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Traumatic Brain Injury Healing Tips

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Stay Away from Ordinary Drugs! Take the Natural Route!

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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.

Healing of a TBI – 4 Ways to Accelerate Healing from a TBI

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Healing:

When you get a traumatic brain injury (TBI), your life will probably never be the same. Although the time of healing depends on the area of your brain that was most affected, it can take up to several months to re-learn some of the most common things that you usually took for-granted; this tends to put TBI patients under a lot of stress. 

Although it is normal to have stress, too much stress can cause other serious health problems, including heart problems. Stress can affect your ability to be focused, think clearly or be organized, as well as it can have a negative impact on relationships with your closest family members and/or friends. Learning how to manage your stress should be one of your paramount concerns. When you are under stress, you will likely start to feel anxious and frustrated.

4 ways to speed up your traumatic brain injury healing:

#1: Learn To Relax:

Learning to relax is never easy, and it may be more complicated in your situation. However, there are certain things you can easily do to train your mind and body to relax. You might want to try out breathing deeply while focusing on your breathing, do some visual imagery, or thinking positive. Although it may take you some time to be able to relax, it will help a lot.

#2: Learn To Reward Yourself:

Rewards can be good and rewards can be bad; it all depends on how you manage them. Say, something like therapy, occasionally going to something like therapy is the last thing we want to go and do.  However, sometimes, we just need a push. Whenever you achieve one of your goals, reward yourself. It doesn’t need to be anything fancy or expensive. Just think about the things that give you more pleasure. It can be as simple as having that amazing cup of coffee you love, read a great book, or watch some specific TV show. Whatever works best for you.

#3: Keep A Regular Schedule:

One of the things that your brain is going to appreciate and that is going to speed up your TBI healing are routines. Just think about children, especially babies. They understand very little,  if you manage to set them to eat and sleep at the same time, everyday, their bodies and mind will quickly adapt. No matter how old you are, your brain keeps working the same way and reacts a lot better when you have routines. Make sure that you have specific times for eating and sleeping.

#4: Regular Exercise:

Getting regular exercise is good for everyone, as you already know. When you’re looking to speed up your TBI healing process, make sure regular exercise is a part of your daily routine. You do not need to workout like a bodybuilder or anything like that. Simply take a walk,  for about 30 minutes every day.

Although you don’t have complete control over your TBI healing, there are things that you can do that can make it quicker.

Check out: How Exercice Can Help Heal The Brain After a TBI

How to Prevent Neurons from Dying after Brain Injury

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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

 

 

How a Brain Injury Tells The Body it is Hurt

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Brain Injury – Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans.

 

Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells’ purpose is to defend and protect the body, ironically the brain’s “call to arms” may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain.

In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain.

“This work describes an entirely new way that the brain talks with the body,” says Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. “Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body’s own excessive immune response.”

Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years.

The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell’s metabolism by breaking down fatty molecules into smaller components that cells use for every day functions.

To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working.

Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2’s involvement but still didn’t tell them about the signal sent from the brain to activate the body’s immune response. According to Haughey, after many failed experiments to determine the brain’s messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of “exosomes” — miniature vesicles released from cells.

“That conversation was the ‘Ah-ha’ moment when it all began to make sense,” says Haughey.

He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell’s surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA.

To test that exosomes were the source of this brain to body communication, Haughey’s research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains.

The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain.

When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury.

Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs — short bits of RNA that don’t code for genes — at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation.

“Given the therapeutic potential of the nSMase target, we’re now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use,” says Haughey.

 

Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.

 

Journal Reference:

Alex M. Dickens, Luis B. Tovar-y-Romo, Seung-Wan Yoo, Amanda L. Trout, Mihyun Bae, Marlene Kanmogne, Bezawit Megra, Dionna W. Williams, Kennith W. Witwer, Mar Gacias, Nino Tabatadze, Robert N. Cole, Patrizia Casaccia, Joan W. Berman, Daniel C. Anthony, Norman J. Haughey. Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions. Science Signaling, 2017; 10 (473): eaai7696 DOI:10.1126/scisignal.aai7696

 

Citation:

Johns Hopkins Medicine. “How the injured brain tells the body it’s hurt.” ScienceDaily. ScienceDaily, 18 May 2017. <www.sciencedaily.com/releases/2017/05/170518104041.htm>.

Sleep is Important in the Healing of TBI

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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

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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:

  1. 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)

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“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

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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.

Positive Thoughts, Positive Results

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Audio:

– “Through my own experience dealing with a TBI, I found it beneficial to think positive, not only to me; but the world around me.” -Ryan

