Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the category “Central Pontine Myelinolysis/ Extrapontine Myelinolysis”

Vision Issues Related to Brain Injury and CPM/EPM:

Hello there.

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

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

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

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

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

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

Visual Snow 2

Visual Snow 3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Hope that helps folks!

Exciting new developments in Electro-stimulation and brain disorders and diseases:

Yes, I am still alive. ;) However, I am still struggling. I am working at getting help for the vision issues that have become significant over the past few months.

Someone sent me this report. It is something you listen to, like a radio show. I am REALLY excited at what this might mean for us. Could this be a cure to issues we experience after a brain injury? I will attempt to contact Dr. Lozano to see if he thinks this could help those like us.

My only concern would be that because there is damage to the circuitry in the brain that stimulation might not be as effective. Really, I believe there is no way to know for sure until you try it–a potential cure to our problems. Can’t help but feel excited and hopeful :)

Can Hacking The Brain Make You Healthier?
by NPR/TED STAFF
August 09, 201310:01 AM

http://www.npr.org/player/v2/mediaPlayer.html?action=1&t=1&islist=false&id=209618161&m=209620407

Hope on the horizon:

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

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

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

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

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

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

Brain injury: What causes an increase in symptoms?

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

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

It irks me.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Have a great night!

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

http://jco.ascopubs.org/content/30/3/229.short

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

http://jco.ascopubs.org/content/30/3/229.short

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.

http://jco.ascopubs.org/content/30/3/229.short

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.
http://www.research.va.gov/news/research_highlights/brain-injury-090808.cfm 

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.

 

 

 

Alternative Treatments for CPM/EPM and Brain Injury:

Hi, there.  I hope all is well, and moving forward for you.

I wanted to include this information from my friend, Adam. I have not researched this product or group myself, so I can’t account for what it says, but it seems like if it does everything that they promote it does, this could be a HUGE step in Brain Injury recovery and prevention of degeneration.

This is from the information that he sent me. It really sounds promising:

I am having a little trouble posting on your blog. Tried to post this
Actually the product I am referring to is at GNC Anatabloc. It has anatabine in it.

See also www.anatabloc.com You can see testimonials all over the internet.
www.gnc.com for one

My sister with lupus and diabetes, my neice with thyroid problems, a friend with MS and 100 other people I know are taking.

Controls and attacks inflammation. See brain studies.

TBI is traumatic brain injury
TBI

According to the Centers for Disease Control, 80,000 people in the United States suffer long-term disability from a traumatic brain injury (TBI) annually. Roskamp Institute scientists conducted a research study of TBI and control mice by administering a-natabine to measure its effectiveness for recovery from injury using scientific accepted methods. TBI mice treated with a placebo and the sham (untreated) mice recovered at a similar rate with deteriorated motor and cognitive functions. The a-natabine treated mice however had a significant recovery the researchers believe, by inhibiting inflation and reducing amyloid production. To quote the published research paper; “A-natabine treatment appeared to completely prevent the loss of spatial memory retention following severe TBI. Further study of this promising treatment is warranted and will include treatment in a mild closed head injury model as well as long term outcome from injury. Dietary supplementation for reducing secondary injury after TBI offers an easy path to clinical application and simplifies the administration of the therapeutic.” This pathological information warrant further studies with ongoing research in exploring other models of TBI using anatabine.

Alzheimer’s disease

Research study findings by Roskamp Institute were presented at Neuroscience 2012 about the impact of a-natabine in treating Alzheimer’s disease (AD). AD is a neurodegenerative disorder that causes problems with memory and behavior due to the increasing death of nerve cells in the brain. Most scientists, supported by research done at Roskamp Institute, agree that excessive amyloid plaque buildup (Abeta peptides) and neurofibrillary tangles (twisted protein fibers named tau) are directly related to the brain nerve cell loss. Data from the study using a well-known mouse model of AD shows that a-natabine treated mice have a significant reduction in the accumulation of plaque in the brain as compared to the control population. Scientists believe this occurs because a-natabine reduces or regulates human neuronal like protein BACE-1 (the rate limiting enzyme responsible for Abeta production). Cognitive tests of an ongoing investigation of a-natabine treated mice show greater cerebral functions and improved abilities as compared to the non-treated sample. Data from the study also show a-natabine’s anti-inflammatory results. A-natabine reduces neuroinflammation and STAT3 phosphorylation in the brain of transgenic AD mice. Additional research is warranted based upon results of this study regarding the potential benefit of a-natabine in the treatment of Alzheimer’s disease

http://www.rfdn.org/inflammaging.html

Here is a summary of the important research done at the Roskamp Institute.

http://www.mullanalzheimer.com/livesite/

http://www.rfdn.org/ms_anatabine.html

A quote re the peer reviewed study from Dr. Michael Mullan, the CEO and President of the Roskamp Institute, “Anatabine continues to demonstrate widespread anti-inflammatory properties in a broad array of pre-clinical models. Given the commonality of inflammatory systems in rodents and humans, there’s much reason to expect that anatabine will demonstrate similar properties in humans. In fact, the team went on to demonstrate that in human blood inflamed with LPS, the presence of anatabine dramatically dampened the inflammatory response, a result also included in the paper.”

After consulting with my cousin, the product that they recommend for inflammation is Neprinol. The difference between the product that Adam is recommending and Neprinol, is that Neprinol actually eats away at scar tissue. It dissolves it. The product that Adam is discussing, prevents inflammation. It makes me think that these two products combined could be a super healing combo for everything from arthritis to brain injury.

I will try to research these products more to find out what validity that they have or what the current research is describing, but these natural remedies tend to hit the market decades before mainstream medicine begins to manufacture information. For instance, my Aunt has been promoting the benefits of probiotics since the early 1980′s. Now, almost every doctor recommends probiotics after you finish an antibiotic. It is key in recovering a good GI system.

 

Todd’s Ride:

Hi, folks.

This is going to be an ultra brief post. Todd’s story is posted on my blog, and he has made remarkable strides!

He is raising funds for CPM/EPM. I do not have all of the details, but please be feel free to check out his donations page.

 

 

My prayers and good wishes are with him and his wife as they go the distance for CPM and EPM.
Good Luck, Todd!

Mutism after Brain Injury and Central Pontine Myelinolysis:

I am writing this post for my friend Michael.

Michael developed central pontine myelinolysis a few years ago. In the course of the past 18 months, he has seen a decline in his abilities. He has had ongoing issues with memory, attention, stuttering, movement issues (shakes, tremors, jerks, and spasms), and now he is having issues with mutism.

