CPM | Hyponatremia and Central Pontine Myelinolysis

29 Jan 2013

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.

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Alzheimer's disease, anatabine, antibiotics, brain injury, CPM, epm, inflammation, Neprinol, probiotics, Roskamp Institute

03 Oct 2012

3 Comments

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

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. )

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!

Brain injury timeout (utsandiego.com)
Concussions: Don’t Ignore the Symptoms (chkdsportsmed.com)
Youth concussions serious business (azdailysun.com)
Drug blocks damage that follows brain injury (futurity.org)
Resources for those with traumatic brain injuries (dvidshub.net)

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Brain damage, CDC, Concussion, concussion symptoms, CPM, CPM/EPM, Magnetic resonance imaging, neurological disorders, Neuron, Traumatic brain injury

08 Sep 2012

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 🙂

5 Stages of Grief (janegarber.com)
Functional and Dysfunctional Grief (christinehammondcounseling.wordpress.com)
From denial to acceptance (redeemingrenato.com)
Five Stages of Grief (somamandalnyc.com)
Five Stages of Grief and Me (jacquelinedevito.wordpress.com)
5 Stages of the Awakening (zengardner.com)

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Acceptance, Anger, CPM, Death, Denial, Depression, epm, Five stages of death, Kübler-Ross model

20 Jul 2012

Ketoacidosis and Central Pontine Myelinolysis:

Thanks to the Ninjadoc, I have been made aware of another way that a person can develop hyponatremia, which increases their risk for CPM.

Ketoacidosis can be caused by several factors: Diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketosis and hypoglycaemic ketoacidosis. (http://qjmed.oxfordjournals.org/content/97/6/365.full)

Type 1 diabetics have an increased likelihood of developing ketoacidosis. It can also occur in those who have eating disorders, such as anorexia. Those with type 2 diabetes can also develop it, but it is not as common as in type-1 diabetes (http://www.ucdenver.edu/academics/colleges/medicalschool/centers/BarbaraDavis/Documents/book-understandingdiabetes/ud15.pdf).

So, what is ketoacidosis and how does this lead to hyponatremia?

This is a bit complicated, but I’ll try to make it so understandable that even I can comprehend what I’m talking about 😉

Ok. Everyone has a pancreas, and the pancreas has MANY jobs, but one of it’s most important jobs is to produce hormones that regulate your blood sugar. Insulin is one of the most important hormones that the pancreas produces. After you eat, your body starts to break down food and liquids into glucose. As more and more glucose is absorbed into your blood stream, your blood glucose levels increase, and your body triggers a release of insulin from your pancreas. The insulin causes glucose to be transported from the blood into muscle cells, liver cells, and other types of cells.

Insulin also prevents the break down of fats in the body.

In type 1 diabetics, there is a dysfunction in the pancreas that prevents a release of insulin or the pancreas does not make insulin. This means that when a person eats and glucose floods the blood stream, it stays in the blood stream.

Also, because there is a lack of insulin in the body, cells miss that signal that tells them to NOT break down fats.

Now, I’m not an expert on ketoacidosis, but basically because the cells are unable to use the glucose in the blood, they start to break down fatty acids into glucose in the cells. It’s kind of like having an on sight manufacturing plant of glucose using fatty acids. Also because insulin is not being produced or when a diabetic person does not take their insulin, the cells do not receive that message to stop or not break down fats/ fatty acids. As more and more fats and fatty acids are broken down, more ketones are produced as a by-product.

Ketones are acidic in nature and the build up of ketones in the blood lead to an acidic PH.

So, ketoacidosis will usually occur when a person does not get enough insulin, which means that their cells are not getting the energy that is needed to maintain function. Those cells are also missing the signal to stop breaking down fats, so that inner cellular factory is breaking down fats in high gear. At this point in the reaction, a person will have a very high blood sugar level (in regards to those who develop it in type 1 or type 2 diabetes), and they will also have high ketone levels. This lowers their blood PH, and is termed as ketoacidosis.

I hope that makes perfect sense 🙂 If not, please don’t hesitate to ask questions, and I will try to find the best answers for you.

A person has to go to the hospital to receive treatment for the ketoacidosis, and the treatment is a decrease in blood sugar and a restoration of the proper electrolytes.

So, at the point that the blood sugar is reaching high levels and ketones are reaching toxic levels, the body starts to try to regulate the system by flushing these toxins through the kidneys. This increases a person’s thirst and urine output which leads to dehydration. Also because there is a high concentration of glucose in the blood, the body tries to correct this imbalance by shifting water from inside the cell to the blood. It is trying to dilute the high levels of glucose by adding water. However, because sodium levels do not change this gives an impression that a person has hyponatremia. They may indeed have hyponatremia or it may just be a fluctuation of the fluid balance from in the cell to the blood.

Now according to the University of Texas Medical Branch, lab work can be misleading in cases of diabetic ketoacidosis. It can show that a person has hyponatremia, but in fact, they just have these shifts in sodium and potassium due to the high glucose levels in the blood (known as pseudohyponatremia), but they also acknowledge that in some cases, a person might in fact develop true hyponatremia as well. Now if that seems complicated to you, don’t worry because it is. It seems in regards to ketoacidosis, you definitely have to have an expert in endocrinology oversee your care. I’m not an expert, but if you are interested in finding out more about how you can develop false hyponatremia (pseudo hyponatremia) and want to know more about it, use the following link: http://www.utmb.edu/pedi_ed/CORE/Endocrine/page_27.htm.

Now this is where things get tricky, I believe that because the causes behind the development of hyponatremia (real or pseudo) are so complex, this can lead to an inappropriate treatment of it. For instance, if a person has pseudo hyponatremia because of the high glucose levels, it is believed that once the glucose levels are corrected then the sodium levels will correct naturally as well too. This means that the water shift from the blood back to the cells will occur naturally, however, if treatment is administered in the form of saline iv solution, this fluctuation could happen too quickly and cause CPM/EPM.

It’s something to be aware of if you have diabetes or if you have another cause of hyponatremia. In other words, it is important to understand the root cause behind why a person has developed hyponatremia and make a logical and educated basis of correction from that cause or there will be a great risk of correcting the sodium levels too quickly and an increased chance of myelinolysis.

I hope that makes sense.

For more information on ketoacidosis related to diabetics, please use the following links:

http://emedicine.medscape.com/article/118361-overview

http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html

http://www.ucdenver.edu/academics/colleges/medicalschool/centers/BarbaraDavis/Documents/book-understandingdiabetes/ud15.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770770/

Have a great night!

(I also want to call out a special call out to my helpers on this article, Ninja doc and Dr. R. They both gave me great insight and helped direct me in areas that were a bit off the mark. THANKS guys 😉 )

Diabetic Ketoacidosis and Receiving Social Security Disability (socialsecurityhome.com)
New Blood Glucose Tracking Technology That Will Save Your Fingers! (epicagear.com)

Posted in What is Hyponatremia? and tagged Blood sugar, CPM, Diabetes mellitus type 1, Diabetes mellitus type 2, University of Texas Medical Branch

03 Jul 2012

Michael’s Story:

I am happy to include Michael’s story. He has been suffering from CPM since 2008. He like others saw initial improvements, but has now experienced a decline.

If you’re reading this, here’s the thing…there is not enough information available about what’s going to happen. It’s not known. The doctors will tell you: you may get worse; you may get better; you may stay the same. Isn’t that true for EVERYTHING? That’s why I feel it important to get stories from people that HAVE it, and are living with it every day out to you. BUT, I want to stress to you that it doesn’t mean that YOU are going to experience those same issues.

I would compare this blog to making a path in a forest. What they know and understand about CPM/EPM is virgin territory. Most research articles just repeat what other research articles tell them, and it always end with basically, we don’t know. I figure the best way to make a path is by asking the natives. It doesn’t mean it’s the only way, but I figure it’s a good start.

