Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “CPM/EPM”

Therapy:

Recently, and by that I mean back in April, I think, I was told by my neurologist that you don’t stop recovering from a brain injury.

He said that there used to be a notion that recovery happens only during the first two years post brain injury. He said that isn’t true. He said, recovery can continue to occur post two years.

I don’t know.

I can’t say that I have seen monumental gains or even noticeable gains. However, I am doing more than I did two years ago.

There came a point about 2 to 2 1/2 years ago when I was busy watching everyone else live their life, and I was spending my days on the couch trying to figure out what to do with my life. I’m sure you are probably doing the same, if you haven’t already moved beyond that point.

I would spend a lot of my time surfing social media, FB, and I was so envious of all of my friends and family that were living lives without a brain injury. They were going on vacation. They were participating in 5k’s, marathons, or even triathlons. Yes, they were going back to school, graduating from nursing school, medical school, or having more children.

My life was at a standstill, and I thought, I could spend the rest of my life sitting on this couch in my living room, or I could do something different.

Several of my doctors recommended therapy…aquatic physical therapy….boxing, biking, and others had been mentioned. I had already completed occupational, cognitive, and speech therapy. My insurance stopped paying for it, and I wasn’t getting anything out of it anyway. I don’t have access to Rock boxing near me, but here is a link for it, just in case you do:

Home

This is a program designed for those of us with movement disorders similar to Parkinson’s.  They have locations through out the U.S. I don’t believe that you need to have a prescription from your doctor, and other than that, I would recommend using the link to find more information.

Aquatic physical therapy is good for those of us who have limited range of motion and balance issues. You would need a prescription for that.

There have been significant improvements with movement issues caused by brain injuries after riding bikes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557094/

http://www.medscape.com/viewarticle/751998

This is a research article that explains how it helps with Tremors and Bradykinesia.

http://commons.pacificu.edu/cgi/viewcontent.cgi?article=1433&context=pa

It is also helps with balance. Now, from what I understand, if you do not have fantastic balance to start off with, go for a stationary bike. One of our CPM friends, Todd, has been biking for years,and he has said for years that it has helped him. Turns out, he’s not the only one seeing improvements with movement issues after cycling.

For me, I started walking. Now, there a gazillion reasons to get out and walk. It lowers BP, raises endorphins, lowers stress, etc. For me, I had to start off with just 1/2 a block. That was it. It was hard. It was a bit depressing because I would compare it to what I had been able to do pre-brain injury. Here’s the thing: DON’T DO THAT!!!! Do NOT compare your current self to your past self. There is absolutely NO good that will come of it.

As my daughter says, “You get what you get. You don’t throw a fit.” Yes, that’s easier said than done, but practice it. Even if we didn’t have a brain injury, comparing our former selves to our current selves, NEVER solves anything. It just doesn’t.

We’ve been given this life, and we’ve been given this struggle, but here’s the thing, if not this, it would have been something else at some other point in time. Cancer. Diabetes. Heart attack. Stroke.

So, we’ve got to suck it up and move on.

These therapies above, they won’t make turn you back into your old self, but they might help you move beyond what you have to deal with today. They will help. They will make you mentally stronger, if not physically stronger. They will give you the determination to succeed against the body that does not work with you as much as it once had.

And it is not easy. I promise you, it will hurt. Your muscles will hurt. You will get tired. You might even get angry, especially if you compare your current self to your old self. Hopefully, you will have a fantastic group of friends, family, and hopefully, a loving spouse to motivate you to keep working. Actually, you need to have a friend or spouse or someone to go with you. Trust me, you don’t want a broken leg or a bump on the head because you lost your balance…at least to start.

My first attempt at this was walking. I added more and more distance, and when I finally mastered about an hour walk a day, I started adding more tedious trails. Again, I did not do this alone. I had a good friend who went with me. It was important. Remember, this is not a contest: Pace yourself.

If you can, especially in the beginning, see a massage therapist. They will help work out the kinks that don’t seem to want to unkink on their own. Take about 400mg of magnesium with about 200mg of calcium. This will also help with cramping.

And maybe take an Aleve or Advil before or after you go, with food, because it can cause gastritis if you don’t eat. This will also help with muscle pain and cramping. Just don’t take those for too long because they can lead to stomach, kidney, and liver problems with long term use.

In the end, 2 years post starting exercising, I STILL have cramping within the first 50 yards of my hike or swim.  (I just started cycling, but I look like a drunk monkey because my balance is so bad- HA!) So, I can’t promise that the cramping or pain will stop, but you will develop the determination and the mental fortitude to keep going despite the pain because WE ARE STRONG. We are survivors!

Please contact me if you want more information on any therapies.

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It’s 4 O’clock in the morning…..

So for those of you new to this brain damage/ CPM/EPM experience, you might soon realize you don’t sleep normally anymore. You might sleep too long. You might not sleep long enough. You might sleep for 2 hours only to find yourself awake until the crack of dawn, so that you can suddenly fall back to sleep at 6:45 am when you need to get up at 7.

What do you do?

For me, I would usually turn to FB to surf cute animal videos and lament on my current insomnia kick, but after several fruitless debates with the general public on topics that I have considerable knowledge, I realized two things: FB stresses me out, and I have no self control in walking away from fruitless debates with the general public. It results in HOURS of going back and forth with people. It results in hours of me trying to find research articles that prove I’m right, that have no sway with the unreasonable.

So, I walked away from FB, at least for now, but tonight, after two hours of sleep, I found myself wide awake. What do I do? My hands twitched for my go to drug, my cell phone. I surfed through my email. Spam. My fingers twitched. Should I log onto FB to just vent my frustration of how much I hate not being able to sleep?

Ugh. I grab my phone and go to medicine cabinet and pop a Xanax along with a TUMS. I need sleep. Now, I just want to mention. You should not combine TUMS or any other antacid with your prescription meds. No. You won’t self destruct if you do, but the absorption of your meds can be greatly hindered by your antacids.

