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traumatic brain injury
Important Facts about a Traumatic Brain Injury
-Most people, after suffering a TBI do make a good recovery.
-Using a seatbelt and wearing a helmet is one of the best ways to help prevent a TBI from occurring.
-One of the most commonly injured areas of the brain is the Frontal lobe, which controls thinking and emotion regulation.
-Males are twice as likely to incur a TBI than females are, according to statistics.
This post’s intention was not to present unfortunate facts about TBIs, below are some of the best ways to further your healing from a TBI.
-There Are Groups with Resources to Help TBI Survivors and Caregivers.
Practice going to occupational, speech, and physical therapy regularly. This helps improve how your mind functions. Since it has been proven that the brain has Nuroplasticity, therapy only helps accelerate your healing.
Beware of overstimulation. Overstimulation to the brain and or body could leave a detrimental effect to you. It is important to someone who has a TBI to regulate their energy as best as they can. A sufficient amount of sleep is paramount in one’s recovery.
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Living with an Invisible Disability – TBI (Traumatic Brain Injury)
Hello, I am David A. Grant, writing for TBITalk.com .
While there are many people who have lived with lifelong disabilities, I am a relative newcomer to being disabled. For the first forty-nine years of my life, I was fully-abled. Everything changed in late 2010. I was cycling in southern New Hampshire when a sixteen-year-old driver t-boned me. In two ticks of a clock, I went from being fully abled to living the life I live today.
This was not the plan I had for myself.
Unlike many who are visibly disabled, I live with what is commonly called an “invisible disability.” Millions of us that live in today’s society face challenges that are not visible to the naked eye. The list of invisible disabilities is long: autism, fibromyalgia, PTSD, depression, multiple sclerosis, and many mental illnesses are all part of this family of unseen disabilities.
Though the Americans with Disabilities Act (ADA) recognize most hidden disabilities, most of us with invisible challenges fly just under the radar screen of society.
When you see someone in a wheelchair, or perhaps walking with a companion animal, it’s pretty clear that that person may be disabled. But not so with people like me. I can drive without assistance. I work on a part-time basis, spend time with my granddaughter, and go about my day as many others do.
However, looks are deceiving
[embedyt] https://www.youtube.com/watch?v=iGaIJYERpwE[/embedyt]
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My cycling accident left me with Post Traumatic Stress Disorder (PTSD). While a common misconception exists that PTSD is exclusive to the military community, many who experience different kinds of trauma also live with the daily challenges that come with PTSD.
My life today feels like an acronym soup, often defined by short bursts of letters that have indescribable effects on my life. In addition to PTSD, I live with PCS (Post Concussive Syndrome) as well as the lasting effects of a TBI (Traumatic Brain Injury).
Like many who have experienced trauma, my life is now split between “before and after.” My life before my accident was average. In fact, some might call it downright dull. I went to work as a self-employed, self-sufficient individual. I’d suit up and show up, pay my bills, spend time raising my children, and move forward toward a future that did not include trauma. In fact, I’d planned to remain busy, happily married, work for another fifteen years, and then retire, doing things that retirees do.
Years ago, I heard a saying that still makes me smile. “If you want to make God laugh, make plans.” If there is an element of truth to this, he must have enjoyed a belly laugh at my plans.
Accepting that I am a disabled adult has been a long and painful process. I have fought the disabled moniker since it was first presented to me in early 2012 when a well-respected doctor let me know that I was “permanently disabled” because of my injury.
How dare he call me disabled? For years, I hated him for that. I am not a big fan of the “H” word, but hate him I did. I fought his diagnosis for many years.
I had completed neuropsychological testing about a year after my injuries in a fact-finding effort to see where my deficiencies remained, and what I could do to speed my recovery. The test results were quite grim. In a couple of key categories, I scored in the bottom 5%.
I, once prideful about my perceived life successes, now sat at the bottom of my cognitive class.
Sure, my tests showed that I was in the lower 5% for complex problem solving and verbal recall. A speeding car had hit me a year earlier. Your scores would have crashed too if you met a teenage driver at 35 MPH with nothing but a plastic helmet to save your life. But disabled? No way. You have got me confused with someone else, someone who might actually be disabled.
