Archive for the tag “Central pontine myelinolysis”

03 Jul 2012

Michael’s Story:

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

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

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

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

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

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

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

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

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

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

Thank you Michael!!

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

19 Jun 2012

2 Comments

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

2012 ICD-9-CM 341.8 Other demyelinating diseases of central nervous system

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.

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM/EPM, Demyelinating disease, Diagnosis codes, International Statistical Classification of Diseases and Related Health Problems

19 Jun 2012

Todd’s Story: CPM

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

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

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

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

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

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

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

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

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

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

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

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

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

Hey,

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

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

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

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

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

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

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

Have a great night.

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

21 Apr 2012

A large number of case reports regarding CPM/EPM:

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

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

11/105. immunoglobulins are effective in pontine myelinolysis.

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

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

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

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

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

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

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

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

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

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

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

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

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

18/105. Central pontine myelinolysis.

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

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

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

20/105. Decreased diffusion in central pontine myelinolysis.

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

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

14 Apr 2012

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

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged basal ganglia, Central pontine myelinolysis, cognitive deficits, CPM/EPM, Hyponatremia, neurological disorders, psychological disturbances

03 Feb 2012

My EPM story: the diagnosis:

Up to this point, I have talked about how I developed hyponatremia, how it was treated incorrectly, and how I tried return to the local hospital (the place that treated my hyponatremia) THREE times to get treatment for my developing issues with EPM.

The last trip to my local ER, I asked for a MRI because I was almost positive that I had developed EPM. Instead, they attempted to admit me for observation because of the reaction I had from their doctors, I decided it would be better for me to travel to meet with my ENT and endocrinologist.

After hearing about my issues, they were also determined to get me into to see a neurologist, despite it was the Thursday before the Fourth of July. Trust me, despite going to a HUGE hospital with hundreds of doctors, trying to get an appointment with one of their 50 or more neurologists was a big deal.

Tom and I had no idea what was going to happen next.

I left my local ER around 7pm. I was pumped full of narcotics and was almost dead to the world. I mean, I really did not know what was going on.

I got home, and I think it was at some point around 3 or 4 am, we started our oddessy. We had our three year old with us, and this trip was unexpected. We had no idea how long we would be gone, or what we would need.

I guess we planned for the worse because we didn’t run out of clothing, etc. Granted, I spent my time in a hospital gown.

So, our trip up to the hospital was awful. I had a splitting headache. I didn’t feel well. My daughter was acting like all three year olds. At first, she slept but around 9am, we stopped to get breakfast.

It became absolutely clear there was a problem when I tried to order breakfast for us. Tom had gone to do something, find a table, I don’t know what, so I was left at the counter alone to order.

I knew what we needed, but I was having trouble understanding what the girl was saying. I was extremely frustrated. All I had to do was give the girl the numbers and tell her what drink we needed with each. Tom’s order was easy. Izabel is a picky eater, so I had to make adjustments with her order, and I had a hard time asking if they had pancakes or cereal. I had a hard time explaining that I needed milk with her meal not coffee. The most frustrating thing was when I wanted to change the kind of cheese on my order. I didn’t want Swiss cheese that normally came on the sandwich, I wanted American cheese.

I kept telling the cashier: I don’t want cheese. I want cheese.

Of course, she looked at me like I was retarded because I was.

I tried to explain further: Not cheese. Yellow cheese.

My entire order was like that; I couldn’t express the changes I wanted to make. I had a hard time asking for coffee with Tom’s meal. I had a hard time finding out if they had cereal, and by the time it came to my order, I was left to pointing irrationally at the pictures on the wall. Number 6, no cheese, cheese. I don’t want cheese. I want cheese.

Yeah.

I KNEW what I wanted. I couldn’t say it. AND, these episodes kept skipping. It wasn’t continuous issues with communicating. Talk about feeling like you’re going completely nuts.

Shortly after we left Arby’s, I started experiencing the crippling stomach pains which I no longer was considering as an issue for porphyria but for my adrenal glands.

With all the physical and mental stress I was having, it isn’t difficult to believe that my adrenal glands were becoming stressed. Maybe it’s not my adrenals, maybe it is AIP, maybe it’s both…I really think only God truly knows, but all I did know is that sugar/glucose would stop the pains.

So, Tom and I went off track to find a CVS or other drug store to pick up a bottle of glucose tabs. This delayed our getting to the hospital, but trust me I don’t think I could survive an attack of crippling abdominal pain.

After a shot of liquid glucose and about 1000mg of glucose via tabs, the pain subsided a bit. I was feeling more nausea, but the painful cramps weren’t as bad.

I swear this trip was CRAZY. I think it took four hours longer than it normally does, and I can not explain WHY it took so long. I mean, there was the stop for breakfast. There was the stop for glucose. We did hit road construction at some point, and then there were at least three potty breaks for Izabel.