I drag myself back into my bedroom, and I stand there, hovering over the bed like some crazy horror movie serial killer, except instead of a knife, I have an IPHONE. I literally sway back and forth debating with myself–pale, crazy eyed, sleep deprived, hair a mess. I sway left—go write on my blog. I sway right–go back to bed.

Finally, I set down my phone. I climb back to bed, staring at the ceiling. It could be an hour before the Xanax kicks in, and I fall asleep. FB ? No, FB? Oh, the dilemma!

I desperately want to tell everyone about my 6 year old daughter’s recent rant.

Izabel: “Mom! Tomorrow, you need to call Mrs. Morrison (her teacher) and tell her I am NOT coming back to school tomorrow. I NEED A BREAK- EXCLAMATION POINT (waiving her hands up and down for emphasis). EXCLAMATION POINT! (Saying the words-“exclamation point”) EXCLAMATION POINT!  EXCLAMATION POINT! Sometimes, a 6 year old kid just needs a break from school,” she reasoned, “I am not learning ANYTHING new.”  She continues on making her very cogent point. Tom, comes from the kitchen, “This seems like a monologue.”

“It is,” I reply. How can you possibly reason with such a dramatic argument from your 6 year old? I didn’t try. Instead, I used a diversionary tactic, “Oh, look dad has dinner.”

I love my six year old daughter. She is hilarious, and this is just one of those stories that my friends on FB love to read about, so my fingers are itching to jump on and tell them, but I’m also thinking of my last debate that left me leaving FB, and how much I went to get back on the conversation and tear apart the people with facts and statistics and research, which will to no where but will cause stress, fatigue, emotional distress, etc.

That brings me to here. Time is ticking towards 5 am now. I am tired but awake, and I’m trying to figure out what’s the next step. Sleep? Or trying to figure out a new series of posts for either a new blog–a spin off that discusses politics, vaccines, other medical topics, etc. or researching more about brain injuries: newer treatment options, medications, alternative medicines, diets, etc.

This is another problem with brain injury–making choices, wanting to do everything but hardly doing anything because you can’t decide. Just look at how long it took to decide to write this post.

It’s working though. The Xanax is kicking in. I’m getting sleepy, and I’ve decided any decisions about what to do next can wait until 8 O’clock in the morning. 🙂

Have a good night, morning, day!

Has it really been a year?

Hello, All!

I hope you’re doing well! I am SO sorry that it has been so long since I last made a post. I am still alive and kicking.

Tonight, I am nursing a sinus headache and because of that, this might be relatively short.

I have no idea what I have posted in the past. I mean, I know generally what I have included, but nothing specific.

So, how have things changed in a year? Seriously, I have no clue because my short term memory is still impacted by the injury. There are obvious changes; my kids are older. I am older.

I still live very much in the now, and this still has significant complications for those I know and care about. People who don’t know me might misunderstand this lack of attention as a lack of interest, but it really is that I don’t have a great method of keeping track of time, people, or events. This means that I forget to call or write people. i don’t make doctor’s appointments that I need, or I show up to doctor appointments at the wrong time or on the wrong dates.

I just went back to work part time. It is hard even completing that job because as policies and procedures change, I find it difficult to remember or adjust to the new stuff. It also takes a significant amount of concentration and patience. In general, I find that it takes about 2 hours before I’m stressed and about four hours before I’m mentally and physically exhausted. It is hard for me to complete tasks prior to work and then spend time at work. After work, I am so stressed that on most nights, it is hard to socialize at all with my family. I become so overwhelmed that even our little dog’s attention becomes too much. I need quiet time. Literally.

I’ve heard autistic children have this same tendency.

I still have a significant number of daily issues with movements, blurry vision, tinnitus, balance issues. I have cramping in my hands, feet, legs and hips. The cramping because significant with repetitive movements, like typing and writing. I have found that a certain blend of medication has given me the most relief with twitches, jerks, and severe shaking. I use a combination of Baclofen, Gabapentin, and Carbidopa/Levodopa. That said, the drugs tend to peak with ongoing use. This leads to a need to increase the dosages. They help, but they aren’t a permanent, absolute fix.

I have talked to people in many different countries who say that they have the same issues.

I do believe it is very important to stay as active as possible. I have daily pain with walking and using weights, so I stopped exercising for several years. It didn’t help. I recently started walking again and using light weights. I still have continuous daily pain. It hasn’t improved with exercise, but the mental aspects did. I felt better mentally. I felt like I accomplished something, but honestly, it really hurts. Almost with every step, I experience pain. You have to push through it. If you can’t change it, you need to accept it. I know that sounds like such a bitter pill to swallow, especially if you have recently been diagnosed with the condition. It is hard, but you do become more accustomed to the pain.

A lot of my fellow CPM/EPM survivors have had the same experience. The activity helps, but prepare for physical discomfort. It is recommended that before you start ANY physical activity that you consult your doctor first. It is also important to start of slow and build from there. Don’t expect miracles and give it time. If you also have balance issues, etc, I definitely recommend that you do NOT exercise alone. There are MANY times during a walk that I slip or trip or just lose my balance. I have no doubt a fall will happen eventually, but on almost all of my walks, I have my friend go with me. You’ll be surprised at how many friends are willing to get out with a friend for an hour or so.

Well, that’s all I can manage for now. As always, I am interested in hearing from you. If you have a question or need help, please leave a comment, and I will try to get back to you as soon as possible.

Many Blessings! Have a great night (and hopefully, I’ll be back sooner rather than later) 😉

Identifying Brain Injury:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

MEG Scan – detects errant electrical activity in the brain. Used in conjunction with FMRI and EEG.
http://www.research.va.gov/news/research_highlights/brain-injury-090808.cfm 

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

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

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

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

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

 

 

 

Concerns:

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

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

Concerns:

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

 

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

 

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

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

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

 

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

 

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

 

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

 

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

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Vision

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

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

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

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

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

MUSCULOSKELETAL DYSFUNCTION

Muscular dysfunction

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

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

SUMMARY

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

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

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

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

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

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

 

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

A diagram of the forces on the brain in concussion

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

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

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

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

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

So, let’s investigate brain injuries further:

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

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

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

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

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

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

English: Complete neuron cell diagram. Neurons...

