Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Concussion”

Vision Issues Related to Brain Injury and CPM/EPM:

Hello there.

I received a comment from Elle. She has vision issues too. She did research and feels that her ongoing vision issues are related to CPM and EPM and is classified as Visual Snow. I do not know much about Visual Snow, but I have to say, it is plausible that Central Pontine Myelinolysis and Extra Pontine Myelinolysis can cause this.

I do not know anything significant about Visual Snow, but there was mention that it is attributed to other demyelinating diseases such as MS. In essence, CPM/EPM are similar in that they both are conditions that effect the myelin. There is also a connection to visual snow and ocular and classic migraines. There also seems to be a connection in this and tinnitus.

Unfortunately, today is not a great vision day for me, and the more I try to read, the more I experience the blurriness of vision. (It is so frustrating!) I tried to access medical literature that described Visual Snow, but it seems under researched.

The following are pictures and videos in regards to what Visual Snow is like for those who have it.

There seems to be a variation on how Visual Snow impacts a person's vision.

There seems to be a variation on how Visual Snow impacts a person’s vision.

Visual Snow 2

Visual Snow 3

Now, the visual condition that I experience is truly just blurry vision. (I do get ocular migraines though which started way before the brain injury.) Unlike the reports about Visual Snow, my blurry vision comes and goes. I had it earlier today, and now (about two hours later) it is gone again. It could come back in a few minutes or it might not come back at all. The blurriness can be slight or it can be extreme.

I did find a report of others with CPM and EPM who have experienced the blurry vision after injury.

http://www.ajronline.org/doi/full/10.2214/AJR.07.7052

A 40-year-old man presented with acute onset walking difficulty, slurred speech, and slight blurring of vision. Other relevant clinical history included chronic alcoholism and poor nutrition. Clinical examination revealed mild lower limb incoordination, dysarthria, and bilateral partial abducent nerve palsy. The blood tests for full blood count, renal functions (sodium, 142 mmol/L; potassium, 4 mmol/L; urea, 4.6 mg/dL; creatinine, 85 μmol/L), blood glucose (6.1 mmol/L), serum osmolality (285 mosm/kg), and liver function tests (albumin, 41 g/L; globulin, 25 g/L; bilirubin, 12 μmol/L; aspartate aminotransferase, 30 U/L; γ-gluta myltransferase, 45 U/L; and alkaline phosphate, 142 U/L) were within normal limits.

Read More: http://www.ajronline.org/doi/full/10.2214/AJR.07.7052

Another article explains the same symptoms in a woman (http://www.imj.ie/ViewArticleDetails.aspx?ContentID=3623):

Case Report
A 41-year-old lady was woken up at 5am with sudden pins and needles and weakness involving the hands, trunk and legs. She had gone to bed completely well the previous night. When she attempted to rise, she was weak and unsteady. She then experienced blurred vision and had difficulty speaking and swallowing. Her symptoms worsened over the course of the day. She was transferred to UCHG after one day. On examination she was fully conscious but dysarthric. She had sluggish tongue movements with no palatal movements and severely impaired swallowing. She had abnormal eye movements identified as opsoclonus, upgaze restriction and bilateral partial ptosis. There was pyramidal weakness in both upper and lower limbs limbs, particularly in the right lower limb. Both knee jerks were pathologically brisk and the right plantar was extensor. Other deep tendon reflexes were normal. The upper and lower limbs were severely ataxic. Sensation was normal in all four limbs.

Another case believed to be caused by CPM/EPM (http://content.lib.utah.edu/utils/getfile/collection/EHSL-FBWNOC/id/599/filename/595.pdf):

The patient’s post-operative course was uneventful until 2 days after surgery when she noticed blurred vision in
both eyes and reported difficulty distinguishing colors.
Neuro-ophthalmic evaluation 5 days later disclosed 20/25 visual acuity at near in each eye. The pupils were equal
and reacted sluggishly to direct light. There was no relative afferent pupillary defect noted. The patient could read
only one of seven Ishihara color test plates with each eye. She could count fingers in her temporal visual fields but
could see only hand motions in her nasal visual fields. Dilated fundus exam was normal in each eye.
Automated visual field testing showed an incongruous, predominantly binasal, hemianopia………..We believe a demyelinating process, isolated extrapontine myelinolysis, caused our patient’s visual loss.

So, CPM and EPM can cause vision issues, and it has been noted in other patients that it can specifically cause blurred vision. I would not be surprised that it can cause a visual snow effect, but considering Visual Snow is just now being recognized as a symptom in the medical community, I doubt that there will be literature supporting it.