So, here we go, another account from a native:

First thing I need to say is that I am an alcoholic, I was not drinking from 2001 to 2007 then I went back out. From, the first week of 2007 to the first week of 2009, I was drinking. I have not had a drink in over three and a half year and I hope I never have another. With that said, here is my recollection of what happen to me and how I got CPM

The last ten days of 2008 I had been throwing up between 4 and 6 times a day. I didn’t feel bad, I didn’t have the flu or anything like that I just could not keep anything down. For those ten days I didn’t drink alcohol, just small sips of water and orange juice. Well on the second day of January I went to visit my mother and she took one look at me and said get in my car I am taking you to the hospital, I think you have had a “stroke” when I got to the hospital they took one look at me and thought the same thing, “stroke” so they put me in a room in the emergency room and started doing the tests. That’s when they found out my sodium level was 106. So they admitted me and started me on two IV’s to replace the lost sodium. Well looking at my medical records, (which all of this information is coming from) my sodium level went from 106 to 124 in 24 hours. So boys and girl, what happens when one of the very best hospitals in the whole world gives you almost double the amount of sodium that they should in a 24-hour time frame, you get… CPM!!! (Non- diagnosed)

So, I want to point out in Michael’s case, it is difficult to say what caused Michael’s hyponatremia. The most probable cause of the hyponatremia was alcohol. I am guessing that he started to develop hyponatremia after drinking and that caused him to get sick for those ten days where he couldn’t hold anything down. Now, it’s also very possible that he just had a stomach flu and after getting sick for so long, not being able to eat and only drinking water and OJ, caused him to develop hyponatremia, but the important thing here is that he had the chronic form. Because he didn’t develop seizures or go into a coma from the hyponatremia, his brain and brain stem had enough time to adjust to the swelling. That said, when you have chronic hyponatremia, it puts you at higher risk for CPM. Back to his story:

With that said about 8 days after I was given CPM by the hospital the first signs started to show up. I ended up at a local hospital in basically a coma for six and a half days. They thought it was alcohol induced because there was quite a bit in my system. When I got out of this local hospital for the next 120 days were complete hell. I walked like a 90 year old man; it would take me two hours to walk half a mile. One day I fell in a snow bank and could not get up for over 45 minutes. I needed help to get in and out of chairs. In and out of cars, ect. My speech was awful; it was like English was my second language. Had to wear non-tie shoes in the winter because I could not tie them. I had little control over my bladder, and my hands shook so bad, drinking anything hot was out of the question.

Then after about 120 to 130 days had past I started to get better and things started to clear up. I could walk better and talk and things went back to normal. The company I was working for went out of business and I went and painted houses with a buddy of mine. Then after about 6-8 month I started to notice numbness and a small shake in my left hand and left leg. Not all the time, just now and then. Then I started dropping the paintbrush, which I never did. So I went to see my PCP. He ignored it few times and then finally said ok lets take a look. So on February 25 2011 I was finally diagnosed withCPM.

Sense I started dropping the paintbrush; I am back with the company that I have work for, for 32 years. I am a salesmen, have been for all of the 32 years, but I stutter, shake, have spasms, I am down to calling on one account, can only work till noon, some days English is my second language, have no memory what so ever, and my fine motor skills are gone. With out my wife I would be back to wearing non-tie shoes, tea shirts and sweat pants. So basically I am back to were I was the first 120 days of hell with this disease.

Thank you Michael!!

Posted in Your Hyponatremia/CPM story: and tagged Central pontine myelinolysis, CPM, Hyponatremia

19 Jun 2012

Todd’s Story: CPM

Todd and I have corresponded for the past year, and I find his story also very motivational, so I’m happy to start sharing it here. Todd’s story shows how alcohol can lead to hyponatremia, and being an alcoholic can further increase your chances of developing CPM. It’s a dangerous combination, alcoholism and hyponatremia.

Now, I want to spend time explaining some of the things I’ve hit upon before regarding alcohol.

You are at risk for developing hyponatremia if you have even one drink….however, it is very unlikely for you to develop it after drinking just one drink.

The more you drink, the more likely you are to develop hyponatremia. If you are an alcoholic, you are at great risk for developing it. You can also develop CPM/EPM if you are an alcoholic without developing hyponatremia. In other words, drinking chronically can lead to demyelination of your pontine area, basal ganglia, or other areas of your brain.

I hope Todd’s story will motivate those who are drinkers to think twice about picking up their next drink.

……Unfortunately, I don’t know how to blog, but anything I share with you is free game, my life is an open book now, I don’t hold any secrets about myself anymore. You description of the causes of CPM was explained to me as the perfect storm:

1. I am an alcoholic
2. I pounded scotch and water.
3. I was taking htc for HBP.
4. I got sick on both ends

I am starting to work on my testimony for my recovery group and will share if when I am done.

I try to wake up everyday trying to figure out why God spared my life? Everyday is a great day is I choose to make it one which I suppose about 50/50…..

Hey,
I finished ready your blog today. I know exactly what you mean because sometimes it takes me an hour to write these short little notes because I do not want to offend anyone. I’m in a quandary, I what to forward the blog address to my health care providers but can’t find the right words. There is a long story behind it: They were my clients and they fired me! My work with them was in the med-mal arena.

Hey,
Housekeeping: I was diagnosed with CPM Late December 2007. I am an alcoholic. I haven’t seen a neurologist in 2+ years, they really never wanted o bother with me. My primary care Doc’s are great. I use to go once a week but now it is once a year. The remnants of the CPM are my involuntary grunting, drooling and uncontrolled belching. I also 90% of the time have a “deer” in the headlights expression. Physically, I’m proud to tell you I am in the best condition of my adult life. Over 4 years of sobriety with 3*** and Copenhagen FREE. I’m into biking and spinning. You have to brag when you can: I burned 818 calories in today’s spinning class, a personal best.

My life partner read your Blog and is super impressed with your research. She will be way more useful than me, because she lived the CPM, I only remember certain aspects of my time in prison.

She obviously has permission to correspond with you but is still getting computer literate (I finally bought her and everyone I love a MAC) and is also busy.
We have 5 children, 2 still at home………

Hey,

I forgot to mention that my speech is not perfect. I do stutter when I get excited and my volume increases and I don’t realize it. I also cannot write that well anymore not that I could in the first place. My mother, an RN, who in retirement took me to her continuing education seminars on brain injuries, when I would look down always reminded me, with brain injuries, always give it at least 4 years for recovery.

p.s. Spinning is the best Cardio ever and it is easy on the knees.

My life partner swears that my better days are the ones when I’m active in exercise. I can remember the first time to the gym: 1/11 of a mile was a victory….then a mile…..then two and now 100 mile bike rides.

Keep up the great work.
I’m still encouraging Linda my life partner to write you, I overheard her discussing the Blog with my oldest daughter about their experience with my CPM and the surrounding events. The only things I remember are the peace of the ICU, before being admitted telling my boy to take me out if they cath me, being able to memorize the 8 questions of “Are you an Alcoholic“. Being on the general floor on the Hospital, constantly asking to be walked, because I new something was wrong. I do not remember having headaches. I’ll keep encouraging her because your story sounds familiar to what happened to me except alcoholism was the proximate cause of my low blood sodium.

Hey,
I just got back from a session of speech therapy. I went for a 4 year/50,000 mile tune up. The good news is in their humble opinion and expertise my speech is great. I would admit that normally I feel 95-98% but somethings dip below 90%, I admit the speech problem is all in my head.
One issue that they identified is my facial expressions.
“deer in the headlights” eyebrows always up and my mouth is constantly open. Two things I was not aware of.
So much for my Neurologist’s suggestion for becoming a professional poker player! At the end of the day I can feel some self confidence with my speech.

Hey,
The “deer in the headlights” look is definitely a CPM issue along with my mouth being unconsciously open 24/7 unless I’m thinking about correcting it. The toughest setback of CPM is the mental aspect: Remembering how things were before CPM, then now. Trying your hardest for minuscule gains is a bitch. Don’t be worried about the muscle issue yet. I cannot specifically say that happened to me but I definitely lost strength. Three hunting seasons ago, I could barely carry a 20 gauge and was so pissed off after the season I went directly to the gym. Three years later, I carry what affectionately call “the cannon”–Weatherby O/U 30inch 12 gauge. After this year a buddy told me to “knock off that disabled shit because you can’t fool me, I saw you dropping everything you shot.” He was right. Bottom line–we know when someone is BSing with us or is sincere. Personally I like the BS too because I like to give it out.

