Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Parkinsonism”

Therapy:

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

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

I don’t know.

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

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

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

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

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

Home

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Todd’s story (symptoms):

I am really impressed with how well Todd is doing. He really has made  such a dramatic recovery. It really gives us hope that if you have CPM, you can make great strides. So, Todd developed CPM in December of 2007/Jan of 2008.

Please see his story regarding the progression of his injury.

The following is a series of questions and answer regarding his symptoms:

I think your “addiction” to cycling is fantastic.

I am trying to do everything in moderation.

I hope you are doing well. If you can, if you can give a detailed account of your experiences to date. It seems like you’ve made a great recovery. Do you attribute that to anything? Any certain treatment? Any medications?

Deep down inside of me, I really believe it was God’s way of telling me “You have had enough scotch and Copenhagen”, although I have relapsed once one scotch and twice on beer, never on Copenhagen.  I once asked a X-Camel Straight smoker (may he RIP) after 17 years nicotine free if he ever missed it?  His verbal response was kind but his nonverbal wanted to rip my head off for asking such a stupid question.

The only medication that may have made a difference was the Carb-levadopa.  I was on that until I saw Dr. Bajwa, the local Parkinson’s expert, we weaned me off. (Jan 2008-Sept 2008).  He also diagnosed me with the Parkinsonism.  I have a functional left hand that has issues with a now overextended thumb.  I do not know if it was because of the CPM or the nasty restraints that I had to wear in the hospital.  At the time, I could not communicate, but I was extremely worried I was going to lose function in my hands because of the restraints.

Do you have any ongoing issues with movements? like cramping, spasms, jerks, etc. Do you have any ongoing issues with memory, concentration or learning? How about issues with vision, heart rate, hearing? Do your symptoms remain constant or do they come and go?

Cramping from my spinning.  Early on I had slight issues with memory.  While in the hospital, I always saw a yellow hew.  I have a constant ringing in my ears, which I do not think is CPM related.  I do experience thoratic pain some nights.  My bum left hand also experiences a dull pain and stiffness.  My facial expression is always straining and I have a constant primitive noise that I make and I stutter when excited.

Do you do any therapy or did you do so after being released from the hospital?

I did Occupational, Physical, speech and recreational while at Bethesda.  I continued with speech for an additional 3-6 months going through 3 therapists.  Last summer I spent $ to get a 4 year/40,000 mile tune up with the last and best of the 3 speech therapists.  Everyone tells me my speech is fine, but that is B as in B, S as in S.

Have you met any doctors that have helped with your condition, neurologists/ GP?

I haven’t seen a neurologist since Bajwa, to get off the Carb-Levadopa.  I take the mini aspirin, B-complex, Multi-Vitamin, chondroitin and glucosamine.

Have  you experienced new symptoms or have you had continuous improvements?

I only thing that may be new is the pain in my left hand.  I started doing what I call “old folkies” yoga in 2008.

“Old Folkies” because at 52, I am the youngest there.  Recently I am trying to do “Real” yoga, “real” because I am the oldest there.  Also am trying to do core and muscle classes at last 2 times a week striving to reach 3-4X a week.  I DEFINITELY do feel better exercising (just do not tell my Life Partner).

Have you met any new people with CPM/EPM?

I have personally met M, which was fabulous.  It was like a first date:  seemed like less than a minute in over 2 hours.  I have wanted to go and meet D (about 20 minutes from my Mom) but didn’t pursue that.

Did you have any treatments immediately following the injury? Like, hyperbariatric treatments, plasmaphoresis, anti inflammatory meds?

The only thing I can remember is the Carb-levadopa and Multivitamins.

Conversation continued (Sorry about some repeats, I didn’t remember asking the questions before):

Do you have issues with understanding with verbal directions or written directions compared to what might have happened prior to the injury?

No, I always had and still do have a great sense of direction.

Do you forget stories or movies or articles or recognize faces but forget the plot?

No, if I did, it would be more age related.

Do you have jerks and twitches?

No.

Do you have issues sleeping?

I do have sleeping issues that I am trying to figure out without seeing a Doctor. In a perfect world, I need 6-7 hours of sleep. I use to wake up to my life partner coming to bed—I sleep through that now. I have been going to bed at 10:30 and waking at 4:00. I have finally decided I am going to get up at 4:00 and try not to nap. I have a clean conscious—If tired, I can fall asleep anytime anywhere in an instant.

Do you find yourself easily distracted?

No.

Have you had issues with managing your finances, forgetting to pay bills or paying them more than once?

The only issue that I have had: We took some money out of an IRA to pay for college tuition. Forgot to tell my accountant.

Do you need help doing any daily activities, like grocery shopping?

No. Although everything is more difficult to do: Dressing, tying shoes, cooking.

Have you had irregular heart rates?

No.

Have you had hallucinations?

No.

Have you had any blackout periods?

No.

Have you had any weight gain?

No.

Have you had any issues with visual problems with blurriness?

No.

(Ringing of the ears does happen with CPM/EPM. It’s a form of tinnuitis. I have it in my left ear. It’s not daily. It comes and goes, but it can be rather painful when it does happen).

Mine is not painful.

Have you had issues with smelling?

No.

Fatigue?

No.

Any hormonal changes, like low thyroid?

No.

Issues with making impulsive decisions?

No.

Issues with writing (typing or handwritten) such as cramping in hands, tremors, etc?

I cannot write legibly anymore although only one check has been returned. A bill comes; I immediately make out a check—old school.

Any issues with swallowing?

No. more so with chewing.

Any issues with understanding what someone is saying to you?

No.

Paranoia?

No.

Depression?

I am a recovering alhocolic.

Sleep Apnea?

No.

Numbness and tingling?

In my left hand—I swear it is because of the hospital restraints.

Balance or coordination issues?