There may be no different choice around it, sorry…
you will enjoy negativity in your lifestyles–maybe on a day by day incidence.
There may be some of those days in which you want you stayed inside, laid on the mattress and played tag with the snooze button. There can be those days in which the people, locations, matters and events in your existence come collectively to shape one massive large mass of ‘suck’. As they are saying, things happen. For us in the ‘healing process’, the technique of navigating the bad that takes place to us can be an thrilling experience.
I am now not saying that the mere sliver of negativity will compel you to hurry without delay to the liquor store, corner tavern or your supplier, but in case you let the terrible things simmer and stew inside the crockpot of the soul chances are going to be almost exact that we are able to smell what we are cookin’ and it’ll not indicate properly for us.
The negative events that we encounter in our day-to-day doings are one of the most not unusual snares that we can fall into in regards to relapse. It’s sincerely crucial to stand what stresses, angers, and frustrates us head-on, but ‘cooking’ inside the juices of adversity and permitting it to run insurrection is ‘no bueno‘. How can we maintain the finger off the cause at the same time as shifting forward and keeping our sanity intact?
Understand the power of superb wondering in healing.
We ‘suppose’ a lot
have you ever ever thought approximately how many thoughts you’ve got in a single day?
Consistent with some estimates, we as people average between 40,000 to 60,000 different thoughts an afternoon. Isn’t that remarkable??  That may be a ton of information that passes thru our gray rely, and it’s miles a secure bet that a honest percent of those mind are the ones that motive us grief and problem to various tiers. Paying payments, elevated workload or college work, family issues, tickets, remembering to take the kids to soccer practice/dance class/lacrosse…the listing can go on and on…
It’s no wonder why there are days when we lay down and experience like we have been hit with the aid of a truck. Bad electricity drains us and breaks us down, and if we permit ourselves to stay stuck within the doom and gloom the manner we view ourselves, others and the world round us starts to bitter. While we live in Debbie Downer mode, we are extra prone to feeling prolonged periods of depression and anxiety because we stay caught in emotions of anger, frustration and hopelessness–and that is horrific in we’re looking to maintain our sobriety.
While we stay stuck in negativity, we’re at greater danger for growing high blood pressure, elevated times of infections, cardiovascular ailment and digestive problems. Moreover, research has shown that continual pressure and negativity can genuinely lower our lifespan with the aid of shortening our telomeres (the “end caps” of our DNA strands, which play a massive role in getting older).
It’s miles truly essential that we include advantageous wondering in recuperation if you want to stay on the level. As with the whole lot that we do in recuperation, staying wonderful in sobriety takes realize how.
Embracing Positivity In recovery
whilst you are careworn with the grind of existence and are weighed down via the negative, you’ll be amazed to analyze that some of the things that we agonize and dread in reality flip out for the pleasant. How many instances has that happened to you?  Our pals at Happify daily proportion the following:
85 percent of the stuff we fear about end up having a tremendous or neutral final results.
Inside the occasion that what we fear about becomes reality, eighty percent of humans say they treated the outcome higher than they thought they could.
In our recuperation, it is important to maintain this in mind. We regularly pay attention around the tables of 12-step meetings the phrase this too shall pass, and at the same time as this pronouncing is properly-worn (and dare we say cliche) it’s miles absolutely the fact. Whether or not we believe it or no longer, we have an enormous power in reserve and we can persevere and pull via matters regardless of what the chances.
Easy recommendations to growth Positivity in your recovery
when we talk of positivity in recuperation, you already possess a number of the tools you want. When you have are in a drug remedy application or have already efficiently finished a treatment program, you had been taught the simple but essential life skills needed to keep your recuperation game on point at the same time as efficaciously navigating the molehills and mountains of daily existence.
You can additionally have picked up some of those abilities on your homegroup, via operating along with your sponsor or through a member of the family or pal. The subsequent are easy ways that you may incorporate and enhance tremendous questioning for your healing.
Meditate
One manner to increase your tremendous questioning in recuperation is through the usage of meditation. Meditation is a powerful device which you have at your disposal, and if you may carve out 15 mins an afternoon you may advantage first-rate advantage. Whether it is simple aware meditation practices or greater formal meditation practices, focusing on your breathing is enjoyable and allows you attention on the here and now and the way you can impact the present. Whilst you exercise meditation frequently, any mind of the past or future fall to the sides and you can place your energies on what you may do right now to be happier.
Take duty in your existence
you know this, but you on my own are liable for your life, and also you on my own have the power to convert your life. This simple truth can be difficult to border in our minds due to the fact we often pinned the blame on others when we had been lively in our dependancy. As stated in advance, we’ve limitless electricity that resides inside us and while the chips are down we may be amazed at how we are able to pull through. Now could be the time to position the capabilities and realize how to proper use.
Stick with the Winners
if you need to come to be greater nice, you want fantastic role models. Another one of the commonplace announcing heard in 12-Step meetings is stay with the winners and the that means is simple. You want to dangle with folks that meet adversity of their existence with energy and fortitude. Whether or not is it your peers in restoration, circle of relatives participants, friends or whomever, discover the ones people in your lifestyles who recognise how to deal with negativity in a wholesome, constructive and sensible way and soak their know-how in like a sponge.
Be of provider to a person
in order to tug out of a tailspin, it is good to get out of your self and be of carrier to someone else. Volunteer your time at a drop-in middle, senior citizen home, or nearby sanatorium. Be a mentor or a sponsor to someone who’s new in recovery.
Smile
To generate positive mind for your healing, every now and then you simply ought to faux it that allows you to make it. You can not sense like it or up to it, however the easy act of placing a grin in your face may additionally help you get out of the doldrums. It’s miles often said that it takes extra muscle tissue and strength to frown than it’s far to grin. Simply the simple act of a grin could make you feel lighter. Provide it a attempt.

 

Diffuse Axonal Injury

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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.

 

  • 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.
  • Mechanism
  • 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.
  • 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.
  • Characteristics
  • 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.
  • 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.
  • Histological characteristics
  • 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.[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.
  • Cytoskeleton disruption-
  • 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).
  • 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.
  • 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.
  • Calcium influx
  • 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.
  • 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.
  • 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”.
  • 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.
  • Diagnosis
  • 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.
  • 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.
  • 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.
  • 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]
  • Treatment
  • 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).
  • History
  • 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.