The Associated Press did a profile of Butzler that chronicles the 18-year-old’s struggle to cope with the retrograde amnesia she suffered after her soccer injury.

http://www.necn.com/05/21/12/Brain-injury-forces-Wis-teen-to-rediscov/landing_health.html?&apID=82fa5718573443f29ea84f197efa3d59

After being taken from the field to a hospital for treatment, Butzler returned to a home, relatives and friends that she didn’t recognize. She suffered from severe headaches from lights, and had trouble walking, according to AP.

Her family used photos to show Butzler her past, and she eased into returning to school, initially just attending a few hours a day, AP reported. She received special help in her classes.

Today Butzler is back to being a great student and she plans to go to nursing school next year.

By Attorney Gordon Johnson

800-992-9447

Noises can also set off seizure activity.  But Michael has more cognitive problems with noise.

What about noises?   For example, the backup alarm on a truck, does that bother you?

It can.  Actually the biggest noise problem I have is when, it’s pretty quiet, like if you’re in for a test and you’re supposed to be doing the test, people coughing, dropping their pencils, that would drive me nuts.  Actually what drives me nutty kind of nuts right now is when I have all four of my kids and they can’t give me just one second because I’m very slow at understanding what they’re asking, comprehending.

Your ability to comprehend and, and have a conversation has a lot to do with how little else is going on at the time?

Yes.

And you’re having no problem with our conversation?

No, because it’s just you and me.

Is there any background noise in this room then that bothers you.

No.

So until I mentioned it you probably didn’t even think about the background noise.

No.  I mean to be honest with you, I didn’t think about it, but now that you bring it up since it’s quiet and I can hear you.  For me it’s fine.

Your problems keeping up in conversation has a lot to do with how many different sensory inputs are going on at once? 

That’s true.  Actually from my accident, let’s see if I can remember which year because my dad didn’t tell me this when I talked to him last night, I believe it was this year I did something to my eardrum so I had very bad hearing out of this ear, so I used my right ear to, I rely on my right ear a lot.

So it is not a problem for you to hear our conversation because we’re the only thing going on in this room, but otherwise if I would be to your right side it would be easier for you to follow?

Yes.

Next in Part Ten – Hesitant Speech Post Seveve Brain Injury

The promising finding comes from the Buck Institute for Research on Aging in Novato, Calif., which put out a press release about its study.

http://www.newswise.com/articles/modifying-scar-tissue-can-potentially-improve-outcome-in-chronic-stroke

The research, published in the May 21 online edition of The Proceedings of the National Academy of Sciences, used spinal cord repair studies as its base.

Scientists, using rats, “infused the stroke cavity with either the enzyme chondroitinase ABC (ChABC) or the protein heparan sulfate proteoglycan glypican (glypican),” according to the press release. “In both cases the treatments improved outcome in the animals – they had less weakness and improved coordination.”

Lead researcher Dr. Justin Hill said both treatments reduced the size of the scar tissue that had formed following the stroke and essentially sparked activity in neurons in areas surrounding the injury, stimulating the growth of new neurites, which are the terminal extensions of nerves.

“We think the scar tissue not only blocks off areas of the brain that are injured during stroke, we also believe the scar tissue secretes factors that impact the function of nearby neurons,” Hill said in a statement. “Dissolving the scar may spur neurons to re-route connections around the area injured during the stroke.”

According to the Buck Institute press release, “researchers found that treatment with glypican increased the expression of fibroblast growth factor-2 (FGF-2) near the site of injury and that ChABC increased brain-derived neurotrophic factor (BDNF) expression, both of which have been shown to increase neuron size and survival.”

The institute said that there is a dire need for treatments for chronic stroke patients. There are 750,000 new strokes annually in the United States, and they are a leading cause of morbidity and mortality.

“Aside from physical and occupational therapy, treatments for the 6 million patients in the U.S. who suffer from chronic stroke are lacking; the vast majority of patients remain in an ongoing state of disability with little hope of return to normal function,” the institute’s press release said.

“There are only a handful of laboratories that are focused on treatments for chronic stroke,” Buck faculty member Dr. David Greenberg said in a statement. “Dr. Hill’s research is groundbreaking in that it is the first to apply this research on spinal cord injury to stroke and uncovers some of the underlying mechanisms involved in improved function.”

The research was supported by grants from the National Institutes of Health.

The Buck Institute is the U.S.’s first independent research organization devoted to Geroscience – focused on the connection between normal aging and chronic disease. Its scientists seek  to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer’s and Parkinson’s, cancer, cardiovascular disease, macular degeneration, diabetes and stroke.

The University of California at Los Angeles last week boasted that for the first time its researchers used “brain-imaging data that was lost to science for a decade” to explore the damage that Phineas Gage suffered to the so-called white matter that links different parts of the brain.

http://newsroom.ucla.edu/portal/ucla/embargoed-for-release-until-wednesday-233846.aspx

In 1848 Gage, a railroad supervisor in Vermont, used a rod to pack blasting powder into a rock, inadvertently setting off an explosion. The 13-pound, 3-foot-7-inch rod he was using shor forward and traveled through his left cheek, and then  out of the top of his head.

Despite that traumatic brain injury (TBI), Gage survived. But he wasn’t the same man he was before the accident, which damaged most of his left frontal lobe. Gage, 25, was no longer a happy-go-lucky fellow. He became moody and “profane,” according to UCLA’s press release.

“Over the years, various scientists have studied and argued about the exact location and degree of damage to Gage’s cerebral cortex and the impact it had on his personality,” according to UCLA.

In last Wednesday’s issue of the journal PLoS ONE, ” Jack Van Horn, a UCLA assistant professor of neurology, and his colleagues note that while approximately 4 percent of the cerebral cortex was intersected by the rod’s passage, more than 10 percent of Gage’s total white matter was damaged. The passage of the tamping iron caused widespread damage to the white matter connections throughout Gage’s brain, which likely was a major contributor to the behavioral changes he experienced,” UCLA said in its press release.