SO, as you can see from Todd’s story. There is hope for living with CPM/EPM. He isn’t the same person he was before the injury, but he’s making strides to make the best of his life now. I still have a lot of questions for Todd, so please don’t consider his story complete at this point, but I wanted to get his story out there.

Have a great night.

Posted in Your Hyponatremia/CPM story: and tagged Alcoholism, Central pontine myelinolysis, CPM, Hyponatremia

21 Apr 2012

A large number of case reports regarding CPM/EPM:

This post is going to list a website that I found regarding dozens of case reports regarding CPM/EPM.

I was really surprised that these case reports, though brief, do correlate to many of my previous descriptions of symptoms associated with CPM/EPM. I do not know where these case reports were cited from, and I wish that there were more detailed accounts, but we have to work with what we have. The following information comes from this link: http://www.lookfordiagnosis.com/cases.php?term=Myelinolysis%2C+Central+Pontine&lang=1&from=10

11/105. immunoglobulins are effective in pontine myelinolysis.

Although the exact pathogenesis of central pontine myelinolysis (CPM) is unknown, correction of hyponatremia, thyreotropin releasing hormone, plasmapheresis, and corticosteroids seem to be effective. Assuming intravenous immunoglobulins (IVIG) to also be effective in CPM, 0.4 g/kg body weight/d immunoglobulins were applied to a 48-year-old patient who developed CPM with double vision, dysarthria, dysphagia, and left-sided hemiparesis 3 weeks after spontaneous normalization of hyponatremia. After 5 days of IVIG, his symptoms markedly improved, confirmed by improvement in the Norris score (42%), Frenchay score (19%), Kurtzke score (20%), Disability score (54%), vital capacity(26%), and peak torque (69%). The promising clinical effect of IVIG was assumed to be caused by the reduction of myelinotoxic substances, the development of antimyelinantibodies, and the promotion of remyelination. In conclusion, IVIG appear to be a promising therapeutic option in CPM. (+info)

12/105. Parkinsonism after correction of hyponatremia with radiological central pontine myelinolysis and changes in the basal ganglia.

Parkinsonism has been rarely described following central pontine and extrapontine myelinolysis. We report a case of parkinsonism developing following rapid correction ofhyponatremia with radiological evidence of central pontine myelinolysis and changes in the basal ganglia. A 56-year-old man developed drooling and bilateral hand tremors 3 weeks after correction of hyponatremia from 103 to 125 mmol/L over 14 h. He had a prominent 6 Hz resting tremor which worsened with action and mild cogwheel rigidity.magnetic resonance imaging (MRI) showed changes consistent with central pontine myelinolysis and increased signal on T1-weighted images in the putamen bilaterally. Histremor responded well to L-dopa therapy. There have been several other cases of parkinsonism developing after central pontine/extrapontine myelinolysis. Increased signal in the basal ganglia on T1-weighted images has been described in another case of central pontine myelinolysis imaged about the same time after sodium correction as our case.(+info)

13/105. Central pontine myelinolysis: association with parenteral magnesium administration.

A 29-year-old woman with diabetes mellitus and nephrotic syndrome was given 30 g ofmagnesium sulfate over 14 hours after a cesarian section. Her serum magnesium level increased to 7.4 mg/dl. Five days later, she became quadriplegic with inability to speak or swallow. Cranial magnetic resonance imaging demonstrated central pontine myelinolysis (CPM). Initial serum sodium was not measured. Although CPM is usually associated with a rapid increase in serum osmolality, most patients who experience a rapid increase inserum osmolality do not develop the clinical syndrome of CPM. Consequently, additional factors may also be important in the pathogenesis of CPM. Parenteral magnesium administration may be a potential contributing factor in the pathogenesis of some cases of CPM. (+info)

14/105. Central pontine myelinolysis: delayed changes on neuroimaging.

The authors report two cases, a 44-year-old woman and a 6-year-old girl who had mental status changes and hyponatremia. serum sodium levels in both of these cases were corrected quickly with further decline in their mental status, and the patients became quadriparetic. magnetic resonance imaging (MRI) studies performed then did not reveal any abnormalities, whereas a repeat imaging study performed 10-14 days after the shift inserum sodium revealed evidence for central pontine myelinolysis and extrapontine demyelination. The clinical manifestations and distribution of lesions seen on the imaging studies demonstrated that the above presentation of neurologic illness is the result ofhyponatremia and its correction. The authors conclude that imaging studies performed early during the illness may be unremarkable, but still a diagnosis of central pontine myelinolysis should be suspected and, most importantly, a repeat imaging study might be required in 10-14 days to establish the diagnosis of central pontine myelinolysis. (+info)

15/105. methylphenidate treatment of neuropsychiatric symptoms of central and extrapontine myelinolysis.

OBJECTIVE: Previous reports describe the presentation and course of theneurobehavioral manifestations of central and extrapontine myelinolysis; as of yet, however, there are no specific recommendations for treatment of these problems. We offer the first report of successful treatment. METHOD: We describe a 55-year-old man with chronic alcoholism who developed central and extrapontine myelinolysis following an episode of heavy drinking and rapid correction of hyponatremia. The patient acutely developed motor, cognitive, emotional and behavioral problems best accounted for by central pontine and bilateral striatal myelinolysis. These neuropsychiatric symptoms were treated with methylphenidate over the course of 1 month in an off-on-off-on fashion. The Neuropsychiatric Inventory and other tests were used to assess treatment response. RESULTS: Marked improvements in the patient’s neuropsychiatric status were noted only during treatment with methylphenidate. CONCLUSIONS: methylphenidate effectively reversed the neuropsychiatric symptoms associated with the patient’s demyelinating lesions. We discuss possible underlying mechanisms of both symptom formation and treatment effect. (+info)

16/105. Slowly progressive dystonia following central pontine and extrapontine myelinolysis.

A 28-year-old woman was hospitalized with dysarthria and oro-mandibular and upper limb dystonia. Approximately 8 years prior to the current admission, the woman became severely hyponatremic due to traumatic subarachnoid hemorrhage-related SIADH. brainMRIs showed a signal increase in the central pons, thalamus and striatum on T2 weighted images compatible with central pontine and extrapontine myelinolysis. From a few months after that event, dystonia progressed slowly over the subsequent 8 years. We speculate that the particular damage chiefly to the myelin structures by myelinolytic process may have caused an extremely slow plastic reorganization of the neural structures, giving rise to progressive dystonia. (+info)

17/105. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.

We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na+: 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of plasma Na+ levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. By the 5th day of admission, she became tetraplegic, presented pseudobulbar palsy, ataxia, strabism, extrapyramidal stiffness and clouding of consciousness. Scintigraphic and MRI investigations demonstrated pontine and extrapontine lesions associated with Gayet-wernicke encephalopathy. After correction of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabilities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelinating lesions, usually considered as a consequence of a too fast correction ofhyponatremia, may occur despite the strict observance of recent guidelines. There is increasing evidence to suggest that pontine swelling and dysfunction may sometimes occur in alcoholic patients even in absence of disturbance in plasma Na+ levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypokaliemia, hypophosphoremia, seizure-induced hypoxemia,malnutrition with vitamin b deficiency) for brain demyelination and to correct them appropriately. (+info)

18/105. Central pontine myelinolysis.

Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. There are no inflammatory changes, and blood vesselsare normal. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis, and the locked-in syndrome.magnetic resonance imaging of the brain, the imaging procedure of choice, shows an area of prolonged T1 and T2 relaxation in the central pons, which may have a characteristic shape. Recovery varies, ranging from no improvement to substantial improvement. To avoid CPM, correction of serum sodium in patients with hyponatremia should not exceed 12 mEq/24 h. We describe a case of CPM in a hyponatremic patient who presented with a cerebellar syndrome with no pyramidal tract involvement and in whom the rate of correction of serum sodium was within the recommended limits. (+info)

19/105. Reversible central pontine and extrapontine myelinolysis in a 16-year-old girl.