During the drive, we were also working with an awesome receptionist for the neurology department to try to get an appointment with a neurologist. All of the neurologists were booked or gone already for the 4th of July weekend.

They could only make the appointment for about a WEEK from that date.

At this point, I still had no true clue as to what having EPM or CPM meant. I really didn’t understand that I was in a life threatening situation.

I believe I had read about it, but it didn’t sink in that this was really what was going on with me.

I was relieved when I got to my first appointment with my ENT. I really thought that he must have left packing in my sinuses and that this was going to be the reason I was having such a horrible headache.

I remember sitting in the waiting room, extremely calm. My little girl was striking up a conversation with another little girl. Tom was looking up the newspaper on his laptop, and I was just waiting.

I tell you. I was still experiencing difficulties speaking. Then they did the torturous search of my nasal cavity and sinuses. They spray your throat and nose with a numbing spray, and I was getting extremely ill from the spray. It’s supposed to taste like bananas. It doesn’t. Some people don’t have any issues with it, but other people, like me, the numbness triggers your gag reflex and you because extremely ill.

Then they slowly insert this 1/4 inch diameter, flexible, rubber hose with a scope on the end up your nose.

It doesn’t seem like they should be able to get that much of the hose up your nose (ha, that rhymes), but they did, and I can’t imagine having an alien abduction be more painful or uncomfortable. Just saying.

The ENT reassured me that things looked good. He assured me that there was no packing in my sinuses. He assured me that the surgical site was looking great. However, he was concerned with my neurological issues. He was glad that I was going to see my endocrinologist. He thought I should be hospitalized, but he wanted me to see the endocrinologist first.

So, by this point, I needed a wheelchair to get around. I was truly nauseous, dizzy. I was having issues with my balance. I had the horrible headache.

My endocrinologist is the most awesome doctor in the world, with a close second for my neurosurgeon and an even closer third with my ENT. Truly, I’ve been to hundreds of doctors, or at least a hundred. I’m not sure if that’s an exaggeration. I’ve seen a lot of doctors, so please believe me when I say, these doctors are amazing.

My endocrinologist was disturbed at my neurological issues. She was concerned at how long they had been going on. I told her that I thought I had CPM. I explained why I thought I had CPM. She didn’t arch her eyebrows. She didn’t give me a smirk or a shrug.

She told me that it would be unlikely for me to have CPM because I was 34. She believed that only babies and old people developed CPM. I became concerned that she wasn’t going to do anything.

She left the room to try to get an emergency consult with a neurologist. She checked back with us in about 10 minutes to let us know that the neurology department had not gotten back with her at that point.

She came back five minutes later to tell me that there weren’t any neurology appointments available, and so she was going to admit me. She felt I needed to have a MRI, NOW, not a day from now, not a week from now, NOW.

I was checked into the hospital and in my room in about an hour.

I was seeing the neurology residents in about 15 minutes after that. I was seeing another neurologist about an hour after that.

I was given another IV, pain medications, and because my endocrinologist totally believes me, she also requested the IV glucose to help with whatever it was, adrenal crisis or porphyria. (Even though my endocrinologist ordered it, the neurology department-unbeknownst to me- did not want me to have the glucose treatment, so that wasn’t started. This caused my abdominal pains to become unrelenting.

By 11pm that night, I was being wheeled down for the MRI. Trust me, even though my endocrinologist and ENT believed that I was experiencing a major problem, this belief was not as well received by the neurology department. I got arched eyebrows. I got the smirks.

I was desperate that they find something on the MRI. I KNOW that sounds funny. I KNOW that sounds crazy, but when you’re in that much pain, when you have that significant of a problem, the last thing you want is for them NOT to find anything. Trust me, when you have that many arched eyebrows and funny looks, if they came back with there’s NOTHING on your MRI, the next place you’ll be heading to is the psych ward.

My relief became absolute. My confidence in myself became iron clad, when the neurology resident came rushing into my room.

Resident: You were right. You were right. You have myelinolysis. THEY DID THIS TO YOU. THEY ARE 100% responsible.

I think I was on the verge of tears. I can’t remember exactly what he said after that. This injury was out of his league, and he assured me that the fellow in neurology would be in to see me in a very short while. He stressed that this was a serious issue and that the fellow was actually coming in from home to see me.

I had my answer. I had my reason. I wasn’t crazy. I didn’t have a stroke. I was right. I WAS RIGHT.

I wish that I could say, that’s it. That’s all that happened, but it’s not. The story does continue. Maybe, now, you’ll see why I’ve chosen to write about this later. It’s easy to become distracted and angry about what happened.

It can consume you.

Plus, it’s a hell of a long story. I mean, these are by far the longest posts that I’ve made, and they take the longest to write. It’s really exhausting, but I really feel, you need to know. You deserve to know. You need to learn to trust what you feel and to fight for what you’re going through. You need to understand that even the most prestigious hospitals in the country are fallible. You need to ask questions and push for answers, even when you meet resistance.