“Because white matter and its myelin sheath — the fatty coating around the nerve fibers that form the basic wiring of the brain — connect the billions of neurons that allow us to reason and remember, the research not only adds to the lore of Phineas Gage but may eventually lead to a better understanding of multiple brain disorders that are caused in part by similar damage to these connections,” the university said.

“What we found was a significant loss of white matter connecting the left frontal regions and the rest of the brain,” Van Horn, who is a member of UCLA’s Laboratory of Neuro Imaging (LONI), said in a statement. “We suggest that the disruption of the brain’s ‘network’ considerably compromised it. This may have had an even greater impact on Mr. Gage than the damage to the cortex alone in terms of his purported personality change.”

LONI is  a joint effort with Massachusetts General Hospital and the National Institutes of Health to document the trillions of microscopic links between every one of the brain’s 100 billion neurons — the so-called “connectome,”according to UCLA.

“And because mapping the brain’s physical wiring eventually will lead to answers about what causes mental conditions that may be linked to the breakdown of these connections, it was appropriate, as well as historically interesting, to take a new look at the damage to Gage’s brain,” the university said in its press release.

Gage’s 189-year-old skull is on display at Harvard Medical School, but is too fragile to undergo medical  imaging again.

So UCLA’s researchers set out to find the last imaging data, from 2001, which had been lost due to various circumstances at Brigham and Women’s Hospital, a teaching affiliate of Harvard, for a decade.

“The authors were able to recover the computed tomographic data files and managed to reconstruct the scans, which revealed the highest-quality resolution available for modeling Gage’s skull,” UCLA said.  ” Next, they utilized advanced computational methods to model and determine the exact trajectory of the tamping iron that shot through his skull. Finally, because the original brain tissue was, of course, long gone, the researchers used modern-day brain images of males that matched Gage’s age and (right) handedness, then used software to position a composite of these 110 images into Gage’s virtual skull, the assumption being that Gage’s anatomy would have been similar.”

Using that methodology, researcher determined that almost 11 percent of Gage’s white matter had been damaged, as well as 4 percent of his cortex.

“Our work illustrates that while cortical damage was restricted to the left frontal lobe, the passage of the tamping iron resulted in the widespread interruption of white matter connectivity throughout his brain, so it likely was a major contributor to the behavioral changes he experienced,” Van Horn said.

“Connections were lost between the left frontal, left temporal and right frontal cortices and the left limbic structures of the brain, which likely had considerable impact on his executive as well as his emotional functions,” he added.

After his accident, Gage worked as a stagecoach driver for several years in South America. He died in San Francisco a dozen years after his freak accident.

Van Horn compared Gage’s condition to that of others with TBI.

“The extensive loss of white matter connectivity, affecting both hemispheres, plus the direct damage by the rod, which was limited to the left cerebral hemisphere, is not unlike modern patients who have suffered a traumatic brain injury,” he said. “And it is analogous to certain forms of degenerative diseases, such as Alzheimer’s disease or frontal temporal dementia, in which neural pathways in the frontal lobes are degraded, which is known to result in profound behavioral changes.”

By Attorney Gordon Johnson

800-992-9447

Seizures are typically thought of a dramatic events where the sufferer is lying on the floor, shaking, foaming at the mouth. While these kind of seizures do occur after brain injury, seizure activity covers a broad spectrum of abnormal brain function all the way to staring spells to other peculiar phenomenon such as smelling things that aren’t there. See http://www.subtlebraininjury.com/seizure2.php  Michael’s seizures are of the petit mal variety.

You also mentioned that you did have seizures.

I had petit mal seizures.

When did that start?

Pretty much right when, right after I regained consciousness.

Are you on seizure medication?

I was on, yes, Tegretol for a long time.

Until just recently?

Actually I went from Tegretol to Depakote.  I got off my Depakote about eight months ago.

Did you ever have a grand mal seizure? 

They said I had one when I was in my coma.

My parents and friends and everybody called them staring fits.  All of a sudden I just blank out, I wouldn’t hear a thing and I’d be staring off in oblivion.  I would come out of it on my own or someone would either touch me or pat me on the shoulder and I would come out and then like, are you okay?  Okay, what were you doing?  I have no clue.

Do you remember what’s happening right at the moment at the beginning of the seizure?

Well, mostly no, but when I went to work for the government at the Census Bureau I had a hard time with the computers and I finally had to quit because of all the light problems.

Now the old fashioned computers, the cursor used to blink more.  Still I’m looking at mine and it’s blinking right now.  But it used to blink in a much more overt way.   Do you have as much trouble with a computer made today as you did?

No, actually the cursors for when I’m using are a lot different but then I don’t write a whole bunch on my computer.  But I do use the internet and it’s a lot different because it’s usually just a line.

That was  sort of like a flashing – – a strobe light?

A flashing.  About two years ago, if I remember right, the transformer in front of my parents’ house blew and we had all, we had cops, police officers, we had emergency units, we had fire units. It affected me so bad I just had to go downstairs and lie down and get out of light and get away from everything.

Now you’re in a room with fluorescent lights, do they cause you any trouble?

No.

Next in Part Nine – Dealing with Noise and Distractions After Brain Injury

In a study published last week, a paralyzed woman and paralyzed man were both able to move and control a robotic arm with their thoughts, their brain signals.

Brown University issued a press release on the fascinating research, which employed brain implants, on Wednesday.

http://news.brown.edu/pressreleases/2012/05/braingate2

“On April 12, 2011, nearly 15 years after she became paralyzed and unable to speak, a woman controlled a robotic arm by thinking about moving her arm and hand to lift a bottle of coffee to her mouth and take a drink,” Brown said in its press release.

“That achievement is one of the advances in brain-computer interfaces, restorative neurotechnology, and assistive robot technology described in the May 17 edition of the journal Nature by the BrainGate2 collaboration of researchers at the Department of Veterans Affairs, Brown University, Massachusetts General Hospital, Harvard Medical School, and the German Aerospace Center (DLR).”