It is also not surprising that a person who experiences a head injury can experience vision changes. If a brain injury is caused by penetration of a foreign object, then it might obvious why a visual change occurs, but even in subtle head injuries, a person can experience a change in vision. There might be a structural change to your eye that causes the change, but there can also be change in the way your brain processes the neural impulses that causes visual disturbances.

This link provides insight to brain injury and visual changes: http://www.brainline.org/landing_pages/categories/vision.html

The following information describes how mild brain injuries, like concussions, can cause ongoing issues, including blurred vision:

As many as 30% of patients who experience a concussion develop postconcussive syndrome (PCS). PCS consists of a persistence of any combination of the following after a head injury: headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances. Fixed neurologic deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2-4 months. Typically, the symptoms peak 4-6 weeks following the injury. On occasion, the symptoms of PCS last for a year or longer. Approximately 20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently by PCS. PCS tends to be more severe in children than in adults. When PCS is severe or persistent, a multidisciplinary approach to treatment may be necessary. This includes social services, mental health services, occupational therapy, and pharmaceutical therapy. http://emedicine.medscape.com/article/433855-treatment

The following describes that there seems to be a connection to those who have a cognitive impact after a brain injury to visual complications:

Vision problems and cognitive deficits may compound one another. The most common complaints related to visual problems associated with brain injuries include light sensitivity, headaches, double vision, fatigue, dizziness, difficulty reading, or loss of peripheral visual fields. You may feel a heightened sensitivity to light and may even need to wear your sunglasses inside. You may have to request that fluorescent lights be turned off. Computer and reading tasks may take longer than usual, and tend to be more confusing and tiring. http://www.brainlinemilitary.org/content/2009/11/recovering-from-mild-traumatic-brain-injury_pageall.html

So again, there does seem to be a parallel in brain injuries in general, and more specific conditions and diseases like MS, CPM and EPM. In other words, no matter if you suffered from a physical brain injury, a concussion, or have a brain disease or syndrome, the symptoms are comparable.

Hope that helps folks!

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Brain injury and Alzheimer’s disease:

I am searching for information regarding brain injuries and the long term implications of having a brain injury. This post was started with the belief that there is a connection between those with brain injuries and Alzheimer’s.

There are those who believe that there isn’t a connection, and there are those scientists who believe that there is. I do not think that everyone with a brain injury will develop Alzheimer’s, but I do believe that those who have a brain injury have a higher risk for it. I also believe that it may take years for that disease to develop after the injury.

The majority of this post is showing the physiological links as to why it might develop in a person who has experienced a brain injury.

I also believe that the best evidence is from those who have experienced the injury and their stories. SO, this post does digress a bit with a few excerpts from posts from another blog that includes the stories of those who have had brain injuries and their experiences.

What is Alzheimer’s Disease? Alzheimer’s is a number of cognitive and behavioral issues that occur over an extended period of time. The cause of it is not exactly known, but the disease is determined by the formation of plaque (dead and dying neurons (brain cells) and proteins) in the brain. It is also composed of “clogged” areas in the brain that are a tangle of nerve cells and proteins. Frankly, certain areas of the brain shrink and are in the process of dying. They can’t determine if you have the disease with certainty until after you die.

English: Combination of two brain diagrams in ...
English: Combination of two brain diagrams in one for comparison. In the left normal brain, in the right brain of a person with Alzheimer’s disease. Diagram of the brain of a person with Alzheimer’s Disease. Diagram of a normal brain. Español: Esquema de un corte frontal de dos cerebros. El de la izquierda es un cerebro sano y el de la derecha uno que padece la enfermedad de Alzheimer. Русский: Изображение нормального мозга и мозга при болезни Альцгеймера (Photo credit: Wikipedia)

So, apparently there are a LOT of factors that researchers contribute to the possibility that a person will develop Alzheimer’s in their life time. Some of these factors are Type 2 diabetes, obesity, watching too much T.V., a person’s height, genetics, stress, etc. Age is the greatest risk factor in developing Alzheimer’s. It seems like a no brainer (ha) that a brain injury would eventually lead to a higher risk of Alzheimer’s.

I’ve already posted previously that Central pontine myelinolysis and EPM have been associated with significant cognitive, emotional, and behavioral issues. I believe that this just makes it even more probable that there would be a higher incidence of Alzheimer’s in those with CPM/EPM, since Alzheimer’s is known to cause:

It results in a progressive deterioration of neurocognitive (such as learning, memory, higher-order language skills, judgment, and reasoning) and functional abilities. As the disease progresses, some patients experience pronounced personality and behavior changes including anxiety, agitation, suspiciousness, delusions, and hallucinations.

I also believe that CPM and EPM will lead to Alzheimer’s or causes symptoms similar to it because they seem to share similar pathophysiology. This is true for brain injuries in general as well.