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

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

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

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

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

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

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

Physical Issues:                   Cognitive Issues:  

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

• Visual problems                • Forgetful of recent information or conversations

• Fatigue                                • Confused about recent events

Sensitivity to light           • Answers questions slowly

• Sensitivity to noise          • Repeats questions

• Numbness/ Tingling

• Dazed or stunned

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

Emotional Issues:                           Sleep Issues:

• Irritability                                        • Drowsiness

• Sadness                                            • Sleeping less

• More emotional than usual             • Sleeping more

• Nervousness                                      • Trouble falling asleep

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

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

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

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

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

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

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

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

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

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

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

Have a great night!

Additional symptoms related to CPM:

 

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

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

 

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

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

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

Table 6

Metabolic aetiologies of dystonia and chorea

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

 

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

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

Here is the quote:

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

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

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

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

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

 

Have a great night 🙂

 

CPM: THE STATISTICS

So after months of trying to find out the answers to this question, I have found a beginning answer. Now, here’s the thing. This is the diagnosis code for CPM, but it doesn’t include a diagnosis code for those who develop EPM only…at least I don’t believe it does. But, it’s a start. 🙂

First the ICD-9 diagnosis code for CPM is

The way I found this is through my friend Jeffery Amitin. He left it in a message he posted in 2008. The ICD-10 code is G37.2:

2012 ICD-10-CM Diagnosis Code G37.2

Central pontine myelinolysis

  • G37.2 is a billable ICD-10-CM code that can be used to specify a diagnosis.
  • On October 1, 2013 ICD-10-CM will replace ICD-9-CM in the United States, therefore, G37.2 and all ICD-10-CM diagnosis codes should only be used for training or planning purposes until then.

Mortality Data

  • Between 1999-2007 there were 209 deaths in the United States where ICD-10 G37.2 was indicated as the underlying cause of death 
  • ICD-10 G37.2 as underlying cause of death data broken down by: gender, age, race, year

ICD-10-CM G37.2 is part of Diagnostic Related Group(s) (MS-DRG v28.0):

  • 058 Multiple sclerosis & cerebellar ataxia with mcc
  • 059 Multiple sclerosis & cerebellar ataxia with cc
  • 060 Multiple sclerosis & cerebellar ataxia without cc/mcc

Convert ICD-10-CM G37.2 to ICD-9-CM

The following ICD-10-CM Index entries contain back-references to ICD-10-CM G37.2:

  • Myelinolysis, pontine, central G37.2

Now, the above information states that the number of deaths related to CPM from 1999 to 2007 were 209 deaths. Now, I believe this is an EXTREMELY low number because it is believed that at least a 1/3 of patients who develop CPM die. The following information for 2010 ALONE, makes me doubt that the number of deaths related to CPM over an 8 year period is only 209.

2010 National statistics – principal diagnosis only

Outcomes by 341.8 Cns Demyelination Nec
341.8 Cns Demyelination Nec Standard errors
Total number of discharges 524 56
In-hospital deaths * *

The above information states that there were 524 DISCHARGES related to CPM…that doesn’t include the number of those who died from CPM.

The other interesting finding in the statistics above is that there WERE NOT ANY DEATHS related to CPM. Now, I really believe that’s not possible at all. Obviously, there’s information that is missing. 😦

Now this makes a little more sense. If you list the number of diagnosis of CPM that is diagnosed in combination with another disorder/disease, then the number of those who impacted jumps dramatically:

2010 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”
341.8 Cns Demyelination Nec
341.8 Cns Demyelination Nec Standard errors
Total number of discharges 2,490 190

The following chart is the number of those who have been diagnosed with CPM over the past 18 years. Considering that the number of cases of hyponatremia have increased over the past 10 years, it is a bit unusual not to see the same type of increase in the number of cases of CPM. Again, I have to wonder if the data reported on CPM, due to the nature that it is usually caused by malpractice, is in accurate. I will continue to try to find out information as it becomes available.

HCUPnet provides trend information for the 18 year period: 1993-2010

Number of discharges
ICD-9-CM all-listed diagnosis code and name 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
341.8 Cns Demyelination Nec 1,956 1,831 2,127 2,386 2,594 2,300 1,906 1,711 1,662 1,666 2,003 2,097 2,103 2,435 2,537 2,299 2,168 2,490

Keep in mind, that the above information is the number of people DISCHARGED. This is not a record of the number of deaths related to CPM.

Please use the following website to find out more information regarding CPM. You have to do research on all hospitals in the nation and use the ICD code 341.8 to locate these charts.

Also, please feel free to contact me with any questions.

 

Deb’s Story:

 

Deb has helped provide insights into symptoms that are related to CPM/EPM. She’s suffered from the condition for four years, and I am including excerpts from comments that she’s left me in my comments section to help journal some of the symptoms that aren’t recorded in the medical literature.

In the beginning:

I had the headache for about a month before my collapse into a coma. I kept going to the Chiropractor thinking there was something wrong with my neck, but as it turned out it was my sodium.