The two people who participated in the study were a 58-year-old woman, dubbed “S3″  and a 66-year-old man, “T2.” Newspaper stories identified the woman as Cathy Hutchinson of Massachusetts and the man as Robert Veillette of Connecticut. Both became paralyzed, with no control of their limbs, after suffering so-called “brainstem” strokes several year sago.

The research’s amazing results were widely covered in newspapers across the county, including USA Today.

http://www.usatoday.com/news/health/story/2012-05-15/robotic-arm/55004238/1?csp=34news

In the research, the participants used neural activity to directly control two different robotic arms  to reach and grasp.

“The BrainGate2 pilot clinical trial employed the investigational BrainGate system initially developed at Brown University, in which a baby aspirin-sized device with a grid of 96 tiny electrodes is implanted in the motor cortex — a part of the brain that is involved in voluntary movement,” Brown said in its press release.

“The electrodes are close enough to individual neurons to record the neural activity associated with intended movement,” the release said.” An external computer translates the pattern of impulses across a population of neurons into commands to operate assistive devices, such as the … robot arms used in the study now reported in Nature.”

The BrainGate2 neural interface system is an implanted micro electrode device. It detects brain signals, which can be translated by a computer into machine instructions, allowing control of robotic devices by thought.

“This technology was made possible by decades of investment and research into how the brain controls movement,” Story Landis, director of the National Institute of Neurological Disorders and Stroke, which helped fund the study, said in a statement. “It’s been thrilling to see the technology evolve from studies of basic neurophysiology and move into clinical trials, where it is showing significant promise for people with brain injuries and disorders.”

The BrainGate participants have had previous triumphs translating their thoughts to action via the brain implants: They were able to control of a cursor on a computer screen and had rudimentary control of simple robotic devices.

“The study represents the first demonstration and the first peer-reviewed report of people with tetraplegia using brain signals to control a robotic arm in three-dimensional space to complete a task usually performed by their arm,” Brown said in its press release.

“Specifically, S3 and T2 controlled the arms to reach for and grasp foam targets that were placed in front of them using flexible supports,” the release said. “In addition, S3 used the … robot to pick up a bottle of coffee, bring it to her mouth, issue a command to tip it, drink through a straw, and return the bottle to the table. Her BrainGate-enabled, robotic-arm control during the drinking task required a combination of two-dimensional movements across a table top plus a ‘grasp’ command to either grasp and lift or tilt the robotic hand.”

The sponsor-investigator for the BrainGate2 pilot clinical trial had plenty to say in a statement.

“Our goal in this research is to develop technology that will restore independence and mobility for people with paralysis or limb loss,” said lead author Dr. Leigh Hochberg, a neuroengineer and critical care neurologist who holds appointments at the Department of Veterans Affairs, Brown University, Massachusetts General Hospital and Harvard.

“We have much more work to do, but the encouraging progress of this research is demonstrated not only in the reach-and-grasp data, but even more so in S3’s smile when she served herself coffee of her own volition for the first time in almost 15 years.”

As Brown pointed out in its press release, after almost 15 years “a part of the brain essentially ‘disconnected’ from its original target by a brainstem stroke was still able to direct the complex, multidimensional movement of an external arm.”

Part of the funding for the research is from the VA, which is trying to help injured vets.

“VA is honored to have played a role in this exciting and promising area of research,” VA Secretary Eric Shinseki said in a statement. “Today’s announcement represents a great step forward toward improving the quality of life for veterans and others who have either lost limbs or are paralyzed.”

The other news out of the research was that Hutchinson controlled the robotic arm more than five years after her BrainGate electrode array was first implanted.

“This sets a new benchmark for how long implanted brain-computer interface electrodes have remained viable and provided useful command signals,” Brown said.

John Donoghue, the VA and Brown neuroscientist who pioneered BrainGate more than a decade ago and who is co-senior author of the study, said the new study was a testament to how much progress has been made in the field of brain-computer interfaces.

“This paper reports an important advance by rigorously demonstrating in more than one participant that precise three-dimensional neural control of robot arms is not only possible, but also repeatable,” Donoghue, who directs the Brown Institute for Brain Science, said in a statement.

“We’ve moved significantly closer to returning everyday functions, like serving yourself a sip of coffee, usually performed effortlessly by the arm and hand, for people who are unable to move their own limbs,” he said. “We are also encouraged to see useful control more than five years after implant of the BrainGate array in one of our participants. This work is a critical step toward realizing the long-term goal of creating a neurotechnology that will restore movement, control, and independence to people with paralysis or limb loss.”

The robots acted as a substitute for each participant’s paralyzed limb in the study.

“The robotic arms responded to the participants’ intent to move as they imagined reaching for each foam target,” Brown said in its release. “The robot hand grasped the target when the participants imagined a hand squeeze. Because the diameter of the targets was more than half the width of the robot hand openings, the task required the participants to exert precise control.”

The study used two advanced robotic arms: the DLR Light-Weight Robot III with DLR five-fingered hand and the DEKA Arm System.

The DLR LWR-III is designed to assist in recreating actions like the human arm and hand and to interact with human users.

DEKA Research and Development developed the DEKA Arm System for amputees, through funding from the United States Defense Advanced Research Projects Agency (DARPA).

In addition to Hochberg, Donoghue, and van der Smagt, other authors on the paper are Daniel Bacher, Beata Jarosiewicz, Nicolas Masse, John Simeral, Joern Vogel, Sami Haddadin, Jie Liu and Sydney Cash.

In a press release last week, UCLA said that a new “rat study” is the first research to demonstrate that “a diet steadily high in fructose slows the brain, hampering memory and learning — and how omega-3 fatty acids can counteract the disruption.”

http://newsroom.ucla.edu/portal/ucla/this-is-your-brain-on-sugar-ucla-233992.aspx

The Journal of Physiology published the findings last Tuesday.

“Our findings illustrate that what you eat affects how you think,” said Fernando Gomez-Pinilla, a professor of neurosurgery at the David Geffen School of Medicine at UCLA and a professor of integrative biology and physiology in the UCLA College of Letters and Science. “Eating a high-fructose diet over the long term alters your brain’s ability to learn and remember information. But adding omega-3 fatty acids to your meals can help minimize the damage.”

