Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “basal ganglia”

Late onset symptoms:

It’s a two-for tonight 🙂

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

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

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

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

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

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

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

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

Here is the link:

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

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

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

 

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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

 

Tremors:

As I mentioned on my previous “personal” post, there’s a lot of information on tremors, and as I recently found out, it’s important to know the distinctions when you are dealing with CPM/EPM.

The real question is: what are some of the characteristics of a tremor associated with CPM/EPM?

This really isn’t an easy question to answer because it seems that movement issues associated with CPM/EPM vary. Not everyone with CPM/EPM will have an associated tremor, just like not everyone will develop locked in syndrome.

Further, there seems to be the initial injury that occurs with CPM/EPM, but as the brain creates new neuro pathways after the damage, then there can be new movement disorders that develop.

For whatever reason, this late onset of symptoms seems to be more likely to develop in a person who has damage in the basal ganglia. When a demyelination occurs outside of the pontine area of the brain, it is known as EPM. So, there seems to be a connection with areas damaged outside the pons and movement disorders.

In three survivors of central pontine myelinolysis, dystonia (in two patients) and rest tremor (in one) were sequelae. The onset of these movements occurred 3 weeks to 5 months after the initial presentation with central pontine myelinolysis. Magnetic resonance imaging revealed basal ganglia lesions suggestive of extrapontine myelinolysis in all three patients. We propose that the movement disorders seen in our cases are clinical correlates of extrapontine myelinolysis.

http://onlinelibrary.wiley.com/doi/10.1002/mds.870070208/abstract

We report on a woman with delayed-onset of belly dancer’s syndrome 5 months after central pontine and extrapontine myelinolysis (CPM/EPM) and severe hyponatriemia. This case demonstrates that basal ganglia lesions in EPM can be the underlying pathoanatomic substrate for the rarely observed belly dancer’s syndrome. The sequential appearance of extrapyramidal symptoms might reflect an ongoing but ineffective or deficient remyelination process. The presence of CPM/EPM should be considered in patients with involuntary dyskinesias of the abdominal wall.

http://onlinelibrary.wiley.com/doi/10.1002/mds.21394/abstract

In order to understand tremors to the fullest it is important to understand why people have tremors and the different types of tremors.

For instance, Parkinson’s Disease can cause a resting tremor. It usually impacts one side of the body early on in the disease and then as the disease progresses the movement issues become apparent in both sides. This type of movement issue can actually start in just one finger and for only brief periods.

There are also people with Parkinson’s who first notice the tremor in their hands when they are holding something, like a paper to read, as time progresses these tremors can become significant at rest as well as with activity.

As the following doctor states, it is really difficult to diagnose tremors because they can vary. I found the following video really detailed on how to diagnose a tremor, and I believe that University Hospital that made this video has the right approach in trying to diagnose it. I wish this is how my appointment with the neurologist went. I tried to explain that doctor that the severity of my symptoms vary, and he seemed completely dismissive. Anyway, check out this video:

http://www.youtube.com/watch?v=pP8jaxommQY

I have not been able to find a video that shows a Parkinson’s like tremor early in the disease.

The following video shows the various types of tremors. However, the video is very short.

The next video that I am posting also describes a postural tremor typically found in multiple sclerosis. It also describes cerebral tremors.

Now, I want to pause to explain that parkinson’s is a disease that describes how a brain cell has difficulty uptaking dopamine in the brain. In regards to MS, there is damage to the myelin sheeth because of an autoimmune reaction. There are other reasons for tremor as well, such as cerebral tremor. This type of tremor occurs at the end of an intentional movement. You try to touch your nose or press a button, but you can’t because your hand shakes. This tremor is caused by an injury to your cerebrum. There is a dystonic tremor. This tremor is caused when your muscles contract severely and cause your arms or legs to shake.

In regards to CPM/EPM, they are not certain why some people have tremors. There have been studies that show some people have issues with their cells uptaking dopamine like in parkinsons; however other studies showed patients with tremors had normal dopamine uptake. In these cases, the researchers speculated that the tremors were caused by new neuro pathways that develop.

I hope that one day, we will have more research that is done for CPM/EPM. In the mean time, it’s important to rule out all causes for your neurological symptoms, and in order to receive the correct treatment it is important to meet with qualified neurologists.

Please feel free to contact me with any questions or any information regarding your neurological issues. It is important to get input from you so that we can know and understand more about this injury.

UPDATED 04/14/2012–I’m including the following link that describes that there are people who experience resting bilateral tremors of both hands, that aren’t a Parkinson’s tremor. http://www.ghpjournal.com/article/S0163-8343(99)00018-3/abstract

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