Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Central pontine myelinolysis”

Reversal Of Demyelination in CPM/EPM/ODS

Hello Everyone!

This is it, a new exciting opportunity for possibly reversing the damage caused by Central Pontine Myelinolysis (Osmotic Demyelination Syndrome), and Extra Pontine Myelinolysis.

I was contacted late last week by Dr. James Yarger with ENDECE biopharmaceutical company. He is researching potential drugs to rebuild damaged myelin sheaths due to Multiple Sclerosis, Central Pontine Myelinolysis and Extra Pontine Myelinolysis.

This is the most promising opportunity for those of us who have suffered from CPM/EPM.  The company is looking for interested participants to try the drugs.

The potential to regain any of our health is a magnificent prospect.

If you are interested in finding out more, I would highly encourage you to reach out to Dr. Yarger.

http://endece.com

You scroll to the bottom of the page to “contact”

Or click:  http://endece.com/contact/

I can not guarantee that this will work, but after years of researching CPM/EPM, this is the only option that we have been given for treatment beyond the first few weeks post injury.

If you have any questions, please feel free to reach out to me.

God Bless!

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It’s 4 O’clock in the morning…..

So for those of you new to this brain damage/ CPM/EPM experience, you might soon realize you don’t sleep normally anymore. You might sleep too long. You might not sleep long enough. You might sleep for 2 hours only to find yourself awake until the crack of dawn, so that you can suddenly fall back to sleep at 6:45 am when you need to get up at 7.

What do you do?

For me, I would usually turn to FB to surf cute animal videos and lament on my current insomnia kick, but after several fruitless debates with the general public on topics that I have considerable knowledge, I realized two things: FB stresses me out, and I have no self control in walking away from fruitless debates with the general public. It results in HOURS of going back and forth with people. It results in hours of me trying to find research articles that prove I’m right, that have no sway with the unreasonable.

So, I walked away from FB, at least for now, but tonight, after two hours of sleep, I found myself wide awake. What do I do? My hands twitched for my go to drug, my cell phone. I surfed through my email. Spam. My fingers twitched. Should I log onto FB to just vent my frustration of how much I hate not being able to sleep?

Ugh. I grab my phone and go to medicine cabinet and pop a Xanax along with a TUMS. I need sleep. Now, I just want to mention. You should not combine TUMS or any other antacid with your prescription meds. No. You won’t self destruct if you do, but the absorption of your meds can be greatly hindered by your antacids.

I drag myself back into my bedroom, and I stand there, hovering over the bed like some crazy horror movie serial killer, except instead of a knife, I have an IPHONE. I literally sway back and forth debating with myself–pale, crazy eyed, sleep deprived, hair a mess. I sway left—go write on my blog. I sway right–go back to bed.

Finally, I set down my phone. I climb back to bed, staring at the ceiling. It could be an hour before the Xanax kicks in, and I fall asleep. FB ? No, FB? Oh, the dilemma!

I desperately want to tell everyone about my 6 year old daughter’s recent rant.

Izabel: “Mom! Tomorrow, you need to call Mrs. Morrison (her teacher) and tell her I am NOT coming back to school tomorrow. I NEED A BREAK- EXCLAMATION POINT (waiving her hands up and down for emphasis). EXCLAMATION POINT! (Saying the words-“exclamation point”) EXCLAMATION POINT!  EXCLAMATION POINT! Sometimes, a 6 year old kid just needs a break from school,” she reasoned, “I am not learning ANYTHING new.”  She continues on making her very cogent point. Tom, comes from the kitchen, “This seems like a monologue.”

“It is,” I reply. How can you possibly reason with such a dramatic argument from your 6 year old? I didn’t try. Instead, I used a diversionary tactic, “Oh, look dad has dinner.”

I love my six year old daughter. She is hilarious, and this is just one of those stories that my friends on FB love to read about, so my fingers are itching to jump on and tell them, but I’m also thinking of my last debate that left me leaving FB, and how much I went to get back on the conversation and tear apart the people with facts and statistics and research, which will to no where but will cause stress, fatigue, emotional distress, etc.

That brings me to here. Time is ticking towards 5 am now. I am tired but awake, and I’m trying to figure out what’s the next step. Sleep? Or trying to figure out a new series of posts for either a new blog–a spin off that discusses politics, vaccines, other medical topics, etc. or researching more about brain injuries: newer treatment options, medications, alternative medicines, diets, etc.

This is another problem with brain injury–making choices, wanting to do everything but hardly doing anything because you can’t decide. Just look at how long it took to decide to write this post.

It’s working though. The Xanax is kicking in. I’m getting sleepy, and I’ve decided any decisions about what to do next can wait until 8 O’clock in the morning. 🙂

Have a good night, morning, day!

Has it really been a year?

Hello, All!

I hope you’re doing well! I am SO sorry that it has been so long since I last made a post. I am still alive and kicking.

Tonight, I am nursing a sinus headache and because of that, this might be relatively short.

I have no idea what I have posted in the past. I mean, I know generally what I have included, but nothing specific.

So, how have things changed in a year? Seriously, I have no clue because my short term memory is still impacted by the injury. There are obvious changes; my kids are older. I am older.

I still live very much in the now, and this still has significant complications for those I know and care about. People who don’t know me might misunderstand this lack of attention as a lack of interest, but it really is that I don’t have a great method of keeping track of time, people, or events. This means that I forget to call or write people. i don’t make doctor’s appointments that I need, or I show up to doctor appointments at the wrong time or on the wrong dates.

I just went back to work part time. It is hard even completing that job because as policies and procedures change, I find it difficult to remember or adjust to the new stuff. It also takes a significant amount of concentration and patience. In general, I find that it takes about 2 hours before I’m stressed and about four hours before I’m mentally and physically exhausted. It is hard for me to complete tasks prior to work and then spend time at work. After work, I am so stressed that on most nights, it is hard to socialize at all with my family. I become so overwhelmed that even our little dog’s attention becomes too much. I need quiet time. Literally.

I’ve heard autistic children have this same tendency.

I still have a significant number of daily issues with movements, blurry vision, tinnitus, balance issues. I have cramping in my hands, feet, legs and hips. The cramping because significant with repetitive movements, like typing and writing. I have found that a certain blend of medication has given me the most relief with twitches, jerks, and severe shaking. I use a combination of Baclofen, Gabapentin, and Carbidopa/Levodopa. That said, the drugs tend to peak with ongoing use. This leads to a need to increase the dosages. They help, but they aren’t a permanent, absolute fix.

I have talked to people in many different countries who say that they have the same issues.

I do believe it is very important to stay as active as possible. I have daily pain with walking and using weights, so I stopped exercising for several years. It didn’t help. I recently started walking again and using light weights. I still have continuous daily pain. It hasn’t improved with exercise, but the mental aspects did. I felt better mentally. I felt like I accomplished something, but honestly, it really hurts. Almost with every step, I experience pain. You have to push through it. If you can’t change it, you need to accept it. I know that sounds like such a bitter pill to swallow, especially if you have recently been diagnosed with the condition. It is hard, but you do become more accustomed to the pain.

A lot of my fellow CPM/EPM survivors have had the same experience. The activity helps, but prepare for physical discomfort. It is recommended that before you start ANY physical activity that you consult your doctor first. It is also important to start of slow and build from there. Don’t expect miracles and give it time. If you also have balance issues, etc, I definitely recommend that you do NOT exercise alone. There are MANY times during a walk that I slip or trip or just lose my balance. I have no doubt a fall will happen eventually, but on almost all of my walks, I have my friend go with me. You’ll be surprised at how many friends are willing to get out with a friend for an hour or so.

Well, that’s all I can manage for now. As always, I am interested in hearing from you. If you have a question or need help, please leave a comment, and I will try to get back to you as soon as possible.

Many Blessings! Have a great night (and hopefully, I’ll be back sooner rather than later) 😉

Hyponatremia: What you should really know to prevent CPM and EPM.

Today has been a rough day for me. I knew that my hyponatremia was treated incorrectly when I developed Extra Pontine Myelinolysis. However, I didn’t realize to what extent my treatment of hyponatremia was mismanaged.

It is absolutely a fundamental point of this blog to try to prevent ANYONE from having to live with this injury. There is no reason anyone should.

So, in this post, I am going to try to simplify the steps of how hyponatremia should be treated.

First, it is important for you to recognize the symptoms. *Please see my earlier posts for those*

Once you realize there is a problem, seek treatment. It is an emergency.

A basic metabolic panel should be ordered to determine if your sodium levels are low.

Next, it is important for the doctor to figure out WHY you have hyponatremia, and how LONG you have had it.

If they can’t figure out the time line, then it is better for them to assume that it is chronic because it is more likely that you will develop CPM if they treat chronic hyponatremia too quickly versus acute. (Acute is when sodium has been too low for less than 48 hours. Chronic is when sodium levels have been low for more than 48 hours).

Acute hyponatremia can cause severe symptoms such as seizures, respiratory distress and coma. The severity of symptoms determines how quickly the levels should be raised. However, it is generally accepted that once your symptoms begin to improve, the treatment should be decreased or halted.

According to Dr. Sterns, an expert on hyponatremia, acute hyponatremia should be treated in the following manner, “should be treated immediately with a bolus infusion of 100 mL of 3% NaCl to acutely reduce brain edema, with up to 2 additional 100-mL 3% NaCl bolus infusions that should be given at 10-minute intervals if there is no clinical improvement.10 We believe that this is a reasonable regimen for all symptomatic patients with acute hyponatremia…” (use the link below to find the information).