She further describes her experience:

My initial symptoms were severe. I was in a coma for 4 weeks. Went into cardiac arrest twice. When I woke I was paralized from the neck down, unable to speak or swallow. I had a feeding tube thru my nose while in my coma, but when I woke and they realized I wasnt able to swallow they put one in my stomache. I was then sent to a nursing home where I did 5 hours of phsyical, occupational, and speach therapy daily. I was in a wheel chair for quite a while. I had horrible pain, sharp shooting pains, and alot of cramping. When I woke from my coma my left foot and leg were cramped up, my foot was up to my knee. My hands, were curled up in balls. To make you understand my mind set, when I saw my neurologist for the first time after I left the hospital, he told me I may be in a wheelchair for the rest of my life. My very first words were “F*** you”. They were faint, and hard to get out, but he had to know what I was thinking. Over the next few months I continued my therapy daily. Eventually I was walking with a wlaker. Then my therapy was cut from 5 days a week to 3. And again over many, many months I began to walk with a cane. My tremers are bad in the AM before my meds, my muscles feels like they are constantly being torn. But now I am duing therapy on my own, I can still only lift 2lbs, I have lost over half of my muscle tissue. They say I may never get that back, also eventually I WILL be back in a wheelchair. I can type with 2 fingers, I used to type 80wpm. I have trouble with my vision, My left eye is now considered a “lazy eye”. When I am tired, or look at the computor for too long it gets a mind of its own. My ligaments in every joint are kinda like broken rubber bands, my joints are what they call “free floating”. So, beginning in Sept I am going to start a series of surgeries on them to tighten the ligaments. I have constant pain, never letting up. Not even for a minute. I go once a week to a Chiropractor because my muscles pull my bones out of place. I also have a massage once a week to help keep me limber. Mind you, I am a former swimmer, loved to run, play volleyball, softball, or pretty much any outdoor sport. Now I have the body of a 80 year old (according to all my docs) and the life of one too. CPM/EPM has stolen everything from me. The only thing I enjoy now is watching my kids screw around in the yard and watching birds. My hands are so weak I can’t even enjoy baking or cooking. Hope this helps, I appreciate your site because I don’t have to say all this stuff on facebook, or even inspire. Sick, just sick to death of this disease. Deb

The following describes her experiences with tremors, a problem that I’ve described in previous posts:

The tremors, Mine are really bad in the AM before my meds. After my meds, they get better. If I am doing anything with my hands for too long they will get bad. I have to have an easy hairstyle because I don’t have the control to “do” my hair. If I hold the hairdryer for too long They will start to shake and cramp. I have an experiment for you; Take your thumb and 1st finger and make a “o” with them. Your thumb should point out at the joint closest to your hand. If it doesn’t you have significant muscle loss. Mine is completely flat, my “o” is more the shape of an egg. Give it a whirl. let me know what you find.

In regards to her experience with how she experienced improvements, but over time, she experienced a decline in her health:

Yes, I have had a decline in my health where things initially improved. I have the same issue with recall, I get so pissed at myself! I can remember things that make me angry or upset just fine, but any happy memories just fade away…… My thumbs face a weird way too when I try to make my “o”. My occupational therapist was the first to notcie it. Also, every morning I cry when getting up, all my joints and muscle are so tight it is rediculous! That’s why I do yoga, it help stretch things back out. What is happening is when you sleep your spasticty is causing your joints and muscles to tighten. So, when you wake in the AM, your body needs to move, if you didn’t move would become “stuck” . I have the reading issues as well, haven’t read a book in almost 4 years. All for now. Deb

………I have been pretty lucky as far as docs go. Since they don’t know much about my disease they take my word for pretty much most of the time. My new issues are my thyroid. I now have hypothryoidism. Never had any issues ever before in my life. My memory sucks as well. I have issues with concentration and my spelling. I could spell anything before, now I have to think thru a word, and sometimes I still get it wrong. I am very spastic, my movements are almost robot like. They have gotten better in some ways, and worse in some ways………

You can read more about spasticity through the blog post I made that included the information that Deb provided.

In regards to the emotional issues related to CPM/EPM, which I touched upon in my previous posts:

….. I know exactly what you are talking about. I still struggle with these things and my cpm/epm happened 3 1/2 years ago. And your right, I never feel truly happy. I can feel good about things that happen to other people. I have lost all of my family (mom, dad, brother, sister) because I just tell it like it is. Things I kept bottled up for 30 years just came flying out of my mouth, I had no control. It was like I was another person. Most of my husbands family has walked away too. They just can’t handle my brutile honesty. Things just blurt right out. I have no control. Before I know what I am saying people are standing there with their mouthes hanging open, just stairing at me. Whatever I am thinking just fly’s out of my mouth! I am almost always so close to tears all it takes is one weird look from someone, anyone and I am crying. In fact yesterday, I told my husband I think I need to find someone to talk to. Someone who justs listens and has no judgement. Since this happened I have felt useless. I have tried every kind of “hobby” you can imagine. Most I can’t do because of my hands, and the rest I just don’t have the patience for. I have been reading your blog on a regular basis, and I think it;s great!……..

Deb has also left several comments on the importance of using sea salt. There is a growing recognition on how sea salt is the better type of salt to use, but I haven’t researched it myself, so I don’t know where the difference is.

…….Also, I have seizures when my sodium gets down to 128. That is the “magic number”. Since my incident, my sodium has been pretty well controlled. I read an article that if you eat sea salt on everything it won’t raise your blood pressure, but also give you what you need. I eat it on everything!!! ……

…….I have been writing to Dr. OZ for 3 years. Also Dr nancy from the Today show. But they don’t want this info out. It would ruin their “salt is bad” campain. They are right, table salt is bad, but sea salt couldn’t be any better for you………..

I hope to post more regarding how CPM/EPM has impacted others, so please feel free to leave me comments, etc if you would like to participate. I really believe this is the only way we”ll ever be able to express our stories in their fullest. Medical journals do not research symptoms or experiences that we suffer from long term. There’s just not enough information regarding our experiences, so we will have to document them ourselves.

THANKS, DEB!!! Hopefully, you will be the first of many 😉

Spasticity

This post is brought to you by my friend Deb. She has CPM/EPM too.  She’s had it for four years, and her story is one of determination and strength. She is truly amazing. I am going to start listing her story under the “Your Hyponatremia/CPM story” section, but this information on spasticity was gathered by her.

