Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Trauma and Injuries”

27 Nov 2012

WHY?

I’ve been trying to stay focused on creating posts that are more about central pontine myelinolysis, what to expect, how to compare it to other brain injuries. I’ve been trying to stay away from writing about me.

Frankly, you can only take so much of listening to someone go on and on about horrible things are in their life. It’s hard living through it too, but most people don’t really care, and they don’t want to feel “bummed” about how bad someone else has it, so I’ve tried to refrain from going on and on about my feelings or my struggles with EPM. Tonight, I have to discuss about what’s going on with me.

So, you might be wondering, what’s wrong?

Today, I was told that the “basic” cognitive testing that I had a few weeks ago, showed that I have significant impairment, but that it’s not consistent. Basically, the doctor felt that my symptoms are being created or exasperated by psychological issues.

I have to say that I agree that stress, fatigue, and anxiety the issues I have worse. Isn’t that true for anyone? Even if you don’t have any brain injury, you’re just perfectly normal, doesn’t stress, fatigue, and anxiety make issues worse?

I’ve never been a strong test taker. Never. I was usually one of the last kids to turn in a test. The last college classes I took, I would run out of time, especially in chemistry. I was usually one of only 4 or 5, still taking a test at the end of the exam period, out of more than a 100 or more. I felt this was because of my perfectionism. In reality, I would just tend to over analyze questions. I would get stuck and read over the same question over and over again because I thought that there were multiple ways to interpret the question.

I have found since I’ve had the brain injury, I’ve had more issues with this. It becomes harder for me to shut off the internal dialogue I have with myself over directions, questions, etc. I will tend to confuse directions for one section of the test with other sections. For example, if you ask me to name all the animals that I can think of, my mental gears start spinning: birds. Well, birds aren’t really animals are they? Aren’t they considered more along the species of reptiles? They have a connection to dinosaurs. Do they want specific animals? Like Robin? Robin is a type of bird. I wish I could look up whether a bird is really an animal. Aren’t animals considered types of mammals? There are marsupials. I wish I could look up the answer. I really don’t want to sound stupid by saying birds if birds aren’t really animals. And what if they want specific animals.  Aren’t animals any living organism? There’s different types of Kingdoms. Shit, I’ve studied this stuff, why can’t think of the right answer? Humans are animals. Maybe I should just say humans. Good answer! My answer is humans. How about insects? FRICK!

SO, that’s just an example of how my mind works in the moment of answering ONE freaking stupid question….and they want me to to name as many animals as possible, as quickly as possible! It’s just not that easy any more. I used to be able to shift gears faster, think through things more quickly, and get to an actual correct response, but I don’t have that ability any more. I get caught, stuck.

Another example, they asked me to count the dots in the following pictures one by one, or maybe they actually said individually. I’m not sure exactly how it was worded. The first problem I have is, is staying focused and tracking the dots. The first group was scattered dots everywhere on a page. There must have been 20 or more. They weren’t organized, and when I started counting them I lost track of where I began, and I wanted to give the right answers, so I double counted them. I thought it was the answer that was important, but it was actually the amount of time that it took that they were monitoring. The next pages they started organizing the dots into groups. My first reaction, well that’s a group of five. There’s two groups of five. There’s three groups of three. It’s a total of 19. Wait, they said count them individually. Maybe this is an illusion.  They have those optical illusions where your mind looks at something and doesn’t process it correctly. Did I miss a dot? So, I counted the dots a second time. No, no I think there aren’t any that I’m missing. Are you sure? Yep, I’m sure. Ok. 19 is the answer.

So, if I had known that the answer didn’t matter, then I would have just blurted out numbers. If I realized that it wasn’t a trick question, I would have been able to respond more quickly. If I had just asked for clarification or asked them to start over once, I figured out what I was supposed to do. Frick!

Trust me. I feel stupid over the testing. I don’t know why that part of my mind is broken. I mean, I did have that problem to some extent prior to the injury, but at some point, my reason would take over, and I would just be able to answer the questions. I would be able to shut down that internal dialogue, and just take a test. At the very least, it didn’t interfere as much as it does now.

In other words, I was never quick at taking tests, but now, I’ve become discouragingly slow. It’s just harder for me to process information, directions, to figure out what I need to do and then do it.

 

I am going to say, in my defense, that I had only had four hours of sleep that night. I really wish that they did testing around the times that I’m normally awake. If I don’t fall asleep until 4 or 5 am, and I’m scheduled to take a test at 9am, I’m practically set up for failure, but they don’t start testing in the afternoon. Two pm would have been the best time for me, but doctors do testing around a typical 9am to 5pm schedule, not a 2pm to 10pm schedule.

So, what does all of this have to do with me?

The testing I did reflected poorly on me, and so my integrity has been questioned.

I am so extremely grateful that I know what my issues are, and that my friends and family believe me and know. My cognitive therapists and occupational therapists believe me and see the struggle that I experience, and they believe me.

It really seems that the testing itself is the only thing that doesn’t work in my favor, but I just don’t think that the tests account for the type of mental distractions that I have because of the brain injury. Well, I had these some of these issues before, it’s just so much worse now.