According to Dr. Sterns, chronic hyponatremia should be treated with “…we suggest a goal of 6 to 8 mmol/L in 24 hours, 12 to 14 mmol/L in 48 hours, and 14 to 16 mmol/L in 72 hours.” (http://www.uphs.upenn.edu/renal/important%20pdf%20III/Sterns%20-%20The%20Treatment%20of%20Hyponatremia.pdf)

The cause of your hyponatremia is extremely important because it absolutely determines what treatment you should receive.

For instance, if a drug has caused your hyponatremia, like a diuretic, then the first course of treatment is to stop taking the diuretic. Sometimes, just discontinuing the medication is enough to reverse the low sodium.

I HIGHLY recommend the following article posted by the Cleveland Clinic that outlines in exact detail which types of treatments based on the cause of the hyponatremia.

There is little question that if you are on a 3% saline solution for treatment, that your sodium levels should be monitored every 1 to 2 HOURS. As soon as your levels start to increase to the point that your symptoms start to resolve, even BEFORE it reaches the 6 to 8 m/mol GOAL, the 3% saline should be halted. This will stop your levels from reaching the “danger zone” which is approximately 8 to 12 m/mol in the first 24 hours with chronic hyponatremia. It is generally accepted that with acute hyponatremia that you can raise the levels a bit faster and not risk CPM or EPM.

ONE OF THE MOST IMPORTANT FACTORS TO REALIZE: IF YOUR LEVELS HAVE BEEN INCREASED TOO QUICKLY, THEN THEY CAN BE DECREASED BACK TO A HYPONATREMIC STATE TO PREVENT CENTRAL PONTINE MYELINOLYSIS. IT IS BELIEVE THAT THIS DROP CAN OCCUR DURING A 5 DAY PERIOD AFTER THE RAPID CORRECTION OCCURRED.

For further information and more detailed description of these steps as well as how to treat certain types of hyponatremia, please access this article: http://www.ccjm.org/content/77/10/715.full

These simple steps could save your life!

Vision Issues Related to Brain Injury and CPM/EPM:

Hello there.

I received a comment from Elle. She has vision issues too. She did research and feels that her ongoing vision issues are related to CPM and EPM and is classified as Visual Snow. I do not know much about Visual Snow, but I have to say, it is plausible that Central Pontine Myelinolysis and Extra Pontine Myelinolysis can cause this.

I do not know anything significant about Visual Snow, but there was mention that it is attributed to other demyelinating diseases such as MS. In essence, CPM/EPM are similar in that they both are conditions that effect the myelin. There is also a connection to visual snow and ocular and classic migraines. There also seems to be a connection in this and tinnitus.

Unfortunately, today is not a great vision day for me, and the more I try to read, the more I experience the blurriness of vision. (It is so frustrating!) I tried to access medical literature that described Visual Snow, but it seems under researched.

The following are pictures and videos in regards to what Visual Snow is like for those who have it.

There seems to be a variation on how Visual Snow impacts a person's vision.

There seems to be a variation on how Visual Snow impacts a person’s vision.

Visual Snow 2

Visual Snow 3

Now, the visual condition that I experience is truly just blurry vision. (I do get ocular migraines though which started way before the brain injury.) Unlike the reports about Visual Snow, my blurry vision comes and goes. I had it earlier today, and now (about two hours later) it is gone again. It could come back in a few minutes or it might not come back at all. The blurriness can be slight or it can be extreme.

I did find a report of others with CPM and EPM who have experienced the blurry vision after injury.

http://www.ajronline.org/doi/full/10.2214/AJR.07.7052

A 40-year-old man presented with acute onset walking difficulty, slurred speech, and slight blurring of vision. Other relevant clinical history included chronic alcoholism and poor nutrition. Clinical examination revealed mild lower limb incoordination, dysarthria, and bilateral partial abducent nerve palsy. The blood tests for full blood count, renal functions (sodium, 142 mmol/L; potassium, 4 mmol/L; urea, 4.6 mg/dL; creatinine, 85 μmol/L), blood glucose (6.1 mmol/L), serum osmolality (285 mosm/kg), and liver function tests (albumin, 41 g/L; globulin, 25 g/L; bilirubin, 12 μmol/L; aspartate aminotransferase, 30 U/L; γ-gluta myltransferase, 45 U/L; and alkaline phosphate, 142 U/L) were within normal limits.

Read More: http://www.ajronline.org/doi/full/10.2214/AJR.07.7052

Another article explains the same symptoms in a woman (http://www.imj.ie/ViewArticleDetails.aspx?ContentID=3623):

Case Report
A 41-year-old lady was woken up at 5am with sudden pins and needles and weakness involving the hands, trunk and legs. She had gone to bed completely well the previous night. When she attempted to rise, she was weak and unsteady. She then experienced blurred vision and had difficulty speaking and swallowing. Her symptoms worsened over the course of the day. She was transferred to UCHG after one day. On examination she was fully conscious but dysarthric. She had sluggish tongue movements with no palatal movements and severely impaired swallowing. She had abnormal eye movements identified as opsoclonus, upgaze restriction and bilateral partial ptosis. There was pyramidal weakness in both upper and lower limbs limbs, particularly in the right lower limb. Both knee jerks were pathologically brisk and the right plantar was extensor. Other deep tendon reflexes were normal. The upper and lower limbs were severely ataxic. Sensation was normal in all four limbs.

Another case believed to be caused by CPM/EPM (http://content.lib.utah.edu/utils/getfile/collection/EHSL-FBWNOC/id/599/filename/595.pdf):

The patient’s post-operative course was uneventful until 2 days after surgery when she noticed blurred vision in
both eyes and reported difficulty distinguishing colors.
Neuro-ophthalmic evaluation 5 days later disclosed 20/25 visual acuity at near in each eye. The pupils were equal
and reacted sluggishly to direct light. There was no relative afferent pupillary defect noted. The patient could read
only one of seven Ishihara color test plates with each eye. She could count fingers in her temporal visual fields but
could see only hand motions in her nasal visual fields. Dilated fundus exam was normal in each eye.
Automated visual field testing showed an incongruous, predominantly binasal, hemianopia………..We believe a demyelinating process, isolated extrapontine myelinolysis, caused our patient’s visual loss.

So, CPM and EPM can cause vision issues, and it has been noted in other patients that it can specifically cause blurred vision. I would not be surprised that it can cause a visual snow effect, but considering Visual Snow is just now being recognized as a symptom in the medical community, I doubt that there will be literature supporting it.

It is also not surprising that a person who experiences a head injury can experience vision changes. If a brain injury is caused by penetration of a foreign object, then it might obvious why a visual change occurs, but even in subtle head injuries, a person can experience a change in vision. There might be a structural change to your eye that causes the change, but there can also be change in the way your brain processes the neural impulses that causes visual disturbances.

This link provides insight to brain injury and visual changes: http://www.brainline.org/landing_pages/categories/vision.html

The following information describes how mild brain injuries, like concussions, can cause ongoing issues, including blurred vision:

As many as 30% of patients who experience a concussion develop postconcussive syndrome (PCS). PCS consists of a persistence of any combination of the following after a head injury: headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances. Fixed neurologic deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2-4 months. Typically, the symptoms peak 4-6 weeks following the injury. On occasion, the symptoms of PCS last for a year or longer. Approximately 20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently by PCS. PCS tends to be more severe in children than in adults. When PCS is severe or persistent, a multidisciplinary approach to treatment may be necessary. This includes social services, mental health services, occupational therapy, and pharmaceutical therapy. http://emedicine.medscape.com/article/433855-treatment

The following describes that there seems to be a connection to those who have a cognitive impact after a brain injury to visual complications:

Vision problems and cognitive deficits may compound one another. The most common complaints related to visual problems associated with brain injuries include light sensitivity, headaches, double vision, fatigue, dizziness, difficulty reading, or loss of peripheral visual fields. You may feel a heightened sensitivity to light and may even need to wear your sunglasses inside. You may have to request that fluorescent lights be turned off. Computer and reading tasks may take longer than usual, and tend to be more confusing and tiring. http://www.brainlinemilitary.org/content/2009/11/recovering-from-mild-traumatic-brain-injury_pageall.html

So again, there does seem to be a parallel in brain injuries in general, and more specific conditions and diseases like MS, CPM and EPM. In other words, no matter if you suffered from a physical brain injury, a concussion, or have a brain disease or syndrome, the symptoms are comparable.

Hope that helps folks!

Michael’s story (symptoms):

I am happy to say that Michael has answered some or all of the same questions that Todd has. I think this will give you a good idea as to how each case of CPM/EPM is unique, but also has similarities, especially with movement, speech, cognitive issues, etc. There is a lot more research that needs to be done, and this is by no means a detailed explanation of everything that they experience, but it gives a general idea of what a person lives with.

I hope you’re ready for a great Christmas break. I hope you have a safe trip to Canada.

I’m hoping you can help me by answering the following questions. I’m trying to organize a list of symptoms that people have with this or how their injury has progressed over time. Feel free to add comments and additional comments about how the injury has impacted you. Take your time. I feel this is going to be one of the only ways to get doctors to understand how it impacts us long term.