So, what is mutism? It’s the inability to speak, talk or make vocal noises. In some cases, this issue may be intermittent.

My friend has this issue. A few years after he suffered from central pontine myelinolysis, he began to have issues with mutism. He will go through periods of hours or days without being able to make any sounds. He is not even able to whistle.

Previous to the mutism, he did have issues with a common symptom to CPM/EPM, which was ataxic in nature, dysarthria (general speech issues, including stuttering, stammering, etc).

I have shared this issue. My dysarthria varies in severity. Actually, some days it is barely noticeable. On other days, it’s difficult to communicate because of the stammering.

There does not seem to be any clear reason for the variations, but I have noticed that stress, fatigue, and even fluctuations in my medications can cause the issue. It does get worse when I have to figure out what I want to say, but if I have something that I’m reading from (reciting words), the problem is less significant. I do not have any scientific evidence as to why this happens but my guess is the way that the brain works at processing information. There must be different neurological pathways for reading out loud versus forming ideas and speaking. There is less thought process in reading words out loud from a page versus forming the words for an idea and speaking it.

I find this idea complex. It makes me pause to consider why it is.

Because of this brain injury, I have issues with getting ideas to mind at all, and at times those ideas seem to evaporate as soon as they form. So, there are periods where I do not have anything in my mind. I am desperately trying to think of something, but my mind is blank. Before I had a brain injury, ideas would just be there. I had a “quick wit”. There was far less thinking required. Sure, I would have to manipulate my ideas, the words the that I wanted to use to make my point, based on the audience, but the thought was there. Now, it takes a significant amount of time to just come up with a thought, to form the sentence, and then be able to communicate it effectively. It’s a rather daunting process when it no longer comes to you naturally.

Anyway, Michael’s issue with mutism developed recently, and is sporadic. So, is his condition unique?

One of the first articles that I found was in regards to children who have developed mutism after having cerebellar surgery. Now, this was interesting because central pontine myelinolysis is an injury that generally impacts the pons. The pons is extremely close to the cerebellum.

Because of the locality of the damage to the pons, I am going to suggest that the white matter of the cerebellum can also be impacted. So according to the following research article, it showed that there were children who would have sporadic mutism after damage to the cerebellum, “Cerebellar mutism syndrome and its relation to cerebellar cognitive and affective function: Review of the literature”. http://www.annalsofian.org/article.asp?issn=0972-2327;year=2010;volume=13;issue=1;spage=23;epage=27;aulast=Yildiz

Recent research studies suggest that neurological and cognitive impairments in CMS (cerebellar mutism syndrome) often persist. A prospective study evaluated the neurological status of patients 1 year post-diagnosis based on the presence and severity of ataxia, language difficulties, and other cognitive deficits. [7] Of the 46 patients who had postoperative CMS initially rated severe, residual deficits were common, including 92% with ataxia, 66% with speech and language dysfunction, and 59% with global intellectual impairment. Of the 52 patients with moderate CMS, 78% had ataxia, 25% had speech and language dysfunction, and 17% had global intellectual impairment. Thus, impairment in these domains was common and was also directly related to the severity of CMS. Riva and Giorgi have shown neuropsychological problems a few weeks after cerebellar tumor resection, and prior to further treatment such as radiotherapy or chemotheraphy. [8] Their results reveal a localization related pattern, with problems of auditory sequential memory and language processing after right-sided cerebellar tumor and deficits in spatial and visual memory after left-sided tumor. Lesions to the vermis led to post-surgical mutism, which evolved into speech and language disorders as well as behavioral disturbances ranging from irritability to those reminiscent of mutism. [8]

Now, there is a belief that these issues with mutism are psychological in nature due to the trauma of the event, like car accident. However, this is definitely not the case with Michael, and there has been additional research showing that children that have a stuttering problem, do have injuries in their brains that have been shown to cause this condition. So, it is my belief that if there is an injury significant enough to cause a coma, that it is more likely that it is not a psychological trauma causing the mutism, but an injury to the brain.

So, if that’s the case, then why does the person experience the mutism intermittently?

In the cases of CPM and EPM, I think it is very possible that the injury can progress. Now, this thought goes against the opinions of most medical doctors. Most medical doctors believe that the injury is static; however, in my opinion, it is not CPM/EPM directly causing the injury, but the immune response to the injury. (I would encourage you to review my beliefs on late onset symptoms of CPM/EPM and brain injuries). Basically, the bodies natural response to injury is repair. In my opinion, it does not matter if this injury occurs in your foot, your heart, or your brain. Your immune system sends up a repair “team” no matter where the injury occurs; however, unlike other areas of the body, the brain does not have any non functioning areas, and as the repairs occur more damage is done to surrounding tissue. It creates a slow and steady deterioration, and as in other major structures of the body, scar tissue forms.

This opinion would also explain why a person who is treated with plasmaphoresis after head trauma (including after CPM/EPM) improves with fewer long lasting effects. Generally, it has been shown in previous studies (previously documented in my blog), that in persons who were treated with auto immune disabling treatments, recovered if not fully, significantly.

I also believe that for those who have awoken from a coma with mutism for months or years after, but eventually regain the ability to speak, it is because the brain has healed or has created new neuro- pathways. The following article describes a girl that suffered from a coma and suffered from mutism for 10 months. Eventually, she regained her ability to speak, but she continued to have issues with speaking, cognitive issues, etc.

The patient initially presened as comatose. A period of mutism subsequent to the coma extended for ten months. Following this protracted period of mutism the child demonstrated rapid and unexpected recovery of functional communication skills, despite the persistence of higher level language deficits.

Read More: http://informahealthcare.com/doi/abs/10.3109/02699059009026154

The following article has information that is about a girl that developed mutism after having an injury to the pons. (Bingo! There does seem to be a correlation and an explanation as to why Michael, who has lesions in his pons, has developed mutism.)

 As she was extubated one week later, she was found to have right hemiplegia and muteness. MRI showed a T2- bright lesion on the tegmentum of the left midbrain down to the upper pons. Right vertebral angiography disclosed an intimal ¯ap with stenosis at the C3 vertebral level presumably caused by a fracture of
the right C3 transverse process later con®rmed in a cervical 3D-CT scan. Her muteness lasted for 10 days, after which she began to utter some comprehensible words in a dysarthric fashion. Her neurological de®cits showed improvement within 3 months of her admission. Transient mutism after brain stem infarction has not been reported previously. We discuss the anatomical bases for this unusual reversible disorder in the light of previous observations and conclude that bilateral damage to the dentatothalamocortical ®bers at the decussation of the superior cerebellar peduncle may have been responsible for her transient mutism.