Although prior studies has showed how fructose harms the body through its role in diabetes, obesity and fatty liver, the UCLA research is the first to demonstrate how such sugar influences the brain.

“Sources of fructose in the Western diet include cane sugar (sucrose) and high-fructose corn syrup, an inexpensive liquid sweetener,” UCLA said in its release. “The syrup is widely added to processed foods, including soft drinks, condiments, applesauce and baby food. The average American consumes roughly 47 pounds of cane sugar and 35 pounds of high-fructose corn syrup per year, according to the U.S. Department of Agriculture.”

The researcher said that sugar in fruit doesn’t have him worried.

“We’re less concerned about naturally occurring fructose in fruits, which also contain important antioxidants,” said Gomez-Pinilla, who is also a member of UCLA’s Brain Research Institute and Brain Injury Research Center. “We’re more concerned about the fructose in high-fructose corn syrup, which is added to manufactured food products as a sweetener and preservative.”

Gomez-Pinilla and research co-author Rahul Agrawal, a UCLA visiting postdoctoral fellow from India, studied two groups of rats that each consumed a fructose solution as drinking water for six weeks. The second group also received omega-3 fatty acids in the form of flax seed oil and docosahexaenoic acid (DHA), which protects against damage to the synapses — the chemical connections between brain cells that enable memory and learning.

“DHA is essential for synaptic function — brain cells’ ability to transmit signals to one another,” Gomez-Pinilla said. “This is the mechanism that makes learning and memory possible. Our bodies can’t produce enough DHA, so it must be supplemented through our diet.”

The rat were give standard food and trained on a maze twice daily for five days before starting the experimental diet.

“The UCLA team tested how well the rats were able to navigate the maze, which contained numerous holes but only one exit,” the press release said. “The scientists placed visual landmarks in the maze to help the rats learn and remember the way.”

The researchers tested the rats’ ability to recall the route and escape the maze six weeks late.

“The second group of rats navigated the maze much faster than the rats that did not receive omega-3 fatty acids,” Gomez-Pinilla said. “The DHA-deprived animals were slower, and their brains showed a decline in synaptic activity. Their brain cells had trouble signaling each other, disrupting the rats’ ability to think clearly and recall the route they’d learned six weeks earlier.”

According to UCLA, the DHA-deprived rats also developed signs of resistance to insulin, which controls blood sugar and regulates synaptic function in the brain. A closer look at the rats’ brain tissue suggested that insulin had lost much of its power to influence the brain cells.

“Because insulin can penetrate the blood–brain barrier, the hormone may signal neurons to trigger reactions that disrupt learning and cause memory loss,” Gomez-Pinilla said.

The research believes that fructose caused the DHA-deficient rats’ brain dysfunction. Eating too much fructose could block insulin’s ability to regulate how cells use and store sugar for the energy required for processing thoughts and emotions.

“Insulin is important in the body for controlling blood sugar, but it may play a different role in the brain, where insulin appears to disturb memory and learning,” he said. “Our study shows that a high-fructose diet harms the brain as well as the body. This is something new.”

Gomez-Pinilla’s advice to humans is keep fructose intake to a minimum, and to eat fresh berries and Greek yogurt instead of the usual desserts, such as hot-fudge sundaes.
sweetener is fine too, he said.

For those who won’t give up their sweets, the researcher advises that they eat food with omega-3 fatty acids, such as salmon, walnuts and flax seeds, or take a daily DHA capsule. Gomez-Pinilla recommends one gram of DHA per day.

“Our findings suggest that consuming DHA regularly protects the brain against fructose’s harmful effects,” said Gomez-Pinilla. “It’s like saving money in the bank. You want to build a reserve for your brain to tap when it requires extra fuel to fight off future diseases.”

The UCLA study was funded by the National Institute of Neurological Disorders and Stroke. Gomez-Pinilla’s lab will next examine the role of diet in recovery from brain trauma.

But a fascinating study has found evidence of  chronic traumatic encephalopathy (CTE), a degenerative disease that’s been found in the brains of deceased football players who suffered concussions, in the brain tissue of blast-exposed military service personnel, according to a story on the Boston University School of Medicine (BSUM) website.

http://www.bumc.bu.edu/busm-news/2012/05/17/study-shows-first-case-series-of-chronic-traumatic-encephalopathy-in-blast-exposed-military-service-personnel-and-mechanism-of-injury-in-blast-neurotrauma/

Investigators from BU and the Veterans Affairs Boston Healthcare System performed the study, which received wide coverage in the media Thursday.

http://articles.chicagotribune.com/2012-05-16/lifestyle/sns-rt-us-brain-traumabre84f121-20120516_1_brain-damage-traumatic-brain-injury-head-injuries

Laboratory experiments conducted by the researchers discovered that exposure to a single blast equivalent to a typical improvised explosive device (IED) results in CTE and long-term brain impairments that accompany the disease.

And in an interesting twist, they also found that the blast wind, not the shock wave, from the IED blast is actually what leads to TBI and long-term consequences, including CTE.

The research, which represents the first case series of postmortem brains from U.S. military personnel who were exposed to a blast and/or a concussive injury, was published online Wednesday by Science Translational Medicine.

http://stm.sciencemag.org/content/4/134/134ra60

Dr. Lee Goldstein, associate professor at BUSM and Boston University College of Engineering, and Dr. Ann McKee, professor at BUSM and director of the Neuropathology Service for VA New England Healthcare System, led the study and are its senior co-authors.

CTE, which can only be diagnosed by studying a person’s brain after death, is a progressive neurodegenerative brain disease that has been reported in athletes with multiple concussions or subconcussive injuries.

“In early stages, CTE is characterized by the presence of abnormal deposits of a protein called tau in the form of neurofibrillary tangles, glial tangles and neuropil threads throughout the brain,” BUSM stated. “These tau lesions eventually lead to brain cell death. CTE has clinical features in common with TBI, including psychiatric symptoms and long-term cognitive disability involving memory and learning deficits. TBI can impact military personnel exposed to an explosive blast and may affect approximately 20 percent of the 2.3 million servicemen and women deployed since 2001.”