Before I go into that further, I want to stress that the pathophysiology of Alzheimer’s has not been completely uncovered. There is more and more being discovered about the disease each day, and the exact cause of Alzheimer’s is not known.

Generally, those who experience a mild brain injury (concussion) will recover without significant complications (at least initially). It has been determined that those who tend to have long lasting issues have had damage to neurons. This damage can impact the functionality of the cells which lead to  improper neurotransmission between the cells. The following passages describe the physiological factors that tend to happen after a mild brain injury:

Immediately after a concussive injury, there is an indiscriminate release of neurotransmitters and uncontrolled ionic fluxes. Potassium (K+) rapidly leaves the cell. Shortly after injury, and for a prolonged period of time, there is an influx of calcium (Ca2+). When the ionic gradients are disrupted, cells respond by activating ion pumps in an attempt to restore the normal membrane potential. Because these pumps require energy to function, more glucose is utilized. This leads to dramatic increases in the local cerebral metabolic rate for glucose. This hypermetabolism occurs in the context of decreased cerebral blood flow , which can contribute to a disparity between glucose supply and demand. In addition to increased glucose utilization, there may be impaired oxidative metabolism and diminished mitochondrial function. As a result, anaerobic (not requiring oxygen) energy pathways may be over-utilized. Elevated lactate can occur as a by-product of anaerobic energy production (and through other mechanisms). In addition, intracellular magnesium levels decrease significantly and remain depressed for several days following injury. This is important because magnesium is essential for generation of adenosine-triphosphate (ATP – energy production). Magnesium is also essential for the initiation of protein synthesis and the maintenance of the cellular membrane potential .

The sustained influx of Ca2+ has at least two important effects: (1) mitochondrial accumulations of Ca2+, and (2) initiation of a pathophysiologic process of axonal injury. The increased mitochondrial Ca2+ can lead to metabolic dysfunction and eventually energy failure. Abnormally high intracellular Ca2+ levels can initiate an irreversible process of destruction of microtubules within axons. Coupled with neurofilament damage that can occur with stretch injury, microtubule damage can impair axoplasmic flow along the length of the axon. When this occurs, axons can swell and separate.

When entire cells die following MTBI (NB: a small number), the mechanism of death relates to the spectrum of necrosis; however, researchers have reported that apoptosis (programmed cell death) appears to contribute to cell mortality in both grey and white matter following MTBI (51). Thus, the mechanisms of cell death might represent a continuum between apoptotic and necrotic pathways (52)It is important to note that cell death is closely related to injury severity. Very mild concussions likely produce virtually no permanent damage to cells resulting in long-term symptoms or problems whereas severe traumatic brain injuries, especially those involving considerable forces, often produce widespread cellular death and dysfunction with clear functional consequences.

The author of the above passages goes on to stress that the following tend to be a major contributor to having a risk for continuous symptoms after a brain injury, “The primary pathophysiologies include ionic shifts, abnormal energy metabolism, diminished cerebral blood flow, and impaired neurotransmission.”

The author of this research article goes on to suggest that there are many researchers that believe there is no correlation between brain injury and Alzheimer’s.

I guess it is important to remember that you should be cautious in regards to the possibility that if you’ve had a brain injury, you could have a higher risk for Alzheimer’s, but it is not a certainty.

The above information was quoted from: http://internationalbrain.org/?q=node/51,  “Mild Traumatic Brain Injury & Risk for Alzheimer’s Disease” Grant L. Iverson, Ph.D., Professor

I would like to note that Dr. Iverson also considered the long standing issues that a person experiences after a brain injury might be caused by psychological factors. I believe that this consideration was due to the fact that Dr. Iverson is a professor in psychiatry. I have read additional articles by other psychologists and psychiatrists that had a similar point of view. They consider that a person who has ongoing issues might be experiencing issues because they are experiencing post traumatic stress from the even that caused the injury. They might exaggerating the injury because of litigation. They might think that they are experiencing deterioration in their abilities, but there really isn’t.

A different research article explains that there is a more substantial link to brain injuries and Alzheimer’s Disease. The author’s of this article explain that it may take up to 17 years or longer for a person to develop Alzheimer’s after the initial injury. They explain that because of this length of time, as well as the memory and dementia issues involved with Alzheimer’s that by the time a person is diagnosed with the disease, they will probably not remember an instance of having a brain injury. They suggest that there needs to be long term follow up with those who have brain injuries, even those with mild injuries, to determine whether or not there is an association.