A rare case of an osmotic demyelination syndrome in a 16-year-old girl is presented. MRI in the acute stage revealed a focal abnormal signal within the basis pontis and both caudate nuclei and putamina. Two years later brain lesions had disappeared on T1- and T2-weighted imaging, indicating that central pontine and extrapontine myelinolysis may be completely reversible. (+info)

20/105. Decreased diffusion in central pontine myelinolysis.

Two patients with central pontine myelinolysis (CPM) were studied with diffusion-weighted MR imaging 1 week after onset of tetraplegia. In both patients, affected white matter showed hyperintensity on diffusion-weighted images associated with a decrease in apparent diffusion coefficient (ADC) values. In one patient studied serially, ADC values normalized by 3 weeks after tetraplegia. Early in the clinical course, diagnosis of CPM can sometimes be difficult. Hyperintensity on diffusion-weighted images may therefore have diagnostic utility. Decreased lesional ADC values support the notion that CPM is a consequence of relative intracellular hypotonicity. (+info)

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM, Hyponatremia, Magnetic resonance imaging

03 Apr 2012

Just another day:

Hello All!

I’m sorry it has been so long since my last post. I have a million excuses as to why, but none of them are really good. I’ll give them to you anyway: I wasn’t home. I’ve been busy. My hands keep cramping. I have the attention span of a gnat. I have lost my train of thought on what to blog about next.

Okay, so some of those might be good reasons.

So, what’s happening with me?

It’s almost 10 months since I developed hyponatremia and subsequent myelinolysis! I can’t believe it’s almost been a year.

I have to say that some of my more concerning symptoms, mainly the speech issues, have become significantly better. Oh, I’m not going to pretend that I’m completely back to normal, but from where I was to now, there’s been a dramatic and miraculous improvement. I am extremely grateful. It gives me a new appreciation for people who live with speech impairments. They say people first judge you on how you look, but the very next thing is how you speak.

Despite the fact that I work at Victoria’s Secret Catalog, I do not have an extraordinary fashion sense…well, I do have a pretty good fashion sense, I just don’t have the financial means to support it. So, the fact that my almost everyday ensemble consists of jeans, a tee shirt, and a pair of worn out Asics sneakers, probably doesn’t scream fashion guru or speak volumes about who I am as a person, that means that the way I speak probably has a little bit more influence on people’s opinion of who I am.

This means the more that I stutter, stammer, and trip over my thoughts, combined with the super sloppy, casual wardrobe choices that I can afford might lead a person to suspect, I’m slightly retarded.

Previous to my impairment, I had the ability to impress people with my wit and vocabulary fluency. I was viewed as more of a nerd who didn’t need to worry about fashion because I had more important things to be concerned with than wardrobe choices.

Ok, so to prove my point…it has taken more than 30 minutes to write this. This isn’t an epic story. It’s not even utterly brilliant. It’s just an explanation of my speech issues. My mind skips like an old vinyl record.

I will literally go from thinking about what I want to write, to trying to find the words that I want to use, to trying to convey what I mean in a way that makes sense to everyone else.

It is so freaking frustrating!!

It really is, and if you have CPM/EPM, than you might understand exactly what I’m describing. If you have a brain injury or learning disability, you might also understand. It’s not WHAT you know or understand, it’s an inability to express what you know and understand.

See, just writing this jogged my memory; I wanted to continue to write about brain injuries and how to find support through the Brain Injury Association.

So, now, I’m thinking…I should be writing about the BIA, but this is the wrong place to write about the BIA. I need to stay focused and try to regain a sense of this post.

Getting back to my original topic…my speech has improved, but I still have ongoing issues, especially when I’m nervous. I would have to say my biggest obstacles are the movement issues (tremors, jerks, spasms and cramps), and cognitive deficits (learning impediments, memory problems, attention problems, and recall).

The movement issues aren’t extreme. I mean a person with late onset Parkinson’s has greater issues than I do. Some person’s with CPM/EPM have greater issues than I do. (I’m going to post a few YouTube videos to demonstrate my point), but I still have movement issues.

Right now, I am having a hard time keeping my left hand steady enough to type. My left thumb keeps twitching rapidly. It’s so annoying. I can’t do anything to stop it. Then it becomes painful. I really have lost function in my abilities to do certain things.

I was at the Columbus Zoo several weeks ago, and I tried to make a video of a leopard stalking an unexpecting rabbit that had wandered into its cage. After about five minutes, I was unable to hold my cell phone up to take the video, my arms were cramping so badly that I couldn’t hold the camera.

These movement issues are getting worse. I am not certain as to why. I know that some people who have experienced damage to the basal ganglia have late onset movement issues with dystonia and Parkinson’s like tremors. I am 90% certain that this is what I’m experiencing.

However, I have autoimmune issues, and I have to wonder if my autoimmune issues are contributing to the neurological manifestations of EPM.

I have a feeling that it will be extremely difficult to get an answer to this, but if I do find out more, I will keep you posted.

The other new symptom that has become apparent is autonomia. I’m not sure if I’m classifying this correctly. It’s actually a dysfunction in your autonomic nervous system. There has been reports of having irregularities in heart rate, blood pressure, central nervous system caused sleep apnea, etc.

When I had my sleep study (after diagnosed with EPM), I had one instance of central nervous system induced sleep apnea. I had taken ambien and I think that influenced my study because I did sleep better than what I normally do, but I do not know if it would make central nervous system induced sleep apnea better or worse.

I had issues prior to EPM with tachycardia. My heart rate has now become extremely erratic. I will have a pulse varying from 45 to 116. Literally, I will watch my pulse go from 59, 65, 80, 95, and then drop back to 50 in 10 to 20 second intervals.

My EKG has also shown “new” abnormalities.

The abnormalities in my EKG appeared when I was seeking treatment for EPM before I had an official diagnosis. I’m almost 100% certain that EPM caused the change in my EKG.

I hope to get further testing that might be able to determine if my issues are being caused by my autonomic nervous system, but it most likely won’t occur until July or August. I will keep you posted.

I have to say one of the most positive experiences I’ve had recently is meeting with my cognitive therapist.

I am seeing Angela C with Kettering Medical Center, Kettering Ohio. I can’t say enough about this person. She has offered me hope for the first time in my recovery.

She completely understands what I’m experiencing, and that is refreshing both physically and mentally. Trust me, not all of the doctors I’ve seen in the past 1o months have been supportive or understanding. Angela gets it. She KNOWS where my deficits are. She understands that I was bright before my injury and that I was inspiring to be a doctor, and she is working with me to manage the deficits that I have to navigate around them to learn ways to succeed.

I am really excited to be working with her! I highly recommend that if you are experiencing any type of brain injury or even ADHD or ADD to find a cognitive therapist to help teach you techniques so that you can become more successful.

One thing that Angela has stressed that I want to share: Be kind to yourself! It’s easy for me to criticize myself when I hit a wall, when I can’t think of a word, or when I become distracted for the 100th time in an hour. She’s teaching me to not beat myself up over it. The more I stress over these mistakes the more I derail myself.

The other thing I’ve been working on: breathing. Yep, I really didn’t know how much I tend to hold on to things when I’m not exhaling. I’m great at inhaling, but exhaling..well, I’ve got to practice. More importantly, breathe in deeply through your nose and exhale loudly and completely through pursed lips…a slow, steady exhale. It really does help.

SO, there you have it folks. I’ve discussed the physical and mental issues that I’m experiencing with EPM at the 10 month point.

I hope it helps 🙂

Have a great night, and feel free to contact me with any questions!!!

Oh, yes the videos…click below to see some of the videos of CPM, EPM issues. Keep in mind, I think these are extremes. My movement issues pale in comparison. I’ll post a few of my movement videos in the future.

http://www.youtube.com/watch?v=nnvcSGj7vY8

http://www.youtube.com/watch?v=58jik7RgZzs&feature=related

http://www.youtube.com/watch?v=v-_xNbZ5ef8&feature=related

Posted in I just have to say this: and tagged autonomic nervous system, BIA, brain injury association, cognitive deficits, cognitive therapy, CPM, epm, heart rate

15 Mar 2012

A new MRI for identifying brain injuries:

Did you know that in it wasn’t until 1843 that a physician linked having dirty hands to passing infections?

