Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “PubMed”

Research and Links:

Technology is a magnificent thing, when it works. Today, I’m using my cellphone to start this post. It most definitely will need to be edited from my home PC. The reason: my laptop won’t allow me to connect to the internet. Frustratingly, I have no idea why, and I have spent most of last night and this afternoon trying to figure it out. Obviously, I haven’t, and after so much time fruitlessly invested, I’m at the moment restraining myself from stomping, throwing, and crushing it into 300-$1.00 pieces.

I should have realized that spending less on a laptop than a cellphone won’t buy you the best laptop on the market, but I really thought I would at least be able get online and write papers. Lesson learned.

Before I started the laptop rant, I was prepared to describe how long it takes me to write these brief posts. Before developing CPM, I could write approximately 3 full pages in 45 minutes. Now, I’m lucky if I can write 8 paragraphs in 2 to 3 hours. Now, that is frustrating!

Since developing CPM, my ability to communicate what I think clearly is significantly compromised. Some hours are better than others, but that also adds to my complete frustration. In this world,  you can’t call your employer and say, “I’m sorry. I’m not able to think through anything today. I won’t be coming to work. Maybe tomorrow.” Obviously, the world doesn’t work that way. It can’t.

Let me stress that, I don’t believe my intelligence has been impacted but my ability to recall information but the ability to communicate my thoughts have. It’s extremely stressful when you can’t say what you feel. At times, when I am under significant stress, I have been reduced to monotone grunts and sputters.  That’s not an exaggeration. I make absolutely no sense.

Ok, so I’ve gone on several rants and haven’t relayed any facts, and that’s really what I want to focus on right now.

I want to start posting some of the links that you can access some of the information I have. I am attaching links for the Toronto study from PubMedhttp://www.ncbi.nlm.nih.gov/pubmed/20142578.  This study is pretty recent, Feb. of 2010.

At this time, I still haven’t received any word from any of the local hospitals from which I requested their hyponatremia statistics. I’m not really surprised, but I will try again tomorrow.

Regarding sports athletes:


The following link is in regards to a study performed on the 2002 Boston Marathon Runners.  Thirteen percent of 488 participants developed severe hyponatremia. Wow, right?!!


Another marathon study for hyponatermia. This was also a 2002 study done by University of Pittsburgh:


A recent study, June 2011, regarding hyponatremia and antidepressants. I really didn’t know that antidepressants would cause hyponatremia, so this study took me by surprise. I know A LOT of people who take antidepressants. It’s actually the most commonly prescribed class of drugs. This is really scary.


The risk in the Elderly:


I found this article, EXTREMELY interesting. It’s a September 2011 interview with the vice president (a doctor) of a hospital consulting company:


Hyponatremia and it’s impact on children:


Hyponatremia and Alcoholics. I also wanted to let you know, it frequently occurs in drug addicts as well:


I am going to pull important information from the following link. I think it really puts into perspective, how alcohol impacts blood sodium levels:


Alcohol consumption can have pharmacological effects on water and sodium metabolism. The effects of alcohol on sodium and water balance may differ with acute alcohol intake, chronic alcohol intake, or acute withdrawal from chronic alcohol abuse.

As the blood alcohol level rises with acute alcohol intake, a transitory increase in the elimination of “free water” (water without salts) by the kidney occurs (Rubini et al. 1955), resulting from inhibition of the release of antidiuretic hormone (ADH). As the plasma alcohol level decreases, urinary flow is reduced (Nicholson and Taylor 1938). Concomitant stimulation of water intake (Sargent et al. 1978) causes significant water gain. This water retention occurs together with sodium retention (Nicholson and Taylor 1938; Sargent et al. 1978) due to increases in the reabsorption of sodium by the kidney.

Animal studies involving chronic alcohol intake have shown significant retention of water, sodium, potassium, and chloride after the first week of daily alcohol ingestion (Beard and Knott 1968). Urine output does not decrease, but fluid ingestion is stimulated.

During acute withdrawal following chronic alcohol abuse, urinary elimination of sodium, chloride, and water increases (Beard and Knott 1968). The augmented urinary flow eliminates the fluid and electrolytes that were retained in excess during alcohol abuse.

I hope this post emphasizes the fact that at some point nearly EVERYONE will develop hyponatremia. I hope that listing these links, you may realize, I am not over exaggerating anything.

I believe it is absolutely fundamental that everyone is educated on the risk factors and what the proper treatment is. Tomorrow, I promise, I will explain everything I know about how hyponatremia should be treated. I will also provide my best insights on how some treatments may induce CPM, and what I believe would be extremely important considerations to discuss with your doctor if you are being treated for it.


