Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Traumatic brain injury”

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.


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!


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.


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.


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.


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.


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.


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.


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.


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!

Identifying Brain Injury:

There has been a lot of attention focused on brain injuries recently. We are finding out more and more every day that minor hits to the head can lead to ongoing issues with cognitive abilities.

It’s been over 18 months since I experienced my brain injury due to extra pontine myelinolysis. It was very shortly after the injury occurred that the MRI images stopped showing the lesions that were originally there, but I continued to experience deficits.

Initially, I had an abnormal EEG, but subsequent EEG’s done 8 to 12 weeks later showed normal.

What does it mean when your images show everything has returned to normal, but you are still experiencing issues? Trust me, I had a doctor tell me that because my tests were now normal that my symptoms were not being caused by the brain injury.

This leaves you in a position of not knowing, and this lack of evidence in  current medical imaging/testing is what so many people with brain injuries face. Whether you were injured after a roadside bomb in Iraq, had minor or major concussions after playing in sports, hit your head after falling off your bike, or suffered from an internal injury like stroke or CPM/EPM, you may experience symptoms long after your injury. In some cases, your symptoms may become progressively worse, but the images don’t show any injury at all. Doctors rely so heavily on what the tests say vs what the patient says that you may face a doctor telling you that there is nothing wrong with you, and that is beyond frustrating and depressing.

This is what has caught headlines as more NFL players are ending their lives over their ongoing decline in cognitive abilities. They have gone through testing, MRI, neuropsychological exams, EEG’s, CT’s, etc and the tests showed that they were normal.

It is the frustration that millions of people face each year as they struggle to find answers and more importantly find help.

The most fantastic news that I have is that technology is starting to advance to the point that doctors can finally start to identify injuries that weren’t detectable by any other methods. This is such a relief to those of us who live with the consequences of brain injury. It is so unfortunate that so many doctors need to have this “physical” evidence instead of trying to help a person deal with the outcome of their injury. In other words, would some of those NFL players that took their lives still be alive today if a doctor told them, “no matter what the tests say, you have an injury and let’s work to fix it” ?  If they got treatment based on the symptoms that they experienced instead of being prescribed anti-depressants and anti anxiety medications, would they be here now? It’s a tough question to answer, but the loss of their lives had a purpose. It has brought awareness and funding to support brain injury research.

The purpose of this post is to bring to light some of the most current research on brain injuries. What are the new tests being done? Where are they being done? Will they help you?

One type of injury that we tend to not discuss often is “chemo brain”. Chemo brain is a term used to describe people who have undergone chemotherapy and experienced cognitive issues, especially with concentration and memory. Doctors have dismissed those symptoms as being depression, anxiety, fatigue, etc. They did not believe that they were caused by a physical condition. However, in December of 2012, several research studies using fMRI, PET and other scans, showed evidence that chemo brain is real.

Often, cognitive complaints were associated with persistent fatigue and depressive symptoms, making it challenging to sort out whether or not the complaints of poor memory, attention, and difficulties with multitasking were related to brain dysfunction or were merely a manifestation of an uncontrolled mood disorder.46 Many who complained were younger patients with breast cancer who had become menopausal prematurely with chemotherapy, and their experiences of vasomotor symptoms, nighttime awakening, and poor sleep might have explained some of their cognitive complaints.7


The study goes on to explain the reasons behind why chemo brain (and in my opinion other brain injuries tend to progress). As I have mentioned prior in my blog and this research paper goes on to suggest, there seems to be an autoimmune response that causes ongoing inflammation and injury to the brain.