No.

Have you noticed any new symptoms developing or anything that got better but is now getting worse?

No.

It sounds like overall, except for a few minor speech issues and movement issues, you have completely recovered. Do you feel that is a correct summary? Oh, and in regards to directions, I wanted to clarify the question….do you have issues if someone tells you something verbally, like a new procedure at work, would you have difficulty remembering the task or understanding the directions? Oh, and how long overall do you feel it took for you to make the recovery to this point? Was it a matter of weeks, months? Oh, and what area of the brain was impacted? Was it the pontine area or the basal ganglia area? And how long has it been since the injury again?
I have the drooling and grunting issues along with my bum left thumb, also.  I am graciously, graciously, graciously……..thankful for my recovery, but I would not use the term “completely”.  I have no issues following directions.  I think it was the pontine, honey, is that right?  My life partner has to do the timeline?  I have no clue–we did 2 days of Tour de Kota on 2010 and in 2012 we did all six.  I was diagnosed with CPM in December 2007/January 2008?

Thank you, Todd!!! I hope that I can get more information regarding real life experiences with CPM/EPM. I think it might be an important reference for doctors who want to know what a person lives with after they leave the hospital. With Todd’s help, I’ll keep you posted of any changes and improvements that he experiences, but regarding this injury, he has had the best recovery, and he didn’t have any treatments except cognitive and speech therapy.

Please feel free to contact me with any questions or comments, and I will get them to Todd or try to find an answer for you.

 

Update:  Some information provided about how life has changed for Todd since his injury according to his significant other:

Well, to elaborate just a little more, the event happened right  before Christmas of 2007 and the way it was explained to me was that the demyelination of the myelin sheath doesn’t allow the nerve signals to properly transmit, therefore causing the symptoms of speech he has described.  Believe that would be the basal ganglia.   I would say those issues are considerably more difficult to deal with than “minor”.  Sometimes speaking is quite labored and will often cause him to speak very little because of the strain.  You can visually see the strain on his neck muscles when speaking.  The grunting is mostly in the am upon waking before his body becomes accustomed to regular movement.  That is why vigorous exercise demonstrably improves the situation and remains a vital component to his continued recovery and/or keeping him where he is at in the recovery process.
 
I believe that the recovery has been slow and steady ever since the event occurred. 
Thank You for input, Linda. I think that is really good to know. I think an outside, yet personal, description of the experience is very helpful.

Mutism after Brain Injury and Central Pontine Myelinolysis:

I am writing this post for my friend Michael.

Michael developed central pontine myelinolysis a few years ago. In the course of the past 18 months, he has seen a decline in his abilities. He has had ongoing issues with memory, attention, stuttering, movement issues (shakes, tremors, jerks, and spasms), and now he is having issues with mutism.

So, what is mutism? It’s the inability to speak, talk or make vocal noises. In some cases, this issue may be intermittent.

My friend has this issue. A few years after he suffered from central pontine myelinolysis, he began to have issues with mutism. He will go through periods of hours or days without being able to make any sounds. He is not even able to whistle.

Previous to the mutism, he did have issues with a common symptom to CPM/EPM, which was ataxic in nature, dysarthria (general speech issues, including stuttering, stammering, etc).

I have shared this issue. My dysarthria varies in severity. Actually, some days it is barely noticeable. On other days, it’s difficult to communicate because of the stammering.

There does not seem to be any clear reason for the variations, but I have noticed that stress, fatigue, and even fluctuations in my medications can cause the issue. It does get worse when I have to figure out what I want to say, but if I have something that I’m reading from (reciting words), the problem is less significant. I do not have any scientific evidence as to why this happens but my guess is the way that the brain works at processing information. There must be different neurological pathways for reading out loud versus forming ideas and speaking. There is less thought process in reading words out loud from a page versus forming the words for an idea and speaking it.

I find this idea complex. It makes me pause to consider why it is.

Because of this brain injury, I have issues with getting ideas to mind at all, and at times those ideas seem to evaporate as soon as they form. So, there are periods where I do not have anything in my mind. I am desperately trying to think of something, but my mind is blank. Before I had a brain injury, ideas would just be there. I had a “quick wit”. There was far less thinking required. Sure, I would have to manipulate my ideas, the words the that I wanted to use to make my point, based on the audience, but the thought was there. Now, it takes a significant amount of time to just come up with a thought, to form the sentence, and then be able to communicate it effectively. It’s a rather daunting process when it no longer comes to you naturally.

Anyway, Michael’s issue with mutism developed recently, and is sporadic. So, is his condition unique?

One of the first articles that I found was in regards to children who have developed mutism after having cerebellar surgery. Now, this was interesting because central pontine myelinolysis is an injury that generally impacts the pons. The pons is extremely close to the cerebellum.

Because of the locality of the damage to the pons, I am going to suggest that the white matter of the cerebellum can also be impacted. So according to the following research article, it showed that there were children who would have sporadic mutism after damage to the cerebellum, “Cerebellar mutism syndrome and its relation to cerebellar cognitive and affective function: Review of the literature”. http://www.annalsofian.org/article.asp?issn=0972-2327;year=2010;volume=13;issue=1;spage=23;epage=27;aulast=Yildiz

Recent research studies suggest that neurological and cognitive impairments in CMS (cerebellar mutism syndrome) often persist. A prospective study evaluated the neurological status of patients 1 year post-diagnosis based on the presence and severity of ataxia, language difficulties, and other cognitive deficits. [7] Of the 46 patients who had postoperative CMS initially rated severe, residual deficits were common, including 92% with ataxia, 66% with speech and language dysfunction, and 59% with global intellectual impairment. Of the 52 patients with moderate CMS, 78% had ataxia, 25% had speech and language dysfunction, and 17% had global intellectual impairment. Thus, impairment in these domains was common and was also directly related to the severity of CMS. Riva and Giorgi have shown neuropsychological problems a few weeks after cerebellar tumor resection, and prior to further treatment such as radiotherapy or chemotheraphy. [8] Their results reveal a localization related pattern, with problems of auditory sequential memory and language processing after right-sided cerebellar tumor and deficits in spatial and visual memory after left-sided tumor. Lesions to the vermis led to post-surgical mutism, which evolved into speech and language disorders as well as behavioral disturbances ranging from irritability to those reminiscent of mutism. [8]