I did all I could to prove him wrong. I moved on with my life, wrote a couple of books, started a new career and continued to stumble forward in this new second life.
I’ve since learned that it is easier to realize perspectives in the rearview mirror. With the passage of time comes a new clarity. Here is where it gets hard.
Humbled, I eventually had to admit that the doctor was right. I am disabled. This is perhaps the biggest single mea culpa of my life. I needed to come to terms with my disability in my own terms and in my own time.
For several years, I tried to live my life as I did before my accident, but there were challenges at every turn. Vertigo created the occasional appearance of drunkenness, though I’ve not had a drink for decades. Slow cognitive processing speeds meant that I lived in a perpetual state of time delay. Sure, you can ask me a question, but don’t hold your breath waiting for me to answer. It may take some time for me to understand what you just asked me. Memory issues mean that I might ask you a question, then ask it again, and perhaps a third time for good measure.
None of these challenges is blatant to the naked eye, but spend a bit of time with me, and you’ll learn soon enough that I’m not as normal as I look. Such is the nature of being invisibly disabled.
I fought my fate for close to seven years until I could not fight it any longer.
It has only been over the last few months that I have accepted what I had been most afraid of. By accepting that I am a disabled adult, something unexpected happened—I have gained freedom. I no longer need to struggle to be who I was before my accident.
I am more at peace with my life than I have been in years. I am slowly learning that even though I am disabled, there is still much that I can do. And quite unexpectedly, I feel relief. I no longer have to prove myself. The internal conflict about who I am and how I fit into today’s world has finally gone quiet.
It is in that newfound calm that I will continue to rebuild my new life.
Stay Away from Ordinary Drugs! Take the Natural Route!
Ordinary drugs have shown limited benefits for brain (serious physical or emotional harm) since they don’t address the main cause of what is driving (hard hit to the head that knocks you out) signs of sickness. Now, no neuro-(serving or acting to prevent harm) treatment options exist that improve signs of sickness after a TBI.[5] Now many (people who work to find information) are starting to study a wide range of natural compounds and vitamins that have promising broad-spectrum, (related to protecting nerves from harm), and anti-swelling activity. Curcumin, green tea, extremely important fatty acids, resveratrol, and vitamin E are some of the compounds with potential medically helpful benefit in the treatment of TBI.[3] The (event(s) or object(s) that prove something) for these substances is still very early (and subject to change) and there is much more research needed to confirm these effects in humans, but they offer possible options in a condition with no known treatment.
CURCUMIN – is an active compound found in the spice turmeric. It has attracted much interest as a possible treatment for many long-lasting sicknesses, including Brain disease (AD), cancer, and heart disease due to its powerful anti-swelling and body-protecting chemical properties.[6] While results are still early (and subject to change), curcumin extracts are showing positive benefit in neuro-recovery, cell membrane (making steady/making firm and strong), and reduction of oxidative stress in animals.[8,9,19,11] Other potential medically helpful effects include increasing brain growth factors, chelating heavy metals, reducing cholesterol, and protecting mitochondria.[3]
The problem with curcumin is that it doesn’t (mix with and become part of a liquid) well in water, making its (mental concentration/picking up of a liquid) through the (tube from the mouth to the anus) limited. It is important to point out that only free curcumin (not other curcumin molecules) can pass the blood brain (something that blocks or stops something). Newer, fat (able to be dissolved in something) creations, such as a curcumin extract called Longvida, appear to improve delivery into the bloodstream, past the blood brain (something that blocks or stops something) and into brain tissue.[12,13] Longvida curcumin was developed for nerve-based sicknesses/problems by (people who work to find information) at UCLA. Curcumin stands as one of the most promising (related to protecting nerves from harm) and medically helpful agents in TBI and PCS due its excellent safety profile and wide ranging (machine/method/way) of action.
(Editor’s note: Also, other brands of curcumin have been created for improved bioavailability, including NutriCure by NAKA. Or,/In a different way, (ancient medicine) doctors recommend cooking turmeric in oil, and combining it with black pepper, to improve bioavailability of its voters/parts.)