Concurrently, an increased understanding of immunology and mind-body interactions (psychoneuroimmunology) has made us more aware that events in the body (tissue trauma and inflammation from surgery, radiation, chemotherapy, and biologic and targeted therapies) can trigger systemic inflammation with secondary effects on the CNS.21,22In parallel, stress and cognitive threats can have direct effects on the hypothalamic pituitary adrenal axis and the sympathetic nervous system, leading to systemic responses that can affect the immune system.23 In addition, immune cells, responding to inflammation can traverse the blood-brain barrier and increase local inflammation in the brain, affecting emotional and cognitive function without the need for direct diffusion of chemotherapy into the brain substance.2325


The technology used to determine differences in the white matter between the control group and those treated with chemotherapy was called magnetic resonance imaging diffusion tensor imaging (DTI). The women that they tested showed decreased testing ability in memory, concentration/ attention.

Finally, the DTI detected decreased white matter integrity in tracts involved in cognition in the women treated with chemotherapy with no changes observed in the two control groups; this suggests a causal relationship between the chemotherapy exposure, cognitive complaints, NP test abnormalities, and white matter changes.


PET scans are also being used to detect chem brain. When I hear accounts of chemo brain, the symptoms they mention are identical to those that I experience. It is so frustrating to have doctors tell me that this is not real, and I know that this is the same frustration experienced by so many of us who are suffering from brain injuries of all varieties. It brings me some relief to know that more research is being done, and technology is starting to show the causes of what we experience. I recommend the following link to learn about PET scans in the use of diagnosing chemo brain: http://www.npr.org/blogs/health/2012/12/28/168141465/another-side-effect-of-chemotherapy-chemo-brain

A friend posted these links about newer imaging used to diagnose brain injuries. I haven’t researched all of these as it takes a significant time for me to read through information, but I really want to get this information out there.

MEG Scan – detects errant electrical activity in the brain. Used in conjunction with FMRI and EEG.

Diffusion Tensor Imaging (used above to diagnose chemo brain):
Problems in the white matter—for example, nerve fibers that are not bundled together coherently or that have lost their fatty “myelin” coating—show up in DTI scans but not in regular MRI scans.
Huang says he hopes to eventually incorporate a third imaging technique, chemical shift imaging (CSI), also called MR spectroscopy imaging. This method reveals the distribution of certain chemicals in the brain—another potential marker for subtle brain injury. http://www.research.va.gov/news/research_highlights/brain-injury-090808.cfm

MRI Neurography – Shows nerves. http://en.wikipedia.org/wiki/Magnetic_resonance_neurography
Magnetic resonance neurography (MRN) is the direct imaging of nerves in the body by optimizing selectivity for unique MRI water properties of nerves. It is a modification of magnetic resonance imaging. This technique yields a detailed image of a nerve from the resonance signal that arises from in the nerve itself rather than from surrounding tissues or from fat in the nerve lining. Because of the intraneural source of the image signal, the image provides a medically useful set of information about the internal state of the nerve such as the presence of irritation, nerve swelling (edema), compression, pinch or injury. Standard magnetic resonance images can show the outline of some nerves in portions of their courses but do not show the intrinsic signal from nerve water. Magnetic resonance neurography is used to evaluate major nerve compressions such as those affecting the sciatic nerve (e.g. piriformis syndrome), the brachial plexus nerves (e.g. thoracic outlet syndrome), the pudendal nerve, or virtually any named nerve in the body.

There is also a new one called high definition fiber tracking. http://schneiderlab.lrdc.pitt.edu/projects/hdft

Finally, there is Tau imaging: http://www.sbir.gov/sbirsearch/detail/102432

I will try to add and complete more of this post as I research further and learn more about the different types of imaging, but it is exciting work for those of us suffering from brain injury. Hope is on the horizon for getting answers and evidence for why we continue to experience the symptoms that we do.





Foreword: I wrote this a few days ago, and I think it gives a pretty accurate description of how frustrating it is to have a brain injury. I wish I had more answers as to what to do for it. Hopefully, as time goes on, there will be more answers, more treatments, more ability to have a normal life or better recovery.

It gives me strength to know that I’m not alone in this. I think it’s important to let you know that even though you might have lived past an injury that they thought you would not survive, even though you are grateful for your life, it doesn’t mean that you don’t grieve over the way your life was.