Thank You, Deb, for your help!! 🙂

Submitted on 2012/06/11 at 2:11 pm

Here is some info on spasticity and how it effects your body;
Spasticity is a muscle control disorder that is characterized by tight or stiff muscles and an inability to control those muscles. In addition, reflexes may persist for too long and may be too strong (hyperactive reflexes). For example, an infant with a hyperactive grasp reflex may keep his or her hand in a tight fist.

What Causes Spasticity?

Spasticity is caused by an imbalance of signals from the central nervous system (brain and spinal cord) to the muscles. This imbalance is often found in people with cerebral palsy, traumatic brain injury, stroke, multiple sclerosis, and spinal cord injury.

What Are the Symptoms of Spasticity?
Increased muscle tone
Overactive reflexes
Involuntary movements, which may include spasms (brisk and/or sustained involuntary muscle contraction) and clonus (series of fast involuntary contractions)
Pain
Decreased functional abilities and delayed motor development
Difficulty with care and hygiene
Abnormal posture
Contractures (permanent contraction of the muscle and tendon due to severe persistent stiffness and spasms)
Bone and joint deformities

How Is Spasticity Diagnosed?

Your doctor will evaluate your medical history in order to diagnose spasticity. He or she will look at what medications you have taken and whether you have a history of neurological or muscular disorders in your family.

Several tests can help confirm the diagnosis. These tests evaluate your arm and leg movements, muscular activity, passive and active range of motion, and ability to perform self-care activities.

How Is Spasticity Treated?

Treatment for spasticity may include medications like Lioresal, Zanaflex, Dantrium, Valium, or Klonopin. Occupational and physical therapy programs, involving muscle stretching and range of motion exercises, and sometimes the use of braces, may help prevent tendon shortening. Rehabilitation also may help to reduce or stabilize the severity of symptoms and to improve functional performance. Local injections of phenol or botulinum toxin may be used to relax specific muscles. Surgery may be recommended for tendon release, to cut the nerve-muscle pathway, or to implant a baclofen pump (intrathecal baclofen therapy).

Learn more about baclofen pump therapy.

How Painful Is Spasticity?

The pain associated with spasticity can be as mild as a feeling of tight muscles, or it can be severe enough to produce painful spasms of the extremities, usually the legs. Spasticity also can cause low back pain and result in feelings of pain or tightness in and around joints.

What Is the Outlook for People With Spasticity?

The outlook varies per person. An individual’s outlook depends on the severity of his or her spasticity and any disorder associated with the spasticity

I am including a few additional videos of spasticity. Please understand that these are demonstrations of extreme spasticity, and there can be ranges from slight to extreme. Also, I am including links to articles that I think are interesting. I live in Ohio where medical uses of marijuana are not allowed, but considering the drugs that I’ve been on in the past year to try to treat my pain, cramping, etc. If it was available legally,  I think I would try it.

The following video shows extreme spasticity:

http://www.youtube.com/watch?feature=fvwp&v=wfYNgYgEUoQ&NR=1

The following video shows a person who is improving from spasticity after therapy and baclofen pump:

http://www.youtube.com/watch?v=V2_3lXMKT7Q

Explanation of spasticity due to central nervous system:

http://www.youtube.com/watch?v=lEtkIIoo-3c&feature=related

Pity Party:

I’m almost at the one year point in recovery. It’s been a long year.

Part of me believes that I should be celebrating everything that I’ve accomplished and lived through in the past year. I probably shouldn’t be here, but part of me hates this “new” me. I am not the same person I was a year ago, and it’s so emotionally and physically distressing.

Frankly, I want to sit down and cry.

I’m sure my cognitive therapist, Angela, would tell me that’s depression, but I think it’s more human nature.

I’ve LOST something, and that something is HUGE. I’ve lost the direction of where my life was going, and I haven’t been able to figure out where this “new” life is taking me.

I’m not going to try to deny that my life wasn’t fantastic before my brain injury. I was sick then, and my life was incredibly hard, but I was able to live with those health issues. I was able to take baby steps towards my goals in life.

After I was told that I had the pituitary tumor and it could be removed, I had a solid belief that my life and health would get better. I wouldn’t be able to regain my 20’s, but I could LIVE through my 30’s.  I could manage the illnesses, and I wouldn’t get worse from that point.

Living through my life with my prior health issues was like climbing Mount Everest. Living through my life after the brain injury is like climbing Mount Everest in roller skates.

It really feels fruitless, and in this current state of mind, I would have to agree with Angela, I am depressed….SUPER depressed.

You might be wondering, why in God‘s name are you depressed right now?? You’ve made it soooo far. You aren’t in a wheelchair. You are able to do things in your life that some people are never able to do: walk, talk, eat.

All of those things are true. On one hand, I do feel incredibly blessed, but on the other hand, I feel horribly “picked” on. Why does my burden seem so much heavier than others?

I wonder if Christopher Reeves felt the same way, or Michael J. Fox? I mean, they were both in the prime of their lives when they developed incurable, life long issues, but unlike me, they turned their health catastrophes into platforms to advance medicine for spinal cord injuries and Parkinson’s disease.

Do I dare compare my life to theirs?

I don’t know enough about either person to know if they lived through anything close to what I have, but where I’m floundering and they succeeded: they turned their lemons into lemonade.

Why can’t I?

I know several people now that have CPM/EPM. I know that NFL players are killing themselves over their brain injuries.

If my goal in life was to help other people through becoming a doctor, then why I haven’t I been able to shift gears and find purpose in making hyponatremia and CPM/EPM household names? Help those with CPM/EPM and other forms of brain injuries?

I’ve spent over a month wallowing in pity, feeling more and more distressed over how my life has changed, and I would be lying if I said by the end of this post that I will spontaneously snap out of my depression and tomorrow everything will be better. I only hope that by tomorrow, I can start to develop new strategies and find help for myself that I can still help others.