I hope this helps you with your struggles or helps to push you forward when you feel like giving up. You aren’t alone.

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

23 Jan 2012

Doctors:

I was finished with all of my pre-med classes and was seated to take the MCAT in June of 2011. That was before being told that I was going to have to have surgery for Cushing’s Disease.

I was actually relieved to find out that I had Cushing’s Disease because suddenly everything made sense. The years of illness made sense.

Doctors try to find an answer that fits everything, but I kept having problems that didn’t fit the diagnosis. It started with endometriosis (and of course irritable bowel and fibromyalgia), but that didn’t make sense. Yes, I had pain with my menses, and I had heavy periods, but endometriosis didn’t really explain weight gain, fatigue, low grade fevers, hair loss, aches and pains, etc. I would also have crippling abdominal pain, nausea, vomiting, and blood in my stools.

I will try not to go into all the details, but over the years, I also developed hypertension. They found high uroporphyrins in my urine and blood, so my doctors believed I had acute intermittent porphyria.

Antiphospholipid syndrome explained the several miscarriage, and my elevations in cardiolipins, etc.

Bottom line, Cushing’s Disease explained everything (elevated uroporphyrins and autoimmune issues), so I was excited. I wouldn’t be cured from the autoimmune issues, but removing the pituitary tumor would take care of the Cushing’s disease, and I would feel better and there would be nothing stopping me from becoming a doctor.

I’m still hopeful that I will get into med school, but I’ve had another set back. After the pituitary surgery, I developed hyponatremia. The hospital corrected my sodium levels too quickly and that led to EPM. That was six months ago.

I’m better than where I was, but I’m a long way from MCAT ready. The MCAT is a thinking test. I not only can’t member what I need to remember, but I can’t think as quickly as I once did.

Because I’ve seen many sides of health care (that of the doctors as well as a patient), I feel conflicted regarding what I’ve been through. Life is not black and white.

I am extremely angry at the doctor’s who treated me, but I also feel an understanding about what’s happened.

I think people expect their doctors to be perfect. They get paid a huge amount of money to know what they are doing. Is it too much to expect that they do?

If you every look at a physician’s desk reference, it’s about 8 inches thick, in a font that’s similar to that used in a Bible, on paper that’s practically see through. It’s been said that about 5000 new diseases are discovered EVERY year.

If that’s the case then why do we feel that a single doctor will know and understand every disease and disorder that we might have?

Is it too much to expect?

That said, hyponatremia is a COMMON metabolic disorder. It is the MOST common metabolic disorder. Over 1.5 million people are treated for hyponatremia each year!

So now I feel caught in the middle. Yes, I do expect doctors to know more than the common person. They get paid to know it. At the same time, how will I feel if I’m on the other side of the clipboard, trying to figure out what this person’s tapestry of symptoms means?

Yes, life is not black or white.

Okay, now let me give you some more important information. Let me direct you to a group of doctors that are supposed to know more than most doctors in regards to CPM/EPM. Keep in mind, as I’ve stated before, there aren’t any “true” experts in the field because CPM/EPM is really rare, but these are doctors that have at least heard of it.

My neurologist, Dr. Noor Pirzada. I was referred to him by Jeffrey Amitin. I had the expectation that Dr. Pirzada had treated several patients with CPM/EPM. However, when I’ve questioned him regarding how many patients he’s treated, he won’t give me a direct answer, but will tell me that it’s very rare. I don’t know what that means exactly, but he’s understanding.

Dr. Noor Pirzada, University of Toledo Medical Center,

3120 Glendale Ave

Ruppert Health Center

Suite 1500 Door F

Toledo Ohio 43614

Phone: 419-383-3760

Fax: 419-383-3364

The following names come from GARD. They may or may not treat patients, but they have at least heard of it.

Dr. Richard Sterns: University of Rochester School of Medicine, Rochester, NY. (He is an expert in the treatment of hyponatremia and knows a lot about CPM/EPM.
Dr. Amyn Rojiani: University of South Florida, Tampa, FL.
Dr. Yeong-Hau Lien: University of Arizona, Tucson, AX

Yeah, I know, that list is really disappointing. If you’ve been treated by an “expert” in CPM/EPM, post it in the comments section.

I will also update it with doctors that I am in the process of contacting. Right now, I have contacted a handful of doctors that have written research papers on CPM/EPM, but I haven’t gotten a lot of information from them as of yet.

Thank you for putting up with my rant on doctors, and I hope this information helps a little bit.

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM/EPM, GARD, Hyponatremia

09 Jan 2012

Treatments: NEW INFORMATION

Ok folks, I’m really hoping to keep this post short and sweet.

My last post had information regarding treatments for CPM/EPM. Guess what, I have found new information suggesting there are treatment options for CPM/EPM.