I don’t know what’s going to happen in my life. It has already changed TREMENDOUSLY. The biggest issues that I have is with the way I think, how I act, not being  able to live my life like the way it was, but this might be as GOOD as it gets, and that is extremely SCARY.


I was right. My occupational therapist said that those who suffer brain injuries can have their brains turn to MUSH. Ok, she didn’t use the word, mush, but that’s pretty much what happens. (She thought that was ridiculous before, but she went to a conference and they acknowledged that it was happening.) The brain calcifies. It can take a few years up to 40. In autopsy, they removed the brain of someone with CPM, and their brain CRUMBLED in their hands.


I’m 35. I have two kids. I wanted to be a doctor, and that was a realistic possibility, and now I’m stuck working about 12-16 hours a week taking sales calls. I have TRIED to pick up my textbooks. I have TRIED meeting with my MCAT study partner. It doesn’t work. My mind doesn’t work. It’s like throwing cooked spaghetti at a wall. It might stick for a few seconds, maybe a few minutes, but then it’s gone.

I want to get better! I want to be back to normal.

It’s exhausting trying, over and over and over. I find comfort in the things that I do remember. I remembered an appointment, and that gives me false confidence that things are better or that I’m better than I am, and so I think, I don’t really need to write this down. I’ll remember it. Or I won’t need to create a reminder on my phone to pick my prescriptions, I’ll be driving by the pharmacy and that will cause me to remember. That’s how it used to be. Everything, would just fall into place as I did something. I would be able to organize things in my mind, as simply as one puts the pieces of a puzzle together. It was so easy.


It does bother me that the other day I could not remember how old I am. I could not.  It bothers me that I don’t realize I bought the same video game from three different places in a 24 hour period.


I don’t want o be like this for the rest of my life. I’ve always been a survivor. I’ve always been able to overcome obstacles. I have lived through SO much: physical, mental, emotional abuse, sexual assaults, long term illness (when they couldn’t figure out why). I’ve worked through it all. I’ve lived through it all. I’ve overcome it all, and just as I was beginning to think I had the possibility that it was going to be better (pituitary tumor removed), I was mistreated and ended up with brain damage. And now, to face the possibility that after losing my mental abilities and that now I face years of losing my mental abilities over the course of 5 to 10 years or longer until I die, until my brain turns to mush.


I am extremely tired of having to deal with the brain injury, of having to make adjustments to my life. I HATE not being me. I hate that I have to make notes to get things done. I hate that I can’t remember if I’ve taken my medications or not, or that I forget to call a prescription in, or that I didn’t fill the prescription box correctly. I hate the side effects that I get from the medications. I hate that they don’t fix the problem. I hate that I have people question my integrity when they don’t know who I am or how much I’ve accomplished and Lived through. I hate that I have to walk into work and feel like a slacker because I’m not able to work 30,40, 60, 80 hours a week. I hate that I watch the same shows over and over again and that I remember the faces but I don’t remember the story.


I hate the stress. I hate the fatigue. I hate that I have to go through this. It’s not fair. It’s not right, and I don’t know what to do about it. I don’t know what I can do about it.

I don’t want to live the rest of my life having other people take care of me. I don’t want to live the rest of my life dependent on medications, physical or occupational therapy. I want to be 35, and live the life of a 35 year old. I want to go back to school. I want to get into medical school. I want to be a doctor. I want to be the strong, independent person I was before the brain injury.


What do you do when what you want to do, who you want to be, is no longer what you can do or can be?


I am not sure what to do next, and I’m trying to be happy with what I have, but I’m not. There is a hole in me that’s so BIG, the disappointment is so tangible, the grief is so pungent, that I feel lost. What do I do next?



I’ve been trying to stay focused on creating posts that are more about central pontine myelinolysis, what to expect, how to compare it to other brain injuries. I’ve been trying to stay away from writing about me.