Read more: http://www.springerlink.com/content/h952wk14rwd65798/

Another case of mutism after brain injury, however this person experienced relief with treatment of diazepam:

A 34-year-old woman with a severe closed-head injury had many impairments including apparent global aphasia. After a diazepam premedication for a motor point block she was heard to speak a few words. A trial of oral diazepam succeeded in restoring speech adequate to make her needs known, which persisted on a maintenance dose of 5 mg t.d.s. The possible diagnoses and reasons for this phenomenon are discussed. We suggest that diazepam may be useful in assessing speech in selected people with severe head injuries.

http://www.ncbi.nlm.nih.gov/pubmed/8877308

The following article is only available fully if you pay for it. However, according to the introduction, a woman developed delayed mutism after she had a brain injury caused by drug related issues:

A 49-year-old woman developed a catatonic mute state a few weeks after methadone overdose. Clinical, radiological and histological findings were consistent with toxic spongiform leukoencephalopathy, which adds a potentially deadly side-effect to a generally considered safe substitution for heroin……..

Mutism

The inability to generate oral-verbal expression, despite normal comprehension of speech. This may be associated with BRAIN DISEASES or MENTAL DISORDERS. Organic mutism may be associated with damage to the FRONTAL LOBE; BRAIN STEM; THALAMUS; and CEREBELLUM. Selective mutism is a psychological condition that usually affects children characterized by continuous refusal to speak in social situations by a child who is able and willing to speak to selected persons. Kussmal aphasia refers to mutism in psychosis. (From Fortschr Neurol Psychiatr 1994; 62(9):337-44)

http://www.bioportfolio.com/resources/pmarticle/38247/Brief-Communication-Delayed-Akinetic-Catatonic-Mutism-Following-Methadone-Overdose.html

The next article describes a girl that had issues with stunts in her brain. Her injury also happened in the cerebellar and tracts in the brain stem. The following has a detailed explanation of the researchers belief why akinetic mutism (AK) occurs:

Actually, in the latter situation, AM seems to be related to lesions that occur along pathways that originate in the mesencephalon ([Fig. 6]) and project widely to dopamine receptors in the spinal cord, brainstem, diencephalon, corpus striatum, and mesiofrontal lobe. The resultant behavioral abnormality causes the patient to remain awake but unable to initiate motor activity in response to sensory stimuli. Pressure transmitted to the diencephalon from the hydrocephalus can cause AM. The underlying mechanism is believed to be damage to the periventricular monoamine projections in the thalamus and hypothalamus caused by the expansion of the third ventricular wall. This is the theoretical basis for use of a dopamine agonist in humans with AM, giving gratifying results.

In posterior fossa surgery, damage of the dentate nuclei is the main factor for AM. Fibers emanate from the damaged dentate nuclei through the superior cerebellar peduncles to the contralateral red nucleus and the thalamus and supplementary motor area connected by the dentatothalamocortical pathway[11] ([Fig. 6]). As already mentioned, the supplementary motor area has proven necessary for the initiation of speech[9]

In contrast to AM secondary to hydrocephalus, in which the injured pathways are dopaminergic and/or monoaminergic, in the cerebellar mutism, the neurotransmitters consist of glutamate and aspartate that are found in cerebellorubral and cerebellothalamic fibers, whereas some GABA-containing cells give rise to cerebellopontine and cerebello-olivary fibers. Some cerebelloreticular projections may also contain GABA.

https://www.thieme-connect.de/ejournals/html/10.1055/s-0032-1313632

Now, I found the following article extremely interesting. It describes brain injuries that occur due to lack of blood flow and/or lack of oxygen. Now, why I found this next article extremely interesting because it documents improvements in symptoms initially, but months to a year or more later, the person’s symptoms progress. This is the same type of progression that has been reported in those with chronic concussions, and the majority of those  that I know with CPM/EPM. I believe that there is a connection that is not clearly understood at this time in regards to how the brain reacts to injury, and it can occur regardless of the injury. (HI stands for hypoxic- ischemic and BI stands for Brain Injury)

Delayed Post-Hypoxic Leukoencephalopathy

In rare cases, early and complete recovery from HI-BI is followed a few days to weeks later by a severe demyelinating syndrome; this syndrome, delayed post-hypoxic leukoencephalopathy, characterized by acute or subacute onset of severe and progressive neuropsychiatric problems such as delirium, psychosis, parkinsonism, and/or akinetic-mutism, and/or quadriparesis, among others. Although this condition is often described as a delayed sequelae of carbon monoxide-induced HI-BI, it has been associated with nearly all causes of HI-BI (Shprecher and Mehta 2010). The neural mechanisms of delayed post-hypoxic demyelination have not been established definitively. However, combinations of toxic exposure (e.g., carbon monoxide, inhaled heroin), genetic (e.g., pseudodeficiency of arylsulfatase A, abnormalities of other genes regulating myelin turnover), and age-associated vascular risk factors have been suggested as possible contributors to this unusual post-hypoxic condition. Regardless of mechanism, this syndrome is characterized neuropathologically by diffuse bihemispheric demyelination that generally spares the cerebellum and brainstem. Neurological and neurobehavioral improvement over the first 3 to 12 month periods following onset of this syndrome is typical, but many survivors experience persistent cognitive impairments (particularly impairments of attention, processing speed, and/or executive function), parkinsonism, and/or corticospinal tract signs. There are case reports describing symptomatic and functional improvement of the cognitive and parkinsonian sequelae of delayed post-hypoxic leukoencephalopathy during treatment with stimulants, amantadine or levodopa. The observation that these agents offer some benefit in this context despite their lack of efficacy for the same sequelae of HI-BI itself may reflect differences in the anatomy of these conditions: in HI-BI there is involvement of both gray and white matter, limiting the target of pharmacotherapies more severely than in delayed post-hypoxic leukoencephalopathy, which involves only white matter.

 

I have to say that this idea of mutism after brain injury is absolutely possible. It seems to be more studied in children who have experienced brain injuries vs adults. There seems to be some professionals who believe that it is a psychological issue and others that believe there is a neurological injury that causes it. I believe that you must rule out the physical injury before you consider the psychological cause. Keep in mind that it was only recently discovered that stuttering has a physical cause. This is because the brain is phenomenally complex, and we do not have the technological advancements nor the physical understanding to map the complexity of the brain. This means that you have to approach the subject with an open mind.