I was shocked to discover that once your sodium levels have been corrected too quickly, you are not destined to CPM/EPM. You doctor has the ability to PREVENT CPM/EPM AFTER your levels have been corrected too quickly. Research has shown that there is an approximate 5 DAY window in which your doctors can LOWER your sodium levels back to abnormal, approximately 120. If they do this after your levels were raised too quickly, within 5 days, CPM/EPM can be avoided!!!

The above information was discussed as early as 2005 and 2007: http://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/104/6/56.pdf and again in : http://www.ccjm.org/content/74/5/377.full.pdf and again in:

This type of treatment has been extremely successful in preventing CPM/EPM. I DO NOT UNDERSTAND WHY DOCTORS DON’T KNOW THIS or DO NOT PRACTICE THIS. I’m really at a loss over why my doctors, who admitted to me that they raised my levels too quickly, did not have the knowledge to do this. It turns my stomach to think that this might not be COMMON knowledge among doctors. WOW.

Since this might not be common knowledge among doctors, PLEASE take it upon yourself to inform them if you are in this situation. You might be able to prevent your brain damage after all!

That said, I also found additional treatment options! I went to one of the major teaching hospitals in this country for treatment of my CPM/EPM, and they DID NOT offer this! They told me that there were NO TREATMENT OPTIONS. Imagine my shock and dismay at finding research to the contrary. It really makes me sick to my stomach to think not only could this have been COMPLETELY PREVENTED, it could have been TREATED. 😦

That said, these treatments have not been clinically proven to work. There haven’t been any control group studies.

I mean, here’s the thing, CPM/EPM is uncommon. It’s not like heart disease or cancer where people can enroll in studies to test therapies, so your doctor may or may not know about these treatments. If they know about them, they are not going to suggest you forgo the treatment since it hasn’t been studied in a controlled study. They will suggest to do the treatment. If you don’t do the treatment, you have an approximate 67% probability of having some type of neurological deficit for the rest of your life.

The research studies did not report ANY side effects (I’m sure there are), so proceeding with these unstudied/ unproven treatments would be the best thing. Furthermore, all of the case studies that were listed had a 100% recovery when given the treatments.

In other words, there needs to be more research regarding CPM/EPM, but in the mean time, if you are facing permanent neurological issues, try these treatments that have shown effective in treating the brain damage. What do you have to lose???!

Here are the additional treatments that I did not mention previously:

1.) plasmaphoresis

2.) TRH (thyrotropin releasing hormone)

3.) immunoglobulins

4.) methylprednisolone (the cleveland clinic journal also listed dexamethasone, but it did not provide information regarding its effectiveness.)

This information comes from :http://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/104/6/56.pdf

It has also been reported in several additional journals.

There are also natural remedies that have been recommended. I will post more information on possible natural treatments as well.

Please feel free to post any information you have in regards to treatments you might have been given for CPM/EPM.

Thank you for reading!

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged Central pontine myelinolysis, CPM/EPM, Hyponatremia

07 Jan 2012

CPM: Treatments

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

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

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

Okay, so CPM/EPM treatments:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Brain injury support groups offer a great help.

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

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

UPDATE:

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

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

Immunoglobulins are effective in pontine myelinolysis.

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

Neurological Department, Neurological Hospital Rosenhügel, Vienna, Austria.

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

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

03 Jan 2012

CPM/EPM–What to expect:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

So, what does this mean?

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

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

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

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

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

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

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

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

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

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

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

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

I will report it and update my blog accordingly.

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

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

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

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

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

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

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

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

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

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

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

Many blessings!

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

31 Dec 2011

To summarize:

Ok, I know I’ve covered a LOT of information over the past few weeks regarding hyponatremia.

There is so much information and it is very complex that it’s hard to not get confused and lost in reading it, so I’m going to try to summarize what I’ve discussed so far.

There at least five categories of hyponatremia: Hypovalemic, Euvolemic, Hypervolemic, Redistributive, and Pseudohyponatrmia.

The most commonly impacted people:

Infants due to diluted formula

Alcoholics

athletes (especially marathon runners)

Those who have liver cancer, liver damage, chirossis of the liver.

The elderly (usually due to malnutrition and dehydration)

Brain injuries, brain tumors

Transplant patients

Burn patients

Person’s who are receiving chemotherapy

Person’s with kidney disease and those who receive dialysis

Person’s who take certain medications like diuretics and anti depressants.

AID’s patients

Person’s who have pneumonia or flu

Anorexics and bulemics.

I’m sure I’m leaving about a dozen other groups affected, but you get the picture. It’s pretty common. Approximately, 1.5 million people are treated for it each year, and that’s probably a low number because I do not believe it includes persons who develop it while being treated for other conditions and develop hyponatremia as a secondary illness. I’ll try to find more information on that in the future.