GREEN TEA – like curcumin, is a well-known and widely used/ate/drank/destroyed herb with broad-spectrum body-protecting chemical activity. Its (related to protecting nerves from harm) properties can be attributed mostly to the power body-protecting chemical molecule called epigallocatechin-3-gallate (EGCG), the amino acid L- theanine, and to a lesser degree (drug that gives you energy).[14] EGCG has been shown to have body-protecting chemical and anti-swelling effects in animal models of brain injury.[15,16,17] One (like nothing else in the world) aspect of green tea is that the L-theanine content may offer protection from excitotoxic injury that happens immediately after a (hard hit to the head that knocks you out).[17] There is a clear need for more research, but promising (event(s) or object(s) that prove something) hints that even regular dietary consumption of green tea may have a (related to protecting nerves from harm) effect if a (hard hit to the head that knocks you out) happens. Some other plant compounds such as resveratrol (found in red wine) and anthocyanidins (found in berries) have also shown (related to protecting nerves from harm) effects.[3] Unlike (related to medical drugs) medicines, these plant extracts have many modes of action and work cooperatingally with each other. They also support the function of the body’s own body-protecting chemical systems and nerve repair systems.[18] There have been some animal trials using plant compounds such as resveratrol, (showing or proving) an anti-swelling and (related to protecting nerves from harm) effect in TBI, but like green tea, there have been no human trials to date.[19,20] Since these molecules are found in many colourful fruits and vegetables, it would be a safe recommendation for people with TBI or PCS to include/combine them into their diets.
OMEGA-3 FATTY ACIDS – have long been thought about/believed extremely important for brain development and function. Docosahexaenoic acid (DHA), and to a lesser degree Eicosapentaenoic acid (EPA), is mostly found in nerve membranes; they influence cell signaling and anti-swelling pathways.[21] Since the human body cannot (in a way that produces a lot with very little waste) convert plant-based extremely important fatty acids to EPA and DHA, fish oil adds to/helpful additions are the best source of the active parts/pieces. (It is important to note that, while using/eating/drinking fish high in omega 3 fatty acids is desirable, the heavy metals and polychlorinated biphenyls (PCBs) found in most fish is a concern, especially for brain function.)[22] Some trials in animal models of TBI have found that DHA and omega-3 addition (to something else) improves thinking-related function, reduces nerve swelling, (makes steady/makes firm and strong) cellular energy production, and increases nerve repair.[23,24] One of these studies showed that pre-injury (something extra you eat or drink) with fish oil also had a (related to protecting nerves from harm) effect.
VITAMIN E – is a commonly studied natural compound for brain health since it has a powerful body-protecting chemical effect, specifically in fatty tissue (i.e. nerves). Some animal studies have found that vitamin E addition (to something else) reduces nerve damage and improves thinking-related performance following repeating, concussive brain injury.[25,26] Interestingly, addition (to something else) before the (hard hits to the head that knock people out) also had a (related to protecting nerves from harm) effect.[26] A good creation should provide all eight molecules of vitamin E, with the highest proportion being the strong gamma-tocopherol, which is carefully thought about/believed the most anti-swelling part. Also, vitamin E works with other body-healing chemicals, such as vitamin C and coenzyme Q10 as part of a body-protecting chemical network. This highlights the need to consume body-healing chemicals together in order to support their proper (related to the body function of living things) function.
CREATINE, L-CARNITINE, ALA AND MORE – There are some other newly-visible (vitamins, minerals, protein, etc.) now being studied for TBI. Creatine, an amino acid found in muscles, has human (event(s) or object(s) that prove something) supporting its benefit in reducing signs of sickness after a (hard hit to the head that knocks you out). Benefits were found for addition (to something else) before and even after the injury, (event(s) or object(s) that prove something) that creatine can be used to prevent and treat nerve-based shortages after a (hard hit to the head that knocks you out). There are other promising adds to/helpful additions being studied, including acetyl L-carnitine, alpha lipoic acid, B12, ginkgo biloba, and magnesium.[27]
HYPERBARIC OXYGEN THERAPY – Another (action that helps a bad situation) suggested to have helpful effects on TBI recovery is hyperbaric oxygen therapy (HBOT), although more research is needed to confirm its benefit.