All parties have to come to an end at some point, even pity parties.

 

Having my Cake:

The past few days, I’ve had a hard time understanding things.

I don’t know if I’ve explained this issue previously, but I’ll take some time to revisit it.

When I first developed EPM, one of the biggest signals to me that there was something majorly wrong was that I wasn’t able to form words.. I wasn’t able to make sense or explain things, and I was also having a very hard time understanding what other people were saying to me. It wasn’t that I couldn’t hear them. I could, but what they were saying wasn’t registering.

In the past 10 months, that has improved, but I still have periods where I have great difficulty understanding things. It just doesn’t register.

These issues tend to happen when I’m under greater stress or really tired. Fatigue and stress don’t cause them; they just get worse.

It’s a catch 22 because when I’m really stressed, well I really want to post what’s going on.

I guess this means, please forgive any rambling or if this doesn’t really make a lot of sense.

First, I want to clarify from my previous post for those who really don’t know me: I don’t drink. I for whatever crazy reason love  to make comments about drinking.  Maybe I’m subconsciously wanting to become an alcoholic, but I don’t have the ability to do it.

Sorry, I shouldn’t make light of being an alcoholic. I know way too many of them, and it’s a hard disease to live with.

That said, I make references to drinking, but I VERY rarely ever drink. I get sick when I drink, and so only drink on very rare occasions and never more than one or two drinks at a time.

It suddenly dawned on me today that people might actually read my blogs and think that I’m really an alcoholic or “drowning” my sorrows in alcohol, and I wanted to clarify. I drank a beer, and literally shed a few tears.

I did not spend the night crying myself to sleep nor did I drink myself into a drunken stupor.

Actually, I drank a beer, cried a few tears, AND ate about 5 tablespoons of Ben and Jerry’s…can’t remember the name of it, but it had cookies in it…chocolate chip cookies. And it was pretty damn good ice cream.

Really folks, I don’t know what’s more depressing the fact that I literally called my last post “drowning my sorrows” or the fact that I had any sorrows to drown.

Moving on, I have no idea what the cake reference was in regards to. I had this post planned in my head around 5pm, and now I can’t remember what it was about.

I wanted to clarify the alcohol references. I’m hoping as I type what I think, I’ll remember what it was I wanted to say about cake.

OH. Bingo.

It’s come to my attention that my memory sucks. Ha. How ironic?! I was going to post about how bad my memory is and I couldn’t remember it…HA. You GOTTA love that. HA! I am literally laughing out loud. 🙂

Hopefully, you are too because if you have CPM/EPM there are very few things that you can really laugh about.

Ok, so settle down because this is the meat of my post:

My memory sucks. I know it sucks way more than most other people know it.

I KNOW my memory sucks, but that doesn’t mean that I don’t remember anything at all. Right?

Previous to my injury I could recall everything. There were very few things that I would need to write down. I could recall great details in everything, everything.

Now, I know that’s not the case. Just ask CVS who has called me for over 3 weeks, 3 times a day to pick up my prescription medications.  They were literally calling me three times a day.

I made it my intention to pick up the prescriptions every day, but I forgot, everyday. There were days that I literally DROVE past the place not once by several times, and I still forgot to pick up the prescriptions.

I started having extreme anxiety over getting the prescriptions, and every night I would sit down on my couch or lay down in my bed and think: SHIT, I forgot those FREAKING prescriptions AGAIN. I’ll have to do it tomorrow.

And then I would forget again tomorrow.

Guess what? I finally picked up the prescriptions. Yep, yesterday. Guess what? The reason I was getting three calls a day was because I had three prescriptions to pick up. Guess what? I could not remember dropping them off. I had NO recollection of dropping them off. I thought I was going to pick up my thyroid medication because I’m almost out of them, and I thought, “CVS is calling me because I called in my thyroid prescription a few weeks ago because I knew I would forget calling it in and I wanted to make sure I had them before I run out”.

Guess what? It wasn’t my thyroid medication.

FREAK. The cycle begins again!

This is just the TIP of the iceberg regarding how my memory has been effected by EPM.

I know I don’t remember things, BUT I also do not want to admit that I don’t remember things!!

So how does this insanity work?

I want my cake and I want to eat it too!

I want people to understand that I have memory issues, but I don’t want to admit that I “forgot” something when I do. Guess how well that is working?

Folks, I really believe that I remember things better than what other people account that I do, but I also realize that have limitations, but I do not want to account for what other people tell me that my limitations are.

And so begins the paranoia and my frustration and my anger and all the crap that you can associate with slowly losing your mind.

My pride and mind is telling me that I remember all of the times that I forget. I think, I may not remember when I need to, but I do remember at some point, and that is good enough.

But then, I was in my car today driving to the health food store, and I couldn’t remember what the two things that I needed to remember were. It wasn’t the things that I was going to buy from the health food store. I really felt I would remember those things, but I needed to do two things today, and I still have no idea what those two things are. Or if there are actually only two things that I really need to remember.

Of course, I got to the health food store and I didn’t remember all of the things I actually went there to buy because I thought, there aren’t that many things, so I won’t forget any of them.  I don’t need to make a list because I can manage just picking up a few things at the store. (See, I even try to delude myself into thinking that my memory issues aren’t that bad.)

So here’s the craziness. I KNOW I HAVE MEMORY ISSUES, I KNOW IT, but I DON’T WANT TO BELIEVE WHEN OTHER PEOPLE TELL ME THAT I’M NOT REMEMBERING CORRECTLY.

I’m NOT WRONG. THEY ARE. And to make things truly crazy, THEY KNOW I HAVE MEMORY ISSUES AND SO THEY ARE LYING TO ME AND ARE TRYING TO TAKE ADVANTAGE OF THOSE MEMORY ISSUES.

Folks, this is how it is. This is how insanity works.

I do not know when people are taking advantage of my brain damage, when I’m wrong, when I’m right, when someone else is lying to me.