Hyponatremia is extremely dangerous. If your blood sodium levels drop very quickly in a 24 to 48 hour period (acute hyponatremia), your brainstem can herniate and/or your brain swells. This can lead to seizures, comas, and of course death.

If you develop chronic hyponatremia, (when your sodium levels drop over a period of 2 days to several weeks) you are less likely to have brain swelling or brainstem herniation, but you become at extremely great risk for developing Central Pontine Myelinolysis or Extrapontine myelinolysis.

The proper treatment is an absolute must. General IV fluids should be avoided if hyponatremia is suspected. Instead, an IV of saline solution ranging from .9% to 3% saline should be used. In some cases, fluid restriction will correct hyponatremia.

A person should have their sodium levels checked a minimum of every 2 to 4 hours.

If they are uncertain of the type of hyponatremia you have, then an MRI should be used to determine if there is cerebral swelling (swelling of the brain) or brainstem swelling. If there’s swelling present on the MRI, then you most likely have an acute form of hyponatremia.

If you have an acute form of hyponatremia, you are at a high risk of dying from immediate brain injury. Because of the risk, it is necessary to raise your blood sodium levels quickly to a safe level. It should be raised 2 to 4 mmol/L in 1 to 2 hours. However, once symptoms improve, the treatment should be halted for at least 24 to 48 hours. No matter what, levels should not be raised more than 15 mmol in 24 hours, in regards to acute hyponatremia.

If a person has chronic hyponatremia, they do not usually display the same severe symptoms. They usually feel sick. They might experience fatigue, nausea, have a severe headache, dizziness, loss of consciousness, delirium, etc. They do not usually have seizures, coma, or death. They are usually more alert compared to a person with acute hyponatremia.

The treatment for someone with chronic hyponatremia is signficantly different from acute hyponatremia because their sodium level MUST be raised slowly. It should be raised no more than .5 to 1 mmol/ L per hour. It should not be raised more than 8 to 10 mmol in a 24 hour period. Some even caution that it should be raised no more than 6 to 8 mmol per 24 hours. If it is raised faster than this, a person can develop Central Pontine Myelinolysis or Extrapontine Myelinolysis.

Expect to be in the ICU for 4 to 5 days at the very least if the treatment is being done correctly.

A person should NOT be given oral prescription medications along with IV saline solutions. The treatment should be fluid restriction if the hyponatremia is not severe or if it is a chronic form. If the fluid restriction does not work (with the chronic form), than a .9% solution should be started. If they have the acute form, then the 3% solution should be used first. Again, if the sodium levels begin to rise to a point where the symptoms begin to subside, then the treatments should be discontinued to see how the body responds.

If a person’s body is not responding to fluid restriction or IV saline solutions, then a person should be given the oral prescription medications. THEY SHOULD NOT BE GIVEN AT THE SAME TIME AS IV SALINE SOLUTIONS. IT SHOULD BE ONE OR THE OTHER–NOT BOTH.

I really think these are the most important aspects to hyponatremia. Please feel free to contact me if you have any questions or want more information over any of the topics I’ve posted so far. If you find out any relevant information regarding hyponatremia that you think I should include, PLEASE contact me or leave a message here. I REALLY appreciate your help.

Thank you for your support!

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

26 Dec 2011

Hyponatremia: More treatment information.

Ok, so I’ve been researching like crazy. I have a friend who has CPM. He was recovering in the hospital from alcoholism. He possibly developed acute hyponatremia, and I have been doing research to find out as much possible about the differences between acute hyponatremia and chronic hyponatremia.

Hyponatremia is really an ugly beast when you try to break it down. It’s complex.

So there are different types of hyponatremia based on how it is induced. There are five different types (classifications) for hyponatremia. (who knew):

1.) Hypovalemic hyponatremia: body water, body sodium and extracellular fluid volume decrease.

2.) Euvolemic hyponatremia: Body water increases but sodium levels remain normal; to put it simply, dilution. There is no edema but extracellular fluid increases slightly.

3.) Hypervolemic hyponatremia: Blood sodium increases, but body water increases more. There is a great increase in extracellular fluid. There is a presence of edema.

4.) Redistributive hyponatremia: This is related to the administration of mannitol, as well as with hyperglycemia. There is no change in body water or blood sodium, but there is a shift from intracellular fluid to extracellular. (Water moves from inside the cell to outside the cell.)

5.) Pseudohyponatremia: The blood sodium and body water are unchanged, but there is an abundance of lipids and proteins in the blood. Two conditions that cause this are hypertriglyceridemia and multiple myeloma.

This information was found from the following website:

http://emedicine.medscape.com/article/767624-overview

I found the above website very informative in drugs that can cause hyponatremia. It also had a lot of important regarding how it should be treated.

For instance, there is chronic hyponatremia in which a person has below normal sodium levels for more than 48 hours. Then, there is acute hyponatremia in which a person has sodium levels lower than normal for less than 24 to 48 hours.