UPDATE: 04/20/12—-I just wanted to include this link. It’s a link for Tufts Medical School. It outlines what happens in hyponatremia. It gives a great explanation for the medical aspects of hyponatremia. I would consider this a really great condensed version of things I’ve written about so far: http://ocw.tufts.edu/data/33/497472.pdf

Hyponatremia: More Facts

Hyponatremia is the most common metabolic disorder. This fact comes from PubMed and other research articles.

What is Hyponatremia? It is blood sodium levels of 135 mEq/L or less. The normal range for blood sodium is 135 to 145 mEq/L.

It sounds pretty innocent in nature. Just consume a little more salt, and you should be fine, right?

It really isn’t that simple. Once your sodium levels drops below 135mEq/L, your brain cells begin to swell with fluid. The swelling of your brain cells causes severe headache, nausea, fatigue, vomiting, confusion, delirium, hallucinations, and coma. Of course, it can also lead to death. One of the other symptoms it causes is cramping. Sodium is an important electrolyte in the regulation of muscle contraction, so when it drops below normal your muscles experience hyper contractility.

So that sounds a little bit more scary, right? No one wants brain swelling.

That’s true, but the really scary thing is how frequently it occurs and who it effects.

One study showed that 38% of hospital admissions were due to hyponatremia. You might not be great with math, but that’s almost half. That figure was the number of people being sent to the hospital due to hyponatremia. An even scarier number, is that 38% of patients who were hospitalized experienced hyponatremia if their hospital stay was longer than ONE day. This study was found on PubMed and was done at St. Michael’s Hospital in Toronto, Canada. The study was performed by the University of Toledo.

In the United States, there are by far, fewer studies being performed for hyponatremia, and the consequences of improper treatment. The main reason, in my opinion, is because the consequences of improper treatment can be significant brain damage, coma, death and/or a permanent paralyzed state known as, locked-in syndrome. This injury is known as CPM/EPM, and it is 100% caused by medical malpractice. (Okay, I have to add an addendum to this. In most cases, CPM/EPM is caused by the error of raising sodium levels too quickly; however, there have been additional studies that suggest that CPM/EPM can be associated with  disorders other than hyponatremia. It is known to happen without hyponatremia in cases of alcoholism, liver transplants, certain lung cancer treatments, leukemia, brain injuries and other transplants. The information regarding these other causes of CPM/EPM are fairly uncommon (except in the case of alcoholics which can be as high as 30% incidence of spontaneous causal).

CPM/EPM is caused when a person’s sodium levels are raised too quickly. This drastic increase causes the previous swollen brain cells to rapidly shrink. The shrinking causes neurons (nerve cells) to be stripped of their myelin.

So, this is the second post that I’ve mentioned myelin, and you may or may not understand the significance of it, so let me explain a little more about it.

Myelin is a fatty white sheath surrounding the axons of nerve cells. It coats the cells. Compare it to an electrical cord. Because my parent’s had an ancient vacuum cleaner, I’m going to use it in this description.

My parent’s Kirby vacuum cleaner was purchased when they were first married. Being the devious and creative children that my brothers and I were, we played extensively with the vacuum cleaner. We would unwind the cord and pretend that it was a rope which we used to cross canyons. We used it as a whip, as a lasso, as a tightrope, a jump rope. The possibilities were endless. Is it any real big surprise then, that this poor cord began to fray and wear. In certain places, the plastic coating surrounding the conducting wires became completely worn away. I actually think my older brother would use the vacuum cord as a chew “toy”. Of course, this happened only when it was unplugged, but you get the idea.

Eventually, the frays in the cord made it difficult (probably even a bit dangerous) to operate. In order to get a current from the electrical outlet to the vacuum motor, the cord would have to be kinked in certain ways. Some times this was effective and the vacuum would work. Other times, the only thing that would happen is you would receive a healthy shock.

Myelin is the in much regards comparable to the sheath that insulates the wires to the vacuum. It allows the current in the wires to travel unmolested from the electrical outlet to the motor. When the cord became damaged, the current could travel to the motor or it could take an alternate path to the hand of the user. Myelin allows the current from the cell body (consider it the electrical outlet) of a neuron to the terminal ends (called axon terminals) rapidly and in the correct direction. There are millions of cells in your brain that don’t have myelin (grey matter). These cells function perfectly fine without this coating. However, the signals that travel these cells move at a considerably slower rate.

If a nerve cell has a myelin sheath, the transmission of signals is more rapid than those without myelin. This might explain why when the myelin sheath is injured, such as in Parkinson’s Disease and CPM/EPM, a person can experience halted, jerky movements.

In closing for today, CPM/EPM is the disorder that is demyelination caused by the rapid swelling and shrinking of brain cells. The rapid swelling occurs because the sodium drops below normal. The rapid shrinking occurs when the blood sodium levels are increased too quickly. The impact this has is hundreds of thousands of short circuits in the wiring of the brain.

I hope this is understandable. Please leave posts with questions, and I will try my best to answer them.


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