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

Do you forget stories or movies or articles or recognize faces but forget the plot? – Yes all the time  

Do you have jerks and twitches? – Yes in my hands, feet, head, and legs…

Do you have issues sleeping? – No I am so tired by the time I get there I pass out.

Do you find yourself easily distracted?- I use to pride my self on how focused I was on being able to complete the task at hand, now if I can sit for ten minutes and stay on one topic I am doing good.

Have you had issues with managing your finances, forgetting to pay bills or paying them more than once? – I only have four bills to pay and my wife has had to take over that because I would always forget to mail them and would wonder why why they would call the house.

Do you need help doing any daily activities, like grocery shopping?- No but I should, I can be in the store for an hour if I go by myself and only need 3 things. I will constantly forget what I am there for.  

Have you had irregular heart rates?- 
No

Have you had hallucinations?- Yes, in the beginning i had a lot of them and it scared the crap out of me. I would be driving on the Highway and I would see people standing in the middle of the road. But now it has calmed down. Only once or twice a week i will see different thing.

Have you had any blackout periods? No

Have you had any weight gain?- No

Have you had any issues with visual problems with blurriness?- Yes, some days are better then others, but my vision is getting really bad. I don’t drive often at night unless I really have to.

(Ringing of the ears does happen with CPM/EPM. It’s a form of tinnitus. 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).- No

Have you had issues with smelling?- No 

Fatigue? – Yes, 

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?- Yes can’t write anymore, my fine motor skills are shot. When typing I have to type slow because my hand twitch and jump all over the place so that can be an adventure. This is not 7 days a week, usually about 5 days.

Any issues with swallowing?-No

Any issues with understanding what someone is saying to you? – Yes, sometimes I have no idea what someone is saying and I just say ok or give them the answer I think that they are looking for.

Paranoia?- No

Depression?- Yes, some days I say why me, 

Sleep disturbances?- No

Sleep Apnea?- No

Numbness and tingling? – Yes, in my hands, back of my head and feet.

Balance or coordination issues?- Yes, some days / most days I walk like I am drunk. 

Do you have any ongoing issues with movements? like cramping, spasms, jerks, etc. Do you have any ongoing issues with memory, concentration or learning? Do your symptoms remain constant or do they come and go?– Yes, Cramps, spasms,jerks, stuttering and drooling come and go on a daily basis. Memory, concentration, learning, numbness of the back of the head, eye sight issues, hand tremors, feet tremors are 24/7  

Do you do any therapy or did you do so after being released from the hospital? – No

Have you met any doctors that have helped with your condition, neurologists/ GP? Yes, finally after going to 7 different neurologist I found one that took the time to listen and figure out how to help with my issue.

Have  you experienced new symptoms or have you had continuous improvements? – Yes new symptoms sense it first started. But the doctors say it is not progressive. 

Have you met any new people with CPM/EPM? – Yes on Inspire a web based forum for people to talk about their medical issues and concerns. Meet a new one this week. 

Did you have any treatments immediately following the injury? Like, hyperbariatric treatments, plasmaphoresis, anti inflammatory meds? – No

What are your current medications that are helping? – Carbidopa-levodopa, Baclofen, Ropinirole, Topiramate, and Tramadol. I take these three times a day. Many many pills………….      

Please feel free to leave questions or comments for me or Michael, and we can try to elaborate on anything listed. 

 

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.

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.

 

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

 

What’s the difference (types of brain injury and their symptoms):

There seems to be a belief that “how” you get an injury makes a difference as to what symptoms you may or may not experience.

If you have a bacterial infection that destroys your heart tissue and that leads to a heart attack, is that different than having clogged arteries that lead to a heart attack?  Of course, there are some differences, the how you had a heart attack, but once the damage is done, the outcome is the same; your heart has been damaged. You will have to live with the damage and its impact to your heart and body.

There is a belief among doctors that brain injuries are universally different depending on how your brain was injured. There is a belief that if you were hit in the head or suffered a concussion, the injury to the brain will not produce the same symptoms as when you have a stroke or an injury due to a chemical imbalance.

I’ve discussed previously that the injury to the brain itself might be a static injury. For instance, once you’ve been in a car accident, your brain will not continue to receive  injury from the car accident itself, but there is  new research that shows that symptoms continue to persist and develop due to the body’s autoimmune response.

There are several ways that a person can get a brain injury.  According to Ohio State University Medical Center, the following is a list of brain injuries and how they differ:

  • Concussion
    A concussion is an injury to the head area that may cause instant loss of awareness or alertness for a few minutes up to a few hours after the traumatic event.
  • Skull fracture
    A skull fracture is a break in the skull bone. There are four major types of skull fractures, including the following:

    Illustration of different types of skull fractures
    Click Image to Enlarge
    • Linear skull fractures
      This is the most common type of skull fracture. In a linear fracture, there is a break in the bone, but it does not move the bone. These patients may be observed in the hospital for a brief amount of time, and can usually resume normal activities in a few days. Usually, no interventions are necessary.
    • Depressed skull fractures
      This type of fracture may be seen with or without a cut in the scalp. In this fracture, part of the skull is actually sunken in from the trauma. This type of skull fracture may require surgical intervention, depending on the severity, to help correct the deformity.
    • Diastatic skull fractures
      These are fractures that occur along the suture lines in the skull. The sutures are the areas between the bones in the head that fuse when we are children. In this type of fracture, the normal suture lines are widened. These fractures are more often seen in newborns and older infants.
    • Basilar skull fracture
      This is the most serious type of skull fracture, and involves a break in the bone at the base of the skull. Patients with this type of fracture frequently have bruises around their eyes and a bruise behind their ear. They may also have clear fluid draining from their nose or ears due to a tear in part of the covering of the brain. These patients usually require close observation in the hospital.
    • Intracranial hematoma (ICH)
      There are several types of ICH, or blood clots, in or around the brain. The different types are classified by their location in the brain. These can range from mild head injuriesto quite serious and potentially life-threatening injuries. The different types of ICH include the following:

      Illustration of Intracranial Hematoma
      Click Image to Enlarge
      • Epidural hematoma
        Epidural hematomas occur when a blood clot forms underneath the skull, but on top of the dura, the tough covering that surrounds the brain. They usually come from a tear in an artery that runs just under the skull called the middle meningeal artery. Epidural hematomas are usually associated with a skull fracture.
      • Subdural hematoma
        Subdural hematomas occur when a blood clot forms underneath the skull and underneath the dura, but outside of the brain. These can form from a tear in the veins that go from the brain to the dura, or from a cut on the brain itself. They are sometimes, but not always, associated with a skull fracture.
      • Contusion or intracerebral hematoma
        A contusion is a bruise to the brain itself. A contusion causes bleeding and swelling inside of the brain around the area where the head was struck. Contusions may occur with skull fractures or other blood clots such as a subdural or epidural hematoma. When bleeding occurs inside the brain itself (also called “intraparenchymal hemmorage”), this can sometimes occur spontaneously. When trauma is not the cause, the most common causes are long-standing high blood pressure in older adults, bleeding disorders in either children or adults, or the use of medications that cause blood thinning or certain drugs of abuse.
      • Diffuse axonal injury (DAI)
        These injuries are fairly common and are usually caused by shaking of the brain back and forth, which can happen in car accidents, from falls or shaken baby syndrome. Diffuse injuries can be mild, such as with a concussion, or may be very severe, as in diffuse axonal injury (DAI). In DAI, the patient is usually in a coma for a prolonged period of time, with injury to many different parts of the brain. (http://medicalcenter.osu.edu/patientcare/healthcare_services/nervous_system/injury/Pages/index.aspx)

Notice in the above list, it does not mention brain injuries caused by stroke. It does not mention injuries caused by infection, like meningitis. It does not mention injury caused from Central Pontine Myelinolysis. It does not mention injury caused by disease, like Multiple Sclerosis.

If you read about any of the above diseases, injuries or disorders, you will find that those who experience injuries to the brain by any means, has similar symptoms.

Those who have MS experience movement issues:

    • Blurred or double vision
    • Red-green color distortion
    • Pain and loss of vision due to optic neuritis, an inflammation of the optic nerve
    • Difficulty walking
    • Paresthesia – abnormal sensation, or pain, such as numbness, prickling, or “pins and needles.”
  • Other symptoms of multiple sclerosis:
    Throughout the course of the illness, an individual may experience any/all of the following symptoms, to a varying degree:

    • Muscle weakness in the extremities
    • Difficulty with coordination (impaired walking or standing may result; partial or complete paralysis is possible)
    • Spasticity – the involuntary increased tone of muscles leading to stiffness and spasms.
    • Fatigue (this may be triggered by physical activity, but may subside with rest; constant, persistent fatigue is possible)
    • Loss of sensation
    • Speech impediments
    • Tremor
    • Dizziness
    • Hearing loss
    • Bowel and bladder disturbances
    • Depression
    • Changes in sexual function

The above list comes from, http://medicalcenter.osu.edu/patientcare/healthcare_services/nervous_system/ms/Pages/index.aspx

Stroke symptoms:

  • movement and sensation
  • speech and language
  • eating and swallowing
  • vision
  • cognitive (thinking, reasoning, judgment and memory) ability
  • perception and orientation to surroundings
  • self-care ability
  • bowel and bladder control
  • emotional control
  • sexual ability

In addition to these general effects, some specific impairments may occur when a particular area of the cerebrum is damaged.