Frankly, you can only take so much of listening to someone go on and on about horrible things are in their life. It’s hard living through it too, but most people don’t really care, and they don’t want to feel “bummed” about how bad someone else has it, so I’ve tried to refrain from going on and on about my feelings or my struggles with EPM. Tonight, I have to discuss about what’s going on with me.

So, you might be wondering, what’s wrong?

Today, I was told that the “basic” cognitive testing that I had a few weeks ago, showed that I have significant impairment, but that it’s not consistent. Basically, the doctor felt that my symptoms are being created or exasperated by psychological issues.

I have to say that I agree that stress, fatigue, and anxiety the issues I have worse. Isn’t that true for anyone? Even if you don’t have any brain injury, you’re just perfectly normal, doesn’t stress, fatigue, and anxiety make issues worse?

I’ve never been a strong test taker. Never. I was usually one of the last kids to turn in a test. The last college classes I took, I would run out of time, especially in chemistry. I was usually one of only 4 or 5, still taking a test at the end of the exam period, out of more than a 100 or more. I felt this was because of my perfectionism. In reality, I would just tend to over analyze questions. I would get stuck and read over the same question over and over again because I thought that there were multiple ways to interpret the question.

I have found since I’ve had the brain injury, I’ve had more issues with this. It becomes harder for me to shut off the internal dialogue I have with myself over directions, questions, etc. I will tend to confuse directions for one section of the test with other sections. For example, if you ask me to name all the animals that I can think of, my mental gears start spinning: birds. Well, birds aren’t really animals are they? Aren’t they considered more along the species of reptiles? They have a connection to dinosaurs. Do they want specific animals? Like Robin? Robin is a type of bird. I wish I could look up whether a bird is really an animal. Aren’t animals considered types of mammals? There are marsupials. I wish I could look up the answer. I really don’t want to sound stupid by saying birds if birds aren’t really animals. And what if they want specific animals.  Aren’t animals any living organism? There’s different types of Kingdoms. Shit, I’ve studied this stuff, why can’t think of the right answer? Humans are animals. Maybe I should just say humans. Good answer! My answer is humans. How about insects? FRICK!

SO, that’s just an example of how my mind works in the moment of answering ONE freaking stupid question….and they want me to to name as many animals as possible, as quickly as possible! It’s just not that easy any more. I used to be able to shift gears faster, think through things more quickly, and get to an actual correct response, but I don’t have that ability any more. I get caught, stuck.

Another example, they asked me to count the dots in the following pictures one by one, or maybe they actually said individually. I’m not sure exactly how it was worded. The first problem I have is, is staying focused and tracking the dots. The first group was scattered dots everywhere on a page. There must have been 20 or more. They weren’t organized, and when I started counting them I lost track of where I began, and I wanted to give the right answers, so I double counted them. I thought it was the answer that was important, but it was actually the amount of time that it took that they were monitoring. The next pages they started organizing the dots into groups. My first reaction, well that’s a group of five. There’s two groups of five. There’s three groups of three. It’s a total of 19. Wait, they said count them individually. Maybe this is an illusion.  They have those optical illusions where your mind looks at something and doesn’t process it correctly. Did I miss a dot? So, I counted the dots a second time. No, no I think there aren’t any that I’m missing. Are you sure? Yep, I’m sure. Ok. 19 is the answer.

So, if I had known that the answer didn’t matter, then I would have just blurted out numbers. If I realized that it wasn’t a trick question, I would have been able to respond more quickly. If I had just asked for clarification or asked them to start over once, I figured out what I was supposed to do. Frick!

Trust me. I feel stupid over the testing. I don’t know why that part of my mind is broken. I mean, I did have that problem to some extent prior to the injury, but at some point, my reason would take over, and I would just be able to answer the questions. I would be able to shut down that internal dialogue, and just take a test. At the very least, it didn’t interfere as much as it does now.