They do use an example of the NFL players that have recently received media attention for their cognitive and physical deficits that they attributed to ongoing concussions from playing football through out their lives.  According to the study, there was a “five-fold increase in the precursor to AD, mild cognitive impairment, and a threefold increase of reported significant memory problems among retirees with three or more reported concussions compared with retirees with no history of concussion.”

The article suggests that Alzheimer’s is caused by a brain injury because of the immune system response.  The immune system responds by sending cells to try to repair the damage and this causes inflammation. This leads to plaque formation in the brain, which causes an additional immune response. Eventually, the process spreads until the entire brain is impacted by the plaque.

This response results in neuronal injury and often in disruption of the blood brain barrier. Microglial cells react to this injury within minutes, and stay activated chronically [31]. Once induced into this state, the microglia become nearly identical to peripheral macrophages, acting as antigenpresenting cells (APC) and secreting proinflammatory cytokines and chemokines [32,33]. (http://www.jneuroinflammation.com/content/pdf/1742-2094-9-185.pdf)

Frankly, the information provided in the research article mentioned in the above paragraph is FULL of the pathophysiology that they use to link brain injury to Alzheimer’s.

I find that stories of people that have brain injuries are the best voice for telling what a person tends to experience while recovering from or living with a brain injury. While trying to find more information on the link between brain injuries and Alzheimer’s, I found a PHENOMENAL website that has a considerable number of stories from those who have a brain injury.

I find the following stories mirror my own experiences. To quote one woman’s experience, Angela:

To say that recovery from brain injury is difficult would do no justice to the anguish that came from realizing that the strengths and skills responsible for leading me in a life of success were severely impaired or nonexistent. It has been devastating to realize what was left. Moving on meant saying goodbye to my best friend of 32 years – “ME” – the most difficult thing I could ever have be asked to do.

In a matter of seconds, I became a stranger to myself.  I miss the old me so much that I question why I would survive the accident only to be forced to live in the shadow of my former self. But I know that the important parts of me were not lost even though it is a constant battle for me to find my way in a world that is moving so fast that I cannot keep up.

I would recommend checking out the dozens of stories that are listed on this site. I find that not only are they informative, but they mirror our experiences. It’s not some doctor trying to explain if what you are experiencing is normal or not, but PEOPLE who have the injury telling you what they’ve experienced in their life. : http://tbivoices.com/ian5.php

Wow, here’s another story that mirrors mine. I was just discussing with my occupational therapist that this has been a HUGE issue with my current job. I can’t remember what we’ve recently learned in training’s. I have a hard time locating information. I can’t remember new things about products that are new. It makes doing  the  job very very hard. Here is an excerpt from another person who went back to work:

For anyone to maintain employment, they not only have to have the skills to do the job, but also the appreciation that work is work, and that a good job may be irreplaceable.  That is far more difficult to remember, when judgment, mood and initiative is impaired after a brain injury.

However, Betty had another problem. She had already known how to be a dental hygienist before her accident and after rehab, was able to do much of what was required of her because it required her to use skills she had learned before her accident.  But the field of dentistry, like any profession, changed, she couldn’t learn the new techniques, acquire the new skills to adapt.

This too has happened to me on numerous occasions:

Those who don’t know much about brain injury are often surprised at how “normal” someone with a brain injury may be.  Only the truly profoundly injured will show the kind of overt dementia that we have been programmed to expect.  Most cognitive challenges are far more subtle than what an Alzheimers or severely learning impaired individual might have.  Much of the brain may be unaffected by even a severe injury, including long term memory and communication ability. Both Angela our first case study and Betty are perfect examples of that.  That Betty communicates so well is both proof of that tendency but also a credit to the extensive and multi-year rehabilitation that she received post injury.

Betty describes a number of classic cognitive problems.  Sequencing (putting things in order) and memory are ongoing problems.  Like most survivors, she has learned to write everything down.

Driving is one of the most troubling aspects of disability for a wide range of brain injured individuals.  It is a uniquely cognitively challenging task, requiring intense attention, visual perception, multi-tasking, capacity to deal with stress and coordinated sensory, reflexive and muscular control.  It took Betty about three years to get her drivers license again after her TBI.  Even now more than 25 years post injury, she must be careful where and when she drivers. http://tbilaw.com/tbivoices/cognitive-challenges-sequencing-staying-on-task-topic/
 

Ok, so I’m  not going to keep quoting all of these stories. Frankly, I do not have the ability to read through them. I become distracted and can’t stay on task. This post has already taken  more than four hours to write over two days 😦  I WOULD DEFINITELY RECOMMEND READING SOME OF THESE STORIES. They are what I think a lot of people experience in their recovery, and that makes them a valuable source of understanding, comfort, and knowledge.