How to Prevent Neurons from Dying after Brain Injury
Electrical stimulation of the brain by applying current to the eye may help retinal nerve cells to survive injury. While these neurons may not be restored to full function, they are prevented from dying. But to achieve survival, their interconnections, the dendritic tree, needs to disconnect rapidly for the protective action to unfold. In a study published in Scientific Reports, researchers from Magdeburg University (Germany) and The Chinese University of Hong Kong report that for rats and mice, repetitive transorbital alternating current stimulation (rtACS) may help preserve visual neurons from cell death after injury.
Because the tissue at the back of the eye, the retina, is part of the brain, researchers can directly observe how brain cells react in the living animal. The researchers repeatedly monitored neurons in both rat and mouse retinas after an optic nerve injury and measured neuronal death after this lesion. Surprisingly, a neuroprotective treatment with electrical alternating current stimulation increased cellular survival in the eye´s retina, but it also induced a fast and complete stripping-off of the neuron’s dendritic tree. The dendrites are like a tree receiving many thousands of signals from other neurons. This enables them to process visual information and then transmit the signals along the optic nerve towards the brain. By retracting its dendrites, the cell withdraws itself from this intercellular communication network and becomes silent — which helps its survival.
The test animals were divided into groups and subjected to both real and sham treatments. For the rats, optic nerve crush (ONC) was used to induce an injury in some of the animals to mimic glaucoma. Some animals and not others (sham) were treated with rtACS, resulting in three test groups: ONC/rtACS, ONC/Sham, and Sham/Sham. Using in vivo confocal neuroimaging (ICON) and measurements of Visual Evoked Potentials (VEP), the researchers could determine whether a neuron had survived and whether it was still functioning. The ONC and the first rtACS stimulation were done on day zero. ICON was performed on day 4, followed by rtACS or sham stimulation. On day 7 post ONC another ICON was performed.
For the mice, a confocal laser ophthalmoscope was used to image the dendritic structures of the retina for three groups of subjects, ONC/rtACS, ONC/Sham and Sham/rtACS. The mice received rtACS on days 0, 3, 6, 9 and 12 after ONC and images were taken on days 3, 7 and 14.
According to lead author Petra Henrich-Noack, PhD, Institute of Medical Psychology, Otto-von-Guericke University, Magdeburg, Germany, “With our experiments, we have detected so far unknown ‘silent survivor cells’ in the brain and it will be exciting to find out whether they later die or can be reactivated.” Surprisingly, neurons in the retina of animals that survived better when treated with rtACS lost their dendritic tree completely within the first 3 days after the lesion. The authors suggest that this early structural isolation might protect the neurons from the “toxic” excitation that is known to appear soon after brain damage.
Story Source:
Materials provided by Institute for Medical Psychology, Otto-v.-Guericke University Magdeburg. Note: Content may be edited for style and length.
Journal Reference:
Petra Henrich-Noack, Elena G. Sergeeva, Torben Eber, Qing You, Nadine Voigt, Jürgen Köhler, Sebastian Wagner, Stefanie Lazik, Christian Mawrin, Guihua Xu, Sayantan Biswas, Bernhard A. Sabel, Christopher Kai-Shun Leung. Electrical brain stimulation induces dendritic stripping but improves survival of silent neurons after optic nerve damage. Scientific Reports, 2017; 7 (1) DOI: 10.1038/s41598-017-00487-z
Sleep is Important in the Healing of TBI
There is a link between the amount of sleep the patient gets and the rate at which their brain heals.
A study of 30 people that were hospitalized for moderate to severe traumatic brain injuries found that sleep quality and brain function improved in tandem, researchers reported in the journal Neurology.
“Patients who still had low levels of consciousness and cognitive functioning would “sleep for a couple of minutes and then wake up for a couple of minutes,” both day and night, says Nadia Gosselin.
The results increase the possibility that patients with brain injuries possibly recover even quicker if hospitals would take measures to restore normal sleep patterns, Gosselin says. Drugs are one option, she says. Another is making sure patients are exposed to sunlight or its equivalent during the day and at night rest in a dark, quiet environment.