Now, there is a belief that these issues with mutism are psychological in nature due to the trauma of the event, like car accident. However, this is definitely not the case with Michael, and there has been additional research showing that children that have a stuttering problem, do have injuries in their brains that have been shown to cause this condition. So, it is my belief that if there is an injury significant enough to cause a coma, that it is more likely that it is not a psychological trauma causing the mutism, but an injury to the brain.

So, if that’s the case, then why does the person experience the mutism intermittently?

In the cases of CPM and EPM, I think it is very possible that the injury can progress. Now, this thought goes against the opinions of most medical doctors. Most medical doctors believe that the injury is static; however, in my opinion, it is not CPM/EPM directly causing the injury, but the immune response to the injury. (I would encourage you to review my beliefs on late onset symptoms of CPM/EPM and brain injuries). Basically, the bodies natural response to injury is repair. In my opinion, it does not matter if this injury occurs in your foot, your heart, or your brain. Your immune system sends up a repair “team” no matter where the injury occurs; however, unlike other areas of the body, the brain does not have any non functioning areas, and as the repairs occur more damage is done to surrounding tissue. It creates a slow and steady deterioration, and as in other major structures of the body, scar tissue forms.

This opinion would also explain why a person who is treated with plasmaphoresis after head trauma (including after CPM/EPM) improves with fewer long lasting effects. Generally, it has been shown in previous studies (previously documented in my blog), that in persons who were treated with auto immune disabling treatments, recovered if not fully, significantly.

I also believe that for those who have awoken from a coma with mutism for months or years after, but eventually regain the ability to speak, it is because the brain has healed or has created new neuro- pathways. The following article describes a girl that suffered from a coma and suffered from mutism for 10 months. Eventually, she regained her ability to speak, but she continued to have issues with speaking, cognitive issues, etc.

The patient initially presened as comatose. A period of mutism subsequent to the coma extended for ten months. Following this protracted period of mutism the child demonstrated rapid and unexpected recovery of functional communication skills, despite the persistence of higher level language deficits.

Read More: http://informahealthcare.com/doi/abs/10.3109/02699059009026154

The following article has information that is about a girl that developed mutism after having an injury to the pons. (Bingo! There does seem to be a correlation and an explanation as to why Michael, who has lesions in his pons, has developed mutism.)

 As she was extubated one week later, she was found to have right hemiplegia and muteness. MRI showed a T2- bright lesion on the tegmentum of the left midbrain down to the upper pons. Right vertebral angiography disclosed an intimal ¯ap with stenosis at the C3 vertebral level presumably caused by a fracture of
the right C3 transverse process later con®rmed in a cervical 3D-CT scan. Her muteness lasted for 10 days, after which she began to utter some comprehensible words in a dysarthric fashion. Her neurological de®cits showed improvement within 3 months of her admission. Transient mutism after brain stem infarction has not been reported previously. We discuss the anatomical bases for this unusual reversible disorder in the light of previous observations and conclude that bilateral damage to the dentatothalamocortical ®bers at the decussation of the superior cerebellar peduncle may have been responsible for her transient mutism.

Read more: http://www.springerlink.com/content/h952wk14rwd65798/

Another case of mutism after brain injury, however this person experienced relief with treatment of diazepam:

A 34-year-old woman with a severe closed-head injury had many impairments including apparent global aphasia. After a diazepam premedication for a motor point block she was heard to speak a few words. A trial of oral diazepam succeeded in restoring speech adequate to make her needs known, which persisted on a maintenance dose of 5 mg t.d.s. The possible diagnoses and reasons for this phenomenon are discussed. We suggest that diazepam may be useful in assessing speech in selected people with severe head injuries.

http://www.ncbi.nlm.nih.gov/pubmed/8877308

The following article is only available fully if you pay for it. However, according to the introduction, a woman developed delayed mutism after she had a brain injury caused by drug related issues:

A 49-year-old woman developed a catatonic mute state a few weeks after methadone overdose. Clinical, radiological and histological findings were consistent with toxic spongiform leukoencephalopathy, which adds a potentially deadly side-effect to a generally considered safe substitution for heroin……..

Mutism

The inability to generate oral-verbal expression, despite normal comprehension of speech. This may be associated with BRAIN DISEASES or MENTAL DISORDERS. Organic mutism may be associated with damage to the FRONTAL LOBE; BRAIN STEM; THALAMUS; and CEREBELLUM. Selective mutism is a psychological condition that usually affects children characterized by continuous refusal to speak in social situations by a child who is able and willing to speak to selected persons. Kussmal aphasia refers to mutism in psychosis. (From Fortschr Neurol Psychiatr 1994; 62(9):337-44)

http://www.bioportfolio.com/resources/pmarticle/38247/Brief-Communication-Delayed-Akinetic-Catatonic-Mutism-Following-Methadone-Overdose.html

The next article describes a girl that had issues with stunts in her brain. Her injury also happened in the cerebellar and tracts in the brain stem. The following has a detailed explanation of the researchers belief why akinetic mutism (AK) occurs:

Actually, in the latter situation, AM seems to be related to lesions that occur along pathways that originate in the mesencephalon ([Fig. 6]) and project widely to dopamine receptors in the spinal cord, brainstem, diencephalon, corpus striatum, and mesiofrontal lobe. The resultant behavioral abnormality causes the patient to remain awake but unable to initiate motor activity in response to sensory stimuli. Pressure transmitted to the diencephalon from the hydrocephalus can cause AM. The underlying mechanism is believed to be damage to the periventricular monoamine projections in the thalamus and hypothalamus caused by the expansion of the third ventricular wall. This is the theoretical basis for use of a dopamine agonist in humans with AM, giving gratifying results.

