Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “TBI”

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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Hope on the horizon:

I am posting this before I lose track of it. I’m sorry I haven’t posted in so long. My mind and abilities have been absorbed by a new position at work. This new position has become most of everything that I am able to do. It takes up so much of mental and physical concentration that it leaves little ability for me to do anything else.

But this is a show that I watched tonight, and it shows the brain damage that basic MRI and CT scan imaging does not show. It shows the invisible injury that we have, that no one else can see. It begins to explain and give answers to, and hope for, what we are experiencing. Because in order to fix a problem, you must first acknowledge one exists.

This segment of 60 minutes shows that even those with minor concussions can and do experience brain injury that can explain the symptoms that we experience, like ongoing memory issues. It can show that we are NOT faking. We are not malingerers!

We do have ongoing issues from our brain injuries. Don’t lose hope! Answers are on the horizon.

The following link takes you to the 60 minutes segment that shows some of the new technology being used in the military to diagnose minor and traumatic brain injury after concussions. They are now detecting injuries that standard MRI and CT scans do not detect.

http://www.cbsnews.com/video/watch/?id=50146231n

Brain injury: What causes an increase in symptoms?

I have never really thought to research, why would a brain injury progress after an injury. Good news, later is better than never.

It finally hit me that I might find research documenting that after a brain injury, damage continues to occur. I truly don’t understand why these connections don’t come to me.

It irks me.

I might have discussed parts of this subject before. I have believed that the reason people like Jeffery, Michael and Deb, or even the NFL players, experience an improvement and then after a few years a decline in their health, an increase in symptoms, is because there is an immune response that causes further damage.

Some people after they have surgery, in a few years, they have further issues caused by scar tissue.

I have a history of endometriosis. I had a surgery for endometriosis, and it was less than two years later that I was experiencing significant pain. When the doctor did an exploratory surgery, he found scar tissue. He also found significant intestinal distention, but he did not know what had caused it.

Anyway, within a 12 to 18 month period, I had formed significant scar tissue because I had the surgery from endometriosis.

Scar tissue forms from the trauma that was inflicted in the first surgery.

It is in my opinion that this is what happens to those who have an improvement and then experience a decline in health, especially with cognitive issues and memory.

This post will investigate research that shows this connection after brain injury, from stroke, trauma, and other brain insults.

The following paragraph explains exactly what we experience and what might be the reason behind it. It explains that there is a recovery period where symptoms show improvements, and then as time progresses, there is an increase in symptoms:

Despite the tremendous interest in neural stem cell biology, there is little mechanistic insight into stem cell survival following common conditions induced by trauma or other brain insults. Recently, many paradigms of brain injury, including TBI, seizures, stroke, hypoxia-ischemia, and neurodegenerative diseases, implicate neural stem cells in the remodeling that occurs following such injuries (Arvidsson et al., 2002; Jin et al., 2001; Kernie et al., 2001a; Miles and Kernie, 2008; Parent et al., 2002; Parent et al., 1997; Zhang et al., 2001). The physiologic relevance of this proliferation remains unknown, but it may in part explain some of the spontaneous recovery that occurs in all of these disease states. Alternatively, aberrant neurogenesis after injury could contribute to ongoing morbidity that impairs functional recovery. In the following sections, we describe the current knowledge and outstanding research questions in the field of injury-induced neurogenesis. We first focus on experimental stroke and the SVZ, and then shift to TBI models and dentate granule cell neurogenesis.    (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864918/)

The above article is difficult for me to understand, so I will have a friend try to decipher it in greater detail and get back to me in regards to the relevance in relation to the injuries that we suffer. I believe it is stating that at this point in time, they have not been able to determine if the cells that repair damage in the course of stroke, etc are beneficial, beneficial in the beginning and then cause damage or have no direct consequence in brain injury. I really am uncertain of their direction in the article. They might point out that this is an area that needs to be investigated further. They might also be saying that these cells are only activated for a short period and then die off, and that it is this dying off period that causes the increase in symptoms. That would be an interesting thought, that I have not considered previously:

Since it is reasonably well established that hippocampal progenitors are activated by injury and result in increased numbers of new neurons within the dentate gyrus, ongoing studies can now be directed at relevance and mechanism. First, it needs to be established whether injury-induced neurogenesis is an adaptive response. There are three possibilities for its ultimate relevance. First, the generation of new neurons might be beneficial and contribute to recovery of learning and memory and possibly other functions impaired by brain injury. Second, neurogenesis may contribute to TBI-related morbidity such as temporal lobe epilepsy, which occurs relatively commonly following moderate and severe TBI. Finally, this reservoir of progenitors may be nothing more than a developmental remnant that is incapable of providing functionally relevant neurons into the sophisticated hippocampal circuitry.

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864918/)

The next article states that there was research as early as 2003 showing that chemotherapy could cause brain injury. They speculated that it was being caused by possible inflammation, damage to the grey matter and damage to the white matter, or that it is possible that an immunological response caused the injury.

 Although the available evidence suggests a fairly diffuse pattern of changes, memory and executive functions could be preferentially affected. Preliminary data also suggest that some individuals might be more vulnerable than others, leading to investigation of genetic and other risk factors. The greatest gap in our knowledge regarding chemotherapy-related cognitive changes is a lack of understanding of the mechanism or mechanisms that account for the observed changes. Several pathophysiological candidates include direct neurotoxic effects leading to atrophy of cerebral gray matter (GM) and/or demyelination of white matter (WM) fibers, secondary immunologic responses causing inflammatory reactions, and microvascular injury. Altered neurotransmitter levels and metabolites could constitute an additional mechanism related to neurotoxic effects. Advanced brain imaging techniques can directly or indirectly assess many of these mechanisms, but to date there has been very limited application of these tools. Morphometric magnetic resonance imaging (MRI), functional MRI (fMRI), diffusion tensor imaging (DTI), and MR spectroscopy (MRS) are noninvasive techniques that could yield important complementary data regarding the nature of neural changes after chemotherapy. Electrophysiological studies and targeted molecular imaging with positron emission tomography (PET) could also provide unique information.

(http://www.ncbi.nlm.nih.gov/pubmed/14613048)

It is a bit surprising that this information was available in 2003, but it took more than 8 years to get the information to the public. I don’t understand why.

Another abstract explains again, that there seems to be an initial injury and then an immune system response results in long term cognitive decline. It goes on to explain that anti-inflammatory agents might be able to prevent or treat this immune response. I’m sorry that I am unable to get full access to this article. Hopefully, at some point in the future, I will be able to include follow up information for these abstracts.

Brain damage following traumatic injury is a result of direct (immediate mechanical disruption of brain tissue, or primary injury) and indirect (secondary or delayed) mechanisms. These secondary mechanisms involve the initiation of an acute inflammatory response, including breakdown of the blood-brain barrier (BBB), edema formation and swelling, infiltration of peripheral blood cells and activation of resident immunocompetent cells, as well as the intrathecal release of numerous immune mediators such as interleukins and chemotactic factors. An overview over the inflammatory response to trauma as observed in clinical and in experimental TBI is presented in this review. The possibly harmful/beneficial sequelae of post-traumatic inflammation in the central nervous system (CNS) are discussed using three model mediators of inflammation in the brain, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β). While the former two may act as important mediators for the initiation and the support of post-traumatic inflammation, thus causing additional cell death and neurologic dysfunction, they may also pave the way for reparative processes. TGF-β, on the other hand, is a potent anti-inflammatory agent, which may also have some deleterious long-term effects in the injured brain. The implications of this duality of the post-traumatic inflammatory response for the treatment of brain-injured patients using anti-inflammatory strategies are discussed.

(http://link.springer.com/article/10.1385%2FMN%3A24%3A1-3%3A169?LI=true)

The following articles I can’t access, but they seem to describe that this immune response is also prevalent and possible related to cognitive deficits after exposure to carbon monoxide poisoning.