“I think bad sleep can have bad consequences for brain recovery,” she concludes.
New Test to Quickly Identify Mild Traumatic Brain Injury
A new test using peripheral vision reaction time could lead to earlier diagnosis and more effective treatment of mild traumatic brain injury, often referred to as a concussion. Identify Brain Injury
A new test using peripheral vision reaction time could lead to earlier diagnosis and more effective treatment of mild traumatic brain injury, often referred to as a concussion, according to Peter J. Bergold, PhD, professor of physiology and pharmacology at SUNY Downstate Medical Center and corresponding author of a study newly published online by the Journal of Neurotrauma.
While most patients with mild traumatic brain injury or concussion fully recover, a significant number do not, and earlier diagnosis could lead to better management of patients at risk for developing persistent symptoms, according to Dr. Bergold and his co-authors.
Lingering symptoms may include loss of concentration and/or memory, confusion, anxiety, headaches, irritability, noise and light sensitivity, dizziness, and fatigue.
“Mild traumatic brain injury is currently diagnosed with subjective clinical assessments,” says Dr. Bergold. “The potential utility of the peripheral vision reaction test is clear because it is an objective, inexpensive, and rapid test that identifies mild traumatic brain injury patients who have a more severe underlying injury.”
Dr. Bergold’s co-authors include colleagues from the University of Texas Southwestern Medical Center; The University of Texas at Dallas; Washington University; the National Institute of Neurological Disorders and Stroke; the Uniformed Services University of the Health Sciences; and SUNY Downstate.
The article published by the Journal of Neurotrauma is titled “Measurement of Peripheral Vision Reaction Time Identifies White Matter Disruption in Patients with Mild Traumatic Brain Injury.”
[embedyt] http://www.youtube.com/watch?v=aKZnMC5vzhU[/embedyt]
Story Source:
Materials provided by SUNY Downstate Medical Center. Note: Content may be edited for style and length.
Journal Reference:
- Kyle B. Womack, Christopher Paliotta, Jeremy F. Strain, Johnson S. Ho, Yosef Skolnick, William W. Lytton, L. Christine Turtzo, Roderick McColl, Ramon Diaz-Arrastia, Peter J. Bergold. Measurement of Peripheral Vision Reaction Time Identifies White Matter Disruption in Patients with Mild Traumatic Brain Injury. Journal of Neurotrauma, 2017; DOI:10.1089/neu.2016.4670
SUNY Downstate Medical Center. “New test may quickly identify mild traumatic brain injury with underlying brain damage.” ScienceDaily. ScienceDaily, 16 February 2017. <www.sciencedaily.com/releases/2017/02/170216120538.htm>.
What is a Diffuse Axonal Injury? (DAI)
“As tissue slides over tissue, a shearing injury occurs. This causes the lesions that are responsible for unconsciousness, as well as the vegetative state that occurs after a severe head injury. A diffuse axonal injury also causes brain cells to die, which cause swelling in the brain.”
DAI is characterized by axonal separation, in which the axon is torn at the site of stretch and the part distal to the tear degrades. While it was once thought that the main cause of axonal separation was tearing due to mechanical forces during the trauma, it is now understood that axons are not typically torn upon impact; rather, secondary biochemical cascades, which occur in response to the primary injury (which occurs as the result of mechanical forces at the moment of trauma) and take place hours to days after the initial injury, are largely responsible for the damage to axons.
Though the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton.[1] It also opens sodium channels in the axolemma, which causes voltage-gated calcium channels to open and Ca2+ to flow into the cell. The intracellular presence of Ca2+ unleashes several different pathways, including activating phospholipases and proteolytic enzymes, damaging mitochondria and the cytoskeleton, and activating secondary messengers, which can lead to separation of the axon and death of the cell.
Tips on How To Recover from a TBI
Recovering from a Brain Injury could be a long and grueling process, especially if you do not have the information to better assist you to heal. In this post, we go over how to help accelerate the healing of your brain.
Recover – Get a lot of rest around evening time, and rest amid the day.