Despite the lack of information and understanding, there does appear to be a physiological link to the pons, the cerebellum, and possibly the basal ganglia and the ability to speak. It is also likely that not all of these injuries progress or heal at the same rate, which means that even after mild brain injuries there is a chance that mutism can develop or resolve.

I would HIGHLY recommend that after a brain injury, even mild brain injury, discuss the use of steroids (anti-inflammatory types of steroids that inhibit the immune system-not testosterone) or possibly plasmaphoresis. There has also been research that shows that hyperbariac oxygen exposure can also speed recovery and provide a better recovery. There seems to be a lot of scientific evidence that shows a person’s immune response is in part if not entirely responsible for late onset symptoms.

There will be more to come on this topic as I locate more information.

 

Related articles

 

What’s the difference (types of brain injury and their symptoms):

There seems to be a belief that “how” you get an injury makes a difference as to what symptoms you may or may not experience.

If you have a bacterial infection that destroys your heart tissue and that leads to a heart attack, is that different than having clogged arteries that lead to a heart attack?  Of course, there are some differences, the how you had a heart attack, but once the damage is done, the outcome is the same; your heart has been damaged. You will have to live with the damage and its impact to your heart and body.

There is a belief among doctors that brain injuries are universally different depending on how your brain was injured. There is a belief that if you were hit in the head or suffered a concussion, the injury to the brain will not produce the same symptoms as when you have a stroke or an injury due to a chemical imbalance.

I’ve discussed previously that the injury to the brain itself might be a static injury. For instance, once you’ve been in a car accident, your brain will not continue to receive  injury from the car accident itself, but there is  new research that shows that symptoms continue to persist and develop due to the body’s autoimmune response.

There are several ways that a person can get a brain injury.  According to Ohio State University Medical Center, the following is a list of brain injuries and how they differ:

  • Concussion
    A concussion is an injury to the head area that may cause instant loss of awareness or alertness for a few minutes up to a few hours after the traumatic event.
  • Skull fracture
    A skull fracture is a break in the skull bone. There are four major types of skull fractures, including the following:

    Illustration of different types of skull fractures
    Click Image to Enlarge
    • Linear skull fractures
      This is the most common type of skull fracture. In a linear fracture, there is a break in the bone, but it does not move the bone. These patients may be observed in the hospital for a brief amount of time, and can usually resume normal activities in a few days. Usually, no interventions are necessary.
    • Depressed skull fractures
      This type of fracture may be seen with or without a cut in the scalp. In this fracture, part of the skull is actually sunken in from the trauma. This type of skull fracture may require surgical intervention, depending on the severity, to help correct the deformity.
    • Diastatic skull fractures
      These are fractures that occur along the suture lines in the skull. The sutures are the areas between the bones in the head that fuse when we are children. In this type of fracture, the normal suture lines are widened. These fractures are more often seen in newborns and older infants.
    • Basilar skull fracture
      This is the most serious type of skull fracture, and involves a break in the bone at the base of the skull. Patients with this type of fracture frequently have bruises around their eyes and a bruise behind their ear. They may also have clear fluid draining from their nose or ears due to a tear in part of the covering of the brain. These patients usually require close observation in the hospital.
    • Intracranial hematoma (ICH)
      There are several types of ICH, or blood clots, in or around the brain. The different types are classified by their location in the brain. These can range from mild head injuriesto quite serious and potentially life-threatening injuries. The different types of ICH include the following:

      Illustration of Intracranial Hematoma
      Click Image to Enlarge
      • Epidural hematoma
        Epidural hematomas occur when a blood clot forms underneath the skull, but on top of the dura, the tough covering that surrounds the brain. They usually come from a tear in an artery that runs just under the skull called the middle meningeal artery. Epidural hematomas are usually associated with a skull fracture.
      • Subdural hematoma
        Subdural hematomas occur when a blood clot forms underneath the skull and underneath the dura, but outside of the brain. These can form from a tear in the veins that go from the brain to the dura, or from a cut on the brain itself. They are sometimes, but not always, associated with a skull fracture.
      • Contusion or intracerebral hematoma
        A contusion is a bruise to the brain itself. A contusion causes bleeding and swelling inside of the brain around the area where the head was struck. Contusions may occur with skull fractures or other blood clots such as a subdural or epidural hematoma. When bleeding occurs inside the brain itself (also called “intraparenchymal hemmorage”), this can sometimes occur spontaneously. When trauma is not the cause, the most common causes are long-standing high blood pressure in older adults, bleeding disorders in either children or adults, or the use of medications that cause blood thinning or certain drugs of abuse.
      • Diffuse axonal injury (DAI)
        These injuries are fairly common and are usually caused by shaking of the brain back and forth, which can happen in car accidents, from falls or shaken baby syndrome. Diffuse injuries can be mild, such as with a concussion, or may be very severe, as in diffuse axonal injury (DAI). In DAI, the patient is usually in a coma for a prolonged period of time, with injury to many different parts of the brain. (http://medicalcenter.osu.edu/patientcare/healthcare_services/nervous_system/injury/Pages/index.aspx)

Notice in the above list, it does not mention brain injuries caused by stroke. It does not mention injuries caused by infection, like meningitis. It does not mention injury caused from Central Pontine Myelinolysis. It does not mention injury caused by disease, like Multiple Sclerosis.

If you read about any of the above diseases, injuries or disorders, you will find that those who experience injuries to the brain by any means, has similar symptoms.

Those who have MS experience movement issues:

    • Blurred or double vision
    • Red-green color distortion
    • Pain and loss of vision due to optic neuritis, an inflammation of the optic nerve
    • Difficulty walking
    • Paresthesia – abnormal sensation, or pain, such as numbness, prickling, or “pins and needles.”
  • Other symptoms of multiple sclerosis:
    Throughout the course of the illness, an individual may experience any/all of the following symptoms, to a varying degree:

    • Muscle weakness in the extremities
    • Difficulty with coordination (impaired walking or standing may result; partial or complete paralysis is possible)
    • Spasticity – the involuntary increased tone of muscles leading to stiffness and spasms.
    • Fatigue (this may be triggered by physical activity, but may subside with rest; constant, persistent fatigue is possible)
    • Loss of sensation
    • Speech impediments
    • Tremor
    • Dizziness
    • Hearing loss
    • Bowel and bladder disturbances
    • Depression
    • Changes in sexual function

The above list comes from, http://medicalcenter.osu.edu/patientcare/healthcare_services/nervous_system/ms/Pages/index.aspx

Stroke symptoms:

  • movement and sensation
  • speech and language
  • eating and swallowing
  • vision
  • cognitive (thinking, reasoning, judgment and memory) ability
  • perception and orientation to surroundings
  • self-care ability
  • bowel and bladder control
  • emotional control
  • sexual ability

In addition to these general effects, some specific impairments may occur when a particular area of the cerebrum is damaged.