This article hints that there is a cognitive impact after exposure to carbon monoxide:

Neuropsychiatric aspects of carbon monoxide poisoning: diagnosis and management Adv. Psychiatr. Treat. 2012 18 (2) 94-101

The next abstract shows that there is a neuropathophysiological impact that occurs after exposure to carbon monoxide:

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes.                              Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.

(http://www.pnas.org/content/101/37/13660.short)

I really feel that this article, though using rats as the subjects, shows that there is the potential for continued progression of symptoms after the initial brain injury. The article suggests that brain cells continue to die up to a year after an injury in rats. If this correlates to what happens to humans, then this would potentially explain continuing cognitive issues. My opinion in this scenario is that cells that were injured, but not necessarily “killed”, continue to atrophy and die. It might be a combination of factors that cause people with brain injuries to see a progression in symptoms after seeing improvements. It is very difficult to determine without research.

Examination of the injured brains revealed substantial and progressive tissue loss with concomitant ventriculomegaly in the hemisphere ipsilateral to injury. The regions with the most notable progressive atrophy included the cortex, hippocampus, thalamus, and septum. Quantitative analysis demonstrated a significantly progressive loss of cortical tissue as well as shrinkage of the hippocampal pyramidal cell layer ipsilateral to injury over 1 year following injury. In addition, reactive astrocytosis in regions of atrophy and progressive bilateral death of neurons in the dentate hilus was observed for 1 year following injury. These results suggest that a chronically progressive degenerative process may be initiated by brain trauma. Thus, there is a temporally broad window within which to introduce novel therapeutic strategies designed to ameliorate the short and long-term consequences of brain trauma.

(http://online.liebertpub.com/doi/abs/10.1089/neu.1997.14.715)

I have not seen a lot of information regarding the merging of these two sciences, but it would interesting to see if there has been:

Until recently, the brain was studied almost exclusively by neuroscientists and the immune system by immunologists, fuelling the notion that these systems represented two isolated entities. However, as more data suggest an important role of the immune system in regulating the progression of brain aging and neurodegenerative disease, it has become clear that the crosstalk between these systems can no longer be ignored and a new interdisciplinary approach is necessary. A central question that emerges is whether immune and inflammatory pathways become hyperactivated with age and promote degeneration or whether insufficient immune responses, which fail to cope with age-related stress, may contribute to disease. We try to explore here the consequences of gain versus loss of function with an emphasis on microglia as sensors and effectors of immune function in the brain, and we discuss the potential role of the peripheral environment in neurodegenerative diseases.

(http://www.sciencedirect.com/science/article/pii/S0896627309006771)

This concludes this post for now, but it does bring interesting insight and raises questions to what really does happen after a brain injury? Does the immune system cause havoc on the brain once a brain injury occurs? How long will take for those effects to be seen? Is brain tissue still dying years after the initial injury? If so, is that caused from the injury itself or from the immune response? What can we do to save what we have? Are there any precautionary measures that we can take to prevent things from degrading? Like an aspirin does with heart disease, would anti-inflammatories protect the brain?

I wish I had more answers than questions. I wish I had more definitive research, but as technology advances and the spot light on brain injuries widens, I think we will find what we can do. I think doctors will become more understanding to what we experience.

Have a great night!

Is a brain injury an acute incident or a chronic disease:

There is so much that we do not understand about the brain. There are thousands of scientists discovering new aspects of the brain everyday. As I’ve said before, the brain is still a mystery and doctors and scientists will be working far into the future to uncover its secrets.

Therefore, I believe that it is ignorant to think that an isolated injury to the brain will not cause resonating effects. At this time, due to limitations in science and limitations of understanding function,it is impossible to know with certainty what, if any, the long term effects will be. Currently, due to the media attention being directed to the NFL players who have experienced symptoms years after multiple concussions and head injuries, doctors and scientists are beginning to realize that there is a possibility that the injury continues to develop after the initial occurrence.

This idea is not widespread, and it is definitely not understood, but because of the media attention it is being looked at further.