Maintain a strategic distance from exercises that are physically requesting (e.g., substantial housecleaning, weightlifting/working-out) or require a considerable measure of fixation (e.g., adjusting your checkbook). They can exacerbate your manifestations and moderate your recuperation.
Stay away from exercises, for example, contact or recreational games, that could prompt to another blackout (it is best to maintain a strategic distance from fast entertainment mecca rides that can exacerbate your side effects or even cause a blackout).
At the point when your medicinal services proficient says you are alright, come back to your typical exercises bit by bit, not at the same time.
Since your capacity to respond might be slower after a blackout, ask your social insurance proficient when you can securely drive an auto, ride a bicycle, or work overwhelming gear.
Converse with your medicinal services proficient about when you can come back to work. Get some information about how you can help your boss comprehend what has transpired.
Consider chatting with your boss about coming back to work step by step and about changing your work exercises or timetable until you recoup (e.g., work half-days).
Take just those medications that your medicinal services proficient has endorsed.
Try not to drink mixed refreshments until your social insurance proficient says you are all around ok. Liquor and different medications may moderate your recuperation and put you at danger of further damage.
Record the things that might be harder than regular for you to recollect.
In case you’re effectively occupied, attempt to do one thing at any given moment. For instance, don’t attempt to sit in front of the TV while settling supper.
Counsel with relatives or dear companions when settling on essential choices.
Try not to disregard your fundamental needs, for example, eating great and getting enough rest.
Maintain a strategic distance from supported PC utilize, including PC/computer games ahead of schedule in the recuperation procedure.
A few people report that flying in planes aggravates their side effects soon after a blackout.
Diffuse Axonal Injury
Audio:
Diffuse Axonal Injury (DAI) A brain injury, in which damage is in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most prevalent and devastating types of traumatic brain injury, DAIs are a major cause of unconsciousness and most likely, leads to vegetative state after severe head trauma. The outcome is frequently a coma, with over 90% of patients with severe DAI never again, regaining consciousness. Those who do wake up often remain significantly impaired.
DAI can occur in every measure of severity from very mild or moderate to very severe
Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury,[1] and is a major cause of unconsciousness and persistent vegetative state after severe head trauma.[2] It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.
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DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.
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Mechanism
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Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults.[5] It usually results from rotational forces or severe deceleration. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse[6] such as in shaken baby syndrome.
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The major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another. Tracts of axons, which appear white due to myelination, are referred to as white matter. Acceleration causes shearing injury: damage inflicted as tissue slides over other tissue. When the brain is accelerated, parts of differing densities and distances from the axis of rotation slide over each other, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter. Two-thirds of DAI lesions occur in areas where grey and white matter meet.
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Characteristics
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Lesions typically exist in the white matter of brains injured by DAI; these lesions vary in size from about 1–15 mm and are distributed in a characteristic way. DAI most commonly affects white matter in areas including the brain stem, the corpus callosum, and the cerebral hemispheres.
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The lobes of the brain most likely to be injured are the frontal and temporal lobes. Other common locations for DAI include the white matter in the cerebral cortex, the superior cerebral peduncles, basal ganglia, thalamus, and deep hemispheric nuclei. These areas may be more easily damaged because of the difference in density between them and the rest of the brain.
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Histological characteristics
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DAI is characterized by axonal separation, in which the axon is torn at the site of stretch and the part distal to the tear degrades. While it was once thought that the main cause of axonal separation was tearing due to mechanical forces during the trauma, it is now understood that axons are not typically torn upon impact; rather, secondary biochemical cascades, which occur in response to the primary injury (which occurs as the result of mechanical forces at the moment of trauma) and take place hours to days after the initial injury, are largely responsible for the damage to axons.
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Though the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton.[1] It also opens sodium channels in the axolemma, which causes voltage-gated calcium channels to open and Ca2+ to flow into the cell.[1] The intracellular presence of Ca2+ unleashes several different pathways, including activating phospholipases and proteolytic enzymes, damaging mitochondria and the cytoskeleton, and activating secondary messengers, which can lead to separation of the axon and death of the cell.