In posterior fossa surgery, damage of the dentate nuclei is the main factor for AM. Fibers emanate from the damaged dentate nuclei through the superior cerebellar peduncles to the contralateral red nucleus and the thalamus and supplementary motor area connected by the dentatothalamocortical pathway[11] ([Fig. 6]). As already mentioned, the supplementary motor area has proven necessary for the initiation of speech[9]

In contrast to AM secondary to hydrocephalus, in which the injured pathways are dopaminergic and/or monoaminergic, in the cerebellar mutism, the neurotransmitters consist of glutamate and aspartate that are found in cerebellorubral and cerebellothalamic fibers, whereas some GABA-containing cells give rise to cerebellopontine and cerebello-olivary fibers. Some cerebelloreticular projections may also contain GABA.

https://www.thieme-connect.de/ejournals/html/10.1055/s-0032-1313632

Now, I found the following article extremely interesting. It describes brain injuries that occur due to lack of blood flow and/or lack of oxygen. Now, why I found this next article extremely interesting because it documents improvements in symptoms initially, but months to a year or more later, the person’s symptoms progress. This is the same type of progression that has been reported in those with chronic concussions, and the majority of those  that I know with CPM/EPM. I believe that there is a connection that is not clearly understood at this time in regards to how the brain reacts to injury, and it can occur regardless of the injury. (HI stands for hypoxic- ischemic and BI stands for Brain Injury)

Delayed Post-Hypoxic Leukoencephalopathy

In rare cases, early and complete recovery from HI-BI is followed a few days to weeks later by a severe demyelinating syndrome; this syndrome, delayed post-hypoxic leukoencephalopathy, characterized by acute or subacute onset of severe and progressive neuropsychiatric problems such as delirium, psychosis, parkinsonism, and/or akinetic-mutism, and/or quadriparesis, among others. Although this condition is often described as a delayed sequelae of carbon monoxide-induced HI-BI, it has been associated with nearly all causes of HI-BI (Shprecher and Mehta 2010). The neural mechanisms of delayed post-hypoxic demyelination have not been established definitively. However, combinations of toxic exposure (e.g., carbon monoxide, inhaled heroin), genetic (e.g., pseudodeficiency of arylsulfatase A, abnormalities of other genes regulating myelin turnover), and age-associated vascular risk factors have been suggested as possible contributors to this unusual post-hypoxic condition. Regardless of mechanism, this syndrome is characterized neuropathologically by diffuse bihemispheric demyelination that generally spares the cerebellum and brainstem. Neurological and neurobehavioral improvement over the first 3 to 12 month periods following onset of this syndrome is typical, but many survivors experience persistent cognitive impairments (particularly impairments of attention, processing speed, and/or executive function), parkinsonism, and/or corticospinal tract signs. There are case reports describing symptomatic and functional improvement of the cognitive and parkinsonian sequelae of delayed post-hypoxic leukoencephalopathy during treatment with stimulants, amantadine or levodopa. The observation that these agents offer some benefit in this context despite their lack of efficacy for the same sequelae of HI-BI itself may reflect differences in the anatomy of these conditions: in HI-BI there is involvement of both gray and white matter, limiting the target of pharmacotherapies more severely than in delayed post-hypoxic leukoencephalopathy, which involves only white matter.

 

I have to say that this idea of mutism after brain injury is absolutely possible. It seems to be more studied in children who have experienced brain injuries vs adults. There seems to be some professionals who believe that it is a psychological issue and others that believe there is a neurological injury that causes it. I believe that you must rule out the physical injury before you consider the psychological cause. Keep in mind that it was only recently discovered that stuttering has a physical cause. This is because the brain is phenomenally complex, and we do not have the technological advancements nor the physical understanding to map the complexity of the brain. This means that you have to approach the subject with an open mind.

Despite the lack of information and understanding, there does appear to be a physiological link to the pons, the cerebellum, and possibly the basal ganglia and the ability to speak. It is also likely that not all of these injuries progress or heal at the same rate, which means that even after mild brain injuries there is a chance that mutism can develop or resolve.

I would HIGHLY recommend that after a brain injury, even mild brain injury, discuss the use of steroids (anti-inflammatory types of steroids that inhibit the immune system-not testosterone) or possibly plasmaphoresis. There has also been research that shows that hyperbariac oxygen exposure can also speed recovery and provide a better recovery. There seems to be a lot of scientific evidence that shows a person’s immune response is in part if not entirely responsible for late onset symptoms.

There will be more to come on this topic as I locate more information.

 

Related articles

 

02/17/2012

This week I had yet another appointment, and this appointment has stuck with me the rest of this week.

First, I want to apologize for not posting more recently than this. If you have CPM/EPM, you will find that your life seems to be full of the unexpected. You will find that there are days that seem normal and days that you wonder how will you be able to live the rest of your life in this manner.

It’s exhausting. It’s frustrating. It’s unfair.

It seems like everyday is chaotic and for someone who used to be so focused and moderately organized, this is driving me freaking crazy!!!

IT’S STRESSFUL!

SO, now I’m starting yet another category for my blog, but I still have to go back and add to hyponatremia, to CPM/EPM, and to my story!!! However, what I experienced this week needs to be addressed before I forget it, and it has really consumed me, so I feel I have to write about it.

C’est la vie!