Effects of a right hemisphere stroke:

The effects of a right hemisphere stroke may include the following:

  • left-sided weakness (left hemiparesis) or paralysis (left hemiplegia) and sensory impairment
  • denial of paralysis or impairment and reduced insight into the problems created by the stroke (this concept is called “left neglect”)
  • visual problems, including an inability to see the left visual field of each eye (homonymous hemianopsia)
  • spatial problems with depth perception or directions such as up/down and front/back
  • inability to localize or recognize body parts
  • inability to understand maps and find objects such as clothing or toiletry items
  • memory problems
  • behavioral changes such as lack of concern about situations, impulsivity, inappropriateness, and depression

Effects of a left hemisphere stroke:

The effects of a left hemisphere stroke may include the following:

  • right-sided weakness (right hemiparesis) or paralysis (right hemiplegia) and sensory impairment
  • problems with speech and understanding language (aphasia)
  • visual problems, including the inability to see the right visual field of each eye (homonymous hemianopsia)
  • impaired ability to do math or to organize, reason, and analyze items
  • behavioral changes such as depression, cautiousness, and hesitancy
  • impaired ability to read, write, and learn new information
  • memory problems

What effects can be seen with a stroke in the cerebellum?

The cerebellum is located beneath and behind the cerebrum towards the back of the skull. It receives sensory information from the body via the spinal cord and helps to coordinate muscle action and control, fine movement, coordination, and balance.

Although strokes are less common in the cerebellum area, the effects can be severe. Four common effects of strokes in the cerebellum include the following:

  • inability to walk and problems with coordination and balance (ataxia)
  • dizziness
  • headache
  • nausea
  • vomiting

What effects can be seen with a stroke in the brain stem?

The brain stem is located at the very base of the brain right above the spinal cord. Many of the body’s vital “life-support” functions such as heartbeat, blood pressure, and breathing are controlled by the brain stem. It also helps to control the main nerves involved with eye movement, hearing, speech, chewing, and swallowing. Some common effects of a stroke in the brain stem include problems with the following:

  • breathing and heart functions
  • body temperature control
  • balance and coordination
  • weakness or paralysis in all four limbs
  • chewing, swallowing, and speaking
  • vision
  • coma

The above information is taken from, http://medicalcenter.osu.edu/patientcare/healthcare_services/stroke/effects/Pages/index.aspx

The next list, is the list that I have found to be defining to those who have brain injuries in general. Notice how similar they are to what we find in things like stroke and MS:

Issues that are attributed to brain damage:

Hearing Issues (problems with understanding spoken word, tinnitus, dizziness, buzzing)
Visual Issues (blurry vision, color issues, blindness)
Heart Issues (problems with maintaining proper blood pressure and heart rates)
Cognitive Issues (memory deficits, learning issues, reading problems, writing problems, word recognition)
Hormone Issues (lack of Growth Hormone, sex hormones, hypothyroidism, and hypopituitarism)
Sexual Issues (lack of desire)
Reproductive Issues (lack of menses in women, lack of gonadotropin hormones)
Psychological Issues (depression, irritability, nervousness, anger, crying, anxiety)
Parkinson’s Disease
Alzheimer’s or Alzheimer’s like disease
Epilepsy (early to late onset of seizures, can occur up to 40 years after injury)
Sleep Disturbances (insomnia, inability to stay asleep, central nervous system sleep apnea)
Early Mortality (high risk of death during first 1 to 10 years after injury, after that life expectancy is 5-7 years less than average non injured person)
Incontinence (urinary or bowel)
Muscle Dysfunction (twitches, spams, jerks)
Mental Fatigue (difficulties working or going to school full time due to concentration deficits)
Speech disturbances (stutters, stammering, not being able to complete thoughts, not using proper words)
Issues with communicating
Movement disorders (problems with coordination, walking, standing, eating, tremors, shaking, swallowing, speaking)
Temperature control issues (too hot or too cold)
Complete paralysis (those with CPM/EPM are known to develop locked in syndrome)
Breathing issues (the brain forgets to tell the body to breathe, especially critical in sleep)
As you can see, people have very similar, if not identical symptoms, no matter how they received the brain damage. I am hopeful that over time doctors will come to realize that whether or not you were hit in the head or had a stroke the process and recupperation needs to be treated the same if not structured from the same basic model and tweaked to meet an individuals need.
Further, it needs to be understood that no matter HOW you got your injury, the immune system responds to the injury in the same manner leading to further complications as a person ages.
Now, I wanted to add some descriptions to the symptoms that you may experience with brain injuries. Iwas excited to find the following description of mental fatigue. I have experienced this as I returned back to work. I have had ongoing issues with this outside of work as well. I simply can not do as much as I did before. The mere act of trying to stay focused for long periods of time leaves me mentally and physically exhausted. My doctors first reaction when I explained this is that it must be a psychological phenomena related to knowing I have a brain injury. When a doctor gives these suggestions, you have to believe they must be right. It must be all in my head (ha-no pun intended). I was happy to find a research article discribing this issue as a part of having a brain injury.

Patients will recover within days to weeks, but a significant minority develop persistent mental fatigue, and it will take a long time before they can accept the situation and find
ways to lead their “new life”. Until then, life can be very mentally tiring and for many it can be a great strain. In the case of a slow recover, things might turn out not to work as smooth and easily as they used to. It is possible for patients to take walks in the forest, but reading, talking on the telephone or attending a meeting could be mentally very tiring and may require a prolonged rest afterwards. It is no longer a pleasure to go to parties, as they can’t take part in conversations, and they soon become extremely tired and want to go home. It might also be shameful for the person to admit that the brain does not work properly. They also tend to experience difficulties concentrating, and it could be difficult to filter what they hear and see. Every unimportant detail is registered. Sensitivity to stress is also very common, even in minor situations which they are normally able to handle.

http://cdn.intechopen.com/pdfs/30498/InTech-Mental_fatigue_a_common_long_term_consequence_after_a_brain_injury.pdf

I will try to include the additional research that I have found regarding brain injuries and what you can expect, no matter what type of injury you have.