In 2009, a paper was published by the Brain Injury Association of the USA, that stated:

Traumatic damage to the brain was therefore seen by the industry as an “event.” A broken brain was the equivalent of a broken bone—the final outcome to an insult in an isolated body system. Once it was fixed and given some therapy, no further treatment would be necessary in the near or distant future, and certainly, there would be no effect on other organs of the body.

The purpose of this paper is to encourage the classification of a TBI not as an event, not as the final outcome, but rather as the beginning of a disease process. The paper presents the scientific data supporting the fact that neither an acute TBI nor a chronic TBI is a static process—that a TBI impacts multiple organ systems, is disease causative and disease accelerative, and as such, should be paid for and managed on a par with other diseases.

If you’re reading that, it might feel like a breath of fresh air. I know that might sound funny because you, like me, might really want to believe that things won’t get worse. You want to believe that what the doctors told you post injury is true, but when things start to progress and you look at the medical community for answers, you receive smug grins, arched eyebrows, and the reminder that these new symptoms weren’t from the injury your received, so this passage feels like a little bit of reassurance and vindication. Someone out there believes that what you’re experiencing IS related to your brain injury, and that is where the relief is.

The paper then continues to show examples of where traumatic events, like severe burns, kidney disease, and lung disease lead to further complications and seemingly unrelated diseases like cardiac disease or lung diseases.

Yes, folks, what are they saying….what happens to one part of the body can impact another system of the body!!!! And if you think about it, the brain is the central processing system for the entire body, so why is it such a stretch for doctors to realize that an injury to the brain, which controls the functions of your lungs, your heart, your kidney’s, your hormones, EVERYTHING in your body, might cause irregularities in heart rates, sleep apnea, water retention, even a decrease in sex drive or reproductive ability. Frankly, I think it would be more surprising to discover that nothing happens after a brain injury.

I read some place that those of us who have developed CPM/EPM die within 5 -10 years after the injury. That said, I can not remember where I found that information. It seems that most of those who died had cardiac issues, like irregular heart rates, uncontrollable hypertension or hypotension, etc. SO, I found the following information extremely relevant as well. Keep in mind, the following applies to brain injuries in general.

In a 2004 study on mortality one year post injury among 2,178 individuals with a moderate to severe TBI, it was reported that individuals with a TBI were twice as likely to die as a similar non-brain injured cohort and had a life expectancy reduction of seven years (Harrison-Felix et al., 2006).

Follow-up studies on causes of death revealed that individuals surviving more than one year with a TBI are 37 times more likely to die from seizures, 12 times more likely to die from septicemia, four times more likely to die from pneumonia and three times more likely to die from other respiratory conditions than a matched cohort from the general population. The greatest proportion of deaths in the study—29 percent—was from circulatory problems.

Shavelle and colleagues found that individuals with a TBI were three times more likely to die of circulatory conditions (Shavelle et al., 2001). Although it is somewhat intuitive that individuals with moderate to severe TBIs would have a higher mortality rate than the normal population, even individuals with mild TBIs have been found to have a small but statistically significant reduction in long-term survival (Brown et al., 2004).

I have also stated that the younger you are the more likely you are to see the most improvements. I have said this so many times to doctors, friends, and my family. It is to be expected that as you age, your brain ages as well. This is common knowledge, but when you are talking to your doctors they tend to negate this fact. I really do not understand why.

That said, I think it that it makes sense that if you experience a brain injury when you’re older, your brain will probably not recover like it would have when you were in your 20’s.  It also makes sense that when you have an injury to your brain, the injured cells will tend to malfunction more as you get older leading to more dysfunction.

I would compare it to an apple that you drop on the ground. The area of the most impact won’t ever be the same. It’s never going to be un-bruised. However, as time goes on, that spot gets worse and worse. It becomes the first spot to rot. Unfortunately, I think that the brain is similar. The injury will never be undone completely and as well age, those weakened spots weaken more and more.