In the end, getting this news just stresses me out even more, but then I begin to regain my composure. I don’t really care what the tests say. I know what’s going on with me, and that’s what matters. I just have to brush off this bad news and regain my focus. Keep on, keeping on.

I know stress, fatigue, and anxiety complicate my problems, but I’ve always been able to work around those issues. They’ve never stopped me from doing what I wanted or needed to do.

They are causing issues now, and I’ve tried everything I can to control those factors, so that I can become more functional, but they aren’t the cause of the deficits that I have, and it has left me exasperated and frustrated.

Let me give you an example of how people can misinterpret a problem. A man is having a drink at a bar.  He’s chatting with his friends, and as he gets up to go home, his friends stop him and ask him if he needs a ride home. They suggest that maybe he call a taxi. He feels insulted because he’s only had one drink. He refuses the taxi. The next night, at the same bar, he sits down to have a drink. After a glass of wine, he gets up to leave and another person suggests that he not drive home. Again, the man scoffs at the suggestion. On the way home, he gets pulled over by a cop. The cop believes that the man is drunk. The man refuses to take sobriety test. He feels angered at the fact that people keep suggesting that he’s drunk. Since he refused to take the sobriety test, the cop takes him to jail to sleep it off. The next morning, they find the man dead in his jail cell. He wasn’t drunk at any time. He had had a stroke.

How do I feel that this story relates to my experiences? It is not uncommon for people to look at someone with a brain injury and because they do not see any physical injury on the outside, they assume that there is an external cause to the problems that you have. You don’t really have memory issues. You’re just stressed. You have trouble with concentration and reading because you’re mind is creating those problems, because you are focused on issues.

It’s so easy to judge someone when you’ve never experienced the same problem. It’s easier to put on a filter and say that these issues are mental when you’ve never lived with them.

I’ve been told by so MANY people that they’ve forgotten to pay bills. It’s normal. I’ve forgotten where I’ve parked. It’s normal. I’ve forgotten to take my medications. It’s normal.

Yesterday, I couldn’t figure out how old I was! I’m 35, and I forgot. I wasn’t sure if I was 33, 34 or 35. I could not figure it out. I forgot my son’s birthday. I forgot the significance of 9/11 (also my son’s birthday).

THIS is NOT normal for me! This was not who I was before the brain injury. I worked full time. I went to school full time. I took care of the bills. I did NOT have these issues. I’ve never ever had to have an 80 year old man have to shuttle around the parking lot trying to find my car because I couldn’t. I could do advanced math in my head without any issue. I could figure out patterns and trends. I could read through law books, Title 21 of the federal code of regulations.  Shakespeare was like a Dr. Seuss book to me. I could spend 6 to 8 hours reading through legal cases. I could spend 10 to 13 hours studying for the MCAT while working 32 hours or more in a week. What I live with now, IS NOT NORMAL FOR ME! I’ve always lived with stress, but it did not cause impairment.

To have some guy read through one to three tests and can tell me that he has my brain injury figured out, TOTALLY pisses me off. The most brilliant scientists in the world do NOT have a great understanding of how the brain works. They don’t!  Were the tests even designed for a person who has a brain injury? Does it take into consideration that the person has an issue with understanding directions, language, or writing.

I had cognitive testing done BEFORE my brain injury, and I would have difficulty completing tasks in an allotted time. I was able to get the puzzles, etc correct, but not within a standard time frame.

I was told by my cognitive therapist today that I was right. A few months ago, I told her that there is a belief that over time a person’s brain can turn to mush after they’ve had a brain injury. In a person who has had CPM/EPM who lives for longer than a few years, when they move the brain at autopsy, it crumbles. It turns to mush.

When I told my cognitive therapist this, she told me that it wouldn’t happen. (She has been working as a cognitive therapist for more than 20 years. She is an expert.) She went to a conference this weekend, and they are finding that these injuries can kill the brain slowly over time, that the brain can calcify after a brain injury. She told me that I was right.

In the end, what can I do? I have to keep moving on, but tonight, I raised my hands up to God and cried. (I don’t cry often because my immune system causes issues after.) I don’t understand, why?! WHY? Why do I have to live through this? I’ve already had a pretty tough life, but to go through this too! Why God? Why do I have to go through this too?

Can’t I just be normal again? God, I would give anything to have my old mind back! I wish I could just put this whole brain injury thing away! I wish I could get back to doing what I wanted to do. I just want to go back to school, get into medical school, work at saving people.

I wish I knew why.  I wish I could just get over it, as if I was getting over a cold. I don’t think they understand how frustrating these things are for me. I don’t think they understand how strong I am, and how hard I’ve worked, and how desperately I want to put all of this behind me, but it isn’t just a mental thing. It’s just not, and I have to learn how to work with the deficits I have and try to make the best of my life and my abilities as they are. I will continue to work with my therapists in trying to get new connections, with my doctors to get on the right medications, and try to become the closest to my old self as I can. I guess that’s all you can do when you’re living with a brain injury.

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Posted in I just have to say this: and tagged , , , ,
14 Nov 2012

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.

 

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