Unless, I carry a voice recorder around everywhere I go, I do not have any proof as to whether or not someone said this or didn’t say that.

I really believe people are taking advantage of my memory disability, but how do I know? What if it is just me? What if I’m not remembering as much as I think I remember?

I have Alzheimer’s, dementia, and paranoia all wrapped into one neat little package called EPM. OR people are exploiting my weakness and disability.

TRY FIGURING THIS ONE OUT FOLKS!! Is it ME or THEM? And how do you tell?

This doesn’t even touch the fact that I am LOSING memories. I’m losing precious events in my life that I CAN NOT remember. I can not remember if I took a close friend out for her birthday lunch. I really can’t remember it, and if I can’t remember that then how many other MUNDANE, unimportant things am I forgetting?

I leave you that little gem to think about because if you don’t have CPM/EPM, but a member of your family or friend does, consider what type of insanity they are facing every day before you get angry when they ask you for the twelfth time today, what’s for dinner?

Just think, almost everyone who is over the ago of 60 is experiencing some form of memory loss or dementia, YOU could be that person one day, and how will you feel when you start to lose your mind?

(To my CPM/EPM friends: I just want to let you know, there is hope with these issues. I’m not saying they are going away, but I’m learning skills to deal with them through, my absolutely amazing cognitive therapist, Angela C. God Bless, her! I think she’s going to buy me a life time supply of post it notes 🙂 Love to Angela 🙂   )

Late onset symptoms:

It’s a two-for tonight 🙂

But, this post will be extremely short! I will try to expand on it as I find out more.

I think I mentioned this in previous posts, but I’ve been told by so many medical professionals that once the CPM/EPM has occurred no further damage will happen, and there won’t be any progression in symptoms.

This information was contradicted by my former mentor, Jeffrey Amitin. He had CPM for about 10 years before he died, and he explained that over the years some things got better, but other symptoms developed later. He was absolutely certain these symptoms were caused by CPM/EPM.

I’ve had others tell me that they’ve experienced the same thing, progression of symptoms. Usually these are issues with movements, but they also described problems with loss of consciousness, etc.

I have also experienced delayed onset of symptoms with cramping, tremors, jerks, spasms, etc.

Again, I was told that these issues could not possibly be related to CPM/EPM because they believe once the injury occurs, there is no further damage.

I have found subsequent articles that disagree with this, and I believe I’ve published them previously in my blog. Well, actually, I published something to that effect tonight about a research article that showed a person developed new symptoms 6 months after the injury.

So, I just found another publication that noted a person who developed significant symptoms 10 MONTHS after the injury!!! Further, the MRI that they did showed a kind of disintegration to the basal ganglia area.

Here is the link:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1074115/pdf/jnnpsyc00004-0119.pdf

Now, I don’t like the link because it does not have all of the article, and I will have to research it further to obtain where it comes from, etc, but I wanted to get this information posted before I “lost” it.

Thanks for reading, and I hope this is a step in the right direction for bringing more awareness about damage that occurs from CPM/EPM after the initial injury heals.

 

What’s wrong with me: psychological impact of CPM/EPM:

A few days ago I posted regarding how CPM/EPM has impacted my emotional abilities as well as my cognitive abilities. At that time, I didn’t have a lot of information regarding if this is a typical symptom of CPM/EPM.

Now, I have to stress what I’m sure I’ve mentioned previously; CPM/EPM is RARE. Hyponatremia is not rare, but developing CPM/EPM after it does not happen very often.

It is because it is so rare, there is not very much information, especially detailed information or studies that diagnose the symptoms. So, if  you approach a doctor to get answers, you might very well be given a blank stare. Let’s face it, if we had heart disease or cancer, we would get more information as to what to expect, but CPM isn’t widely seen by the medical profession, and even more importantly there aren’t long term studies or follow up of these patients. You’ll also find a lot of discrepancy in the research articles that are written.

I’ve been to several doctors who have never seen a patient with it.

What does this mean for us?

Don’t set high expectations for doctors who treat you, and as I’ve said before with CPM/EPM, ANYTHING GOES. NO one can tell you with absolution what is happening to you or things that have changed after you developed CPM/EPM isn’t normal or typical, because they DON’T KNOW. They really don’t.

I hope that over time, more research will be done for us who suffer from it, but in the mean time, I hope you find that my blog provides the most detailed information on what to expect.

SO, here’s what I found:

There is a link to emotional issues after CPM/EPM. There’s also a very solid link to cognitive issues. I’m also still trying to find links to the impulsiveness.

The following two links provide brief descriptions in their abstracts about having behavioral changes as well as cognitive changes. Now, here’s the thing; these articles require you to pay for access. I am citing their links, but I will only be able to post them after I gain access to them when I go to my local university, which is what I recommend if you don’t want to pay for them. Simply write down the name of the article, the publication date, etc and go to your local or major university library to access them, usually for free.

http://www.ncbi.nlm.nih.gov/pubmed/10514953

The following link provides information on the cognitive deficits a person experienced after developing CPM/EPM (but again to access full article requires payment):

http://www.tandfonline.com/doi/abs/10.1080/13554799808410619#preview

The following research article gives a fantastic description of how the damage occurs, but I will post that under the information regarding hyponatremia and the CPM section that describes how the damage occurs. The following quotes, I’m including gives an example of why I believe articles are pretty vague, but does give a more detailed account of the cognitive symptoms that we may experience:

A more recent study examined 12 individuals with CPEPM related to a variety of medical causes. In this more diverse population, four patients died in the acute  phase, and two were lost to follow-up. The remaining six were reported to have “good motor and cerebellar recovery.” However, all five of the patients who received neuropsychological testing had evidence of subcortical/frontal dysfunction, and most of these (4/5) were unable to return to work.