I will continue to try to find more information on brain injuries, but please feel free to contact me regarding YOUR stories. I believe that until there is more information presented by more people, we will struggle to find doctors who understand that a brain injury is not an acute injury but a life long disease.

UPDATE:

This link was provided by a person who has found the connection between Alzheimer’s and the autoimmune response to brain injury. You will find it interesting:

http://www.dana.org/news/features/detail.aspx?id=40308

Related articles

Drawing a connection between general brain injuries and CPM/EPM:

A diagram of the forces on the brain in concussion

A diagram of the forces on the brain in concussion (Photo credit: Wikipedia)

I’ve said it before, but I believe it needs to be addressed further. Doctors do not know that much about CPM/EPM. Because there are only 2,000 to 2500 cases that are definitively diagnosed as CPM/EPM each year, there aren’t any “experts” that we can turn to. Because of this, it is necessary to draw understanding from what we know about brain injuries in general.

The brain is the most complex part of a human body, and the most interesting thing to remember is that we do not know that much about it.

Previously, it was believed that if you did not pass out from an injury (hit, fall, car accident) then a brain injury did not occur. Now, we know that is not always the case.

You can have short term to long term cognitive, physical or emotional issues from a simple bump on the head or even from whiplash.

So, let’s investigate brain injuries further:

The first type of more common and less recognized form of brain injury is a concussion. Concussion occurs when your brain is jostled, which results in impaired functioning. It can occur from a fall, a hit, a car accident, even from shaking (shaken baby syndrome). Generally, a concussion is determined from the symptoms that a person experiences. In other words, you may or may not have any outward physical signs of trauma, like bumps, bruising or bleeding. You may not even have a direct hit to the head. You may experience an impact to the body that leads to a jolt to the head that causes injury to the brain.

Concussions cause microscopic injuries that are generally not detectable by CT scans and do not cause pronounced bleeding of the brain. It is believed that the damage in the brain is from cellular damage. It is also believed that the damage to the brain is widespread. This is why if there is bleeding, it will not typically show on a CT scan because it is not significant enough to pool in one area to be detectable.

So, concussions result from injuries to the way the brain cell (neuron) functions vs having damage to the blood vessels in the brain that causes more significant bleeding. This type of injury is similar to the cellular type of injury that those with central pontine myelinolysis or EPM. You will also find this type of physiological type of injury with MS too.

The brain cells (neurons) may be severed completely in concussions or there may be physiological damage that is done that impacts the way the cell functions. So, the brain cell itself may be damaged or the way it works may be damaged.

What do I mean by that? I would compare it to when you have a neck injury that causes paralysis or a neck injury that just causes numbness and tingling to an extremity. If you have paralysis, the damage is complete and there’s little or no function to the impacted sites, and it can not be repaired. The wiring is cut and the signals can’t get through. If you have an injury that causes numbness and tingling, there is some information being processed, but it is not being processed correctly. This would be comparable to having a short circuit in an electrical wire. Sometimes, the information will get from point A to point B, sometimes it won’t. In these instances, sometimes your body can repair the damage.

(The following is a picture of a neuron…the cells that compose your brain tissue. )

English: Complete neuron cell diagram. Neurons...

I would recommend checking out the following link for a little more information regarding the physiology of concussions (http://www.cordingleyneurology.com/contuseconcuss.html)

Based on what type of injury occurs, concussions can be mild (a person does not lose consciousness) or severe (a person can lose consciousness or even slip into a coma).

So how do you know if a concussion is mild or severe?

Generally, hospitals will look at the person’s symptoms to determine how severe a concussion is and also on if the person lost consciousness and for how long. That said, symptoms may or may not develop right when the injury takes place, and because of typical limitations on insurance plans, hospital staffing, and resources, most emergency rooms will dismiss the person to the care of family or friends within a few hours if the did not lose consciousness from the injury.

It is suspected that there are 1.6 to 3.8 million sports related concussions each year. Each year approximately 1.4 million people seek care for brain injuries. It’s obvious from the numbers I just mentioned that a significant number of people, especially those who participate in sports, do not seek medical treatment for the injuries that they have.

It can mean that a person does not suspect that their injury is significant enough to require treatment, or it might be that people do not realize a connection between their symptoms to the injury that they experience. I believe it is the latter.

This means it is important to recognize the symptoms of a concussion. Typical indicators of a concussion:

Physical Issues:                   Cognitive Issues:  

• Headache                            • Feeling mentally
• Nausea                                  “foggy”
• Vomiting                             • Feeling slowed  down
Balance problems             • Difficulty Concentrating
• Dizziness                              • Difficulty Remembering

• Visual problems                • Forgetful of recent information or conversations

• Fatigue                                • Confused about recent events

Sensitivity to light           • Answers questions slowly

• Sensitivity to noise          • Repeats questions

• Numbness/ Tingling

• Dazed or stunned

•Seizures may also occur immediately or even up to a year or more later.