Now the key with acute hyponatremia is the rate at which it decreases over 24 to 48 hours. For instance, a person may be diagnosed with hyponatremia on day 1 with a level of 130, but by day 2 have a level of 118, and by day 3 have a level of 110. Would this be considered chronic or acute? If sodium levels continue to fall over a period of time, a few days to a few weeks, it is considered chronic, despite where it started or how quickly it initially dropped. It is the overall period of time it has continued to drop.

This goes back to one of my earlier posts. It is actually believed that the longer it stays low the safer it is medically for the person. What I mean by that, it is less likely for a person to go into a coma or for a person to have their brain stem herniate due to swelling directly caused by a rapid drop in sodium.

There is a fine line between low and too low and how long it should stay that low. There is a large number of studies that say if you can stabilize the hyponatremic state, it is safer long term for the person. However, at that point, it becomes critical that the person’s sodium levels be raised to normal at an extremely slow rate (.5mmol/hr or less and no more than 8 mmol/24 hours)!!!

If a person develops acute hyponatremia, their sodium levels drop extremely low the first 24 to 48 hours. This is most common in persons who drink an excessive amount of water. This is also common in infants when parents water down their formula.

What do I mean by extremely low? The levels go from 135 to 110 or lower in the first 24 to 48 hours.

In persons who have their sodium levels drop this significantly, in this short of a period, they have an extremely high risk of developing brainstem herniation and/or cerebral swelling, and/or coma. Their functions are extremely impaired very quickly.

In persons who develop chronic hyponatremia, their initial physical symptoms are far less significant than those who develop acute hyponatremia. If a person, is conscious and can talk coherently, chances are they have chronic hyponatremia. If the person is unconscious, having seizures, thinks they’re a monkey, they probably have acute hyponatremia.

The difference of how to treat these patients vary greatly based on which type of hyponatremia they have. The chronic hyponatremic patient must have their sodium levels raised slowly. The acute hyponatremic patient must have their levels raised rapidly, at least initially.

*****The acute hyponatremic patient has a greater risk for developing brainsterm herniation, coma, and cerebral swelling, so they must have their levels raised quickly to control this swelling. As I mentioned previously, raising the sodium levels, decrease the swelling in the brain. That said, the levels can’t be raised too quickly!

It is recommended that sodium levels be increased by 4-6 mmol/L during the first 1 to 2 hours. (http://emedicine.medscape.com/article/767624-treatment#a1126). ONCE SYMPTOMS BEGIN TO IMPROVE THIS THERAPY SHOULD BE SLOWED OR CEASE!!! In other words, once a person has stabilized there should be a reduction to this high dose treatment to prevent CNS abnormalities. It is further recommended that a person should not have their levels increased more than 12 to 15 mmol during that first 24 hours. Once it has reached that point, it should not be increased further for a total of 48 hours.*****

It is extremely difficult for a medical professional to determine which type of hyponatremia you or your loved one might have. You can help them determine this by letting them know if there were any issues the day or so before you were brought to the hospital. Were you feeling sick or experiencing headaches, fatigue or cramps in the 24 to 48 hours before you made it to the hospital?

Most people experience unexplained cramps in their hands or feet as the one of the first symptoms of hyponatremia; however, they don’t realize it, so they delay seeking treatment until the symptoms progress.

IF your doctor is unable to determine what type of hyponatremia you have by your symptoms or time frame alone, then they should perform an MRI or CT scan to check for swelling in the brain or brainstem!!! Please, be aware of this crucial step. If a person shows brainstem or brain swelling, then they should be treated for acute hyponatremia. This type of injury is less common in persons who have the chronic form!

There is so much to this puzzle, and it becomes more complex the more I research. It also leaves questions. For instance, it is known that alcoholics are more likely to develop CPM; however, I have not been able to determine what type of hyponatremia alcoholics develop most often, chronic or acute. If the develop chronic, then that is in accord with the research I have found thus far because those with chronic hyponatremia have the highest risk for developing CPM. If alcoholics develop acute hyponatremia, this would go against research that says those with acute hyponatremia rarely develop CPM.

So, the more I research, the more questions I have.

Please be patient as I learn more and pass the information to you. Please leave any questions or point out any inconsistencies you might find in my posts. No matter what, please continue to pass the information forward. It will be nearly impossible to protect people from this threat without your help.

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia, Vasopressin

23 Dec 2011

Hyponatremia: Other’s personal accounts and blogs

I want to encourage you to post your experience or notify me of blogs that you might find in regards to hyponatremia.

There is not much research regarding hyponatremia, especially when you compare it to other diseases and disorders. There is far fewer studies in regards to CPM/EPM. In order to get a better idea how CPM/EPM impacts people, both short term and long term. Your personal testimony is essential in getting awarness for this cause.