I know that does not sound very encouraging, but that’s why scientists and doctors need to focus on figuring out why it happens and what can be done to make the person the most functional after the injury. The following paragraph addresses this issue:

Age is clearly a factor in brain injury disease. Older patients show a greater decline over the first five years following a TBI than younger patients (Marquez de la Plata et al., 2008). Also, the greatest amount of improvement in disability has been noted in the youngest group of survivors.

Because I found the following information SO incredibly descriptive of some of the things that I have gone through, I decided to just add it to the post. So, the following information is directly from the Brain Injury Association of the USA paper that has been used through this entire post:

Epilepsy
Traumatic brain injuries are a major cause of epilepsy, accounting for 5 percent of all epilepsy in the general population (Hauser et al., 1991). Individuals with a TBI are 1.5-17 time (depending on the severity of the TBI) more likely than the general population to develop seizures (Annegers et al., 1998). TBI is the leading cause of epilepsy in the young adult population. Seizures will be observed over a week after a penetrating TBI in 35-65 percent of individuals. In a study of 309 individuals with moderate-severe TBI followed as long as 24 years post injury, 9 percent were being treated for epilepsy (Yasseen et al., 2008). As the time from injury to the time of the first post TBI seizure may be as long as 12 years (Aarabi et al., 2000), there is a need for heightened awareness of the development of epilepsy on the part of the patient, family and treating medical personnel.

Vision

Visual disturbances are common after a TBI, occurring in 30-45 percent of individuals (Sabates et al., 1991). In a review of 254 individuals, two and five years post injury, 42 percent continued to complain of visual difficulties at five years (Olver et al., 1996). Optic atrophy can begin shortly after the brain injury and lead to a marked decreased acuity and blindness. Persistent 4 visual field deficits also pose a significant safety risk due to the inability to see to the side. High flow carotid cavernous fistulas causing the direct flow from the internal carotid artery system into the cavernous venous sinus may develop weeks after a TBI. If not recognized and treated, permanent visual loss may progressively develop (Atkins et al., 2008).
Sleep
Sleep complaints are common following TBI. Subjective complaints of sleep disturbances have been reported in 70 percent of TBI outpatients (Chesnut et al., 1999, Max et al., 1991, McLean et al., 1984). Disturbed sleep, as measured by polysomnogram, was reported in 45 percent of a group of 71 individuals averaging three years post injury (Masel et al., 2001). Hypersomnia is associated with decreased cognition and decreased productivity, and certainly with a greater risk for accidents. National Highway Traffic Safety Administration data showed that approximately 56,000 auto crashes annually were cited by police officers where driver drowsiness was a factor (Strohl et al., 2005).
Alzheimer’s Disease
Alzheimer’s disease (AD) is an enormous public health problem in the United States where 5.2 million Americans are living with that disease. The direct and indirect cost of this disease is estimated to be $148 billion annually. (http://www.alz.org/index.asp). Although the cause of Alzheimer’s is unknown, numerous studies have shown that a brain injury may well be a risk factor for the development of Alzheimer’s disease (Jellinger et al., 2001, Plassman et al., 2000). In a large study of World War II veterans, Plassman and colleagues found that any history of head injury more than doubled the risk of developing AD, as well as the chances of developing non-Alzheimer’s dementia. They also found that the worse the head injury, the higher the risk for AD. A moderate head injury was associated with a 2.3 fold increase in the risk, and a severe head injury more than quadrupled that risk (Plassman et al., 2000). In their excellent review on this issue, Lye and Shores (Lye and Shores, 2000) suggested many possible etiologies for this connection: damage to the blood brain barrier causing leakage of plasma proteins into the brain, liberation of free oxygen radicals, loss of brain reserve capacity, as well as the deposition of beta amyloid plaque (present in Alzheimer’s disease). Even individuals with no known cognitive impairment after their TBI have a risk of an earlier onset of dementia due to Alzheimer’s disease (Schofield et al., 1997).