Effects of a right hemisphere stroke:

The effects of a right hemisphere stroke may include the following:

  • left-sided weakness (left hemiparesis) or paralysis (left hemiplegia) and sensory impairment
  • denial of paralysis or impairment and reduced insight into the problems created by the stroke (this concept is called “left neglect”)
  • visual problems, including an inability to see the left visual field of each eye (homonymous hemianopsia)
  • spatial problems with depth perception or directions such as up/down and front/back
  • inability to localize or recognize body parts
  • inability to understand maps and find objects such as clothing or toiletry items
  • memory problems
  • behavioral changes such as lack of concern about situations, impulsivity, inappropriateness, and depression

Effects of a left hemisphere stroke:

The effects of a left hemisphere stroke may include the following:

  • right-sided weakness (right hemiparesis) or paralysis (right hemiplegia) and sensory impairment
  • problems with speech and understanding language (aphasia)
  • visual problems, including the inability to see the right visual field of each eye (homonymous hemianopsia)
  • impaired ability to do math or to organize, reason, and analyze items
  • behavioral changes such as depression, cautiousness, and hesitancy
  • impaired ability to read, write, and learn new information
  • memory problems

What effects can be seen with a stroke in the cerebellum?

The cerebellum is located beneath and behind the cerebrum towards the back of the skull. It receives sensory information from the body via the spinal cord and helps to coordinate muscle action and control, fine movement, coordination, and balance.

Although strokes are less common in the cerebellum area, the effects can be severe. Four common effects of strokes in the cerebellum include the following:

  • inability to walk and problems with coordination and balance (ataxia)
  • dizziness
  • headache
  • nausea
  • vomiting

What effects can be seen with a stroke in the brain stem?

The brain stem is located at the very base of the brain right above the spinal cord. Many of the body’s vital “life-support” functions such as heartbeat, blood pressure, and breathing are controlled by the brain stem. It also helps to control the main nerves involved with eye movement, hearing, speech, chewing, and swallowing. Some common effects of a stroke in the brain stem include problems with the following:

  • breathing and heart functions
  • body temperature control
  • balance and coordination
  • weakness or paralysis in all four limbs
  • chewing, swallowing, and speaking
  • vision
  • coma

The above information is taken from, http://medicalcenter.osu.edu/patientcare/healthcare_services/stroke/effects/Pages/index.aspx

The next list, is the list that I have found to be defining to those who have brain injuries in general. Notice how similar they are to what we find in things like stroke and MS:

Issues that are attributed to brain damage:

Hearing Issues (problems with understanding spoken word, tinnitus, dizziness, buzzing)
Visual Issues (blurry vision, color issues, blindness)
Heart Issues (problems with maintaining proper blood pressure and heart rates)
Cognitive Issues (memory deficits, learning issues, reading problems, writing problems, word recognition)
Hormone Issues (lack of Growth Hormone, sex hormones, hypothyroidism, and hypopituitarism)
Sexual Issues (lack of desire)
Reproductive Issues (lack of menses in women, lack of gonadotropin hormones)
Psychological Issues (depression, irritability, nervousness, anger, crying, anxiety)
Parkinson’s Disease
Alzheimer’s or Alzheimer’s like disease
Epilepsy (early to late onset of seizures, can occur up to 40 years after injury)
Sleep Disturbances (insomnia, inability to stay asleep, central nervous system sleep apnea)
Early Mortality (high risk of death during first 1 to 10 years after injury, after that life expectancy is 5-7 years less than average non injured person)
Incontinence (urinary or bowel)
Muscle Dysfunction (twitches, spams, jerks)
Mental Fatigue (difficulties working or going to school full time due to concentration deficits)
Speech disturbances (stutters, stammering, not being able to complete thoughts, not using proper words)
Issues with communicating
Movement disorders (problems with coordination, walking, standing, eating, tremors, shaking, swallowing, speaking)
Temperature control issues (too hot or too cold)
Complete paralysis (those with CPM/EPM are known to develop locked in syndrome)
Breathing issues (the brain forgets to tell the body to breathe, especially critical in sleep)
As you can see, people have very similar, if not identical symptoms, no matter how they received the brain damage. I am hopeful that over time doctors will come to realize that whether or not you were hit in the head or had a stroke the process and recupperation needs to be treated the same if not structured from the same basic model and tweaked to meet an individuals need.
Further, it needs to be understood that no matter HOW you got your injury, the immune system responds to the injury in the same manner leading to further complications as a person ages.
Now, I wanted to add some descriptions to the symptoms that you may experience with brain injuries. Iwas excited to find the following description of mental fatigue. I have experienced this as I returned back to work. I have had ongoing issues with this outside of work as well. I simply can not do as much as I did before. The mere act of trying to stay focused for long periods of time leaves me mentally and physically exhausted. My doctors first reaction when I explained this is that it must be a psychological phenomena related to knowing I have a brain injury. When a doctor gives these suggestions, you have to believe they must be right. It must be all in my head (ha-no pun intended). I was happy to find a research article discribing this issue as a part of having a brain injury.

Patients will recover within days to weeks, but a significant minority develop persistent mental fatigue, and it will take a long time before they can accept the situation and find
ways to lead their “new life”. Until then, life can be very mentally tiring and for many it can be a great strain. In the case of a slow recover, things might turn out not to work as smooth and easily as they used to. It is possible for patients to take walks in the forest, but reading, talking on the telephone or attending a meeting could be mentally very tiring and may require a prolonged rest afterwards. It is no longer a pleasure to go to parties, as they can’t take part in conversations, and they soon become extremely tired and want to go home. It might also be shameful for the person to admit that the brain does not work properly. They also tend to experience difficulties concentrating, and it could be difficult to filter what they hear and see. Every unimportant detail is registered. Sensitivity to stress is also very common, even in minor situations which they are normally able to handle.

http://cdn.intechopen.com/pdfs/30498/InTech-Mental_fatigue_a_common_long_term_consequence_after_a_brain_injury.pdf

I will try to include the additional research that I have found regarding brain injuries and what you can expect, no matter what type of injury you have.

Please keep in mind, no matter what type of injury you have, it does not mean that you will have all of these symptoms. It does not even mean that you will have life long consequences because of it. The severity of the injury, the location of the injury, and the initial treatment that you receive following the injury all determine the outcome that you will have following your injury. I believe fully that you can go on to lead a productive life depending on many factors that I will address later in the future.

 

UPDATE 11/14/12—I found this research article, which explains a significant number of the physical issues after a brain injury. It provides more of the physiological description of why the injury will cause the symptoms, like epilepsy, visual and auditory disturbances, cognitive dysfunctions.I was extremely happy that this article states that a person’s IQ remains relatively intact after these types of brain injuries (this is what I have experienced), but they continue to have issues with memory, learning, and retrieval.

http://jnnp.bmj.com/content/73/suppl_1/i8.full

Cognitive and neuropsychiatric sequelae

After resolution of PTA, overall IQ and posterior cognitive functions of language and visuospatial skills are often relatively intact and the residual neuropsychological deficits may not be easily detected by simple tests of cognitive function. A formal neuropsychological assessment of the patient’s memory, attention, and executive skills and their mental speed is thus mandatory, particularly late after severe injury when these problems play a major role in limiting independence.

Organic disorders of behaviour9 are often seen in tandem with cognitive dysfunction, and are usually described by a carer. Personality changes, of imprecise localising value, include egocentricity, childishness, irritability, aggressiveness, poor judgement, tactlessness, stubbornness, lethargy, disinterest, reduced drive and initiative, and often reduced rather than increased sexual interest. Occasionally more dramatic positive and impulsive, or negative and abulic, behaviours prevail.

Psychiatric sequelae including low mood, depression, and anxiety disorders are common after TBI, and often delayed in onset. Psychiatric illness, fewer years of formal education pre-injury, and a more dependent outcome predispose to the development of these problems.10 Depression may respond to a selective serotonin reuptake inhibitor or venlafaxine, and psychiatric referral may be necessary. Occasionally obsessive–compulsive disorders and psychoses occur in the absence of obvious premorbid psychiatric history, and the risk of suicide is increased.

The moment of Now:

Oh, the beauty of having a brain injury, is that you truly don’t remember what has happened previously.  I have no idea if I’ve visited this topic or not. I’ve no idea.

It’s now over a year since I suffered my brain injury, and tonight I feel myself feeling a bit depressed over the idea that I have not gone farther than I have.

I have so many friends and family members who tell me that I’m just being negative. They tell me that if you think that you aren’t going to get better then you won’t. They tell me that it’s your mindset that influences where you go with your life.

I have to say to them, Screw off. I say that with love, but no one I know has a brain injury. No one. I wouldn’t want them to have one either.

It’s not easy. It’s unbelievably hard.

Do they even know what I go through on a daily basis?

I never know exactly what I said, if I said it, if I did it, if I didn’t do it. My mind does not work!!!!

You get over breaking a toe. You just don’t  learn to “live” with having a brain injury.

You can learn to live without an arm or a foot. You can learn to live with an illness. I had.

I wasn’t healthy before the brain injury, but I could DO things. I could fight through the pain, the fatigue, the frustration, the nausea, the headaches…all the physical issues, I was able to fight through it. I was able to work 60 to 80 hours while being sick. I could go to work and then spend my days off studying for the MCAT while I was sick.

But, when you have a brain injury, well that’s having your mind broken. The chemistry in your brain is screwed up. They way you think is broken. The way you process information is broken.