Click the following link to learn more regarding the history of hand washing: http://www.accessexcellence.org/AE/AEC/CC/hand_background.php

Originally, hysteria was categorized as an ailment that inflicted women after having babies. It apparently caused a host of symptoms such as, “anxiety, nervousness, fullness in the lower abdomen, erotic fantasies, paralytic states and fainting…”

Until the mid 1800’s to early 1900’s, it was believed that a woman experienced these issues because her uterus was “floating” around her body and choking her. Doctors treated it by causing orgasms in women. This was an actual selling point for vibrators. They “cured” hysteria. Use the following link to learn more, http://ije.oxfordjournals.org/content/30/4/904.full

So, what’s my point? Modern medicine and treatments are NEW. We know more about the human body and health than what our ancestors did, but there is still so much we need to learn, discover and understand.

This post is dedicated to a new technology that is in process to help those with minor and major brain injuries. This new advancement is promising as it is supposed to detect actual damage in neuro fibers in the brain. In my earlier blog posts, I mentioned how the injuries related to CPM/EPM are like having a short circuit in an electrical wire. This new type of MRI(High Definition Fiber Tracking) actually detects those short circuits! Where normal MRI’s and CT scans will show inflammation and bleeds, this MRI scan actual shows the neuron damage and can potentially predict how successful recovery will be.

This is exciting news for us!!! This might give us a definitive proof for the cognitive issues that we experience. It might show us how likely we will be to recover and to what extent. YEAH!!

For additional information on the upcoming information regarding this new MRI(High Definition Fiber Tracking) use the following links:

http://abcnews.go.com/Health/wireStory/finding-unseen-damage-traumatic-brain-injury-15830461

The following is a research article written about the MRI:

Click to access Pittsburgh%20HDFT%20TBI%20Diagnosis%20report.pdf

I had to copy the image (below) from the above link, just because it is that freaking awesome!!

New MRI

I really believe that this technology could greatly benefit those of us who are suffering from the “unseen injury”. Be patient friends, because this new scan will probably not be covered by insurance companies nor will it be offered in the next few months. I’m guessing it won’t be available for another year or more. (If you are interested in possibly getting it earlier, there are research studies being done at the University of Pittsburgh now.)

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged brain injury, CPM, epm, HDFT, hysteria, minor brain injury, MRI, Pittsburgh University, unseen injury

15 Mar 2012

3 Comments

Brain Injury:

This might seem utterly ridiculous, but up to this point, I did not realize I HAVE a brain injury. EPM and CPM causes a BRAIN INJURY. Maybe it would be more appropriate to state, that I didn’t realize what it meant to have this injury.

Of course, I’ve known that I have had damage to my brain, but that already happened, and for whatever reason, I did not consider that injury along the same line of having an injury caused in a car crash or stroke, etc.

The injury was in the past. It happened. It’s over.

This is the reaction that I’ve had from all of my doctors up to this point. Every doctor that’s treated me for issues related to EPM has stressed to me that the injury has happened. It will not happen again. The damage has been done and from that point forward I will only get better.

Many of my doctors have stressed that because my MRI has shown improvements, healing, then it’s just a matter of time before I’m 100% normal again.

Let me stress, this is NOT true. As, I’ve mentioned on numerous occasions, the MRI detects inflammation in the brain and even though the inflammation does dissipate in the months after CPM/EPM, it does not mean that you are going to be 100% back to normal. You may or you may not. The MRI images do NOT correlate to the symptoms you experience with this injury.

My MRI images have shown improvements. My doctors have told me that I am certain to get better, and I have been left struggling with wondering; Why am I not back to my normal self? It’s almost 9 months post injury, why am I not normal yet?

Further, NONE of my doctors touched upon the issues that have been most concerning to me, deficits in my cognitive abilities. It is extremely difficult for me to stay on task. I have short term memory problems. I have problems with reading and writing. I have difficulty thinking of words. I have attention deficits. The list goes on.

I recently was in training for work, and after 30 minutes, I couldn’t retain any more information.

Have you ever made manicotti? If you aren’t familiar with it, is a large cylindrical shell. In most cases, you stuff the shell with a cheesy filling. The shell is hollow and open on both ends. My ability to retain information is like a stuffing a manicotti shell. You can keep adding filling, but it’s just going to leak out the other side.

I might have retained some of the information from our recent training, but at this point, I’d say 70 to 80% is gone. I might remember parts of what I learned at points in time, but I almost guarantee that I couldn’t sit down and recall everything.

Here’s something that I don’t think I’ve discussed previously; I have found that my past memories have become extremely vivid and are constantly at the forefront of my mind. It’s so frustrating. I don’t know why these things are so blaring and concrete. I have no control over when they occur. I have no idea why they occur. They aren’t even significant events, but just random memories that are mundane and non influential.

Not all of them are mundane, and I have to say that’s even worse. Events that I would rather not think about come to my mind as well, bringing with me emotional turmoil and grief.

So why is it that I can remember sitting in the backseat of our beat up brown SAAB, as a kid, in the middle of the summer and arguing with my brother’s about Garbage Pail Kid cards, as we waited for our mother to come out of the grocery store around the age of 8, but I couldn’t remember to call my doctor’s office to schedule an appointment for the 4th day in row?

Folks, the stuff that filters through my mind on a daily basis in such GREAT detail about my past..from the weather and temperatures to clothes that I was wearing. It’s mind numbing. Why am I remembering these things constantly, but can’t retain 1/10th of events happening now?

After doing the research on my last post, Cognitive Therapy, I realized why. I HAVE A BRAIN INJURY!

CPM and EPM did more than just cause a temporary damage. I am utterly clueless why my current doctors who are treating me for this have been so adamant about not acknowledging this! I’ve spent the past 8 and a half months struggling to come to terms and prove that this isn’t something I’m making up. I’M NOT FAKING THIS, and now I understand why these things are happening to me.

I’ve had doctors tell me it was stress. It was from fatigue. I’m faking these issues. It’s test anxiety. It’s not related to EPM. It’s long term ADHD. It’s from having high cortisol.

I’ve struggled to understand why these issues became a problem after I developed EPM. I’ve questioned my sanity. I’ve questioned the severity of these issues. I’ve wondered if I was exaggerating these problems.

I’ve had people try to tell me it’s normal. It’s what happens when you get older.

If you are reading this, then I’m here to tell you, those people are FULL of it.

Let me stress, the reason you have the issues that you do is because you have had a trauma to your brain!! The damage is not necessarily ongoing (though that is also questionable), but the cognitive issues ARE or at least can be.

I now have answers and understanding to why these issues are occurring AND I can share with you, hope.

I had no idea as to how much support there is for brain injuries. There is actually a tremendous wealth of information regarding what might be considered “minor” brain injury.

Now, I’m not going to classify EPM and/or CPM as a minor brain injury. There are people who are living their lives completely incapacitated, requiring 24 hour support. That’s not minor. On the other end of the spectrum, you have people like me, who have are “functionally disabled”. You can live your daily life with little or no assistance, but you have not returned to your former self.

The following information I found online from Dr. Thomas Kay a renowned neuropsychologist who has specialized in minor brain injuries:

There is a known natural course of recovery for concussion, and the vast majority of persons appear to recover completely. (“Appear” is italicized because there is increasing evidence that there may be sub-clinical residual damage that can become manifest under certain circumstances, or can accumulate and cross a threshold after a series of presumably fully recovered concussions.)

There are predictable clinical deficits that occur immediately after most concussions: problems with attention, concentration, and short term memory; irritability; headaches; dizziness and balance problems; sensory sensitivity). These are often referred to as the “post-concussion syndrome.” However, because only some of these symptoms come from an injury to the brain, while others come from non-brain body systems, I prefer to avoid the phrase “post-concussion syndrome,” and try to refer to “post-concussive symptoms.”