This week I traveled 4 hours to meet with a neurologist who is a movement disorder specialist. I also had a MRI and something else….what was it. For real!! Another five minutes gone to trying to figure out what it was that I actually did while I was there. I only had three appointments. Oh, yes, the skin biopsy.

I thought I was going to go to the neurologist to get a TREATMENT for my tremors, jerks, shakes, twitches, spasms, etc. In other words, my neurological problems with movement.

I guess this is where I made my mistake. I had already met with a neurologist who is treating me for EPM, and she was sending me to get treatment for my EPM movement issues. She told me that she was sending me to a movement specialist neurologist for this purpose. I assumed that this was going to be the reason for the appointment: I was going to get medicine for my neurological issues related to EPM.

If I thought that I was going to be examined to determine on whether or not my movement issues were related to EPM, I would have been more prepared. I would have brought materials on EPM.

Here’s the thing: EPM IS RARE. CPM IS RARE. MOST DOCTORS HAVE NEVER TREATED A PATIENT WITH THIS INJURY, and it’s not that they are stupid or trying to be judgmental, they are purely ignorant!

This doctor was the same way.

I had no idea what the true intention for this appointment was, and this set me up for disaster.

This doctor did a complete neurological exam. He was pretty thorough.

After the examination, he told me: Well, you have an essential tremor and it is not related to your EPM. It’s fairly mild, but I can give you medication to treat it. I would also like you to test for Wilson’s disease. You don’t have any of the symptoms for Wilson’s, but it is a cause for tremors in a person who is younger. I don’t think you have it, but we’ll do the test as a precaution.

Before, having EPM, I would have just nodded my head and left. I would have spent the rest of the day biting my lip and waiting to say the things I wanted to say.

I don’t know what would have been better. I really don’t.

I literally started arguing with the doctor. He told me that because my MRI images were normal that the tremors weren’t caused by EPM.

Ok, folks, you know I’ve done research. I’ve spent the past 8 MONTHS researching this injury, and my first question to the doctor was: how many patients have you treated with this? His answer: ONE!!!

I then went on to say: My MRI still shows the injury (and it does). This is what my other neurologist has told me. However, if you were more familiar with EPM/CPM, you would understand that there is no correlation to the findings on an MRI and a person’s symptoms.

The doctor didn’t cotton to my pointing this out to him.

We literally started to ARGUE.

He basically told me that he wasn’t going to have me lecture him on this, but then I explained to him that I wasn’t pulling this information from WebMD. My information comes from credible medical research documents, and that I was preparing to go to medical school.

He warmed up a little bit at that point.

He tried to explain to me that the ONE patient that he’s treated with this disorder had the Parkinson’s like tremor that is associated with EPM/CPM. He told me that he had a video that he took on that patient. This particular person had both significant injury to the pontine region as well as the extra pontine regions AND that this person’s MRI still showed the injury.

He believed that my movement issues have nothing to do with EPM. He thought they were random.

He told me that I did not have Parkinson’s, and I did not have a Parkinson’s tremor.

Okay, so what’s wrong with what he was telling me, and how could I have better handled it? How could have this appointment gone better? What should I have done?

First, I should have been prepared. Really. I’ve been to hundreds of appointments. When you have something rare or not clearly understood, you need to come ready for everything. You need to have any research that you’ve found regarding your disorder. Make copies of your labs, of your reports, of research that you have found.

I had no idea what a Parkinson’s tremor was and how it was different from the tremors that I have. I will make a separate post on tremors and how they differ. Of course, with everything that is medical, there is disagreements on what is and isn’t a Parkinson’s tremor.

Basically, if you have a tremor or movements that impact one side of the body (at least in the beginning stages) that are present when you ARE NOT moving, they suspect Parkinson’s.

The tremor that the movement neurologist suspected is something called essential tremor. This type of tremor is usually found in both sides of the body. It generally becomes worse when you are moving. For instance, if you are trying to get food to your mouth or trying to get a cup to your mouth, but your hands shake so severely that your food falls off your fork or you spill liquids from your cup, they suspect essential tremors.

Now, I had no CLUE what the difference was. I had no idea that there was a difference. All I knew was that this issue became extreme when I developed EPM.

If I was prepared for this appointment, then I would have been able to produce information regarding my tremors. I would have also been able to represent the different types of tremors that are associated with EPM.

I did not know until after the appointment that this doctor really did not know what he was talking about: EPM/ CPM can have both, either, or neither…Parkinson-like or bilateral tremors.

In other words, my “essential” tremors, are probably caused by the EPM.

Furthermore, the doctor told me that there were no reasons to think that these tremors would not be long lasting if they were indeed caused by EPM. He believed that because the MRI images were improving then my symptoms would also improve.

I can not say whether or not this is true. I would have to point out to anyone who states that because your MRI images get better does NOT mean that your symptoms will improve. Further, if your MRI images DO NOT improve, that does NOT mean that you will not improve. The MRI, at this time, WILL NOT show anything more than that you had this injury.

The doctor also tried to state that symptoms will NOT get worse after the injury has happened. THIS IS TOTALLY NOT TRUE. DOCTORS DO NOT KNOW WHAT WILL HAPPEN WITH CPM/EPM!!! They do NOT KNOW.  People do see a progression in their symptoms even AFTER 8 and 9 months.

There has not been enough research in this area to know with any certainty what will happen. I know of 4 individuals with CPM/EPM that had improvements, but after a period of 1 to 2 years, their symptoms worsened. I really believe that this is related to just normal aging.

I would compare it to my cell phone that I dropped in the toilet. (It was an unused toilet at the time). I made the mistake of turning it on as soon as I fished it out. Now, anyone who is familiar with electronics knows this was a mistake. It basically fried it. However, I did not want to go out and buy a new phone. So, I took it apart. I sprayed it down with electronic cleaner. I let completely dry out and put it back together. IT WORKED! 🙂 BUT, there were certain keys that did not work, the pound and star button. I was perfectly fine with that because I didn’t really use those buttons that much any way.