What good is a computer monitor or keyboard if your hard drive does not work?

A year ago, I had hope that this injury would get better. I have seen some improvements. I am not stuttering as much. I am not walking into walls. Ha, that’s funny! I can’t even remember the things that I used to do when I initially had the brain injury to give you an idea as to how it’s improved.

I think that’s part of the problem. I live in the now. I can not make plans because I can not envision how things will be in a week, a month, a year. I do not have the capability of saying…oh, I can’t do that because I will be doing this instead. Because in my mind, the canvas is blank, the calendar is mentally empty. I can’t say that in a year I will be in medical school or in a year, I’m going to take a vacation.

In my life, there is no next year.

I do not remember what commitments I have until I pull out my phone and check my calendar or reminders.

My son might tell me that he will be going to a party next weekend. Sure, that sounds fine. Right now, that does sound fine. I can’t remember that I wanted to get his pictures taken with his sister. It doesn’t register in this minute of my life. In a few days, I might have another plan set in my mind, like going out to dinner as a family.

Things hit me as a realization….Just now, I realized that Halloween is this week. This triggered the memory that I took off that day off from work. Why did I take that day off? I must have had a reason. I don’t have a costume. I don’t have a party that I’m going to. Trick or Treat is the day before. I don’t know.

This is just one example of how things just happen in my life. I live in the present. I don’t remember the past, and I have no idea how to plan for the future.

In this moment of now, I feel a loss. I feel melancholy. I feel jealous of those who do not know what it means to live like this. I feel ashamed that I feel so bad about the life that I should be grateful for. I feel alone because no one I know shares this life with me. And I feel hate over the fact that this injury was caused by someone else, and that person will be going to sleep tonight without any regard for what I’m living with and what I will have to live with for the rest of my life.

I’ve tried to regain my life. I’ve tried counseling. I’ve tried therapy. I’ve tried medicines. I’ve tried dozens of doctors. I’ve tried just doing it. I’ve tried exercise. I’ve tried forgetting about it. I’ve tried organizing. Now, I have to try to live with it, and to learn to live with it, and be happy with the fact that I have lost everything I was working for before the injury. I have to try to figure out how to make the most of the life that I have now, and to make that mean the most to me.

I figure out there must be a reason, and I pray with time that reason will become apparent so that I can try to make myself believe that this injury was for the greater good.

I’m certain that I am not the only who has a brain injury that feels this way. I know that there are so many people in the world that are living with the same feelings, and with that I have to say despite the negative tone in this post, I still have hope for tomorrow. What can we do but keep on keeping on?

This is a journey and even if the path is rocky, it’s still worth the view.

Brain injury and Alzheimer’s disease:

I am searching for information regarding brain injuries and the long term implications of having a brain injury. This post was started with the belief that there is a connection between those with brain injuries and Alzheimer’s.

There are those who believe that there isn’t a connection, and there are those scientists who believe that there is. I do not think that everyone with a brain injury will develop Alzheimer’s, but I do believe that those who have a brain injury have a higher risk for it. I also believe that it may take years for that disease to develop after the injury.

The majority of this post is showing the physiological links as to why it might develop in a person who has experienced a brain injury.

I also believe that the best evidence is from those who have experienced the injury and their stories. SO, this post does digress a bit with a few excerpts from posts from another blog that includes the stories of those who have had brain injuries and their experiences.

What is Alzheimer’s Disease? Alzheimer’s is a number of cognitive and behavioral issues that occur over an extended period of time. The cause of it is not exactly known, but the disease is determined by the formation of plaque (dead and dying neurons (brain cells) and proteins) in the brain. It is also composed of “clogged” areas in the brain that are a tangle of nerve cells and proteins. Frankly, certain areas of the brain shrink and are in the process of dying. They can’t determine if you have the disease with certainty until after you die.

English: Combination of two brain diagrams in ...
English: Combination of two brain diagrams in one for comparison. In the left normal brain, in the right brain of a person with Alzheimer’s disease. Diagram of the brain of a person with Alzheimer’s Disease. Diagram of a normal brain. Español: Esquema de un corte frontal de dos cerebros. El de la izquierda es un cerebro sano y el de la derecha uno que padece la enfermedad de Alzheimer. Русский: Изображение нормального мозга и мозга при болезни Альцгеймера (Photo credit: Wikipedia)

So, apparently there are a LOT of factors that researchers contribute to the possibility that a person will develop Alzheimer’s in their life time. Some of these factors are Type 2 diabetes, obesity, watching too much T.V., a person’s height, genetics, stress, etc. Age is the greatest risk factor in developing Alzheimer’s. It seems like a no brainer (ha) that a brain injury would eventually lead to a higher risk of Alzheimer’s.

I’ve already posted previously that Central pontine myelinolysis and EPM have been associated with significant cognitive, emotional, and behavioral issues. I believe that this just makes it even more probable that there would be a higher incidence of Alzheimer’s in those with CPM/EPM, since Alzheimer’s is known to cause:

It results in a progressive deterioration of neurocognitive (such as learning, memory, higher-order language skills, judgment, and reasoning) and functional abilities. As the disease progresses, some patients experience pronounced personality and behavior changes including anxiety, agitation, suspiciousness, delusions, and hallucinations.

I also believe that CPM and EPM will lead to Alzheimer’s or causes symptoms similar to it because they seem to share similar pathophysiology. This is true for brain injuries in general as well.

Before I go into that further, I want to stress that the pathophysiology of Alzheimer’s has not been completely uncovered. There is more and more being discovered about the disease each day, and the exact cause of Alzheimer’s is not known.

Generally, those who experience a mild brain injury (concussion) will recover without significant complications (at least initially). It has been determined that those who tend to have long lasting issues have had damage to neurons. This damage can impact the functionality of the cells which lead to  improper neurotransmission between the cells. The following passages describe the physiological factors that tend to happen after a mild brain injury:

Immediately after a concussive injury, there is an indiscriminate release of neurotransmitters and uncontrolled ionic fluxes. Potassium (K+) rapidly leaves the cell. Shortly after injury, and for a prolonged period of time, there is an influx of calcium (Ca2+). When the ionic gradients are disrupted, cells respond by activating ion pumps in an attempt to restore the normal membrane potential. Because these pumps require energy to function, more glucose is utilized. This leads to dramatic increases in the local cerebral metabolic rate for glucose. This hypermetabolism occurs in the context of decreased cerebral blood flow , which can contribute to a disparity between glucose supply and demand. In addition to increased glucose utilization, there may be impaired oxidative metabolism and diminished mitochondrial function. As a result, anaerobic (not requiring oxygen) energy pathways may be over-utilized. Elevated lactate can occur as a by-product of anaerobic energy production (and through other mechanisms). In addition, intracellular magnesium levels decrease significantly and remain depressed for several days following injury. This is important because magnesium is essential for generation of adenosine-triphosphate (ATP – energy production). Magnesium is also essential for the initiation of protein synthesis and the maintenance of the cellular membrane potential .

The sustained influx of Ca2+ has at least two important effects: (1) mitochondrial accumulations of Ca2+, and (2) initiation of a pathophysiologic process of axonal injury. The increased mitochondrial Ca2+ can lead to metabolic dysfunction and eventually energy failure. Abnormally high intracellular Ca2+ levels can initiate an irreversible process of destruction of microtubules within axons. Coupled with neurofilament damage that can occur with stretch injury, microtubule damage can impair axoplasmic flow along the length of the axon. When this occurs, axons can swell and separate.

When entire cells die following MTBI (NB: a small number), the mechanism of death relates to the spectrum of necrosis; however, researchers have reported that apoptosis (programmed cell death) appears to contribute to cell mortality in both grey and white matter following MTBI (51). Thus, the mechanisms of cell death might represent a continuum between apoptotic and necrotic pathways (52)It is important to note that cell death is closely related to injury severity. Very mild concussions likely produce virtually no permanent damage to cells resulting in long-term symptoms or problems whereas severe traumatic brain injuries, especially those involving considerable forces, often produce widespread cellular death and dysfunction with clear functional consequences.

The author of the above passages goes on to stress that the following tend to be a major contributor to having a risk for continuous symptoms after a brain injury, “The primary pathophysiologies include ionic shifts, abnormal energy metabolism, diminished cerebral blood flow, and impaired neurotransmission.”

The author of this research article goes on to suggest that there are many researchers that believe there is no correlation between brain injury and Alzheimer’s.

I guess it is important to remember that you should be cautious in regards to the possibility that if you’ve had a brain injury, you could have a higher risk for Alzheimer’s, but it is not a certainty.

The above information was quoted from: http://internationalbrain.org/?q=node/51,  “Mild Traumatic Brain Injury & Risk for Alzheimer’s Disease” Grant L. Iverson, Ph.D., Professor

I would like to note that Dr. Iverson also considered the long standing issues that a person experiences after a brain injury might be caused by psychological factors. I believe that this consideration was due to the fact that Dr. Iverson is a professor in psychiatry. I have read additional articles by other psychologists and psychiatrists that had a similar point of view. They consider that a person who has ongoing issues might be experiencing issues because they are experiencing post traumatic stress from the even that caused the injury. They might exaggerating the injury because of litigation. They might think that they are experiencing deterioration in their abilities, but there really isn’t.