A subset of persons who suffer concussions, or mild traumatic brain injuries, have long term residual symptoms, and a smaller subset remains highly dysfunctional. There is a long standing, often bitter, debate about why some people do not recover completely from concussion or mild traumatic brain injury. At one extreme, some advocates maintain that all problems are due to permanent brain injury. At the other extreme, skeptics maintain that anyone who fails to recover from a concussion/MTBI either has psychological problems or is malingering, and maintain that it is not possible to sustain permanent neurological damage from a concussion.

He goes on to state:

It is important to realize that multiple factors other than neurological ones can contribute to the appearance of brain injury, or exacerbate the apparent severity of brain injury. These include pain, sleep deprivation, depression (which is extremely common), anxiety, PTSD, and the results of medication (especially narcotic analgesics).

The evaluation of MTBI is complex, and needs to sort out the various contributing factors. Comprehensive evaluation should be delayed until the natural course of recovery has been completed (often up to a year), and major psychological complications have receded. Briefer screenings can track cognitive recovery. Patients who are depressed will often perform much lower on cognitive tests, than when they are not depressed.

Tests of effort are also an essential part of neuropsychological testing. Multiple studies have shown a tendency for a high percentage of persons with MTBI to fail tests of effort, and underperform on cognitive tests. In my opinion, tests of effort may be failed for a variety of reasons having to do with motivation. In order for neuropsychological test data to be interpreted as valid, tests of effort must be passed. (Failure of tests of effort does NOT necessarily mean a person does not have a brain injury.)

Clinical treatment of persons with MTBI will depend on the relative contribution of neurological, physical, and psychological factors. The neuropsychological approach I take is determined entirely by the presentation, dynamics, and needs of each individual person. I conceptualize treatment of MTBI as the restoration of an effective sense of self. Limits on this restoration may or may not be set by neurological injury. Each individual is different.

I am going to elaborate on this post in the near future, but before I end tonight, I just wanted to share this exciting news. Yes, folks, we have a brain injury, and if you are experiencing these issues than you are not alone and there are people who will believe you and your issues. Most importantly, now you have a source for help. 🙂

Keep checking back on this post for the next few days because when time and energy allow, I will be updating with more detailed information for support and direction.

The Updates:

This is I believe an amazing quote:

Brain injury is not an event or an outcome. It is the start of a misdiagnosed, misunderstood, under-funded neurological disease.

This quote is from the Brain Injury Association of America:

http://www.biausa.org/

I really believe it is absolutely true. I’m hoping it is not true for you, but it describes me to a T.

Update: This person found my site and after reviewing it, I really found the information extremely beneficial. I recommend checking it out: http://brainhealthresources.wordpress.com/2012/05/09/there-is-help-for-battered-athletes-and-tbi-patients/

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged cognitive deficits, cognitive therapy, concentration, CPM, epm, learning disabilities, minor brain injury, short term memory, Thomas Kay PhD

20 Jan 2012

1 Comment

Discharged:

I think one of the hardest moments I faced after developing CPM/EPM was being discharged from the hospital. I literally had a bit of a break down. I don’t think my reaction was abnormal.

I was already beginning to see some improvements during the week I was hospitalized for CPM/EPM. At the same time, I was still really screwed up. I was NOT anywhere close back to my formal self.

I had only had the injury for about 10 days. I was aware from the very little access to information online that I would not be considered out of danger for at least 3 weeks from the date of injury. Some research suggests that you can be at risk for dying for up to 12 weeks. There’s just not enough research and answers fluctuate.

Everyday I woke up in the hospital I felt a sense of relief, but every time I went to sleep I felt anxiety. Would this be the time that I would not wake up or wake up and not be able to move?

At the same time, the doctors were monitoring my symptoms intently, but they were truly unable to do anything but watch me.

They were afraid to give me things like pain medications or even something as benign as glucose IV fluids because they were concerned with how they would impact my neurological functions.

Despite their not doing much of anything but observing, I felt a comfort in knowing I was there. If something bad happened, I knew that something could be done immediately.

I was also extremely dismayed at leaving because I was NOT normal. At that point in time, my list of neurological issues was extensive. I had problems losing my balance, walking into walls, developing hypotension when I was standing and hypertension when I was sitting. How was I going to get back to a “normal” life if I couldn’t even stand up for long periods of time without getting super sick?

One of my biggest issues at that time was my speech problems. It was extremely obvious, and I have a phone sales position. How could I perform my job if I couldn’t speak properly?

I’m sure if you are reading this, you are experiencing something similar to this or deficits that may be greater. It is terrifying. There aren’t any “real” answers. There is a lot of unknown.

This will probably lead to anxiety and depression when you are released from your hospital or hospice. It’s like losing an anchor in the middle of a hurricane.

What should you expect?

First, make a list of your questions. Is the hospital or rehabilitation center setting up ongoing occupational, speech, and physical therapy at home? Who will be in charge of your ongoing treatment? Will it be your general practitioner? Will it be a neurologist from the hospital who was treating you? Who should you consult regarding your work notes, disability claims, insurance questions? What will your insurance company cover? What will your co-pays be? Will you need 24 hour support, live in aid or daily assisted living? What type of medications will you need and those side effects? Is there any doctor associated with the hospital that has experience with CPM/EPM? Can you drive? Are there any specific physical limitations that should be avoided? Is there a support group they know of (you probably won’t find one for cpm/epm, but you might find one for neurological disorders or brain injuries?

Is there a source for your care givers? For instance, you may experience things like paranoia, dementia, irritability. These are normal psychological effects of it. If you become unstable, who should they call? If your symptoms become worse, what should they do?

If you were employed before your injury, you need to get in touch with your human resources department. If you are a caregiver of someone who has CPM/EPM, you will need to contact their employer to let them know what the situation is and find out about their disability policies. In most cases, you can fill out FMLA forms to help protect their/your job. If you are a caregiver, you will want to find out about becoming power of attorney.

In most cases, you were not anticipating this to occur, and it is a huge surprise. You might have been perfectly healthy previous to this injury, but now you’re facing the chance of having life long injuries. You probably did not have things like your living will, durable power of attorney, health care power of attorney.

IF you are reading this as a precaution, and you’ve never developed hyponatremia or your CPM/EPM, then I recommend taking the initiative and getting these basic legal affairs taken care of. Let’s look at the facts, you may never develop CPM or EPM, but you do have a fair risk of developing hyponatremia.

Further, you are going to die at some point, whether it’s a car accident in 3 weeks or a heart attack tomorrow. It’s inevitable. You need to be certain that you have everything ready for your family and your friends.

At the very least, you need to discuss your plans with your family and friends. It’s never a comfortable subject. No one wants to face the reality of losing someone they love, but it’s worse to leave the heavy burden to your family and friends when they are suffering from the pain of not having you in their life.

If you need help, most lawyers will consult with you free. There are legal forms that are available online. At the very least, you can create a document at home, typed or written that express your wishes. You simply take that letter to a notary (usually a bank will have a notary) and sign and date it in front of them. It has to be signed and dated in front of the notary to be valid.

This is just a stepping stone on what to do. I hope this helps, and if you think of any additional advice to add, please feel free to do so.

Take care!

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged CPM, durable power of attorney, epm, living will, medical power of attorney, occupational therapy, physical therapy, speech therapy

07 Jan 2012

CPM: Treatments

I hope you are doing well. It has been several days since I posted last. I could list several crazy reasons: I was in the hospital having a sleep study. They didn’t have WiFi at the hospital, so I couldn’t use my laptop. Tom was sick. However, honestly, the biggest reason is I didn’t know how to continue with this topic.

It might seem obvious that it is easy for me to get distracted and get off topic. (I hope not). I think my last post on CPM/EPM might have demonstrated this a little more than normal.

I covered a lot of material in my last post. Several of the topics I mentioned, I feel, could be made in to separate posts. I might try to do this at a later time, which means that I might have some topics come up more than once. Please be patient.

Okay, so CPM/EPM treatments:

There really aren’t any treatments, as far as a cure. You will find this information on any resource regarding CPM. For your convince, I’ve included this quote from, http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001779/.

There is no known cure for central pontine myelinolysis. Treatment is focused on relieving symptoms.

The following quote is from a study that suggests the following has been used in the treatment of it:

Case reports have suggested that steroids, intravenous immunoglobulin, and thyrotropin-releasing hormone may be helpful; however, there are no findings from a large-scale trial to support the use of these therapies.