So, I was happy, but several months later, other keys started not working properly. Some numbers would repeat a dozen times when I pushed them once. Sometimes, letters wouldn’t show up.

And this is my point, truly the brain works in a fairly similar way. We don’t understand how it works completely. Medicine is really archaic in this field. However, we know as we age the body breaks down. They don’t work as well. This is true for the brain. So, if you already have an injury in the brain, yes, you are likely to see improvements, but it’s like my cell phone, you just don’t know how long those improvements will last, and you are most likely to see these areas degrade over time as your brain ages.

Getting back to my appointment:

I tried to explain that the delay in new symptoms is believed to be caused NOT BY CPM/EPM INJURY directly, BUT BECAUSE YOUR BRAIN TRIES TO REBUILD CONNECTIONS, and it is believed that these new pathways can cause the new symptoms.

Therefore, people have seen NEW symptoms months and EVEN years after the injury. The doctor I saw agree with this, but he felt that new symptoms would not be seen after 1 or 2 months after injury.

See this article for a description on how this isn’t true:

Journal of Clinical Neuroscience 19 (2012) 179–180

And this one:

Journal of  Neurology (1995) 242:450-454
© Springer-Verlag 1995

Regarding the types of tremors that are experienced in CPM/EPM injuries, most are considered Parkinson’s like, resting tremors; however there are also studies that show that both types of tremors can be present, parkinson’s and tremors that worsen with movements.

Here is information from Wikipedia http://en.wikipedia.org/wiki/Central_pontine_myelinolysis:

 Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis andlocked-in syndrome.[14]

Okay, the following is what I have. I do have a bilateral resting tremor that gets worse with movement:

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. His tremor responded well to L-dopa therapy.

(http://www.ncbi.nlm.nih.gov/pubmed/10833626)

I could go on all day quoting journals regarding tremors and EPM/CPM. Here’s another:

Rigidity was present in all four limbs, with orofacial dystonia and dystonic posture of hands and feet and with tremor in both hands.

http://dmc.academia.edu/MahmudurSiddiqui/Papers/893372/Selective_Extrapontine_Myelinolysis_in_Osmotic_Demyelination_Syndrome_in_a_Case_of_Previously_Undiagnosed_Sheehans_Syndrome_with_Recurrent_Hyponatraemia_-_A_Rare_Association

If I had been better prepared, I would have been able to bring these things to his attention.

More importantly, I showed him two videos of my tremors. He believed these videos demonstrated that I indeed have essential tremors. And I cannot disagree with this statement. I don’t know. I’m not an expert in tremors.

That said, I only recently started recording my tremors, and more importantly, I have spasms and jerks in certain fingers, in my legs, or feet, but these jerks are fleeting. So, I will have three or four twitches in my finger and there’s no way that I can record those particular movements without making a video diary of my every waking moment. I never know when these movements will occur.

This is extremely frustrating because by this point in my appointment, there was no trying to communicate with the doctor. I was too emotionally involved and so was he.

His take away message was: you’re going to be fine. You aren’t going to get worse. You are going to get better. You should try this medication to help with the essential tremor that you have, and I am almost positive that your tremors are not related to EPM. Even if they are, the medicine should help them. You do not have Parkinson’s.

Now, this seemed to be a crux in the conversation that I haven’t hit upon previously. He kept stressing that I did not have Parkinson’s. He stated that he was an expert for Parkinson’s.

I really did not understand why he kept bringing up Parkinson’s disease. I DO NOT HAVE PARKINSON’s. I did not think that I had Parkinson’s. I believe that I have Parkinsonism. Now, I’ve previously discussed Parkinsonism. From the knowledge that I have, it is any tremor that a person has, along with dystonia, and dyskinesia, and possible issues with your voice. I am not an expert on this. I know what I’ve read, and I promise to research this further and try to post on this more when I post specifically on tremors.

What’s wrong with his message:

HE HAS ONE FREAKING PATIENT WHO HAS HAD CPM/EPM. He certainly hasn’t spent the past 8 months researching every possible thing you can find on it.

He made incorrect comparison’s: Parkinson’s and EPM. People with EPM/CPM DO NOT HAVE PARKINSON’s. They have a Parkinson’s like tremor, and that isn’t even true for everyone with EPM/CPM. He did not understand that there IS NO SET STANDARD for CPM/EPM. It’s like saying someone who has colon cancer will have the same symptoms and issues as someone with esophageal cancer. It’s like saying there is only one cause for heart disease.

He was unwilling to say: I DON’T KNOW. I will need to evaluate you further. Please spend time making more videos of your issues and feel free to contact me when your symptoms change or if you have a video of something different. He didn’t even ask me when I took the videos I made.

I tried to explain that my symptoms vary in severity from day to day. Truthfully, they vary from hour to hour. Right now, I barely have any tremor at all. However, an hour ago, I did. I have twitches and spasms even at night when I’m trying to go to sleep, at rest. They make it difficult to fall asleep. I don’t have this problem EVERY night, but probably three or four times a week.

So, what could I have done?

I should have made a journal of these things. I should be keeping a daily record of my symptoms, the times, places, how much caffeine have I consumed, etc. Doctors really like data. They like it when you have detailed information for them to look at.

I really haven’t documented my symptoms and when I have them. I should be keeping more videos. I feel embarrassed to pull out my cell phone or video recorder to make these videos in public places when I’m experiencing these problems. I believe that those localized spasms that I get in my fingers or feet don’t last long, so I shouldn’t bother trying to record them.

I AM MY ONLY ADVOCATE. NO ONE ELSE IS GOING TO DO IT. You really need to take this to heart if you are reading my posts.