In the study, researchers performed pathological analyses on brain tissue from four military service personnel with known blast exposure and/or concussive injury.

The researchers compared their findings with brain tissue from three young amateur American football players and a professional wrestler, who all had suffered repeated concussions,  and four brain  samples from comparably-aged normal controls with no history of blast exposure, concussions or neurological disease.

“The investigators found that CTE neuropathology in the brains of blast-exposed military veterans was similar to that found in young athletes with repetitive concussion and consistent with what has previously been observed in brain samples from other athletes with a history of repetitive concussive injury,” according to BUSM.

“Our results showed that the neuropathology from blast exposure, concussive injury, or both were virtually indistinguishable from those with a history of repeat concussive injury,” said McKee, who is the director of the Brain Banks for BU’s Alzheimer’s Disease Center and the Center for the Study of Traumatic Encephalopathy, which are based at the Bedford VA Medical Center.

According to McKe, the findings seem to show that TBI caused by different factors may trigger similar disease pathways in the brain.

“The neuropsychiatric symptoms of CTE that have previously been associated with athletes diagnosed with CTE could also be attributed to military personnel who were exposed to blast,” said Goldstein, who also is affiliated with the BU Photonics Center and served as the study’s lead author.

According to BUSM, to research the impact of a single-blast exposure,  investigators worked with  experts in blast physics, experimental pathology and neurophysiology at Boston University, VA Boston Healthcare System, White River Junction VA Medical Center, New York Medical College, Fraunhofer Center for Manufacturing Innovation, University of Massachusetts Lowell, Lawrence Livermore National Laboratory, Massachusetts General Hospital and the University of Oxford.

‘The data demonstrated that one blast comparable to that experienced by military service personnel in the field resulted in both neuropathological and behavioral evidence of CTE,” BUSM said, which is a pretty frightening finding.

And these long-term impairments in brain function, affecting learning and memory, were seen just two weeks after exposure to a single blast.

The blast wind from an IED can reach a velocity of up to 330 miles per hour, which is more than the biggest gust of wind  ever recorded on earth.  That wind violently jerks the head, resulting in brain damage.

The researchers also looked into how they could prevent the brain injury. They found that  immobilizing the head during a blast prevented the learning and memory problems associated with CTE that took place when the head wasn’t immobilized.

“Our study provides compelling evidence that blast TBI and CTE are structural brain disorders that can emerge as a result of brain injury on the battlefield or playing field,” Goldstein said in the BUSM piece. “Now that we have identified the mechanism responsible for CTE, we can work on developing ways to prevent it so that we can protect athletes and our military service personnel.”

By Attorney Gordon Johnson

800-992-9447

One of the often missed symptoms of brain injury are vision problems.  While those surviving a severe brain injury, like Michael may get diagnosis of this problem, they can occur even in milder cases.  Visual problems can come from an injury to the eye itself, to the optic nerve, to the cranial nerves that control the muscles of the eye or from an injury to the part of the brain that sees.  Michael’s problems appear to originate in the muscles that control the eye.

Talk to me about the problems you have with your vision.

Well, I, my eyes will cross.  I had this one all the way and that one verging.  I had to get two eye, two muscle transplants; the first one was for this side to pull it over and then six months later I had another one to pull this one eye over.  But the bad thing about it is now all I do is I can see straight and if I look just right I only see one.  But I mostly see two of everything unless I have my glasses.

You were saying about your mother warning you about.

Oh, my mom, you know, it’s, they tell you when you’re young, don’t cross your eyes and have someone hit you in the back of the head because it’ll stick that way; it’s true.  I must have crossed my eyes the split second I had the accident and hit the  head rest because my eyes stuck.

You don’t actually think the reason your eyes stuck crossed was because they were crossed at the time, do you?

I have no idea.  That sounds like the most logical and funny reason we could come up with.

Tell me about visual issues right now.

Right now I can’t stand sunlight, too much sunlight.  I close my eye, my right eye a lot so I can see just one of things.  I do that when I drive sometimes.  So if you see a beige Dodge Intrepid driving on the highway, park.

Okay, let’s go back and talk about the timeline of your recovery. What you told us was that you were with your parents for about a year after you got out of the nursing home?

Yes.

Then what?

Well, in the fall of ’94, I think, I went back up to school and it was either the fall of ’94 or the fall of ’95.

So that would have been 18 months to –  30 months after the accident?

Yeah, I can’t really remember. I think it was fall of ’94.  I really rushed myself because people asked, why did you come back so quick.  Easiest answer I could tell them was I thought I was in love with somebody.

So the girl that you followed to Wisconsin –   stayed here after you got hurt?

Yes.  She stayed, we stayed together for another four years.

Did she involve herself in your rehabilitation at all?

No.  She was up here working the summer and then school and then she was in school and then she worked that summer so she was all, she was up here.  The people that really worked with me, like I said, was my dad, my mom and I’d say somewhat my sister, too.

Next in Part Eight – Petit Mal Seizures After Severe Brain Injury

As the NIH explains in a recent press release (which this blog is based on), variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer’s disease. But the gene’s role in the disease has been unclear. But researchers funded by the NIH have found that in mice, having the most risky variant of ApoE damages the blood vessels that feed the brain.

http://www.nih.gov/news/health/may2012/ninds-16.htm

The researchers found that the high-risk variant, ApoE4, triggers an inflammatory reaction that weakens the blood-brain barrier, a network of cells and other components that lines brain’s brain vessels. Normally, this barrier allows nutrients into the brain and keeps harmful substances out.

“The ApoE gene encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body,” according to the NIH. ” The gene exists in three varieties. ApoE2 is thought to play a protective role against both Alzheimer’s and heart disease, ApoE3 is believed to be neutral, and ApoE4 confers a higher risk for both conditions. Outside the brain, the ApoE4 protein appears to be less effective than other versions at clearing away cholesterol; however, inside the brain, exactly how ApoE4 contributes to Alzheimer’s disease has been a mystery.”

