said.

“He has ringing in the ears,” added his wife, Mary.

“Other than that, I would consider myself healthy,” he said. “The practices are the practices they had. Smelling salts, flashlight in the eye, shake your hand and go back out.”

Baumgartner sounds ambivalent about his feelings toward the league. He says he holds no grudge against the NFL – “I don’t blame them at all” -- but he also likens the players to thoroughbred racehorses.

“We raced until we couldn’t race anymore, and kind of got put out to pasture. We’re sitting like glue. Or dog food.”

The study did not include kickers like Dempsey, who drives twice a week to Tulane University for therapy, but mostly stays home.

Dempsey, who was born without toes on his kicking foot, said he was expected to run down the field and make tackles in a way that today’s kickers rarely do.

He said he recalls three head shots – “because people have told me about it” – including one that had him veer off mistakenly to the opponents’ bench.

His wife, Carlene, says the “senior moments” began turning more serious in 2010, although in retrospect there were signs six years earlier, she said.

Dempsey could still sign autographs, but if he was asked to include a personal message, he couldn’t spell it out.

Recently, Dempsey recalled playing Baltimore Ravens linebacker Ray Lewis.

“He said, ‘Boy, he hit me hard.’ That was new. Somewhere in his mind he had delusions of playing against Ray Lewis,” Carlene said. “And then he gets mad. It frustrates him.”

Lewis was four years old when Dempsey retired in 1979, making $50,000 that year.

There are other problems as well. “He’s getting his times mixed up. He can’t really tell time anymore,” said Carlene.

Dr. Daniel Amen, who studied the images of 135 brains of former NFL players, is convinced that Dempsey’s dementia is the result of “many hits to the head.

“There’s no question in my mind. We see this pattern. You were not made to start putting on a helmet and start slamming against other people,” said Amen. “We look at blood flow and activity. If you think of a healthy scan, it’ll look like a big grape. His looks more like a raisin.”

Until 2010, Amen said, the NFL had turned their heads away from the problem, denying disability to players with clear head trauma.

“In the kindest way, you could say they were in active denial,” he said. Amen said.

Now the league has poured money into funding studies into CTE and other brain injuries. But Amen argues that the lawsuit has distracted from research into medical treatment that has shown promise in making the lives of many older, brain-injured ex-NFLers better.

“That’s exciting. Still, most of the conversation this week is, not can we make them better. It’s ‘Did the NFL know? Were they lying?’”

In the meantime, Dempsey goes twice a week to Tulane, one of seven league-approved programs that provide evaluation and therapy to NFL alumniwho need it.

He takes his homework with him – alphabet sheets he uses to relearn his letters – and does physical and cognitive exercises there.

Though he lives just a few miles away, Dempsey won’t be attending any of the Super Bowl events in New Orleans, Carlene said.

“He was asked to, but as a family we decided we wouldn’t even mention it to him, rather than put him up front and center on a stage that I don’t think he can handle anymore,” Carlene said.

“There was a time when he would take charge and take over. He can’t do that anymore.”

Link to the Times Picayune.

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