A different research article explains that there is a more substantial link to brain injuries and Alzheimer’s Disease. The author’s of this article explain that it may take up to 17 years or longer for a person to develop Alzheimer’s after the initial injury. They explain that because of this length of time, as well as the memory and dementia issues involved with Alzheimer’s that by the time a person is diagnosed with the disease, they will probably not remember an instance of having a brain injury. They suggest that there needs to be long term follow up with those who have brain injuries, even those with mild injuries, to determine whether or not there is an association.

They do use an example of the NFL players that have recently received media attention for their cognitive and physical deficits that they attributed to ongoing concussions from playing football through out their lives.  According to the study, there was a “five-fold increase in the precursor to AD, mild cognitive impairment, and a threefold increase of reported significant memory problems among retirees with three or more reported concussions compared with retirees with no history of concussion.”

The article suggests that Alzheimer’s is caused by a brain injury because of the immune system response.  The immune system responds by sending cells to try to repair the damage and this causes inflammation. This leads to plaque formation in the brain, which causes an additional immune response. Eventually, the process spreads until the entire brain is impacted by the plaque.

This response results in neuronal injury and often in disruption of the blood brain barrier. Microglial cells react to this injury within minutes, and stay activated chronically [31]. Once induced into this state, the microglia become nearly identical to peripheral macrophages, acting as antigenpresenting cells (APC) and secreting proinflammatory cytokines and chemokines [32,33]. (http://www.jneuroinflammation.com/content/pdf/1742-2094-9-185.pdf)

Frankly, the information provided in the research article mentioned in the above paragraph is FULL of the pathophysiology that they use to link brain injury to Alzheimer’s.

I find that stories of people that have brain injuries are the best voice for telling what a person tends to experience while recovering from or living with a brain injury. While trying to find more information on the link between brain injuries and Alzheimer’s, I found a PHENOMENAL website that has a considerable number of stories from those who have a brain injury.

I find the following stories mirror my own experiences. To quote one woman’s experience, Angela:

To say that recovery from brain injury is difficult would do no justice to the anguish that came from realizing that the strengths and skills responsible for leading me in a life of success were severely impaired or nonexistent. It has been devastating to realize what was left. Moving on meant saying goodbye to my best friend of 32 years – “ME” – the most difficult thing I could ever have be asked to do.

In a matter of seconds, I became a stranger to myself.  I miss the old me so much that I question why I would survive the accident only to be forced to live in the shadow of my former self. But I know that the important parts of me were not lost even though it is a constant battle for me to find my way in a world that is moving so fast that I cannot keep up.

I would recommend checking out the dozens of stories that are listed on this site. I find that not only are they informative, but they mirror our experiences. It’s not some doctor trying to explain if what you are experiencing is normal or not, but PEOPLE who have the injury telling you what they’ve experienced in their life. : http://tbivoices.com/ian5.php

Wow, here’s another story that mirrors mine. I was just discussing with my occupational therapist that this has been a HUGE issue with my current job. I can’t remember what we’ve recently learned in training’s. I have a hard time locating information. I can’t remember new things about products that are new. It makes doing  the  job very very hard. Here is an excerpt from another person who went back to work:

For anyone to maintain employment, they not only have to have the skills to do the job, but also the appreciation that work is work, and that a good job may be irreplaceable.  That is far more difficult to remember, when judgment, mood and initiative is impaired after a brain injury.

However, Betty had another problem. She had already known how to be a dental hygienist before her accident and after rehab, was able to do much of what was required of her because it required her to use skills she had learned before her accident.  But the field of dentistry, like any profession, changed, she couldn’t learn the new techniques, acquire the new skills to adapt.

This too has happened to me on numerous occasions:

Those who don’t know much about brain injury are often surprised at how “normal” someone with a brain injury may be.  Only the truly profoundly injured will show the kind of overt dementia that we have been programmed to expect.  Most cognitive challenges are far more subtle than what an Alzheimers or severely learning impaired individual might have.  Much of the brain may be unaffected by even a severe injury, including long term memory and communication ability. Both Angela our first case study and Betty are perfect examples of that.  That Betty communicates so well is both proof of that tendency but also a credit to the extensive and multi-year rehabilitation that she received post injury.

Betty describes a number of classic cognitive problems.  Sequencing (putting things in order) and memory are ongoing problems.  Like most survivors, she has learned to write everything down.

Driving is one of the most troubling aspects of disability for a wide range of brain injured individuals.  It is a uniquely cognitively challenging task, requiring intense attention, visual perception, multi-tasking, capacity to deal with stress and coordinated sensory, reflexive and muscular control.  It took Betty about three years to get her drivers license again after her TBI.  Even now more than 25 years post injury, she must be careful where and when she drivers. http://tbilaw.com/tbivoices/cognitive-challenges-sequencing-staying-on-task-topic/
 

Ok, so I’m  not going to keep quoting all of these stories. Frankly, I do not have the ability to read through them. I become distracted and can’t stay on task. This post has already taken  more than four hours to write over two days 😦  I WOULD DEFINITELY RECOMMEND READING SOME OF THESE STORIES. They are what I think a lot of people experience in their recovery, and that makes them a valuable source of understanding, comfort, and knowledge.

I will continue to try to find more information on brain injuries, but please feel free to contact me regarding YOUR stories. I believe that until there is more information presented by more people, we will struggle to find doctors who understand that a brain injury is not an acute injury but a life long disease.

UPDATE:

This link was provided by a person who has found the connection between Alzheimer’s and the autoimmune response to brain injury. You will find it interesting:

http://www.dana.org/news/features/detail.aspx?id=40308

Related articles

Is a brain injury an acute incident or a chronic disease:

There is so much that we do not understand about the brain. There are thousands of scientists discovering new aspects of the brain everyday. As I’ve said before, the brain is still a mystery and doctors and scientists will be working far into the future to uncover its secrets.

Therefore, I believe that it is ignorant to think that an isolated injury to the brain will not cause resonating effects. At this time, due to limitations in science and limitations of understanding function,it is impossible to know with certainty what, if any, the long term effects will be. Currently, due to the media attention being directed to the NFL players who have experienced symptoms years after multiple concussions and head injuries, doctors and scientists are beginning to realize that there is a possibility that the injury continues to develop after the initial occurrence.

This idea is not widespread, and it is definitely not understood, but because of the media attention it is being looked at further.

In 2009, a paper was published by the Brain Injury Association of the USA, that stated:

Traumatic damage to the brain was therefore seen by the industry as an “event.” A broken brain was the equivalent of a broken bone—the final outcome to an insult in an isolated body system. Once it was fixed and given some therapy, no further treatment would be necessary in the near or distant future, and certainly, there would be no effect on other organs of the body.

The purpose of this paper is to encourage the classification of a TBI not as an event, not as the final outcome, but rather as the beginning of a disease process. The paper presents the scientific data supporting the fact that neither an acute TBI nor a chronic TBI is a static process—that a TBI impacts multiple organ systems, is disease causative and disease accelerative, and as such, should be paid for and managed on a par with other diseases.

If you’re reading that, it might feel like a breath of fresh air. I know that might sound funny because you, like me, might really want to believe that things won’t get worse. You want to believe that what the doctors told you post injury is true, but when things start to progress and you look at the medical community for answers, you receive smug grins, arched eyebrows, and the reminder that these new symptoms weren’t from the injury your received, so this passage feels like a little bit of reassurance and vindication. Someone out there believes that what you’re experiencing IS related to your brain injury, and that is where the relief is.

The paper then continues to show examples of where traumatic events, like severe burns, kidney disease, and lung disease lead to further complications and seemingly unrelated diseases like cardiac disease or lung diseases.

Yes, folks, what are they saying….what happens to one part of the body can impact another system of the body!!!! And if you think about it, the brain is the central processing system for the entire body, so why is it such a stretch for doctors to realize that an injury to the brain, which controls the functions of your lungs, your heart, your kidney’s, your hormones, EVERYTHING in your body, might cause irregularities in heart rates, sleep apnea, water retention, even a decrease in sex drive or reproductive ability. Frankly, I think it would be more surprising to discover that nothing happens after a brain injury.

I read some place that those of us who have developed CPM/EPM die within 5 -10 years after the injury. That said, I can not remember where I found that information. It seems that most of those who died had cardiac issues, like irregular heart rates, uncontrollable hypertension or hypotension, etc. SO, I found the following information extremely relevant as well. Keep in mind, the following applies to brain injuries in general.

In a 2004 study on mortality one year post injury among 2,178 individuals with a moderate to severe TBI, it was reported that individuals with a TBI were twice as likely to die as a similar non-brain injured cohort and had a life expectancy reduction of seven years (Harrison-Felix et al., 2006).

Follow-up studies on causes of death revealed that individuals surviving more than one year with a TBI are 37 times more likely to die from seizures, 12 times more likely to die from septicemia, four times more likely to die from pneumonia and three times more likely to die from other respiratory conditions than a matched cohort from the general population. The greatest proportion of deaths in the study—29 percent—was from circulatory problems.

Shavelle and colleagues found that individuals with a TBI were three times more likely to die of circulatory conditions (Shavelle et al., 2001). Although it is somewhat intuitive that individuals with moderate to severe TBIs would have a higher mortality rate than the normal population, even individuals with mild TBIs have been found to have a small but statistically significant reduction in long-term survival (Brown et al., 2004).

I have also stated that the younger you are the more likely you are to see the most improvements. I have said this so many times to doctors, friends, and my family. It is to be expected that as you age, your brain ages as well. This is common knowledge, but when you are talking to your doctors they tend to negate this fact. I really do not understand why.