Please keep in mind, no matter what type of injury you have, it does not mean that you will have all of these symptoms. It does not even mean that you will have life long consequences because of it. The severity of the injury, the location of the injury, and the initial treatment that you receive following the injury all determine the outcome that you will have following your injury. I believe fully that you can go on to lead a productive life depending on many factors that I will address later in the future.

 

UPDATE 11/14/12—I found this research article, which explains a significant number of the physical issues after a brain injury. It provides more of the physiological description of why the injury will cause the symptoms, like epilepsy, visual and auditory disturbances, cognitive dysfunctions.I was extremely happy that this article states that a person’s IQ remains relatively intact after these types of brain injuries (this is what I have experienced), but they continue to have issues with memory, learning, and retrieval.

http://jnnp.bmj.com/content/73/suppl_1/i8.full

Cognitive and neuropsychiatric sequelae

After resolution of PTA, overall IQ and posterior cognitive functions of language and visuospatial skills are often relatively intact and the residual neuropsychological deficits may not be easily detected by simple tests of cognitive function. A formal neuropsychological assessment of the patient’s memory, attention, and executive skills and their mental speed is thus mandatory, particularly late after severe injury when these problems play a major role in limiting independence.

Organic disorders of behaviour9 are often seen in tandem with cognitive dysfunction, and are usually described by a carer. Personality changes, of imprecise localising value, include egocentricity, childishness, irritability, aggressiveness, poor judgement, tactlessness, stubbornness, lethargy, disinterest, reduced drive and initiative, and often reduced rather than increased sexual interest. Occasionally more dramatic positive and impulsive, or negative and abulic, behaviours prevail.

Psychiatric sequelae including low mood, depression, and anxiety disorders are common after TBI, and often delayed in onset. Psychiatric illness, fewer years of formal education pre-injury, and a more dependent outcome predispose to the development of these problems.10 Depression may respond to a selective serotonin reuptake inhibitor or venlafaxine, and psychiatric referral may be necessary. Occasionally obsessive–compulsive disorders and psychoses occur in the absence of obvious premorbid psychiatric history, and the risk of suicide is increased.

Brain injury and Alzheimer’s disease:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This too has happened to me on numerous occasions:

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

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

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

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

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

UPDATE:

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

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

Related articles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Vision

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

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

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

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

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

MUSCULOSKELETAL DYSFUNCTION

Muscular dysfunction

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

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

SUMMARY

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

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

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

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

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

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

 

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!

Additional symptoms related to CPM:

 

I’ve previously described movement issues like dystonia, Parkinson like tremors, other tremors, and random jerking movements, but this is something I have not heard about previously, choreic.

I had no idea what the word meant or what it is related to before a few days ago, so please feel free to add any input you might have about it.

 

The dictionary definition is: “An involuntary spasmodic twitching or jerking in muscle groups not associated with the production of definite purposeful movements.”

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
Basically, these movements are involuntary movements and jerks, so I guess in a way, I have discussed this issue before. I have jerks a lot.
If I get really stressed there seems to be this movement that my left leg does. It’s weird, and if I every experience it for a long period, I will upload a video of it. It really feels like I should have control of it. It seems ridiculous that I can’t, but it’s like my body has a mind of its own and this is one thing that I never had an issue with before. It really bugs me, but others don’t seem to notice. I guess some might consider it a  nervous tic.
I believe that the following videos really do what the motions are like for those who have these types of jerks.
This is kind of what I have experienced, so I’m posting it. I don’t have issues with my face so much as I do with kind of a rolling to my left and a rocking of my left leg and rolling of my body. It  really seems like I’m jittery or nervous or can’t sit still.  I don’t experience it very often and the periods that I go through are brief. I believe this is a positive sign.
With the following video, the little girl developed this because of scarlet fever, not huntington’s disease. She was able to recover almost completely so the following videos show her before and after:
Another good example. I believe these kind of show the extremes. Some people just seem fidgety. Others are extremely disabled.
The information that I have found has been sparse when it comes to directly attributing these choreic movements to CPM/EPM. However, it has been documented. It may not be an immediate appearing symptoms. In some cases it did not appear until months after CPM/EPM was first diagnosed. I have read that this in not an uncommon theme regarding EPM. It seems that movement disorders with EPM can appear months after the injury. I really noticed my issue develop at a doctor’s appointment. I was becoming extremely agitated, and I realized that my left kept moving as well as my left shoulder. I kept crossing and uncrossing my leg as well as moving in my chair. I’ve noticed those movements at other times of stress.
Thankfully, I don’t think it is getting worse for me.
The following information is a chart that describes that chorea can be caused by electrolyte issues:
J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

Table 6

Metabolic aetiologies of dystonia and chorea

Hyperthyroidism
Hypocalcaemia (hypoparathyroidism)
Hypoglycaemia
Hyperglycaemia
Hypernatraemia
Hyponatraemia
Hypomagnesaemia
Osmotic demyelination syndrome (central pontine myelinolysis)
Splenorenal shunt

 

Literature also seems to suggest that these reasons that these choreic movements occur is because of injury the putanem or basal ganglia. It suggests that there is a decreased amount of GABA, and there there are issues with Dopamine and glutamate.

Frankly, folks, I simply can’t read through this very detailed information from the following journal link, but it goes into great explanation why both dystonia and chorea are found in a variety of brain damage injuries, including CPM/EPM, Huntington’s disease, and many others.