The NIH study appeared recently in Nature, and was led by Dr. Berislav Zlokovic, director of the Center for Neurodegeneration and Regeneration at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles.

“Understanding the role of ApoE4 in Alzheimer’s disease may be one of the most important avenues to a new therapy,” Zlokovic said.

“Our study shows that ApoE4 triggers a cascade of events that damages the brain’s vascular system,” he said, referring to the system of blood vessels that supply the brain.

According to NIH, Zlokovic and his team studied several lines of genetically engineered mice, including one that lacks the ApoE gene and three other lines that produce only human ApoE2, ApoE3 or ApoE4.

Mice normally have only a single version of ApoE, the NIH said. The researchers found that mice whose bodies made only ApoE4, or made no ApoE at all, had a leaky blood-brain barrier. With the barrier compromised, harmful proteins in the blood made their way into the mice’s brains, and after several weeks, the researchers were able to detect loss of small blood vessels, changes in brain function, and a loss of connections between brain cells.

“The study demonstrates that damage to the brain’s vascular system may play a key role in Alzheimer’s disease, and highlights growing recognition of potential links between stroke and Alzheimer’s-type dementia,” said Roderick Corriveau, a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research. “It also suggests that we might be able to decrease the risk of Alzheimer’s disease among ApoE4 carriers by improving their vascular health.”

The researchers also found that ApoE2 and ApoE3 help control the levels of an inflammatory molecule called cyclophilin A (CypA), but ApoE4 does not.

Levels of CypA were raised about five-fold in blood vessels of mice that produce only ApoE4. The excess CypA then activated an enzyme, called MMP-9, which destroys protein components of the blood-brain barrier.

Treatment with the immunosuppressant drug cyclosporine A, which inhibits CypA, preserved the integrity of the blood-brain barrier and lessened damage to the brain. An inhibitor of the MMP-9 enzyme had similar beneficial effects. In prior studies, inhibitors of this enzyme have been shown to reduce brain damage after stroke in animal models.

“These findings point to cyclophilin A as a potential new drug target for Alzheimer’s disease,” said Suzana Petanceska, a program director at NIH’s National Institute on Aging (NIA), which also funded Zlokovic’s study.

“Many population studies have shown an association between vascular risk factors in mid-life, such as high blood pressure and diabetes, and the risk for Alzheimer’s in late-life,” she said. “We need more research aimed at deepening our understanding of the mechanisms involved and to test whether treatments that reduce vascular risk factors may be helpful against Alzheimer’s.”

Alzheimer’s disease is the most common cause of dementia in older adults, and affects more than 5 million Americans, the NIH noted.

A hallmark of the disease is a toxic protein fragment called beta-amyloid that accumulates in clumps, or plaques, within the brain. Gene variations that cause higher levels of beta-amyloid are associated with a rare type of Alzheimer’s that appears early in life, between age 30 and 60.

But it’s the ApoE4 gene variant that is most strongly linked to the more common, late-onset Alzheimer’s disease. Inheriting a single copy of ApoE4 from a parent increases the risk of Alzheimer’s disease by about three-fold. Inheriting two copies, one from each parent, increases the risk by about 12-fold.

Zlokovic’s study and others point to a complex interplay between beta-amyloid and ApoE4. On the one hand, beta-amyloid is known to build up in and damage blood vessels and cause bleeding into the brain.

On the other hand, Zlokovic’s data suggest that ApoE4 can damage the vascular system independently of beta-amyloid. He theorizes that this damage makes it harder to clear beta-amyloid from the brain. Some therapies under investigation for Alzheimer’s focus on destroying amyloid plaques, but therapies designed to compensate for ApoE4 might help prevent the plaques from forming, he said.

By Attorney Gordon Johnson

800-992-9447

 

 

You have tingling in your left arm?

Yes, I get that all the time.

Tell me about that.

Well I’m right handed and I’ll be sitting watching TV or even walking and I have a nervous habit to where I go like this because I can’t sometimes feel my fingers and that drives me kind of, well but there’s nothing my doctors or any of the doctors I’ve seen can do about it.

Were you right handed before?

I’m right handed.

Did you know how to type before you got hurt?

I don’t think so.  I hunt and peck now.

Are you able to use your left hand well enough to hunt and peck with it?

I can’t use it very long because it’ll go numb.

What else makes it go numb?

When I hold it up.  When I have it on angle like this, it’ll start to go numb so I have to shake down.  That’s mostly or when I put, when I sleep on it it’ll go numb and I’ll wake in the morning and I won’t have any feeling in it.

Where else in your body do you have weakness or this partial paralysis?

Well I have a huge weakness in my legs. I sometimes they get so bad I, I still use a cane.

Are you using a cane today?

No, I didn’t have my cane today.  Actually, I’m doing really good with my legs.  Usually when I use the cane, it’s in the fall and then all winter.

It’s a warm summer day today.

Yeah and I’m doing just fine.  We hope.

Do you remember relearning to walk?

Bits and pieces.  I remember, like I said, those bars I had to walk through and even after I left Elizabethtown and came up to Louisville and had outpatient therapy, um, even then, um, that was one of the big things and I, I had a really hard time on the steps.

Are you able to go up and down the stairs now?

It takes me a long time.

Now we’re on a lower level of the library here.  Is there an elevator that you could use?

There is, there could be an elevator I could use.  I just held on tight with both hands and walked down.

Look for the elevator on the way up?

Probably.

What about relearning to walk?  You told us that you remember the parallel bars.

I remember I had a walker for a while and that, I definitely asked them not to put wheels on it, they put them regularly.  And then I went from a walker to a four cane and then I went to a single cane.  I still use that off and on, especially on, I’m very sensitive to weather now.

Today you came here without your cane?

Right.

There’s some stairs that you had to come down What was that like?

That was hard.  I had to, uh, really concentrate because it’s easier going up for me than going down.  I really had to adjust my weight and kind of lean back.

