Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the month “July, 2012”

I can’t do it all:

















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












Ketoacidosis and Central Pontine Myelinolysis:


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now this is where things get tricky, I believe that because the causes behind the development of hyponatremia (real or pseudo) are so complex, this can lead to an inappropriate treatment of it. For instance, if a person has pseudo hyponatremia because of the high glucose levels, it is believed that once the glucose levels are corrected then the sodium levels will correct naturally as well too. This means that the water shift from the blood back to the cells will occur naturally, however, if treatment is administered in the form of saline iv solution, this fluctuation could happen too quickly and cause CPM/EPM.
It’s something to be aware of if you have diabetes or if you have another cause of hyponatremia. In other words, it is important to understand the root cause behind why a person has developed hyponatremia and make a logical and educated basis of correction from that cause or there will be a great risk of correcting the sodium levels too quickly and an increased chance of myelinolysis.
I hope that makes sense.

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




Have a great night!

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












I think I cried for an hour straight.






CPM/EPM- Locked-In Syndrome:

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

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

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

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

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

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

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

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

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

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

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

I found this paragraph interesting:

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

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

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

This is a similar story to Terry’s.


The following video is also heartbreaking:


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


I found this story also inspiring:



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

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

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

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


Michael’s Story:

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

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

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

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

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

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

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

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

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

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

Thank you Michael!!


Rinse, Wash, Repeat:















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