Chronic Traumatic Encephalopathy (CTE) has recently garnered the attention of both the medical and lay press. At one time referred to as dementia pugilistica or “punch drunk,” CTE is a distinct neuropathological entity caused by repetitive blows to the head and was at one time deemed to be a disease seen only in old retired professional boxers. CTE is an insidious disease beginning with deterioration in concentration, memory and attention, eventually affecting the pyramidal tract resulting in disturbed gait, coordination, slurred speech and tremors (McCrory et al., 2007). The sporting world has recently been shaken by autopsy-confirmed findings of CTE in retired professional football players (Omalu et al., 2006). As repetitive head injuries occur in a wide variety of contact sports beginning at the high school level, there is a pressing need for further study of this entity.5

Neuroendocrine
A TBI is associated with a host of neuroendocrine disorders. Hypopituitarism is found in approximately 30 percent of individuals, over a year post injury, with moderate to severe TBIs (Schneider et al., 2007). Although individuals who develop post-traumatic hypopituitarism acutely may have resolution of that problem over time (Aimaretti et al., 2004), 5 percent of those patients in that study had normal pituitary functioning at three months but developed deficits at one year (Aimaretti et al., 2005). Growth hormone (GH deficiency/insufficiency is found in approximately 20 percent of moderate to severe TBIs (Agha and Thompson, 2006). GH deficiency is associated with an increased risk of osteoporosis, hypercholesterolemia and atherosclerosis. These patients have a significant increase in mortality from vascular disease (Rosén and Bengtsson, 1990). Hypothyroidism is found in approximately 5 percent of individuals post TBI (Agha and Thompson, 2006). Associated signs and symptoms are weight gain, dyspnea, bradycardia and intellectual impairment (Agha and Thompson, 2007). A recent study has shown a connection between hypothyroidism in females and the development of Alzheimer’s disease (Tan et al., 2008). Gonadotropin deficiency is found in approximately 10-15 percent of individuals post TBI (Agha and Thompson, 2006). Adult males will note decreased libido, muscle mass and strength. A correlation has been found between low free testosterone levels and cognitive function, although there is no clear consensus on testosterone supplementation therapy and cognition (Papaliagkas et al., 2008). Hypogonadal women will develop secondary amenorrhea and increased risk for osteopenia.
INCONTINENCE
A TBI frequently affects the cerebral structures that control bladder storage and emptying functions, resulting in a neurogenic bladder. Fox-Orenstein and colleagues reviewed the records of more than 1,000 individuals admitted to rehabilitation centers after a TBI. One-third of the individuals were incontinent of bowel. Twelve percent were incontinent at discharge, but 5 percent were still incontinent at the one year follow-up. In their review of medical complications in 116 individuals with moderate to severe TBI, Safaz and colleagues found that 14 percent had fecal incontinence over one year post injury (Safaz et al., 2008). Fecal incontinence is not only socially devastating, but it will have medical consequences, including skin breakdown, pressure ulcers and skin infections (Foxx-Orenstein et al., 2003). Urinary incontinence is also an enormous social and medical problem. Chua, et al., (Chua et al., 2003) reviewed the records on 84 patients admitted to a rehabilitation unit within six weeks of injury. Sixty-two percent were incontinent. This improved to 36 percent at discharge; however, 18 percent remained incontinent at six months. Safaz and colleagues found urinary incontinence in 14 percent of their cohort over a year post injury (Safaz et al., 2008). Urinary incontinence is associated with the development of frequent urinary tract infections and decubitus ulcers. 6
PSYCHIATRIC DISEASE