 

 

Michael didn’t look for the elevator on his way up.  In fact he helped carry my tripod up for me. Below are some pictures that do show his off balance kilter when he walks.

Next in Part Seven – Vision Problems Secondary to Brain Injury

http://www.hhs.gov/news/press/2012pres/05/20120515a.html

Health and Human Services Secretary Kathleen Sebelius this week outlined details of the called for in the National Alzheimer’s Project Act (NAPA), which President Obama signed into law in January 2011. Federal officials issued a press release on the plan Tuesday.

The National Plan to Address Alzheimer’s Disease sets forth five goals, including the development of effective prevention and treatment approaches for Alzheimer’s disease and related dementias by 2025.

In February, the administration announced that it would take immediate action to implement parts of the plan, including making additional funding available in fiscal 2012 to support research, provider education and public awareness.

On Tuesday Sebelius announced additional actions, including the funding of two major clinical trials, jump-started by the National Institutes of Health’s (NIH) infusion of additional 2012 funds directed at Alzheimer’s disease; the development of new high-quality, up-to-date training and information for our nation’s clinicians; and a new public education campaign and website to help families and caregivers find the services and support they need.

To help accelerate the national initiative, the President’s proposed fiscal 2013 budget provides a $100 million increase for efforts to combat Alzheimer’s disease. These funds will support additional research ($80 million), improve public awareness of the disease ($4.2 million), support provider education programs ($4.0 million), invest in caregiver support ($10.5 million), and improve data collection ($1.3 million).

“These actions are the cornerstones of an historic effort to fight Alzheimer’s disease,”  Sebelius said. “This is a national plan — not a federal one, because reducing the burden of Alzheimer’s will require the active engagement of both the public and private sectors.”

The plan was unveiled at the Alzheimer’s Research Summit 2012: Path to Treatment and Prevention.  The plan was developed with input from experts in aging and Alzheimer’s disease issues and calls for a collaborative approach across federal, state, private and non-profit organizations.

More than 3,600 people or organizations submitted comments on the draft plan.

As many as 5.1 million Americans have Alzheimer’s disease and that number is likely to double in the coming years. At the same time, millions of American families struggle with the physical, emotional and financial costs of caring for a loved one with Alzheimer’s disease.

The initiatives announced include the funding of new research projects by the NIH will focus on key areas in which emerging technologies and new approaches in clinical testing now allow for a more comprehensive assessment of the disease.

“This research holds considerable promise for developing new and targeted approaches to prevention and treatment,” according to the press release.

Specifically, two major clinical trials are being funded. One is a $7.9 million effort to test an insulin nasal spray for treating Alzheimer’s disease.

A second study, toward which NIH is contributing $16 million, is the first prevention trial in people at the highest risk for the disease. That $100 million study was the topic of a Page One story in The New York Times Wednesday, as well as coverage in papers such as The Wall Street Journal.

http://www.nytimes.com/2012/05/16/health/research/prevention-is-goal-of-alzheimers-drug-trial.html

http://online.wsj.com/article/SB10001424052702303505504577406431528720826.html

That test will involve a drug from Genentech Inc., crenezumab, and most of the participants will “come from the world’s largest family to experience Alzheimer’s, an extended clan of 5,000 people who live in Medellin, colobia, and rmeote mountain villages outside that city,” The Times reported.

As for as the Obama plan, the Health Resources and Services Administration has awarded $2 million in funding through its geriatric education centers to provide high-quality training for doctors, nurses, and other health care providers on recognizing the signs and symptoms of Alzheimer’s disease and how to manage the disease.

The Obama initiative also includes giving easier access to information to support caregivers. As part of that, the HHS’ new website, www.alzheimers.gov, offers resources and support to those facing Alzheimer’s disease and their friends and family.

“The site is a gateway to reliable, comprehensive information from federal, state, and private organizations on a range of topics,” Tuesday’s press release said. “Visitors to the site will find plain language information and tools to identify local resources that can help with the challenges of daily living, emotional needs, and financial issues related to dementia. Video interviews with real family caregivers explain why information is key to successful care giving, in their own words.”

The plan also includes an awareness campaign, with TV ads encouraging caregivers to seek information at the new website debuting. This media campaign will be launched this summer, reaching family members and patients in need of information on Alzheimer’s disease.

In 2013, the National Family Caregiver Support Program will continue to provide essential services to family caregivers, including those helping loved ones with Alzheimer’s disease. This program will enable family caregivers to receive essential respite services, providing them a short break from care giving duties, along with other essential services, such as counseling, education and support groups.

By Attorney Gordon Johnson

800-992-9447

 

Let’s talk about your therapy.  You were getting therapy at the nursing home in Elizabethtown?

Yes.

Do you remember any of that?

            Bits and pieces.

What do you remember?

I remember I used to have to walk.  I guess they were the walking bars you had in between you to hold you up.  I remember being in occupational therapy.  My dad actually went on the Internet and checked out something for me.  The whole side, my whole left side was paralyzed and my dad found that it was a form of Bell’s Palsy.  So I had to recondition all that.

My speaking at first, there were problems with it, but I recovered that actually rather quite rather quick and so I didn’t have occupational therapy  or speech therapy for too long.

You have an injury in your brain that affects your cognition, effects memory, effects emotions.  But lets start with the more physical natures of the injury you suffered. You weren’t able to walk initially?

            No, I still have problems.

You had some left sided paralysis?

            Yes

So let’s first talk about the paralysis and then we’ll talk about the walking.Do you have a memory of when you had profound problems in the left side?

All I can really remember was my arm was stuck like this and it took a long time for them to be able to get it down.

Do you remember the physical therapy working with your left arm?

Working with my left arm, yes, because it was very tough for them to get it down.

Talk to me about that therapy.

Actually for me, that was very painful because for them they had to keep on pulling it down because I would sleep – I still sleep a little bit with this arm up but they had to keep pulling it down to stretch the muscles and that for me was very painful.

What do you understand to be the cause of  the spasticity you had in that left arm?