In other words, I was never quick at taking tests, but now, I’ve become discouragingly slow. It’s just harder for me to process information, directions, to figure out what I need to do and then do it.


I am going to say, in my defense, that I had only had four hours of sleep that night. I really wish that they did testing around the times that I’m normally awake. If I don’t fall asleep until 4 or 5 am, and I’m scheduled to take a test at 9am, I’m practically set up for failure, but they don’t start testing in the afternoon. Two pm would have been the best time for me, but doctors do testing around a typical 9am to 5pm schedule, not a 2pm to 10pm schedule.

So, what does all of this have to do with me?

The testing I did reflected poorly on me, and so my integrity has been questioned.

I am so extremely grateful that I know what my issues are, and that my friends and family believe me and know. My cognitive therapists and occupational therapists believe me and see the struggle that I experience, and they believe me.

It really seems that the testing itself is the only thing that doesn’t work in my favor, but I just don’t think that the tests account for the type of mental distractions that I have because of the brain injury. Well, I had these some of these issues before, it’s just so much worse now.

In the end, getting this news just stresses me out even more, but then I begin to regain my composure. I don’t really care what the tests say. I know what’s going on with me, and that’s what matters. I just have to brush off this bad news and regain my focus. Keep on, keeping on.

I know stress, fatigue, and anxiety complicate my problems, but I’ve always been able to work around those issues. They’ve never stopped me from doing what I wanted or needed to do.

They are causing issues now, and I’ve tried everything I can to control those factors, so that I can become more functional, but they aren’t the cause of the deficits that I have, and it has left me exasperated and frustrated.

Let me give you an example of how people can misinterpret a problem. A man is having a drink at a bar.  He’s chatting with his friends, and as he gets up to go home, his friends stop him and ask him if he needs a ride home. They suggest that maybe he call a taxi. He feels insulted because he’s only had one drink. He refuses the taxi. The next night, at the same bar, he sits down to have a drink. After a glass of wine, he gets up to leave and another person suggests that he not drive home. Again, the man scoffs at the suggestion. On the way home, he gets pulled over by a cop. The cop believes that the man is drunk. The man refuses to take sobriety test. He feels angered at the fact that people keep suggesting that he’s drunk. Since he refused to take the sobriety test, the cop takes him to jail to sleep it off. The next morning, they find the man dead in his jail cell. He wasn’t drunk at any time. He had had a stroke.

How do I feel that this story relates to my experiences? It is not uncommon for people to look at someone with a brain injury and because they do not see any physical injury on the outside, they assume that there is an external cause to the problems that you have. You don’t really have memory issues. You’re just stressed. You have trouble with concentration and reading because you’re mind is creating those problems, because you are focused on issues.

It’s so easy to judge someone when you’ve never experienced the same problem. It’s easier to put on a filter and say that these issues are mental when you’ve never lived with them.

I’ve been told by so MANY people that they’ve forgotten to pay bills. It’s normal. I’ve forgotten where I’ve parked. It’s normal. I’ve forgotten to take my medications. It’s normal.

Yesterday, I couldn’t figure out how old I was! I’m 35, and I forgot. I wasn’t sure if I was 33, 34 or 35. I could not figure it out. I forgot my son’s birthday. I forgot the significance of 9/11 (also my son’s birthday).

THIS is NOT normal for me! This was not who I was before the brain injury. I worked full time. I went to school full time. I took care of the bills. I did NOT have these issues. I’ve never ever had to have an 80 year old man have to shuttle around the parking lot trying to find my car because I couldn’t. I could do advanced math in my head without any issue. I could figure out patterns and trends. I could read through law books, Title 21 of the federal code of regulations.  Shakespeare was like a Dr. Seuss book to me. I could spend 6 to 8 hours reading through legal cases. I could spend 10 to 13 hours studying for the MCAT while working 32 hours or more in a week. What I live with now, IS NOT NORMAL FOR ME! I’ve always lived with stress, but it did not cause impairment.