No one else is going to go to bat for you, and if you are willing and able, you need to make as many records as you can regarding your situation. It can and will help you out. It might help your doctor more fully understand your situation. More importantly, you can post it here on my blog and help others with CPM/EPM.

I also shouldn’t have bothered correcting this doctor when I didn’t have access to the medical journals or very good videos of my symptoms. Now, this doctor has formerly based his opinion. He isn’t going to bother to do anything else with me. If I ever need to go back to him, I will have to have a huge collection of evidence proving him wrong.

Let me stress, it’s not important to prove him wrong for the sake of being right, but because I will not get help from him unless that happens. I also won’t get the correct medications for the types of neurological issues that I have.

It’s also important to realize that it’s important to realize when you’ve lost a battle. It’s your choice on whether or not you are going to waste your precious time and health on trying to bring this person up to speed on CPM/EPM.

As more and more records become easier to access, hospitals will become able to share information on your medical history. This means that this doctor may be able to pollute the opinions of future doctors that I see, even at different hospitals, in different cities or states.

So, you really need to make a decision on whether or not you are going to spend your time and resources on “educating” a doctor on your condition.

If you choose to, I think it’s really important to “educate” him on the first appointment. First impressions make the biggest impact, and this is most certainly true for your doctors.

In other words, you need to be prepared for EVERYTHING on that first appointment. You have to have research articles on the types of symptoms and issues that you have, especially when those symptoms are rare. You need to have videos and if at all possible, personal testimony from family and friends (hopefully someone can go with you for your appointment that can attest to your issues and their severity). It’s great if you have a journal of your symptoms from each day.

You need to ask your doctors questions like: how many patients have you treated or seen with CPM/EPM? And it’s important for you to make a decision on whether or not you are going to continue to see this person if the appointment does not go well. Be prepared. Don’t be afraid to ask questions.

I’m sorry if this post was a bit repetitive. I believe that when I have something that I feel especially strongly about, I tend to repeat it. I will try to edit in the future for those type of repetitions.

For now, I’m going to retire. and as always, please feel free to write me with any questions or your personal story.

Getting a diagnosis:

Please bear with me tonight, I had my wisdom teeth removed today, so I’m taking pain killers. Let’s just say, I’m a bit off my game.

Most people who are treated for hyponatremia are already in the hospital for a secondary issue, like burns or liver transplants, etc. I believe persons who are being treated for other conditions are at a higher risk for a delay in diagnosis for hyponatremia. This would make it most likely for them to develop chronic hyponatremia (chronic, meaning longer than 48 hours, up to a few weeks). This will put them at higher risk for developing CPM/EPM.

That said, it is harder to diagnose these individuals with CPM/EPM because they are already ill. Most will be experiencing issues with nausea, headaches, vomiting, etc. They may even already be in a coma, so the symptoms will be attributed to other issues.

If you’re already in the hospital with a major disease, injury, or disorder and then develop hyponatremia followed by CPM/EPM, you will probably have significant damage. To be honest, you probably won’t make it.

If you do live through those major health issues, you will be lucky to get a diagnosis of CPM/EPM. Here’s why: in most cases, if you are already in the hospital for something like severe burns, to help manage the pain, the hospital will sometimes put you into a medically induced coma. If you are in a coma, it is difficult for the hospital to know if you are experiencing neurological issues.

When they awaken you from the coma, they might deduce that the issues you are having are due to the induced coma. If you have cancer, they might believe the issues (nausea, headache, balance issues) are due to the cancer especially if you have something like a brain tumor and especially if you are having chemotherapy treatments.

Depending on your doctor’s expertise and the symptoms you present with, you may not get a diagnosis of CPM/EPM right away.

CPM/EPM can appear on a MRI as early as two to three days; however, it may not appear on a MRI for up to two to four weeks. In less severe cases of CPM/EPM, your symptoms can begin to improve within a week after the injury. This makes it even more difficult to detect because doctors are even more likely to attribute the symptoms to the primary reason for hospitalization, so they don’t look for it.

To complicate things further, most individuals will begin to experience a disappearance of the lesions on the MRI as early as 4 to 6 weeks. In most cases, the lesions can completely disappear in 4 to 6 months. Despite the healing of the lesions, symptoms may or may not approve accordingly. In most research papers that I read, most lesions will disappear but a person will have ongoing issues with dystonia, speech issues, cognitive and learning issues, tremors, etc. Generally, the symptoms that remain after the lesions have disappeared are related to motor functions and cognitive functions. There can also be on going issues with behavioral and psychological deficits.

This leads to a misdiagnosis, or you may not ever get a diagnosis.

So, what do you do?

Get your medical records. Look for hyponatremia (keep in mind that CPM/EPM does not always occur with hyponatremia), but it is most common with it.

You can also request a MRI. A really good neurologist and/or radiologist can see something called sequelae. Basically, this is, for lack for better words, scar tissue. It is usually very difficult to see in our current scans. So, if you really believe CPM/EPM is responsible for your issues, you might have to see several neurologists or radiologists.

Some doctors will diagnose you based on symptoms and your clinical history alone.

For arguments sake, let’s say you really don’t have CPM/EPM. If you have symptoms that aren’t typical for the disorders or diseases that you experienced, you should pursue getting answers anyway.

I’ve been a patient for more than 8 years. I’ve been diagnosed with other health issues/ disorders before I was injured from CPM/EPM. From past experience, it is common for doctors to attribute any new symptoms that you may have to the previous diagnosis. Basically, they think that since you have one disease or disorder that you will not be unlucky enough to develop another. They might also attribute these new symptoms to being a psychological issue. They will state that this new issue is due to the stress of having a previous illness.