The impact and cost to society by psychiatric disorders is among the most important healthcare issues of today. Current estimates in the U.S. suggest that the collective cost of psychiatric diseases could be one-third of the total healthcare budget (Voshol et al., 2003). It is critical to note that psychiatric and psychological deficits are among the most disabling consequences of a TBI. Many individuals with a mild TBI, and the overwhelming majority of those who survive a moderate to severe TBI, are left with significant long-term neurobehavioral sequelae. The costs to society in terms of lost productivity, as well as the costs for medical treatment are enormous. In addition to the aggression, confusion and agitation seen in the acute stages, a TBI is associated with an increased risk of developing numerous psychiatric diseases, including obsessive compulsive disorders, anxiety disorders, psychotic disorders, mood disorders and major depression (Zasler et al., 2007b). Individuals with a TBI appear to have higher rates of depressive disorders, anxiety disorders and substance abuse or dependence (Hibbard et al., 1998, Holsinger et al., 2002, Koponen et al., 2002, Silver et al., 2001) and often have suicidal plans or suicidal behavior in the context of these illnesses (Kishi et al., 2001). TBI is associated with high rates of suicidal ideation, (Kishi et al., 2001, León-Carrión et al., 2001) suicide, (Silver et al., 2001) and completed suicide (Teasdale and Engberg, 2001). In chronic TBI, the incidence of psychosis is 20 percent. The prevalence of depression is 18-61 percent, mania is 1-22 percent, PTSD is 3-59 percent and post TBI aggression is 20-40 percent (Kim et al., 2007). Koponen, et al, (Koponen et al., 2002) studied 60 individuals, 30 years post injury. Fifty percent developed a major mental disorder that began after their TBI. Another 11 percent developed a major mental disorder later on in their lifetime. Twenty-three percent had developed a personality disorder. In a long-term follow-up study of 254 individuals at two and five years post TBI, it was found that there was a higher incidence of cognitive, behavioral and emotional changes at five years than at two years post TBI. Thirty-two percent of those working at two years were unemployed at five years (Olver et al., 1996). A traumatic brain injury clearly may cause decades long, and possibly permanent, vulnerability to psychiatric illness.

SEXUAL DYSFUNCTION
Sexuality, both physiological and functional, plays an enormous role in our lives. Sexual dysfunction is a large issue in the general population and is a major ongoing problem in the TBI population. Studies have shown 40-60 percent of individuals complain of sexual dysfunction after a TBI (Zasler et al., 2007a). Transient hypogonadism is common acutely following a TBI, yet it persists in 10-17 percent of long-term survivors. Beyond just the fertility and psychosocial issues presented by hypogonadism, muscle weakness and osteoporosis may have a significant impact on long-term function and health with consequences exacerbated by immobility of long durations following a TBI (Agha and Thompson, 2005). 7

MUSCULOSKELETAL DYSFUNCTION

Muscular dysfunction

Spasticity is characterized by an increase in muscle tone that will result in abnormal motor patterns. This spasticity may well interfere with an individual’s general functioning, and limit self care, mobility and independence in the activities of daily living. Spasticity requires life long treatment. Untreated, spasticity will eventually lead to muscle contractures, tissue breakdown and skin ulceration.

Skeletal dysfunction
The incidence of fractures in a TBI is approximately 30 percent. TBI patients with fractures, especially fractures of the long bones, are at risk for heterotopic ossification (HO), which may not develop for as long as three months post injury. HO is defined as “the development of new bone formation in soft tissue planes surrounding neurologically affected joints,” and has an incidence of 10-20 percent following a TBI (Colorado, 2006). Safaz and colleagues found HO in 17 percent of their cohort over a year post injury (Safaz et al., 2008). If left untreated, HO will eventually lead to abnormal bony fusions (ankylosis) and subsequent functional limitations.

SUMMARY

Historically, individuals living with a brain injury have been referred to as brain injury survivors. No one knows how that term came to be used in this situation. Perhaps the concept of merely staying alive was used because as little as 30 years ago, the majority of individuals with a moderate to severe TBI succumbed soon after their injury. Perhaps it was used to imply that the individual outlived their injury and persevered despite the hardship of the trauma. This term, however, does not address the reality of brain injury. Cancer survivors are survivors because it is believed they are cured—and they indeed have outlived their disease. Many individuals who sustain a TBI recover 100 percent. They have truly survived their injury. However, in the U.S. alone, every year, over 125,000 individuals who sustain a TBI become disabled. This paper discusses only a small percentage of the causes of disability and the ongoing and developing medical conditions individuals with TBI face. Presently, more than 3 million individuals in the U.S. are disabled due to the myriad of sequelae of a TBI (Zaloshnja E, Miller T, Langlois JA, Selassie AW. Prevalence of long-term disability from traumatic brain injury in the civilian population of the United States, 2005.The Journal of Head Trauma Rehabilitation 2008;23(6):394-400.) Their brain trauma has resulted in a condition that is disease causative and disease accelerative. As a result of their brain trauma, these individuals now have life-long brain injury disease. Their disease should be reimbursed and managed on a par with all other diseases. Only then will the individuals with this disease get the medical surveillance, support and treatment they deserve. Only then will brain injury research receive the funding it requires. Only then, will we be able to
truly talk about a cure. 8