Ironically, I am including the link of a research scientist who was afflicted with CPM after a bought of hyponatremia. She developed hyponatremia after running the Vermont 100.

http://www.wvmtr.org/hyponatremia.htm

Please post them or email them to me, or if you have a problem getting them to post here, let me know. I am truly a blogging novice, so I am learning as I go. If you want to share your story here, I will do everything I can to make that happen.

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

21 Dec 2011

Hyponatremia: more on treatment

***I wanted to emphasize that this post contains a lot of my non professional opinion. I am not completely ignorant regarding human physiology, but I am not a medical doctor or physiology professor. I do not recommend that my opinion be used as a professional opinion, but please feel free to discuss them with your doctor or other medical professional.*****

At times, it’s hard to figure out exactly how to start the next topic. It’s kind of like when you’re about to enter a lake in which you know the water is icy cold. Do you jump in head first? Do you walk in and try to slowly adjust? Do you just change your mind altogether and wait for warmer water?

I don’t think there’s a right answer.

Writing a blog is kind of like that. It’s hard to know how to approach the next topic. I guess with time, it will become easier.

I really wanted to address how important it is once you’ve developed hyponatremia that the correction be made unbelievably slowly.

Every doctor and every nurse that cared for me in the ICU made this abundantly clear. They all had the same consensus, if we raise your sodium levels too quickly, you can die, go into a coma, develop brain damage.

I have an Aunt who is a doctor, and she emphasized the importance that it be raised slowly. It seemed like it was pretty universal that it was going to take a long time, and if they didn’t do it correctly, I could be universally screwed.

So, how is it that everyone knew how important it was, warned against its rapid correction, but it still happened?

For me, it was a series of errors. I hope these posts prevent anyone from going through the same fate.

However, I have read over the course of weeks that there is a division between some on how the treatment should progress.

There are some that believe once your sodium drops, your life is in danger and corrections need to be made to adjust your levels to a safe zone, slowly but as quickly as possible. In other words, they should raise your levels the maximum amount allowed per every 24 hours.

However, others believe that it is safer to let a person stay in a hyponatremic state, as long as the person isn’t dying. Now, that’s a tricky situation because if your sodium levels are below 135, you risk going into a coma and dying. There’s no guarantee.

The professionals that believe your levels should be maintained at the hyponatremic state, argue that the brain cells are already swollen. If you raise the sodium at this point, it is believed that rapid fluctuations in sodium cause the myelin damage in CPM/EPM, so if you keep it at a hyponatremic state for an extended period (maybe a few days), then the brain cells have time to adjust naturally.Fluid flows out of the cells, and it becomes less of an issue with demyelination when the sodium levels are corrected.

That said, there aren’t studies being done to prove or disprove these ideas. It really is kind of like playing Russian roulette, but there’s no one who wants to risk pulling that trigger with the stakes literally being a person’s life. There’s also not a lot of funding going towards animal studies for this disorder.

My idea (which has absolutely no medical validity): put the person into a medically induced coma, lower their body temperature to hypothermia for several days. Then, slowly raise the sodium, and then their body temperature.

Here’s my reasoning: the body does not respond well to rapid fluctuations of any kind. In patients who have experienced brain trauma, the patients have been placed in medically induced comas and their body temperature has been lowered. This has had success in reducing the amount of brain damage a person experiences.

I believe these principles can be applied to brain damage that is caused by fluctuations in sodium. The body’s system all slow in a hypothermic state. This includes the reactions experienced in the brain. If you raise the sodium levels before returning the body to a normal rate, you might be able to prevent the rapid fluctuations in cells.

My ideas are probably improbable, so I would side with the professionals who recommend keeping a person in a state of hyponatremia for several days before attempting to raise their sodium levels to normal.

In order to do this in a more safe manner, I would recommend placing the person in a medically induced coma vs. hoping the person does fall into a coma because of the hyponatremia.

The studies that have shown a person who has a stabilized blood sodium level (their levels aren’t dropping lower, but aren’t rising steadily), is less likely to develop CPM/EPM.

I think this post might raise more questions than answers, but that tends to happen in medicine. I hope you will be able to make an informed decision on how your care for hyponatremia is managed.

(Addendum: This is extremely important, so I will post it again on a separate page of it’s own. It’s actually been reported in several case studies that there has been a huge success in preventing CPM/EPM, AFTER the sodium levels have been raised too QUICKLY, then the sodium levels should be dropped back to the 120 mmol/L level(hyponatremic state) within 5 days of the rapid increase. This has been shown extremely successful in preventing CPM/EPM. However, it means that you or your caregiver need to be aware of the rises in your sodium levels because your doctor might not admit to incorrectly raising the levels).

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia

16 Dec 2011

Hyponatremia: YOU’LL WANT TO READ THIS. Statistics.