Emotional Issues:                           Sleep Issues:

• Irritability                                        • Drowsiness

• Sadness                                            • Sleeping less

• More emotional than usual             • Sleeping more

• Nervousness                                      • Trouble falling asleep

I HIGHLY, HIGHLY recommend checking out the following link to learn more about the effects of concussion and other brain injuries (this is a great tool for those who have a brain injury as well as those who live with them)— http://www.brainline.org/landing_pages/TBI.html

Check out the following on how scientists are determining the function of how the brain works : http://connectedsocialmedia.com/5697/future-lab-mapping-the-network-in-the-brain/

It is also important to understand that you may not develop all of these symptoms, and the symptoms may not appear immediately after the injury. It may take days or weeks before the symptoms appear. It may happen a few hours after the injury. And unlike other brain injuries, these injuries do not typically appear on CT scans or MRI scans.

You may experience the following longer lasting issues in your daily life:

• Increased problems paying attention/concentrating
• Increased problems remembering/learning new information
• Longer time required to complete tasks
• Increased symptoms (e.g., headache, fatigue) during school/work
• Greater irritability, less tolerance for stressors
Until a full recovery is achieved, you may need the following supports:

• Time off from school/ work
• Shortened day
• Shortened classes (i.e., more frequent breaks)
• Rest breaks during the day
• Allowances for extended time to complete work/assignments/tests
• Reduced homework/work load
• No signiicant classroom or standardized testing at this time
Physicians and school personnel should monitor the student’s symptoms
with cognitive exertion (mental effort such as concentration, studying) to
evaluate the need and length of time supports should be provided.

The information above is from the CDC: http://www.cdc.gov/concussion/HeadsUp/physicians_tool_kit.html

Generally, a person will recover from mild concussions in a few weeks, but it is also important to remember that concussions can “build”. If a person, experiences a concussion and it is mild, and then experiences an additional injury, days,weeks or even months later, the injury can be catastrophic. It can actually lead to death. For this reason, there are new policies being implemented in schools and college athletic programs throughout the country that bench players for weeks or months following minor concussions.

Until concussions are understood more fully, I believe this should be a mandatory step for the protection of the individual.

Ok, so how does this relate to CPM/EPM? Concussions can impact any area of the brain, but as mentioned above the type of injury found in a concussion is believed to impact the physiology of the brain cells. It impacts how brain cells relay chemical signals, and this is true for CPM/EPM too. This is why there are similarities in the emotional, behavioral, cognitive and sleep symptoms of CPM/EPM and concussions.

I plan to research brain injuries further to hopefully discover answers as to why our experiences are so vast and different, and hopefully to determine what we can anticipate in how the injury responds to treatments.

Have a great night!

Dying to play Football:

This post is a bit of a stretch from my norm, but I really think it deserves a look.

I encouraged my son to start playing football in 2nd grade. I thought it would be a great way to build character, endurance, and I really thought it would help me as a single mom teach Zachary more about respect and discipline. Ok, and let’s face it, everyone wants their child to become an athletic super star.

I’ve always encouraged Zachary to dream big, and now that he’s finishing his freshman year of high school, he is dreaming big. He does want to play college level football for Ohio State University. It’s been his dream since he was in the fourth grade, and following that he dreams of playing for the NFL. I have never discouraged him. I believe he can do anything he wants to do, but after I sustained my brain injury, I’m looking at his “career” in football in a whole new light.

Tonight, I read another account of a retired NFL player committing suicide. My heart goes out to his friends and family, and I really believe that his physical trials after playing football need to be addressed.

Here’s the reality folks, a brain injury is a brain injury, and though there are MANY ways to have trauma to the brain, it really is all the same.

Let me clarify, I’m not saying that EVERYONE who has a brain injury has the same symptoms, but an injury to the brain is an intense injury, and it is an invisible injury to the rest of the world.

If you saw someone in a wheelchair, you have an immediate awareness that this person has a disability, but there are no external indicators that tell you a person has a brain injury. You really have no way of telling.

Trust me, before my injury, I would speak to people through my job, and I would immediately assume that they were really, really stupid. Some people, I talked with, I knew they had an injury because their speech was impacted, but for those where it wasn’t apparent as soon as they started speaking, I seriously judged their intellect.

I know better now.

Whether you were in a car accident, you fell down and hit your head, you were in sports like boxing or the NFL, or you just got into one too many fights, it’s important to realize that you may have life long issues related to these occurrences. AND please be aware, even just one event can cause these life long issues.