The next quote also describes another study that was researched:

Almost half (12/25) died either during the acute phase (2) or after hospital discharge (10). One was lost to follow-up. At final follow-up (mean 2.2 years; median: 1 year; range: 0 – 8 years), 29% (7/24) were normal; 17% (4/24) had mild cognitive or extrapyramidal deficits; and 54% (13/24) had a poor outcome (died or were dependent).

To clarify the above study: 2 people died immediately, 10 died after hospital discharge (but it doesn’t say from what); one died but not sure from what; 7 were “normal”, but it doesn’t clarify what that means; and 4 had deficits. Now, if you do the math these numbers don’t add up to 25…so what does that mean? There must be a mistake or error somewhere, and I think that helps to emphasize my point. The research articles on CPM/EPM are vague.

The next quote provides information from this research article on some of the cognitive impairments experienced:

A patient with only EPM (lesions in
the basal ganglia) had severely impaired attention, verbal and visual memory, visuospatial function, frontal
executive function, recognition memory, free recall
memory, and naming, with preservation of other language-related functions.
29
All these deficits are consistent with previous reports in patients with basal ganglia
lesions. In the other case, the patient had CPEPM (lesions in the pons, caudate, lentiform nucleus, thalamus,
and internal capsules).
28
At 1 week, the patient had
prominent deficits in attention and concentration (e.g.,
high distractibility, slow visual scanning), memory (immediate verbal recall and memory for daily events),
visuomotor functioning, and fine motor speed.

The above information really defines what I’ve been experiencing. My lesions were in the basal ganglia, so I have to say it’s pretty accurate in my regards.

The study goes on to explain that there were additional cognitive dysfunctions that occurred after the initial damage occurred and resulted in “pathological crying and laughter at 6 months after symptom onset, all consistent with a brainstem process.”

Doesn’t that sound a bit familiar. I’m not sure exactly what the pathological crying means. I’m guessing they mean it was inappropriate.

THE ABOVE QUOTES COME FROM THIS ARTICLE: http://neuro.psychiatryonline.org/data/Journals/NP/4399/jnp00411000369.pdf

It is very insightful, but I recommend breaking it up into sections because it can become a bit overwhelming.

So this is the information that I have found up to this point, but I’m sure there will be further information to come. There’s so much to go through..dud links…search results that don’t have anything to do with what you want, etc. Consider this post, like all of mine, a work in progress.

I hope it helps, and if you find something, message me with the link so I can add it. I REALLY appreciate your feedback. Truly the only way we can find out what is happening with CPM/EPM is through your feedback of what’s happening to you, so LEAVE comments, and details, etc. You’ll be helping other people!!

UPDATED: 04/20/12….Ok, so folks, so I have been trying to find more references to the psychological impacts of CPM/EPM.  The following link is in reference to a man who developed CPM/EPM after quitting drinking. They performed an MRI that showed lesions in his brain correlating to CPM. His behavior and symptoms progressed, and he began to develop angry outbursts, etc. They performed another MRI that showed demeylination was spreading further in the basal ganglia and the pons.

Two days after the admission, he showed violent behavior, agitation and irritability, getting angry on the slightest provocation without any mental changes or Parkinson symptoms or aggravation of his dysarthria. At first, we considered his symptoms to be alcohol withdrawal psychosis and started antipsychotics to control him, but his symptoms worsened. We performed MRI again 5 days after he developed psychiatric symptoms. The second MRI showed extended lesions in the bilateral basal ganglia and pons, as compared with the previous MRI.

The previous quote and information comes from: http://alcalc.oxfordjournals.org/content/43/6/647.full

This research article states that damage specifically associated with the basal ganglia areas are documented to cause behavioral and cognitive changes:

Abnormality of the basal ganglia is known to cause various cognitive dysfunctions and abnormal behavior via the involvement of the corticostriatothalamic or cortical–subcortical circuit through the basal ganglia (Carlsson,1988), while the role of pontine pathology for cognitive function and personality remains unclear.

UPDATE: 11/14/12

I have found this great research article that sites long term effects of brain injuries. In subsequent posts, I have decided that is safe to draw correlations between all brain injuries, so the following article describes what may happen psychologically after developing a brain injury. I have found that I have experienced a number of these issues, especially with distancing myself emotionally from people. There seems to be an emotional disconnect on a personal level, but I have the ability to cry over anything I experience regarding my brain injury. I don’t have all the answers for what is happening on a psychological level, but the following article does describe a lot:

http://apt.rcpsych.org/content/5/4/250.full.pdf —Psychiatric Sequelae of Acquired Brain Injury-Ken Barrett, APT 1999, 5:250-258

 

I am adding this quote from another research article that I found:

A patient with central pontine myelinolysis (CPM) underwent neurological and mental status examination, as well as neuropsychological testing, during the acute stage of the disease. After correction of the hyponatremia, a gross change in his neuropsychiatric status was observed. The patient underwent extensive neurological, psychiatric, and neuropsychological testing during the acute phase of the disease and at follow-up 4 months later. All major neurological and neuropsychiatric symptoms present at onset were fully reversible. Neuropsychological examination revealed deficits in the domains of attention and concentration, short-term memory and memory consolidation, visual motor and fine motor speeds, and learning ability. Although improved, neuropsychological testing still revealed remarkable deficits at follow-up. We conclude that neuropsychological deficits can accompany CPM, and that these deficits do not necessarily diminish simultaneously with the radiological or clinical neurological findings but may persist for a longer period of time, or even become permanent. In his recovery the patient started to manifest new neurological symptoms consisting of a mild resting tremor of both hands and slow choreoathetotic movements of the trunk and the head, which we considered to be late neurological sequelae of CPM. The significance of CPM in the differential diagnosis of acute behavioral changes after correction of hyponatremia is stressed, even if correction is achieved slowly and carefully.

This really explains the problems that I’ve experienced, and even mentions that you can have late onset symptoms related to CPM/EPM. The above quote comes from http://www.ncbi.nlm.nih.gov/pubmed/10514953

 

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