I have been trying to locate statistics for hyponatremia for months. I have searched hundreds of websites. I have tried contacting local hospitals. FINALLY, I’ve had a breakthrough, and it’s a HUGE breakthrough.

There is a research tool funded by the government and due to the Freedom of Information Act hospitals must post their annual diagnostic statistics.

I’m a novice at researching facts on this website, so as I am able to locate more information, I will be certain to post it. Without further adieu, here is the golden nugget for hyponatremia.

First, let me explain that hyponatremia is coded as hyponatremia/and or Hyposmolality. The ICD-9-CM code for this is 276.1. This is the medical billing code used by doctors and hospitals to receive payment from insurance companies or medicaid/medicare. Please use the following link to confirm the diagnositc codes:

http://www.icd9data.com/2011/Volume1/240-279/270-279/276/default.htm

To make this a little more accesible, I will simply copy and paste the essential information from the above site:

2011 ICD-9-CM Diagnosis Code 276.1convert to ICD-10-CM

Hyposmolality and/or hyponatremia

abnormally low sodium levels in the blood; salt depletion.
Abnormally low blood sodium level.
Hypernatremia; lower than normal levels of sodium in the circulating blood.

Let me point out that the above information, contains an error. Hypernatremia is not LOWER than normal sodium levels. I believe this is simply an editing error and that the above description should read: Hyponatremia; lower than normal levels of sodium in the circulating blood. I believe this is a logical deduction considering the title of the code is a description of hyposmolality and/or hyponatremia, not hypernatremia. I would also like to reassure you that hyposmolality is another way to describe hyponatremia.

There are further codes that describe other electrolytic disorders, like hyperkalemia (high potassium), etc.

That said, check out the following information from this link:

http://hcupnet.ahrq.gov/HCUPnet.jsp

This link has the motherload for statistics for hyponatremia, and it is astounding!

The following is taken directly from the above link:

HCUPnet provides trend information for the 17 year period: 1993-2009

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
276.1	Hyposmolality	1,035,284	1,114,170	1,100,355	1,011,519	975,253	922,323	773,223	753,530	905,743	923,473	1,005,420	1,105,431	1,239,144	1,265,353	1,362,216	1,602,836	1,735,847

YES, you are reading that right. In most years, more than a MILLION people per year are diagnosed with hyponatremia. WOW! I would also like to point out that the incidence of hyponatremia has been STEADILY increasing since 1999! I think this speaks volumes for why hyponatremia/CPM and EPM should be a household name.

The following are the maximum amount of error that’s possible each year with this diagnosis. What does that mean?

It means that the statistics, for example, in 2009 has a possible range in error of being a maximum of 1,788,305 and a minimum of
1,683,389. Each year, there is a maximum number of errors that can positively or negatively impact the reported data. The following table documents the number of possible errors. Please feel free to post any questions associated with this.

Number of discharges – Standard Errors

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
276.1	Hyposmolality	35,104	36,817	37,056	36,746	36,207	35,803	20,986	19,120	21,021	22,157	23,650	27,058	34,350	34,636	31,387	44,683	52,458

The next description is the how they determined the above chart regarding possible errors.

Weighted national estimates from HCUP Nationwide Inpatient Sample (NIS), Agency for Healthcare Research and Quality (AHRQ), based on data collected by individual States and provided to AHRQ by the States. Statistics based on estimates with a relative standard error (standard error / weighted estimate) greater than 0.30 or with standard error = 0 in the nationwide statistics (NIS, NEDS, and KID) are not reliable. These statistics are suppressed and are designated with an asterisk (*). The estimates of standard errors in HCUPnet were calculated using SUDAAN software. These estimates may differ slightly if other software packages are used to calculate variances.

Bottom Line:

There are an extremely large number of people being hospitalized each year for hyponatremia. This number is on the rise, and it is of the utmost importance to spread the facts about hyponatremia, the proper treatment and what occurs if it is not treated properly (CPM/EPM).

Please continue to read this blog. Forward the information to friends and family. Post links to your FaceBook pages, Twitter, etc. Please, help spread the word and save people’s lives.

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Freedom of information legislation, Hyponatremia, International Statistical Classification of Diseases and Related Health Problems

Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Central pontine myelinolysis”

Michael’s Story:

Todd’s Story: CPM

A large number of case reports regarding CPM/EPM:

11/105. immunoglobulins are effective in pontine myelinolysis.

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

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

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

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

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

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

18/105. Central pontine myelinolysis.

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

20/105. Decreased diffusion in central pontine myelinolysis.

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What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Central pontine myelinolysis”

2012 ICD-10-CM Diagnosis Code G37.2

2010 National statistics – principal diagnosis only

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

11/105. immunoglobulins are effective in pontine myelinolysis.

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

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

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

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

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

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

18/105. Central pontine myelinolysis.

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

20/105. Decreased diffusion in central pontine myelinolysis.

HCUPnet provides trend information for the 17 year period: 1993-2009

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