(http://radiographics.rsna.org/content/29/3/933.full)

You may be given prescriptions for movement disorders (tremors, shakes, twitches). These are usually the same type of drugs that treat parkinsons. You may be given pain meds. You might need to see a pain management specialist. You may need anti anxiety/anti depressants. You may need medicines for insomnia or for central nervous system sleep apnea.

You may need on going physical and occupational therapy. You will probably need speech therapy.

You will probably be given anti-depressants or anti- anxiety medicines because let’s face it, the pill you are forced to swallow is unbelievably bitter.

I know that sounds a bit scary. It is. It is terrifying because the doctors have no way to know what is going to happen to you, so they won’t be able to provide you with much information.

If they’re honest with you, they will tell you that you could slip into a coma at any point in time, die, or slip into something called locked in syndrome.

In a series of 44 patients, myelinolysis
occurred after a mean of 6.3 days (range 3–11)
and resulted in a “locked-in” syndrome in 23
patients.

The above information was provided by: http://www.ccjm.org/content/74/5/377.full.pdf

Personally, I think the locked in syndrome is the most terrifying because you will lose all ability to move. It’s a FULL body paralysis. The only thing that you will be able to move is your eyes, but you’re aware of what is happening.

Some studies state that you are at risk to develop these severe health issues (coma, death or locked in syndrome) up to 12 weeks after developing CPM/EPM. Other studies, suggest that it is up to 8 weeks. Frustratingly, there is not enough information regarding CPM/EPM to know for sure.

In most cases, the hospital will keep you under observation for at least 7 days depending on how severe your symptoms are. In other cases, you may be hospitalized for up to 21 days for observation. If you go into a coma or locked in syndrome, you may be hospitalized for 4 to 12 weeks, if not longer.

Here’s the thing, if you are being released in this 7 to 21 day period, I highly recommend that you remain in contact with your doctors that were monitoring your for the CPM/EPM. If you experience ANY changes after being discharged, GO TO THE ER. Err on the side of caution with CPM/EPM. Being wrong is better than being dead.

If you’ve developed CPM/EPM, you’re already unlucky. You’ve already fallen into the less than 1% to 5% range by developing it, and NO ONE really knows what will happen, so err on the side of caution if you experience ANYTHING that gives you concern.

I want to stress that it’s important to return to the hospital that was treating you because most hospitals have never treated a patient with CPM/EPM. Most doctors have only read about it in textbooks. If your hospital treated you, then they might have experience with it.

Your life has just been changed tremendously. If you’re reading this, then you are EXTREMELY luck and terribly unfortunate at the same time. You are terribly unfortunate in developing CPM, but EXTREMELY lucky that you are even alive.

It’s going to take time to adjust to your new abilities, and your journey is just beginning.

Now, here’s the thing. No ONE knows what is going to really happen with you.

Depending on the severity of your symptoms, you may improve significantly. Some research suggests that you may recover COMPLETELY. However, I question this on the basis that research is vague.

In long-term
follow-up of 32 survivors of the acute phase of
central pontine myelinolysis, 11 had no functional deficit, 11 had minor neurologic
deficits, and 10 had severe deficits requiring
dependent (ie, long-term) care.

The above quote comes from the article used previously. Use the ccjm.org link above to access it.

The widely used study above suggests, that 1/3 of patients will recover, a 1/3 of patients will have symptoms but live independently, and a 1/3 will need to have assisted living.

This study was vague. It didn’t say how long the patients had CPM. Was it 3 months, 6 months, 10 years after developing it?

I would like to suggest that unless you die, you are going to improve. I would like to suggest that everyone who has CPM (except for those who die) will improve to some degree to an almost normal, pre-injury state. However, it is not known if this type of improvement is absolute or to what degree you will improve.

The study quoted above, also explained that depending upon the location of the lesions, a person might experience a decline in neurological abilities. I know several persons who have it, and after a period 2 to 3 years, they begin to experience a deterioration in their neurological symptoms.

Some studies have stated that the majority of persons who have CPM, die within 5 to 10 years after developing. More than half commit suicide.

Please be aware, if you are a care giver for someone who has CPM, that more than half commit suicide.

Because of this alarming statistic, I highly recommend getting your loved one supportive psychological therapy. I also recommend that they participate in online support groups.

Brain injury support groups offer a great help.

I looked for months, and found only a handful of people who have CPM through inspire.com. We’re kind of outcasts since there are so few of us, so we don’t really fit into any other neurological support groups.

I hope to change that at some point in time, but right now, please contact me with questions. Please post your story for others to read. Together, I hope we can prevent people from going through this horrible experience.

UPDATE:

It is always depressing to learn that there are TREATMENTS for CPM/EPM, and to know that I could have been fixed if I received one of these treatments! I hope and pray that if you have CPM/EPM or know of someone who has been diagnosed that you will get this information during a period when it can provide relief. The following quote comes from an abstract, so if you provide this information to the doctor, they should be able to get the treatment information:

Clin Neuropharmacol. ;23 (2):110-3 10803802 Cit:11

Immunoglobulins are effective in pontine myelinolysis.

[My paper] J Finsterer, E Engelmayer, E Trnka, M Stiskal

Neurological Department, Neurological Hospital Rosenhügel, Vienna, Austria.

Although the exact pathogenesis of central pontine myelinolysis (CPM) is unknown, correction of hyponatremia, thyreotropin releasing hormone, plasmapheresis, and corticosteroids seem to be effective. Assuming intravenous immunoglobulins (IVIG) to also be effective in CPM, 0.4 g/kg body weight/d immunoglobulins were applied to a 48-year-old patient who developed CPM with double vision, dysarthria, dysphagia, and left-sided hemiparesis 3 weeks after spontaneous normalization of hyponatremia. After 5 days of IVIG, his symptoms markedly improved, confirmed by improvement in the Norris score (42%), Frenchay score (19%), Kurtzke score (20%), Disability score (54%), vital capacity (26%), and peak torque (69%). The promising clinical effect of IVIG was assumed to be caused by the reduction of myelinotoxic substances, the development of antimyelin antibodies, and the promotion of remyelination. In conclusion, IVIG appear to be a promising therapeutic option in CPM.

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM, CPM/EPM, Locked-in syndrome, neurological disorders

03 Jan 2012

CPM/EPM–What to expect:

English: Central pontine myelinolysis, MRI FLAIR (Photo credit: Wikipedia)

I hope for those who are reading this, you are in good health or your loved one is.

If you developed a chronic form of hyponatremia, you are at risk for CPM if your sodium levels were raised too quickly.

Too quickly is not an absolute term. There are person’s who disagree on what “too quickly” means in regards to the treatment of hyponatremia.

Some specialists believe that too quickly is greater than 8 mmol in a 24 hour period. Other specialists would consider “too quickly” as 12 mmol in a 24 hour period.

I would recommend the safer the better no more than 8 mmol in a 24 hour period.

Bottom line, if your levels were raised more than 8 mmol in a 24 hour period, and you started to experience symptoms of CPM/EPM in a period of 3 to 10 days after your treatment for hyponatremia, it was raised “too quickly” for your system.

If it is raised more than 8 mmol in a 24 hour period, you are at risk for CPM/EPM. It doesn’t mean you will absolutely develop it.

I caution you to watch for symptoms during the next 3 to 10 days after treatment if you know your levels were raised at this rate or faster.

When you first start to develop CPM/EPM, your symptoms can vary, but will usually begin with muscle weakness, possible fatigue, headache, muscle stiffness, twitches/spasms/ jerks, trouble swallowing, issues with balance and coordination, visual issues, speech issues (stuttering, slurring or inability to form words), cognitive difficulties, issues with understanding speech, reading, and/or writing. Most importantly, a person can develop complete paralysis (locked-in syndrome), coma, and/or death.

I know, that’s enough to make your heart skip beats. Try to stay calm. This is a huge list of symptoms, and it does not mean that you will develop each one. You are at risk for them.

It is a serious condition, and you need to go to a well equipped hospital immediately, if you were recently released after receiving treatment for hyponatremia and have started to develop any of these symptoms.