To have some guy read through one to three tests and can tell me that he has my brain injury figured out, TOTALLY pisses me off. The most brilliant scientists in the world do NOT have a great understanding of how the brain works. They don’t!  Were the tests even designed for a person who has a brain injury? Does it take into consideration that the person has an issue with understanding directions, language, or writing.

I had cognitive testing done BEFORE my brain injury, and I would have difficulty completing tasks in an allotted time. I was able to get the puzzles, etc correct, but not within a standard time frame.

I was told by my cognitive therapist today that I was right. A few months ago, I told her that there is a belief that over time a person’s brain can turn to mush after they’ve had a brain injury. In a person who has had CPM/EPM who lives for longer than a few years, when they move the brain at autopsy, it crumbles. It turns to mush.

When I told my cognitive therapist this, she told me that it wouldn’t happen. (She has been working as a cognitive therapist for more than 20 years. She is an expert.) She went to a conference this weekend, and they are finding that these injuries can kill the brain slowly over time, that the brain can calcify after a brain injury. She told me that I was right.

In the end, what can I do? I have to keep moving on, but tonight, I raised my hands up to God and cried. (I don’t cry often because my immune system causes issues after.) I don’t understand, why?! WHY? Why do I have to live through this? I’ve already had a pretty tough life, but to go through this too! Why God? Why do I have to go through this too?

Can’t I just be normal again? God, I would give anything to have my old mind back! I wish I could just put this whole brain injury thing away! I wish I could get back to doing what I wanted to do. I just want to go back to school, get into medical school, work at saving people.

I wish I knew why.  I wish I could just get over it, as if I was getting over a cold. I don’t think they understand how frustrating these things are for me. I don’t think they understand how strong I am, and how hard I’ve worked, and how desperately I want to put all of this behind me, but it isn’t just a mental thing. It’s just not, and I have to learn how to work with the deficits I have and try to make the best of my life and my abilities as they are. I will continue to work with my therapists in trying to get new connections, with my doctors to get on the right medications, and try to become the closest to my old self as I can. I guess that’s all you can do when you’re living with a brain injury.


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.


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:


Related articles

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:

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.


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 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

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.
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

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.

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


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.


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

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.


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!

I can’t do it all:


I’ve been at a breaking point for weeks now. It seems like when you think you can’t handle one more thing, five more things are forced upon you.

All of the things that I’ve been going through over the past few weeks are related to having a brain injury, and it has made me SO angry, and so upset because there is nothing that I can do about it.

I’m stuck living with it, and there’s nothing more that I can do to fix it. Don’t get me wrong, I am trying to fix it still. I’ve just started taking several new medications to help with the things like pain in my hands, cramping, shaking, etc. I’m going to start taking medicines for ADHD to see if that will help with my focus, and I will start taking anti-depressants to see if that can help make me happy that I have a brain injury and have lost everything I was working so hard to achieve over the past few years.

You know, I’m just going to say this. I think people, doctors, therapists, all believe that when life hands you shit, you should smile about it and exclaim how fantastic it is and not feel horrible that you’ve been handed a whole load of shit.

If you lose the love of your life or a child, and spend the next few months crying over that, they believe that you need antidepressants. They believe you are depressed. I wonder what people did before they had antidepressants?

They mourned, and it was an expectation. They wore black. They stayed inside. They didn’t participate in normal social activities, but somewhere along the way, we began denying ourselves this process, and began to feel that if you were upset that the man/woman you lived with for 50 years died, that you should start taking antidepressants to help get you through it.

Now, I don’t have all the answers. I don’t. I could simply argue that people would have used anti-depressants if they had them available. We have advancements in medicine that make these wonderful new medicines available, so why shouldn’t we take advantage of them?

But, I think there is a need to find the middle.