Here is the quote:

As discussed earlier, dystonia and chorea most commonly result from striatal dysfunction, and hypoxia-ischaemia has been shown to alter several neurotransmitter systems in the striatum. Glutamate is the main neurotransmitter in cortical neurons projecting to the striatum and may contribute excitotoxic injury. Hypoxia-ischaemia has been shown to increase striatal extracellular glutamate, and decrease glutamate transporter concentrations. Direct lesioning of the globus pallidus with excitatory amino acids in monkeys produces cocontraction of opposing muscle groups on reaching, as in dystonia.9Extracellular dopamine concentrations rise and concentrations of dopamine metabolites fall after hypoxia-ischaemia.710Dopamine may also potentiate the excitotoxic properties of glutamate, and depleting the striatum of dopamine before hypoxia-ischaemia decreases the degree of striatal injury. In the neonatal rat model of cerebral hypoxia-ischaemia, striatal D1 and D2 dopamine receptor numbers fluctuate until 9 to 11 weeks after injury, at which time the D1 receptor number has returned to normal but the reduction in D2 receptors persists.11 Hypoxia-ischaemia also results in areas of complete loss of preproenkephalin mRNA in the dorsal striatum of the rat brain.12 Enkephalin, together with GABA, is an inhibitory neurotransmitter in the projections from the putamen to the external pallidum. Hypoxic-ischaemic necrosis of medium sized spiny striatal neurons may be responsible for decreased concentrations of the inhibitory neurotransmitter, GABA. By contrast, the striatal cholinergic system remains relatively preserved or even upregulated after hypoxia-ischaemia, as evidenced by an increase in cholinergic fibres and cell bodies, and an increase in acetylcholine release.13This is interesting in that anticholinergic medications often ameliorate dystonic movements.

http://jnnp.bmj.com/content/65/4/436.full

J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

I will try to add more to this post in the future if I can, but right now, I can’t. Please feel free to leave questions or suggestions as you like.

 

Have a great night :)

 

The Stages:

It’s been hard the past few months, and I think that shows in my “personal” posts. I’ve been told by some that I’ve been a bit negative about what I’m going through. I’ve been told by others that I’m depressed.

It is really hard to live through what I’ve lived through, and I found out that all of those things that I’ve experienced are normal.  For those of you who might now be used to going through difficult times in your life, having CPM/EPM might be a slap in the face. I’ve gone through really difficult times, and it was still a slap in the face for me. It seems that most people tend to not quite understand everything you are experiencing, so I thought this post would be dedicated to getting a better grasp on what to expect. It’s  not just what your significant other might live through, but it’s the steps or processes that you might live through too.

I think once you get on the other side of this process, then you can really start to live the rest of your life as it is now or prepare for the future. I want to stress that these steps do not have any specific order. They are NOT an exact science. You might experience one of these steps. You might experience all of these steps. You might live in a cycle of these steps. There’s no guarantee, but I hope it helps you understand what to expect and gives you a few resources on how to cope with it.

You are your own person, so don’t expect anyone to try to identify what you are living through. They can’t know what you are living through, but it’s important to understand that they are living with or around you and because they love you, seeing you in pain will give them pain of their own.

They aren’t trying to make your life miserable, so try to be patient. They are doing the best that they can to give you the support that you need, but it isn’t easy for them. You will find that they will go these same stages too because it is a trauma to their life just in a different way.

I hope that makes sense.

The stages are known as the five stages of death, but it’s actually a more accurate way to describe as the five stages of trauma. In other words, it’s classically known as the five stages of death and dying, but you will find that people live through these same stages when ever there is a major impact to their life…loss of a limb, brain injury, loss of a job, an end to a relationship, terminal illness, etc.

The five stages:

Denial.

Anger.

Bargaining.

Depression.

Acceptance.

For me, I don’t think I went through denial. I think I went into shock and fear. I didn’t understand fully what having CPM/EPM meant. I could recite the worst possible scenarios that could happen, and I felt lucky after I passed through the first 12 weeks without dying, but I was still scared because there is that unknown.

I really didn’t want to make adjustments to my routines because I really thought in time things would get better. Maybe that was denial, but my doctors gave me the hope that I would recover in a year or so, and that I would see major improvements in that time. I did experience huge improvements in the first 12 weeks, even in 6 to 9 months, but now things have leveled off, and I believe in things like memory they are getting worse. So, I don’t know if that’s denial.  I had different expectations.

I definitely experienced anger. I am still experiencing anger. I have to say there are days that I will get in the shower and cry. Yes, I know it’s strange to cry in the shower, but it is one of the few times where I can be alone..no kids, no puppy, no phone calls, and I have time to focus on what I am going through. And what I am going through sucks. It sucks. So, this morning, I was thinking about how this stupid doctor screwed up my treatment for something that EVERY doctor is supposed to know how to treat, and now I am going through SO much stress and anxiety. All I wanted to do was be a doctor, and there was no guarantee that it would happen, but I had made it so far through so much, and so I become extremely ANGRY. Yes, I am. I am hurt and because I am so hurt, I am angry. That doctor will go to sleep tonight and he may only think about what he is going to do this weekend. Is he going to fall asleep tonight and think about how I lost my life? No, probably not.

It’s stressful living this life. It’s hard right now, and I have no idea what I am going to do with my future or how much of a future I have. And so Anger is something that I am learning to live with but that anger comes from the pain and hurt over what has happened to me. I just want to go back to being normal and I can’t.

Bargaining, well I’ve begun to do that. I was in Chicago a few weeks ago, and I found an Irish vendor. It was basically Irish and Catholic trinkets of all kind. I went through the medals of all the saints, and I found the medal of St. Jude. St. Jude is the saint of lost causes, especially when dealing with health issues. So, I had to get the medal. I had to wear it daily. It didn’t take long for me to lose it. I have no idea what I did with it. But, it’s really sad because even though I haven’t stepped inside a church (except for a recent baptism and wedding) in YEARS, I had to buy this medal of St. Jude and wear it and pray with all my heart: Please let me get better. Please let my legal issues work out. Please let me get better. I will help the poor, post an article in the newspaper. Whatever, I can do to fix this I will do it.

I had no idea that this was all “normal” for what I was going through. I mean I think I went through something similar while I was in the hospital. It was a: please don’t let me die, kind of prayer.  It was a scary time, but the only thing I did was pray a bit. It wasn’t the same as when I bought and wore a St. Jude medal recently. It wasn’t until that point that I really started the bargaining: if you make me better, I will……

Heck, if you ask anyone, including me, you’ll understand that I’ve been dealing with depression. I think it goes hand in hand with the anger, hurt, and frustration. It’s a slap in the face when you’re told to just be patient that things can get better, but then you hit a stagnant point. This just haven’t moved, and I don’t have any patience. I really don’t.

It is depressing facing the fact that you are not like other people. Your life has changed, and it’s not for the better. You are facing so many bad circumstances and you have no control over it. How are you going to be able to live the rest of you life like this? Are you going to be able to watch your children get older? You might be facing unemployment or financial uncertainty or be dependent upon friends and family to just do the basic things in your life.

This is depressing.