It is not worth risking your life. If you are not certain if you are really experiencing these symptoms or not, but were recently treated for hyponatremia and “feel” as if something isn’t quite right, go and get it checked out.

The best way to determine if you have CPM/EPM is to have a T1 and T2 weighted MRI with contrast performed. It must be done with contrast.

***PLEASE KEEP IN MIND, THE DAMAGE ASSOCIATED WITH CPM/EPM MAY OR MAY NOT SHOW UP ON THE MRI FOR 2 TO 4 WEEKS!!! AN MRI IS NOT AN ABSOLUTE WAY TO DETECT IT. IT IS THE BEST WAY TO DETECT THE DAMAGE. ALSO, THE IMAGES CAN START TO SHOW SIGNS OF IMPROVEMENT IN 4 TO 6 WEEKS!!!****

Yeah, I know, this makes it really difficult to diagnose. By the time you begin to develop symptoms, they might not be able to see the damage on the MRI. If your doctor waits too long to take an MRI, the lesions can heal. JUST BECAUSE THE LESIONS HEAL DOES NOT MEAN THAT YOUR INJURY IMPROVES.

This can lead to a misdiagnosis of Parkinsons. Some of the longest lasting symptoms a person may experience are movement issues (tremors, jerks, spasms, etc). So, it is not uncommon for a person to be misdiagnosed as having Parkinsons.

It is also not uncommon for a person to be incorrectly diagnosed as having a stroke, especially in the elderly.

So, what does this mean?

It means that you should spread the word regarding CPM/EPM. The more the public becomes aware of CPM/EPM, the less it will occur. In this case, prevention is the best way of defeating this disorder.

It is important for people to be aware of the symptoms associated with CPM/EPM. It is important for you to obtain your medical records if you developed any of the previously mentioned symptoms after your treatment to determine how quickly your sodium was raised.

If you experienced any of the above symptoms and your sodium level was raised faster than 8 mmol in a 24 hour period, it is very possible that you developed CPM/EPM.

If you’re making this discovery long after your treatment, you will still want to contact your doctor to request an MRI.

I would highly recommend contacting a neurologist who is experienced in treating CPM/EPM. Trust me, this is easier said than done. I will post information on some of the doctors who are associated with treating CPM/EPM, but please be aware that these doctors are few and far between.

That’s because there are approximately only 2000 cases “documented” each year. Now this number is under dispute. I received this number from the website I reported in my earlier post for hyponatremia. (I will insert it again in the near future). However, my friend, Jeffrey, who was trying to develop a CPM awareness support group, received information from the National Institute of Health that this number could be as high as 30,000 to 50,000.

WOW! That’s a huge difference. How could this be possible?

Well, it’s possible because CPM/EPM is almost 100% caused by medical malpractice, and more than half of those who develop it, die. Those who develop hyponatremia and CPM/EPM are usually being treated for other disorders, such as traumatic brain injury or major burns, etc. In other words, hyponatremia is common as a secondary illness.

To protect the hospital and doctors from a malpractice lawsuits, it is believed that in cases where hyponatremia is a secondary condition that leads to CPM/EPM, the hospital and doctor will list the cause of death as being from the burn, the brain injury, cancer, etc.

For those people who do not die, it is suspected that the hospital/ doctor will tell the patient or their families that the reason they are experiencing these new physical symptoms is because they are having side effects or reactions to the illness or treatments.

Even if there are 30,000 to 50,000 people who develop CPM each year, that is not a huge number of people. Consider the reported fact that at least 1.5 to 1.7 million people develop hyponatremia each year, this means that less than 5% of those will develop CPM/EPM. The reported statistical data suggests that only .03% to .15% of those who develop hyponatremia will develop CPM/EPM. According to recent statistics (which again can be very vague), approximately 500 to 2500 were reported in 2010-2011. I believe that these statistics aren’t extremely accurate due to the drastic variations that were reported from one year to the next.

It is extremely difficult to know for sure what is accurate and what isn’t. I will try to resume the research Jeffrey was uncovering, but his unexpected death due to complications from CPM has made it difficult.

I will report it and update my blog accordingly.

So, what does this mean? YOU need to be your own advocate. You need to access your medical records and determine if your levels were raised too quickly. If you are currently in the hospital, track your sodium levels as they raise it. Be sure you question your doctors regarding your treatment. If you are conscious and able, access information regarding the medicines that you are being given.

If you were recently released from the hospital, TRACK your symptoms. If you start experiencing any subtle changes, go to a DIFFERENT hospital from where you were treated for hyponatremia and demand that they do a MRI.

I literally had to drive to a different city and a major hospital. No one believed that I could have CPM/EPM.

Be adamant. It is also helpful if you provide the new hospital with the records for your treatment.

In most cases, you won’t have issues with being admitted for the problems you are experiencing because it is painfully obvious that there is an issue. Be sure that you have a representative who can speak for you, such as a friend or family member. Make sure you have your living will and/or power of attorney up to date.

It is not uncommon for a person to experience a temporary recovery from their HYPONATREMIA symptoms once their sodium levels are corrected. It is a brief window of relief before you begin to experience different neurological symptoms from CPM/EPM.

The window, as mentioned previously, is approximately 3 to 10 days after your sodium levels have been stabilized. It is the quiet before the storm.

I would use this time frame to prepare if your levels were corrected too quickly. It’s better to be safe than sorry. Try to get as many of your affairs in order as possible, and obtain your medical records from the hospital.

Remember, there are only a very few who experience issues with CPM/EPM, but if your sodium levels were raised too quickly then you are at a greater risk for it.

This is by far, one of my longest posts to date. I understand I’ve repeated some of the information over and over again, but you will only have this opportunity once. It’s absolutely necessary for you to do everything right from the start because there is no room for errors once you start down this road.

I hope this finds you in good health, but if you are one of those being impacted by CPM/EPM, please take comfort in that you are not alone. I hope my message can help you or your family cope with this road bump.

Many blessings!

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM, Hyponatremia, National Institute of Health

Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “CPM”

Reversal Of Demyelination in CPM/EPM/ODS

Hyponatremia Recent Stats:

2011 National statistics – principal diagnosis only (hyponatremia only -from all hospitals in US)

2012 National statistics – principal diagnosis only

Alternative Treatments for CPM/EPM and Brain Injury:

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

The Stages:

Ketoacidosis and Central Pontine Myelinolysis:

Michael’s Story:

Todd’s Story: CPM

A large number of case reports regarding CPM/EPM:

11/105. immunoglobulins are effective in pontine myelinolysis.

12/105. Parkinsonism after correction of hyponatremia with radiological central pontine myelinolysis and changes in the basal ganglia.

13/105. Central pontine myelinolysis: association with parenteral magnesium administration.

14/105. Central pontine myelinolysis: delayed changes on neuroimaging.

15/105. methylphenidate treatment of neuropsychiatric symptoms of central and extrapontine myelinolysis.

16/105. Slowly progressive dystonia following central pontine and extrapontine myelinolysis.

17/105. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.

18/105. Central pontine myelinolysis.

19/105. Reversible central pontine and extrapontine myelinolysis in a 16-year-old girl.

20/105. Decreased diffusion in central pontine myelinolysis.

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What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “CPM”

2011 National statistics – principal diagnosis only (hyponatremia only -from all hospitals in US)

2012 National statistics – principal diagnosis only

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11/105. immunoglobulins are effective in pontine myelinolysis.

12/105. Parkinsonism after correction of hyponatremia with radiological central pontine myelinolysis and changes in the basal ganglia.

13/105. Central pontine myelinolysis: association with parenteral magnesium administration.

14/105. Central pontine myelinolysis: delayed changes on neuroimaging.

15/105. methylphenidate treatment of neuropsychiatric symptoms of central and extrapontine myelinolysis.

16/105. Slowly progressive dystonia following central pontine and extrapontine myelinolysis.

17/105. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.

18/105. Central pontine myelinolysis.

19/105. Reversible central pontine and extrapontine myelinolysis in a 16-year-old girl.

20/105. Decreased diffusion in central pontine myelinolysis.

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