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Cytoskeleton disruption-
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Immunoreactive axonal profiles are observed as either granular (B,G,H) or more elongated, fusiform (F) swellings in the corpus callosum and the brain stem (H) at 24h post traumatic brain injury. Example of APP-immunoreactive neurons (arrow heads) observed in the cortex underneath the impact site (E,G). No APP staining was observed in healthy control animals (D).
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Axons are normally elastic, but when rapidly stretched they become brittle, and the axonal cytoskeleton can be broken. Misalignment of cytoskeletal elements after stretch injury can lead to tearing of the axon and death of the neuron. Axonal transport continues up to the point of the break in the cytoskeleton, but no further, leading to a buildup of transport products and local swelling at that point. When it becomes large enough, swelling can tear the axon at the site of the break in the cytoskeleton, causing it to draw back toward the cell body and form a bulb. This bulb is called a retraction ball, the hallmark of diffuse axonal injury.
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When the axon is transected, Wallerian degeneration, in which the part of the axon distal to the break degrades, takes place within one to two days after injury. The axolemma disintegrates, myelin breaks down and begins to detach from cells in an anterograde direction (from the body of the cell toward the end of the axon),and nearby cells begin phagocytic activity, engulfing debris.
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Calcium influx
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While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca2+ into the cell and unleashing a variety of degrading processes. An increase in Ca2+ and Na+ levels and a drop in K+ levels is found within the axon directly after injury. Possible routes of Ca2+ entry include sodium channels, pores torn in the membrane during stretch, and failure of ATP-dependent transporters due to mechanical blockage or lack of energy. High levels of intracellular Ca2+, the major cause of post-injury cell damage, destroy mitochondria,and trigger phospholipases and proteolytic enzymes that damage Na+ channels and degrade or alter the cytoskeleton and the axoplasm. Excess Ca2+ can also lead to damage to the blood brain barrier and swelling of the brain.
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One of the proteins activated by the presence of calcium in the cell is calpain, a Ca2+-dependent non-lysosomal protease. About 15 minutes to half an hour after the onset of injury, a process called calpain-mediated spectrin proteolysis, or CMSP, begins to occur.[19] Calpain breaks down a molecule called spectrin, which holds the membrane onto the cytoskeleton, causing the formation of blebs and the breakdown of the cytoskeleton and the membrane, and ultimately the death of the cell.[18][19] Other molecules that can be degraded by calpains are microtubule subunits, microtubule-associated proteins, and neurofilaments.
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Generally occurring one to six hours into the process of post-stretch injury, the presence of calcium in the cell initiates the caspase cascade, a process in cell injury that usually leads to apoptosis, or “cell suicide”.
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Mitochondria, dendrites, and parts of the cytoskeleton damaged in the injury have a limited ability to heal and regenerate, a process which occurs over 2 or more weeks. After the injury, astrocytes can shrink, causing parts of the brain to atrophy.
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Diagnosis
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Diffuse axonal injury after a motorcycle accident. MRI after 3 days: on T1-weighted images the injury is barely visible. On the FLAIR, DWI and T2* weighted images a small bleed is appreciated.
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DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically. However, there are characteristics typical of DAI that may or may not show up on a CT scan. Diffuse injury has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are visible in the corpus callosum or the cerebral cortex. MRI is more useful than CT for detecting characteristics of diffuse axonal injury in the subacute and chronic time frames. Newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative. Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness.
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MRI is more sensitive than CT scans, but MRI may also miss DAI, because it identifies the injury using signs of edema, which may not be present.
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DAI is classified into grades based on severity of the injury. In Grade I, widespread axonal damage is present but no focal abnormalities are seen. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage encompasses both Grades I and II plus rostral brain stem injury and often tears in the tissue.[23]
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Treatment
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DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure (ICP).
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History
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The idea of DAI first came about as a result of studies by Sabina Strich on lesions of the white matter of individuals who had suffered head trauma years before.[24] Strich first proposed the idea in 1956, calling it diffuse degeneration of white matter, however, the more concise term “Diffuse Axonal Injury” was eventually preferred. Strich was researching the relationship between dementia and head trauma and asserted in 1956 that DAI played an integral role in the eventual development of dementia due to head trauma. The term DAI was introduced in the early 1980s.