That said, I think it that it makes sense that if you experience a brain injury when you’re older, your brain will probably not recover like it would have when you were in your 20’s.  It also makes sense that when you have an injury to your brain, the injured cells will tend to malfunction more as you get older leading to more dysfunction.

I would compare it to an apple that you drop on the ground. The area of the most impact won’t ever be the same. It’s never going to be un-bruised. However, as time goes on, that spot gets worse and worse. It becomes the first spot to rot. Unfortunately, I think that the brain is similar. The injury will never be undone completely and as well age, those weakened spots weaken more and more.

I know that does not sound very encouraging, but that’s why scientists and doctors need to focus on figuring out why it happens and what can be done to make the person the most functional after the injury. The following paragraph addresses this issue:

Age is clearly a factor in brain injury disease. Older patients show a greater decline over the first five years following a TBI than younger patients (Marquez de la Plata et al., 2008). Also, the greatest amount of improvement in disability has been noted in the youngest group of survivors.

Because I found the following information SO incredibly descriptive of some of the things that I have gone through, I decided to just add it to the post. So, the following information is directly from the Brain Injury Association of the USA paper that has been used through this entire post:

Epilepsy
Traumatic brain injuries are a major cause of epilepsy, accounting for 5 percent of all epilepsy in the general population (Hauser et al., 1991). Individuals with a TBI are 1.5-17 time (depending on the severity of the TBI) more likely than the general population to develop seizures (Annegers et al., 1998). TBI is the leading cause of epilepsy in the young adult population. Seizures will be observed over a week after a penetrating TBI in 35-65 percent of individuals. In a study of 309 individuals with moderate-severe TBI followed as long as 24 years post injury, 9 percent were being treated for epilepsy (Yasseen et al., 2008). As the time from injury to the time of the first post TBI seizure may be as long as 12 years (Aarabi et al., 2000), there is a need for heightened awareness of the development of epilepsy on the part of the patient, family and treating medical personnel.

Vision

Visual disturbances are common after a TBI, occurring in 30-45 percent of individuals (Sabates et al., 1991). In a review of 254 individuals, two and five years post injury, 42 percent continued to complain of visual difficulties at five years (Olver et al., 1996). Optic atrophy can begin shortly after the brain injury and lead to a marked decreased acuity and blindness. Persistent 4 visual field deficits also pose a significant safety risk due to the inability to see to the side. High flow carotid cavernous fistulas causing the direct flow from the internal carotid artery system into the cavernous venous sinus may develop weeks after a TBI. If not recognized and treated, permanent visual loss may progressively develop (Atkins et al., 2008).
Sleep
Sleep complaints are common following TBI. Subjective complaints of sleep disturbances have been reported in 70 percent of TBI outpatients (Chesnut et al., 1999, Max et al., 1991, McLean et al., 1984). Disturbed sleep, as measured by polysomnogram, was reported in 45 percent of a group of 71 individuals averaging three years post injury (Masel et al., 2001). Hypersomnia is associated with decreased cognition and decreased productivity, and certainly with a greater risk for accidents. National Highway Traffic Safety Administration data showed that approximately 56,000 auto crashes annually were cited by police officers where driver drowsiness was a factor (Strohl et al., 2005).
Alzheimer’s Disease
Alzheimer’s disease (AD) is an enormous public health problem in the United States where 5.2 million Americans are living with that disease. The direct and indirect cost of this disease is estimated to be $148 billion annually. (http://www.alz.org/index.asp). Although the cause of Alzheimer’s is unknown, numerous studies have shown that a brain injury may well be a risk factor for the development of Alzheimer’s disease (Jellinger et al., 2001, Plassman et al., 2000). In a large study of World War II veterans, Plassman and colleagues found that any history of head injury more than doubled the risk of developing AD, as well as the chances of developing non-Alzheimer’s dementia. They also found that the worse the head injury, the higher the risk for AD. A moderate head injury was associated with a 2.3 fold increase in the risk, and a severe head injury more than quadrupled that risk (Plassman et al., 2000). In their excellent review on this issue, Lye and Shores (Lye and Shores, 2000) suggested many possible etiologies for this connection: damage to the blood brain barrier causing leakage of plasma proteins into the brain, liberation of free oxygen radicals, loss of brain reserve capacity, as well as the deposition of beta amyloid plaque (present in Alzheimer’s disease). Even individuals with no known cognitive impairment after their TBI have a risk of an earlier onset of dementia due to Alzheimer’s disease (Schofield et al., 1997).

Chronic Traumatic Encephalopathy (CTE) has recently garnered the attention of both the medical and lay press. At one time referred to as dementia pugilistica or “punch drunk,” CTE is a distinct neuropathological entity caused by repetitive blows to the head and was at one time deemed to be a disease seen only in old retired professional boxers. CTE is an insidious disease beginning with deterioration in concentration, memory and attention, eventually affecting the pyramidal tract resulting in disturbed gait, coordination, slurred speech and tremors (McCrory et al., 2007). The sporting world has recently been shaken by autopsy-confirmed findings of CTE in retired professional football players (Omalu et al., 2006). As repetitive head injuries occur in a wide variety of contact sports beginning at the high school level, there is a pressing need for further study of this entity.5

Neuroendocrine
A TBI is associated with a host of neuroendocrine disorders. Hypopituitarism is found in approximately 30 percent of individuals, over a year post injury, with moderate to severe TBIs (Schneider et al., 2007). Although individuals who develop post-traumatic hypopituitarism acutely may have resolution of that problem over time (Aimaretti et al., 2004), 5 percent of those patients in that study had normal pituitary functioning at three months but developed deficits at one year (Aimaretti et al., 2005). Growth hormone (GH deficiency/insufficiency is found in approximately 20 percent of moderate to severe TBIs (Agha and Thompson, 2006). GH deficiency is associated with an increased risk of osteoporosis, hypercholesterolemia and atherosclerosis. These patients have a significant increase in mortality from vascular disease (Rosén and Bengtsson, 1990). Hypothyroidism is found in approximately 5 percent of individuals post TBI (Agha and Thompson, 2006). Associated signs and symptoms are weight gain, dyspnea, bradycardia and intellectual impairment (Agha and Thompson, 2007). A recent study has shown a connection between hypothyroidism in females and the development of Alzheimer’s disease (Tan et al., 2008). Gonadotropin deficiency is found in approximately 10-15 percent of individuals post TBI (Agha and Thompson, 2006). Adult males will note decreased libido, muscle mass and strength. A correlation has been found between low free testosterone levels and cognitive function, although there is no clear consensus on testosterone supplementation therapy and cognition (Papaliagkas et al., 2008). Hypogonadal women will develop secondary amenorrhea and increased risk for osteopenia.
INCONTINENCE
A TBI frequently affects the cerebral structures that control bladder storage and emptying functions, resulting in a neurogenic bladder. Fox-Orenstein and colleagues reviewed the records of more than 1,000 individuals admitted to rehabilitation centers after a TBI. One-third of the individuals were incontinent of bowel. Twelve percent were incontinent at discharge, but 5 percent were still incontinent at the one year follow-up. In their review of medical complications in 116 individuals with moderate to severe TBI, Safaz and colleagues found that 14 percent had fecal incontinence over one year post injury (Safaz et al., 2008). Fecal incontinence is not only socially devastating, but it will have medical consequences, including skin breakdown, pressure ulcers and skin infections (Foxx-Orenstein et al., 2003). Urinary incontinence is also an enormous social and medical problem. Chua, et al., (Chua et al., 2003) reviewed the records on 84 patients admitted to a rehabilitation unit within six weeks of injury. Sixty-two percent were incontinent. This improved to 36 percent at discharge; however, 18 percent remained incontinent at six months. Safaz and colleagues found urinary incontinence in 14 percent of their cohort over a year post injury (Safaz et al., 2008). Urinary incontinence is associated with the development of frequent urinary tract infections and decubitus ulcers. 6
PSYCHIATRIC DISEASE

The impact and cost to society by psychiatric disorders is among the most important healthcare issues of today. Current estimates in the U.S. suggest that the collective cost of psychiatric diseases could be one-third of the total healthcare budget (Voshol et al., 2003). It is critical to note that psychiatric and psychological deficits are among the most disabling consequences of a TBI. Many individuals with a mild TBI, and the overwhelming majority of those who survive a moderate to severe TBI, are left with significant long-term neurobehavioral sequelae. The costs to society in terms of lost productivity, as well as the costs for medical treatment are enormous. In addition to the aggression, confusion and agitation seen in the acute stages, a TBI is associated with an increased risk of developing numerous psychiatric diseases, including obsessive compulsive disorders, anxiety disorders, psychotic disorders, mood disorders and major depression (Zasler et al., 2007b). Individuals with a TBI appear to have higher rates of depressive disorders, anxiety disorders and substance abuse or dependence (Hibbard et al., 1998, Holsinger et al., 2002, Koponen et al., 2002, Silver et al., 2001) and often have suicidal plans or suicidal behavior in the context of these illnesses (Kishi et al., 2001). TBI is associated with high rates of suicidal ideation, (Kishi et al., 2001, León-Carrión et al., 2001) suicide, (Silver et al., 2001) and completed suicide (Teasdale and Engberg, 2001). In chronic TBI, the incidence of psychosis is 20 percent. The prevalence of depression is 18-61 percent, mania is 1-22 percent, PTSD is 3-59 percent and post TBI aggression is 20-40 percent (Kim et al., 2007). Koponen, et al, (Koponen et al., 2002) studied 60 individuals, 30 years post injury. Fifty percent developed a major mental disorder that began after their TBI. Another 11 percent developed a major mental disorder later on in their lifetime. Twenty-three percent had developed a personality disorder. In a long-term follow-up study of 254 individuals at two and five years post TBI, it was found that there was a higher incidence of cognitive, behavioral and emotional changes at five years than at two years post TBI. Thirty-two percent of those working at two years were unemployed at five years (Olver et al., 1996). A traumatic brain injury clearly may cause decades long, and possibly permanent, vulnerability to psychiatric illness.