Eventually, you will move to acceptance. This is one of the more peaceful stages of your trauma. You start to realize that your life has changed and that there isn’t much that you can do to control the situation. It isn’t right. It isn’t fair, but you can not move beyond the other steps until you reach this one. And it can’t just be a process of saying that you are hurt or listing the horrible way the injury has impacted your life. You have to get to a point where you actually feel and accept the injury.

Literally for the past year, I have been very vocal about my experience and how it has changed my life, but that didn’t mean that I accepted what was going on with me personally. I was in denial about how permanent these changes are. I still hold out hope that things will get better, but I’ve come to accept that I will NEVER be the same person. I have been changed, physically, mentally, emotionally by my experiences. I have come to accept that I will have to write things down to make sure I can track how much I’ve spent. I will have to label places around my house and make a conscious effort to keep placing things where they belong. I will have to trust my son when he tells me that he didn’t take money from my purse or the cashier when she tells me that I received the correct change.

IT IS EXTREMELY HARD FOR ME TO DO THIS. EXTREMELY. I’m an unbelievably independent person. I’ve always had an unbelievable memory that I took for granted. I’ve never had to label things, etc. But now I am accepting that those changes have to be made, and I will have to commit myself to doing them.

It’s hard. It’s not fair. It sucks. I shouldn’t have to do it. I’m still very angry about it. It’s depressing, but I am going to have to accept it, learn to live with it and adjust or I will never be able to move past it, and I’m ready to move past it.

I really hope you find support in this post. I would have never realized that these steps are a process, and keep in mind that with any major change in your life just because you go through the cycle of these steps once doesn’t mean that you won’t go through them again.

Take care :)

CPM/EPM- Locked-In Syndrome:

I am sorry that I have not reported on this critical symptom of CPM/EPM previously. I thought I had covered it previously, but I’m not finding any previous posts about it. Please forgive me if I have posted about it, but this should be a much more informative post.

Locked in syndrome is an issue that occurs with brain injury, so it is not just a symptom related to CPM/EPM alone. It can happen with stroke and also with head trauma. It is characterized by the inability to move ANYTHING, except for the eyes. Generally, a person is able to open and close their eyelids and look vertically up. However, they are unable to speak. Sometimes, they are unable to make any sounds at all. Even though they have significant paralysis, their cognitive functions seem to be close to normal or near normal.

It is difficult to determine how many people are actually impacted by locked in syndrome because most of those impacted die before it can be definitively diagnosed. It is also suspected that a number of patients might not be diagnosed because they make an astounding recovery.

Now, again, locked in syndrome is not solely caused by CPM, but it is generally related to an injury to the pontine area of the brain. It is believed that strokes are the primary cause of locked in syndrome. It can also be caused by infection and other demyelination causes.

I found this to be extremely interesting. Firstly, a person may not be able to move even their eyes, so it is believed that a number of persons who are impacted by locked in syndrome might be misdiagnosed as being in a vegetative state, ie that they have little or no cognitive function. It is also sometimes confused with coma.

Due to the complex nature of locked in syndrome, it makes it difficult to determine the true number of people that are impacted. That’s pretty scary, especially when you take into consideration cases like Terry Schiavo.

It was never clearly determined if Terry Schiavo was in a vegetative, completely brain damaged state or if she had some cognitive function and had significant paralysis. It has been determined that she had an electrolyte imbalance, possibly related to an eating disorder, but there is also concern that her injuries were caused by an attack from her husband. It truly is a mystery, but that’s the scary part with people being in an locked in state. It is extremely difficult to determine the extent to their injuries.

For more on Terry Schiavo, I found this website to be very informative: http://www.wnd.com/2005/03/29516/

Now there are different levels of paralysis with locked in syndrome. A person can be completely paralyzed in which there is no ability for movement, even their eyes are paralyzed. There is classic which a person retains the ability to move their eyes (vertically or blink), and then there is incomplete locked in syndrome. In this version, a person has very limited movement.

A person who has more movement has a better chance of recovery.

I found the following website extremely detailed in describing locked in syndrome and what to expect: http://cirrie.buffalo.edu/encyclopedia/en/article/303/

I found this paragraph interesting:

Alertness often fluctuates, especially during the acute phase (Gutling et al., 1996). Several authors reported that cognitive functions were generally preserved although cognitive impairment may be present (Smith et al., 2008; Smith and Delargy, 2005; Ruff et al., 1987). Attention and memory disorders are observed in nearly half the cases, especially in individuals with a post-traumatic LIS (León-Carrión et al., 2002; Ruff et al., 1987; Garrard et al., 2002). Emotional lability is a common symptom (Garrard et al., 2002). Apathy is sometimes observed and may persist in some cases (Beaudoin and De Serres, 2008). Recovery of cognitive functions is often observed in individuals during the first year (Brunoet al., 2008).

I think the above is true for most brain injuries. There seems to be cognitive issues with memory, attention and learning. There is also that psychological factor that is involved in brain injury as well. These are issues that I have experienced but have had difficulty locating in the literature describing CPM/EPM…not the cognitive issues but the psychological aspects, so I found this to be “proof” that this behavior isn’t unlikely with CPM/EPM.

I found this video EXTREMELY relevant. I really think that this is what happened to Terry Schiavo. I have been told by a friend recently that a similar situation is happening NOW to their family member.

This is a similar story to Terry’s.

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

The following video is also heartbreaking:

http://www.youtube.com/watch?v=6gqSYIDsKjs

The following is a story of a women who has locked in syndrome, and how she finds that her life is still important and worth living. It’s very inspiring.

http://www.youtube.com/watch?v=A3uEMyVnThI&feature=related

I found this story also inspiring:

http://www.youtube.com/watch?v=ZR2GQikB7I4

http://www.youtube.com/watch?v=3IO6i0syM8Q

I really think it’s important for people to realize that if you or someone you love develops this condition, it does not mean that you life is over, and it is important to WAIT before pulling feeding tubes or other life supportive measures.

I pray that any of you reading this are just looking for information, and are not experiencing this personally. It is an extremely difficult condition to live with and to watch your loved ones experience, especially in the beginning, but as technology becomes more advanced, I believe there will be more hope and further recovery for even the most devastating cases of locked in syndrome.

In closing, I believe the most important thing for a significant recovery is early recognition and an immediate start to rehabilitation. It is also important to get all senses involved through the use of bitter liquids, sounds, movements, etc.

Please feel free to comment regarding your personal experiences with locked in syndrome or questions.

 

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