Follow your gut instinct! Only you know what you are going through. If you keep getting the run around from one doctor, find a new one…BUT whatever you do, do NOT tell this new doctor that he is your second opinion. Trust me, I know. It is hard to find a doctor who will go against what another doctor has diagnosed.

It shouldn’t be that way, but it is. You may be very blessed and have a doctor whom you do trust, if that’s the case, level with them.  If he’s a great doctor, he will look into new possibilities.

In the end, you should find a diagnosis that answers ALL the questions, fits ALL the symptoms. In your situation, look at the symptoms of your initial disorder/disease, and check out CPM/EPM symptoms. You have to a detective. You also have to be your own advocate.

If you’re able, look for information online. We are in a fantastic technological age where information is just a few key strokes away. Take advantage of it, but try not to be consumed by it. Easier said than done, I know.

I was trying to get into med school before I developed CPM/EPM. It happens to the best of us that the more we read about disorders or diseases, you start to believe you have every disorder that you read about.

To keep this from happening, I would recommend with coming up with your list of symptoms and the dates that they began BEFORE you start doing any research. Take your time in coming up with this list. It’s easy to forget little things, and you don’t want to begin adding things after you start researching because you’ll end up in the same position where you start thinking you have every disease imaginable.

Things to look for on the MRI. Previously, I mentioned that T1 and T2 MRI‘s showed high signal intensity; however, only T2 shows high signal intensity, but T1 shows low signal intensity. This means in T2 MR images, the areas of damage are bright, and in T1 the same areas of damage are darker than surrounding areas. This information might come in handy when you get your medical records. If you review your radiology reports, you might find these things defined, and this is what it means.

Sequelae: an abnormal condition that results from a previous injury or disease. If you are reading it on your radiology report, then it means that there was a previous injury that has caused an abnormality on your MRI.

An EEG may or may not show abnormalities. If there are abnormalities, than it is usually present in theta and delta activity. Usually these abnormalities will also improve in the following months.

J Neurol Neurosurg Psychiatry1998;65:119-121 doi:10.1136/jnnp.65.1.1, Parkinsonism and dystonia in central pontine and extrapontine myelinolysis: 

…….bilateral hyperintense areas within the putamen, caput nuclei caudati, and lateral thalamus (figure). Subsequent control images made up to six months after the onset of the condition showed a marked decrease of these signal intensities. An EEG disclosed diffuse slow background activity and bilateral theta and delta activity which improved gradually during the subsequent months.

Next article:J Neurol Neurosurg Psychiatry2011;82:326-331 doi:10.1136/jnnp.2009.201764 Clinical and functional outcome and factors predicting prognosis in osmotic demyelination syndrome (central pontine and/or extrapontine myelinolysis) in 25 patients

The higher incidence of extrapontine lesions in recent series and ours may be due to the availability of better-quality MRI picking up subtle lesions. Also, the extent of involvement in the imaging depends on the interval at which imaging is done after the onset of ODS.2 21 The MRI done early (1–6 days) in six (24%) of our patients failed to show any abnormality. However, in all these patients, a repeat MRI done 1–2 weeks later showed positive findings. Therefore, we concur with the other authors that a repeat MRI after 1–2 weeks in all clinically suspected cases of ODS is very helpful.2 Also, diffusion MRI can pick up early lesions when conventional MRI is still negative.

CT was done in seven cases and was positive in two (28.5%). All had MRI-detectable lesions (n=23). Six required repeat MRI as the initial one did not reveal any lesion. The mean interval between the first and repeat imaging was 10.6 days in these patients (range 9–17 days). There were T1W hypointense and T2W and FLAIR sequence hyperintense lesions involving pons (76%), basal ganglia (76%) and thalamus (20%) (figures 1 and 2). Contrast enhancement was not seen in any of the cases. Diffusion-weighted imaging (n=3) showed a restricted diffusion in two cases. The radiological findings are summarised in table 3.

Figure 1

Okay, so since I’ve gone on a bit. Please trust me when I say, that this information comes up in pretty much every research paper. This is also a few more types of imaging that have been used to detect CPM/EPM that I wasn’t aware of previously. I do not know anything about what this means, so I will have to get back to you when I know for sure what it refers to, but TcTrodat-1 and 1-IBZM spect images show higher correlations with the severity of clinical features in EPM than MRI alone. (Annals of Nuclear Medicine 2009 23, 409-412.

In summary: MRI is the best method to diagnose CPM/EPM. It usually may not show the lesions until 1 to 4 weeks after injury. The CT scan is the worst at detecting damage. The spect images mentioned above might be a better way showing the damage that correlates to symptoms. The MRI signals usually detect the injury for a few months, but then shows improvements that do not necessarily correlate with the severity in symptoms. This is also true for EEG abnormalities. You may have an abnormal EEG, but improvements usually show within months but do not necessarily correlate to the symptoms you experience. Finally, trust your symptoms. If you had issues with hyponatremia while being hospitalized for a different condition, be sure to access your medical records and consult with one or more neurologists or radiologists to try to determine whether or not CPM/EPM is responsible for issues that seem unrelated to your original conditions.

I’m sorry for the length of this post. I hope it doesn’t ramble too much and that you find the information useful.

Many blessings!

 

UPDATE: 04/20/12….I just wanted to leave a little bit more information regarding imaging. I mentioned above the FLAIR imaging, and I wanted to explain exactly what that is.

Fluid-attenuated inversion recovery (FLAIR) Magnetic Resonance images stands for FLAIR MRI. It can be used in a two dimensional form or 3D form.  This type of imaging can produce an image without showing the fluid in the brain. This type of imaging is used to detect lesions in the brain, and is very useful in diagnosing demyelinating lesions. It is supposed to be a great way to determine lesions caused by MS. I do not have a lot of information regarding CPM/EPM lesions, but it is being used in diagnosing it along with standard MRI’s.

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