For weeks, I’ve been struggling with the stress of dealing with lawyer stuff, family issues, work issues, health problems and then the disheartening realization that I am still unable (at this time) to return to studying for the MCAT. AND it really hit home this week that this totally SUCKS, and it’s completely unfair, and there is nothing that I can do about it.

I have SO much stress directly related to having a brain injury, and it could have been prevented. It SHOULDN’T have happened!!!

No matter what happens, I will never receive enough compensation to make up for what I have lost, and at this point, I don’t think I’ll receive any compensation for what I have lost.

So, I was at my cognitive therapist appointment and tearing up at the idea that they want me to do more there as well. I’m just so fried mentally, emotionally, etc that the idea of doing these worksheets that a 7 year old would have no problem doing about caused me to have a complete breakdown.

And then to make it even worse, my therapist looked over at me and told me that I would need to start taking antidepressants or I would need to give up things that I was already doing or wanted to do. She told me that I needed to stop doing things in order to get better because if I was so overwhelmed when I came in to work with her, then I would not be able to do anything that they needed me to do.

Of course this makes sense. If I’m so stressed out that the thought of doing mental tasks that they require me to do sends me into a tizzy, then they really can’t do anything for me.

This ramped up my anxiety and stress by 80. I mean, my therapist understands me, and she has helped me so greatly over the past several months. She KNOWS and UNDERSTANDS what I’m going through. She has the answers, and she’s a fantastic person and a wonderful friend, and if there is anyone who is going to help me get back to “normal” then it is her.

What am I going to do if I lose her too?

So, I’m left with the choice of going on antidepressants or stopping therapy. There really is no choice. I’ve already made the call to my doctor.

I have to say that even I don’t cotton to the idea of going on antidepressants, I understand why my cognitive therapist wants me to do it. I’m functioning on the edge of about completely losing it every day. She can’t work with that. And, I spend a good portion of my therapy time discussing how crazy my life is and how stressful it is, and that adds extra stress to her life.

As she put it, she sees a younger version of herself in me (sans the brain injury), and it is physically and mentally exhausting to see me make the same mistakes that she made.

In the end, she said, I can’t do it all, and I spent the night wondering what was I supposed to give up. How was I supposed to give something  up? I can’t very well go home, and say to my kids or Tom, well, I’m sorry. I’m unavailable for anything any longer, fend for yourselves. I can’t call the lawyer and say, sorry if you need answers to the questions that you want me to answer, figure it out on your own. I can’t call my disability insurance company and say, too bad if you need medical records, I have brain damage so screw you. I can’t walk into work and say, I’m just going to stare at a wall for the next 5 hours, don’t bother me.

So what am I supposed to stop doing? I have no flipping clue.

That night, I went to my psychologists office, and I’m going through all the same stressful things that I went over at my cognitive therapists office. I was overwhelmed. I am overwhelmed. What am I supposed to do?

Can you imagine my surprise when she told me that I needed to start taking medicines for ADD? She felt that I had a long standing issue with ADD, but that the brain damage has just pushed it over the edge. She believes that taking medicines for ADD would really help ground me and help keep me on task.

At this point, I will try anything. Truly, I think I will try anything. So, I added that to the list of things to see my doctor for. But, then she told me something else, she told me that I needed to give something up, that I can’t do it all. It was hard enough for someone who didn’t have a brain injury to try to accomplish what everyone wants or expects me to accomplish, so I shouldn’t put that extra pressure on myself to be perfect or to do everything that everyone wants me to do.

Here it was, two people, two extremely smart, extremely wise women telling me that I was going to have to stop trying to do everything. I have to accept that I can’t do the same things that I used to do, no matter how unfair it was. I have to stop telling myself, I used to be able to… Having that mentality, holding onto the past, will keep me from moving forward in the future. Wow, right?!

I have to learn to accept and be able to say: I can’t do it all.


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).


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.


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.


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






Sports in General:


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


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