Okay before you start walking around with a helmet strapped to your head, in most cases, one bump to the head won’t cause permanent damage, but it is anticipated that more than 1.2 million people or more experience mild traumatic brain injury.

To differentiate, a person with a Traumatic Brain Injury usually needs to be hospitalized for their injury, and in regards to a Mild Traumatic Brain Injury, a person sustains ongoing issues after receiving a hit to the head, but did not require hospitalization. However, it is believed that there could be a significantly higher number of people with MTBI. The following quotes come from the CDC. In 2003, they were approaching congress to obtain more funding to study MTBI:

First, no standard definitions exist for MTBI and MTBI-related impair­
ments and disabilities. The existing Centers for Disease Control and Prevention (CDC)
definition for TBI surveillance is designed to identify cases of TBI that result in hospital­
ization, which tend to be more severe. MTBI is most often treated in emergency depart­
ments or in non-hospital medical settings, or it is not treated at all. Few states conduct
emergency department-based surveillance, and current efforts do not capture data about
persons with MTBI who receive no medical treatment. Additionally, neither hospital- nor
emergency department-based data can provide estimates of the long-term consequences
of MTBI.

In 2003, the Center for Disease Control defined Mild Traumatic Brain Injury as this:

The Definitions Subgroup developed a conceptual definition of
MTBI based on clinical signs, symptoms, and neuroimaging; and an operational defini­
tion to be used in identifying cases of MTBI in administrative databases, medical
records, and survey and interview results. The Methods Subgroup evaluated surveillance
databases and identified those that would best capture the types of data needed to determine the full magnitude of MTBI and related impairments and disabilities.

The conceptual definition of MTBI is an injury to the head as a result of blunt trauma or
acceleration or deceleration forces that result in one or more of the following conditions:
● Any period of observed or self-reported:
◆ Transient confusion, disorientation, or impaired consciousness;

◆ Dysfunction of memory around the time of injury;

Loss of consciousness lasting less than 30 minutes.

● Observed signs of neurological or neuropsychological dysfunction, such as:
◆ Seizures acutely following injury to the head;
◆ Among infants and very young children: irritability, lethargy,
or vomiting following head injury;
◆ Symptoms among older children and adults such as headache,
dizziness, irritability, fatigue or poor concentration, when
identified soon after injury, can be used to support the diagnosis
of mild TBI, but cannot be used to make the diagnosis in the
absence of loss of consciousness or altered consciousness.
Research may provide additional guidance in this area.
Based on this conceptual definition, separate operational definitions of MTBI are
recommended for cases identified from interviews and surveys, administrative health
care data sets, and patient medical records.

The conceptual definition of a prevalent case of MTBI is any degree of neurological or
neuropsychological impairment, functional limitation, disability, or persistent symptom
attributable to an MTBI.
The operational definition of a prevalent case of MTBI-related impairment, functional
limitation, disability, or persistent symptoms is any case in which current symptoms are 3
reported consequent to MTBI or made worse in severity or frequency by the MTBI,
or in which current limitations in functional status are reported consequent to MTBI.
Symptoms and limitations are described on pages 19-21. (http://www.cdc.gov/ncipc/pub-res/mtbi/mtbireport.pdf)

Ok folks, so what does all of that MEAN?

The CDC realized that in regards to mild trauma to the head, those hits that don’t require hospitalization, are being ignored in the medical community as causing a problem. They understand that these is a serious lack of understanding regarding the brain trauma that occurs after something as simple as whiplash in a car accident or a hit in the head during a boxing match. In order to try to obtain information for those that are being injured, but aren’t being hospitalized, the CDC created the above definitions for hospitals and doctors to use to try to document these cases. So, the above information is a guideline set up by CDC, so that they could start researching this issue further.

They set up the definitions in two parts. The first part is more of the physical symptoms that present and establish that a person might have experienced a MTBI, and the second part is the cognitive effects a person might experience after having a MTBI.

They are stating that doctors should pay attention to both definitions, the conceptual and operational.

This means, YOU should pay attention to both as well because if you fall down and are disoriented, you might experience ongoing issues. However, that does not mean that you WILL experience ongoing issues.

It is anticipated that approximately 30% of those who experience a hit to the head will experience temporary issues, but only 5 to 7 percent of that 30% will have permanent ongoing neurological or cognitive issues.

It is also believed that MTBI’s tend to build, and this brings us back to our NFL football players. If you had just one hit to the head or maybe two or three, the chances of your having a permanent brain injury are pretty remote, but if you started playing football in 2nd grade, and continued to sustain hits through high school, college, and then into the NFL, well by the time you’re in your early 40’s, your brain is going to start turning to jelly. Ok, not literally jelly, but figuratively.