The only thing I could come up with and this is, like I said from what my dad told me, is how the angle of the vehicle hit and how hit my head.

Do you now have normal  use of your left side?

            I’d say it’s about 75 percent.

Show us what you’re range of motion looks like with your left arm.

Well my range of motion, I mean, it’s better than it was but I still… I’ve had my back operated on.  My left side still goes numb.

What kind of feeling do you have now.

When I had my back operated on, because I had one of my ribs pressing on – there’s a main thing that goes and they’re pressing on it and pressing on the nerve to where I couldn’t feel, so they go and fix that.  That, that was very dramatic for me because I could be sitting there watching TV or talking with somebody and all of sudden my whole left side go numb and I would freak.

Are the back problems, are those injuries you suffered in the accident?

They don’t know for sure.  The doctor said more than likely it is, but he can’t guarantee it.

How many years have you had problems with tingling in your lower, lower part of your left side?

            I still have them, since the accident.

There could be a number of causes and one could be that, it could be this injury to one of your discs in your lower back.

            Yes.

Is that what they did surgery on?

Yeah. One of my discs was bulging out and that’s where it was and it was pressing the vein between it and the rib.

When you say vein, do mean the nerve root?

            The nerve root.

After they did the surgery did that tingling stop or did it last?

It’s not as bad anymore.  It still happens but not as often, not as much.  I still have problems.

Establishing causation to conditions that require interventions decades is always complex, but there can be no doubt that a collision serious enough to do this much damage to Michael’s skull and brain, has the potential to injure or weaken any part of his body.  While he is old enough to have chronic problems, the vulnerability which he had as a result of the accident, in all likelihood put him in a spot to have these problems prematurely. It is also probable that because he had the partial paralysis, that symptoms of a bulging or herniated disk might have been missed or misattributed.

Next in Part Six – Partial Paralysis Related to Severe Brain Injury

By Attorney Gordon Johnson

800-992-9447

 

Part Four – Who Michael Was Before TBI

 

Let’s talk about who you were be, and what your dreams, aspirations were, before you got hurt.  You were a college student?

            Actually, UWO was my third college.

Did you have any idea what you wanted to become after you graduated from college?

I really and truly had no idea.  This might sound kind of weird, but my object was to go to school for as long as I could, get a huge debt and die.

I remember having somewhat the same thoughts at 22, when I started law school.

And is that what you said before your injury?

That’s what I said before.  The girl I was dating, when I had my accident, constantly reminded me of what I said about that because she thought it was kind of funny.

What other schools did you go to?

            I went to EKU for a semester.

That’s Eastern Kentucky University.

It was Eastern Kentucky University and then I went to the University of Louisville and I was kicked out, flatly asked to leave.

Poor grades?

That and I was drunk all the time.

How did you wind up at the University of Wisconsin in Oshkosh?

I followed a girl that I was dating at the time. And at University of Wisconsin Oshkosh they have a program.  I was diagnosed with being dyslexic before I had my car – I didn’t know, I was 21 when I got diagnosed, and they have a program (for that) so that’s where I went and got involved with that.

You started in the fall the year before your accident

I started in, yes the fall of whenever. (His accident was in March of 1993).

Do you remember you ever taking exams at University of Wisconsin Oshkosh?

I can remember most of the exams that I had I think were essays, because of my major.

What was your major at the time?

            Human Services.

Now you said you followed a girl.  Was she from Louisville and came up here for school?

She actually was born in Neenah.  She went to live down in Texas, Katy, Texas for a while.  Yeah, that’s right.  And then she came to Louisville with her mom.  She went to the Louisville Presbyterian Seminary and then her mom had her transferred to Linciner, Wisconsin and she got diagnosed up in UWO.  Then she talked me into coming and getting diagnosed.

What was she diagnosed with?

            Dyslexic.

How long had you dated her?

I dated her for eight years. I dated her for four years before the accident and four years after.

Did you ever get married?

            No.  I’ve been married, but I didn’t marry to her.

You weren’t married before the accident?

            No.

What did you like to do in terms of recreational activities?

            Well when I was at the University of Louisville, I drank.

When you say drank, typical college student type drinking?

I’d say I was on the verge of being an alcoholic.  That’s how to describe it – every week night, pretty much six to seven days of the week I was drunk. I lived with my parents.  I was part of a fraternity and I did have enough common sense to stay in there when I was inebriated and not drive home.

Were you interested in sports?

Well I’m from Kentucky.  Basketball is the big thing in Kentucky and I played basketball mostly recreational and in grade school.

Did you play in high school?

            No.

Where’d you go to high school?

            de Sales, Saint Francis de Sales.

And that’s a Catholic school in Louisville?

            Catholic, because my grade school was Saint Agnes.

What other interests did you have in high school?

Well actually, I can’t really remember.  Now it’s a lot different.  I like to read which I never did beforehand.  I read everything from philosophy to fiction, to biographies.  I collect.  When I’m stressed I really focus on those.  The cards and books and comic books.  but now I like to go on the computer and I have a – one son myself and I’m getting married in September and I’m going to be getting three more children. That’s what I do now is watch them during the summer.

Our interview of Michael was done in two parts, separated by about 10 months. The first was done in June of 2011, the second part in April of 2012. The interview was originally scheduled in a library conference room, but had to be terminated because a meeting was scheduled for such conference room before we had finished.

Next In Part Five – Recollections of Therapy for Severe Brain Injury

http://www.ksla.com/story/18332368/two-investigations-underway-in-oil-rig-fatal-fall

Zachary “Ty” Stewart, 22, was flown to Louisiana State University in Shreveport, La., after the accident on the derrick in south Caddo Parish, KSLA reported. He died at the hospital.

There are two separate investigations of the fatal accident taking place, according to KSLA. One is being done by the company that owns the well, Savanna Energy of Calgary, Canada, and the other by the Occupational Safety and Health Administration (OSHA).

Caddo Parish officials said that Stewart had been wearing a safety harness, KSLA reported. But it was unclear if he was wearing it when he fell and it broke, or if he didn’t have it on.