ACKNOWLEDGEMENTS
The Brain Injury Association of America gratefully acknowledges Brent Masel, M.D., as the author of this position paper. The Association also thanks Mark J. Ashley, Sc.D., Gregory J. O’Shanick, M.D., and Christopher Nowinski for their contributions. The Board of Directors of the Brain Injury Association of America adopted this position paper at its meeting on February 27, 2009, in Washington, D.C. The Association will continue to review the topic of brain injury as a disease as scientific and public policy progress dictates.
Electronic copies of this statement may be obtained from the Brain Injury Association of America’s website: http://www.biausa.org.
The paper may be cited as follows: Masel, B. Conceptualizing Brain Injury as a Chronic Disease. Vienna, VA: Brain Injury
Association of America, 2009.

In order to find the following references for the above information, please use the following link to access the guide in its entirety: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CCYQFjAA&url=http%3A%2F%2Fwww.biausa.org%2F_literature_49034%2FBrain_Injury_As_a_Disease_Position_Paper&ei=GM6JUMKBNbHlyAGI54DIDA&usg=AFQjCNFL04VqG2OMLtMj4BolSg8oLMOJxQ

I will keep trying to find more information, but I really feel that this describes a lot of what I have experienced. I believe it is an accurate research article that you should present to your doctor if you have had a brain injury or know of someone who has.

UPDATE: I found this information posted regarding the long term outcome of brain injury. It does discuss some of the issues that were listed above. I also states that damage to the basal ganglia can lead to late onset Parkinson’s disease. I found this interesting because I had injury to this area, and I’ve been told by numerous doctors that my jerking, etc wold not be related to the CPM injury that I have. I did have a radiating pain throughout my body after the initial injury. This radiating pain went away, but in its place, I’ve had issues with random cramping, jerks, and spasms. The doctors didn’t think that the spasms etc were related to my brain injury because I didn’t have the symptoms initially. This is proof that it can and does happen, and it can take up to forty years post injury to have it develop.. That’s crazy!!!

Neurodegenerative disorders such as dementia of the Alzheimer’s type (DAT) and Parkinsonism are related to mild and moderate TBIDAT is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. A moderate TBI increases the risk of DAT with a hazard ratio (HR) of 2.32. In case of a severe TBI the HR for DAT is 4.51. For the sake of ease, one could say that the risk for DAT in patients with a moderate TBI is 2.32 times compared to those who have not suffered a TBIParkinsonism may develop years after TBI as a result of damage to the basal ganglia. It is characterized by tremor or trembling, rigidity or stiffness, slow movement (bradykinesia), inability to move (akinesia), shuffling walk, and stooped posture. The association between TBI and parkinsonism has not been studied as extensively as inDAT. However significant associations between PD and TBI have been established. Professional career boxers have in increased risk for dementia pugilistica also called chronic traumatic encephalopathy or the punch-drunk syndrome. Mild cases may present with slurring dysarthria, gait ataxia, disequilibrium and headache. Symptoms begin anywhere between 6 and 40 years after the start of a boxing career, with an average onset of about 16 years. Mental and physical abilities may decline resulting in dementia and parkinsonism.  (http://cirrie.buffalo.edu/encyclopedia/en/article/338/)  “Brain Injury: Long term outcome after traumatic brain injury”” Gerard M Ribbers, MDPh.D.

 

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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