So that brings us back to, you can’t see the injury, and most people don’t understand what’s happening to them. You fell off your bike, and you weren’t wearing a helmet, and you haven’t been quite the same since. You might go to your doctor. They might order a few tests, but brain injuries do not always show on a MRI or CT scan, or by the time a doctor orders it, the inflammation that the images detect has subsided, and you probably start to feel just a little bit crazy.

You don’t feel the same. You can’t think as clearly as you did before, but your doctor does not see anything in your scans. YOU FEEL LIKE YOU’RE GOING NUTS. Then, you get depressed. No one believes you. Your doctors are telling you there’s nothing wrong. Your spouse doesn’t understand what’s happening to you. You get depressed, and you don’t feel like life is worth living.

Folks, it’s time to understand that you aren’t alone, and no matter how you received your injury, you have an injury. It’s an unseen injury, but you aren’t crazy, and you deserve and need to get help, cognitively, psychologically and physically.

Ray Easterling, former Atlanta Falcons defensive back, died from suicide this weekend. He suffered from memory issues, headaches, dementia, and other health issues.

The NFL is being sued because it is believed that the league was aware that continuous concussions were causing these injuries, but they did not make players aware of the risks, and in some cases denied players ongoing health coverage to help with their medical problems (http://msn.foxsports.com/nfl/story/Ray-Easterling-death-ruled-suicide-Atlanta-Falcons-041912).

http://www.youtube.com/watch?v=pJCEbHJ1oBY&feature=fvst

In 2007, there was a fund created by the NFL to cover medical costs of retired NFL players, however this fund does not cover older NFL team players, and they do not choose to cover everyone’s costs. There is a panel that decides whether or not a former NFL players medical costs will or will not be covered. (http://www.nytimes.com/2011/02/21/sports/football/21duerson.html)

For information on the 88plan:     https://www.nflplayercare.com/Default.aspx

Another great website regarding medical assistance for former NFL players:  http://www.gridirongreats.org/

It is important to understand that the name used for the brain injuries that these football players had is Chronic traumatic encephalopathy (CTE), but this is the name of a disease related to chronic brain injury, either TBI or MTBI.

Other NFL players that have committed suicide after brain injury (CTE):

Andre Waters (2006)

Dave Duerson (2011)

Rick Rypien (age 27)

Michael Current

Shane Dronett

Corwin Brown (suffering from brain injury, attempted suicide, but luckily survived)

Owen Thomas (COLLEGE FOOTBALL player with Penn State had the same injury as the NFL players above).

Please note that the above football players lost their lives, but thousands of others are living with TBI and MTBI, and are at risk.

It is also important to note that it is not just football players, but cheerleaders, boxers, martial artists, kick boxers, soccer players, etc that can also receive these injuries. It’s also important to understand that something as simple as being in a car accident that causes whiplash can cause this injury.

It’s really important to spread the word regarding how this unseen injury is impacting people in their every day, and to understand that if you experience things that just aren’t right for you (unexplained headaches, nausea, memory loss, fatigue, visual or hearing disturbances, attention problems, etc…SEEK HELP. You might be wondering what your next step is after you have been told by a doctor that nothing is wrong; call your local hospital and ask about neurocognitive testing with a psychologist or a neuropsychologist. In most cases, your insurance will cover this type of testing, but you might need a doctors referrel.

In the end, DON’T GIVE UP. YOU ARE NOT ALONE!!

PLEASE, if you are experiencing issues that you don’t understand and need help: LEAVE A MESSAGE here or you can also contact the http://www.biausa.org (that’s the brain injury association).

I really recommend online support groups. It’s AMAZING to talk to people who are LIVING with the same types of issues that you are.

If you are experiencing suicidal thoughts, call 1-800-suicide (1-800-784-2433) or you can go online to crisischat.org. OR go to your nearest emergency room.

In the end, you are not alone, and even though your life has changed and it’s not easy, you can get help and you can learn ways to live and adjust to your injury.

GOD BLESS!

Here are a following broadcasts regarding concussions and mild head injury in sports:

Football:

http://www.youtube.com/watch?v=VfO6Yyr4dmw

http://topics.nytimes.com/top/reference/timestopics/subjects/f/football/head_injuries/index.html

Soccer:

http://www.youtube.com/watch?NR=1&feature=endscreen&v=klESLYtbRe8

Sports in General:

http://www.youtube.com/watch?v=T3FLRDxbLXg&feature=related

Head trauma related to the pituitary gland and how head trauma impacts your hormone function:

http://www.youtube.com/watch?v=Q8DXiCr3-jE&feature=related

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