SEXUAL DYSFUNCTION
Sexuality, both physiological and functional, plays an enormous role in our lives. Sexual dysfunction is a large issue in the general population and is a major ongoing problem in the TBI population. Studies have shown 40-60 percent of individuals complain of sexual dysfunction after a TBI (Zasler et al., 2007a). Transient hypogonadism is common acutely following a TBI, yet it persists in 10-17 percent of long-term survivors. Beyond just the fertility and psychosocial issues presented by hypogonadism, muscle weakness and osteoporosis may have a significant impact on long-term function and health with consequences exacerbated by immobility of long durations following a TBI (Agha and Thompson, 2005). 7

MUSCULOSKELETAL DYSFUNCTION

Muscular dysfunction

Spasticity is characterized by an increase in muscle tone that will result in abnormal motor patterns. This spasticity may well interfere with an individual’s general functioning, and limit self care, mobility and independence in the activities of daily living. Spasticity requires life long treatment. Untreated, spasticity will eventually lead to muscle contractures, tissue breakdown and skin ulceration.

Skeletal dysfunction
The incidence of fractures in a TBI is approximately 30 percent. TBI patients with fractures, especially fractures of the long bones, are at risk for heterotopic ossification (HO), which may not develop for as long as three months post injury. HO is defined as “the development of new bone formation in soft tissue planes surrounding neurologically affected joints,” and has an incidence of 10-20 percent following a TBI (Colorado, 2006). Safaz and colleagues found HO in 17 percent of their cohort over a year post injury (Safaz et al., 2008). If left untreated, HO will eventually lead to abnormal bony fusions (ankylosis) and subsequent functional limitations.

SUMMARY

Historically, individuals living with a brain injury have been referred to as brain injury survivors. No one knows how that term came to be used in this situation. Perhaps the concept of merely staying alive was used because as little as 30 years ago, the majority of individuals with a moderate to severe TBI succumbed soon after their injury. Perhaps it was used to imply that the individual outlived their injury and persevered despite the hardship of the trauma. This term, however, does not address the reality of brain injury. Cancer survivors are survivors because it is believed they are cured—and they indeed have outlived their disease. Many individuals who sustain a TBI recover 100 percent. They have truly survived their injury. However, in the U.S. alone, every year, over 125,000 individuals who sustain a TBI become disabled. This paper discusses only a small percentage of the causes of disability and the ongoing and developing medical conditions individuals with TBI face. Presently, more than 3 million individuals in the U.S. are disabled due to the myriad of sequelae of a TBI (Zaloshnja E, Miller T, Langlois JA, Selassie AW. Prevalence of long-term disability from traumatic brain injury in the civilian population of the United States, 2005.The Journal of Head Trauma Rehabilitation 2008;23(6):394-400.) Their brain trauma has resulted in a condition that is disease causative and disease accelerative. As a result of their brain trauma, these individuals now have life-long brain injury disease. Their disease should be reimbursed and managed on a par with all other diseases. Only then will the individuals with this disease get the medical surveillance, support and treatment they deserve. Only then will brain injury research receive the funding it requires. Only then, will we be able to
truly talk about a cure. 8

ACKNOWLEDGEMENTS
The Brain Injury Association of America gratefully acknowledges Brent Masel, M.D., as the author of this position paper. The Association also thanks Mark J. Ashley, Sc.D., Gregory J. O’Shanick, M.D., and Christopher Nowinski for their contributions. The Board of Directors of the Brain Injury Association of America adopted this position paper at its meeting on February 27, 2009, in Washington, D.C. The Association will continue to review the topic of brain injury as a disease as scientific and public policy progress dictates.
Electronic copies of this statement may be obtained from the Brain Injury Association of America’s website: http://www.biausa.org.
The paper may be cited as follows: Masel, B. Conceptualizing Brain Injury as a Chronic Disease. Vienna, VA: Brain Injury
Association of America, 2009.

In order to find the following references for the above information, please use the following link to access the guide in its entirety: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CCYQFjAA&url=http%3A%2F%2Fwww.biausa.org%2F_literature_49034%2FBrain_Injury_As_a_Disease_Position_Paper&ei=GM6JUMKBNbHlyAGI54DIDA&usg=AFQjCNFL04VqG2OMLtMj4BolSg8oLMOJxQ

I will keep trying to find more information, but I really feel that this describes a lot of what I have experienced. I believe it is an accurate research article that you should present to your doctor if you have had a brain injury or know of someone who has.

UPDATE: I found this information posted regarding the long term outcome of brain injury. It does discuss some of the issues that were listed above. I also states that damage to the basal ganglia can lead to late onset Parkinson’s disease. I found this interesting because I had injury to this area, and I’ve been told by numerous doctors that my jerking, etc wold not be related to the CPM injury that I have. I did have a radiating pain throughout my body after the initial injury. This radiating pain went away, but in its place, I’ve had issues with random cramping, jerks, and spasms. The doctors didn’t think that the spasms etc were related to my brain injury because I didn’t have the symptoms initially. This is proof that it can and does happen, and it can take up to forty years post injury to have it develop.. That’s crazy!!!

Neurodegenerative disorders such as dementia of the Alzheimer’s type (DAT) and Parkinsonism are related to mild and moderate TBIDAT is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. A moderate TBI increases the risk of DAT with a hazard ratio (HR) of 2.32. In case of a severe TBI the HR for DAT is 4.51. For the sake of ease, one could say that the risk for DAT in patients with a moderate TBI is 2.32 times compared to those who have not suffered a TBIParkinsonism may develop years after TBI as a result of damage to the basal ganglia. It is characterized by tremor or trembling, rigidity or stiffness, slow movement (bradykinesia), inability to move (akinesia), shuffling walk, and stooped posture. The association between TBI and parkinsonism has not been studied as extensively as inDAT. However significant associations between PD and TBI have been established. Professional career boxers have in increased risk for dementia pugilistica also called chronic traumatic encephalopathy or the punch-drunk syndrome. Mild cases may present with slurring dysarthria, gait ataxia, disequilibrium and headache. Symptoms begin anywhere between 6 and 40 years after the start of a boxing career, with an average onset of about 16 years. Mental and physical abilities may decline resulting in dementia and parkinsonism.  (http://cirrie.buffalo.edu/encyclopedia/en/article/338/)  “Brain Injury: Long term outcome after traumatic brain injury”” Gerard M Ribbers, MDPh.D.

 

Additional symptoms related to CPM:

 

I’ve previously described movement issues like dystonia, Parkinson like tremors, other tremors, and random jerking movements, but this is something I have not heard about previously, choreic.

I had no idea what the word meant or what it is related to before a few days ago, so please feel free to add any input you might have about it.

 

The dictionary definition is: “An involuntary spasmodic twitching or jerking in muscle groups not associated with the production of definite purposeful movements.”

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
Basically, these movements are involuntary movements and jerks, so I guess in a way, I have discussed this issue before. I have jerks a lot.
If I get really stressed there seems to be this movement that my left leg does. It’s weird, and if I every experience it for a long period, I will upload a video of it. It really feels like I should have control of it. It seems ridiculous that I can’t, but it’s like my body has a mind of its own and this is one thing that I never had an issue with before. It really bugs me, but others don’t seem to notice. I guess some might consider it a  nervous tic.
I believe that the following videos really do what the motions are like for those who have these types of jerks.
This is kind of what I have experienced, so I’m posting it. I don’t have issues with my face so much as I do with kind of a rolling to my left and a rocking of my left leg and rolling of my body. It  really seems like I’m jittery or nervous or can’t sit still.  I don’t experience it very often and the periods that I go through are brief. I believe this is a positive sign.
With the following video, the little girl developed this because of scarlet fever, not huntington’s disease. She was able to recover almost completely so the following videos show her before and after:
Another good example. I believe these kind of show the extremes. Some people just seem fidgety. Others are extremely disabled.
The information that I have found has been sparse when it comes to directly attributing these choreic movements to CPM/EPM. However, it has been documented. It may not be an immediate appearing symptoms. In some cases it did not appear until months after CPM/EPM was first diagnosed. I have read that this in not an uncommon theme regarding EPM. It seems that movement disorders with EPM can appear months after the injury. I really noticed my issue develop at a doctor’s appointment. I was becoming extremely agitated, and I realized that my left kept moving as well as my left shoulder. I kept crossing and uncrossing my leg as well as moving in my chair. I’ve noticed those movements at other times of stress.
Thankfully, I don’t think it is getting worse for me.
The following information is a chart that describes that chorea can be caused by electrolyte issues:
J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

Table 6

Metabolic aetiologies of dystonia and chorea

Hyperthyroidism
Hypocalcaemia (hypoparathyroidism)
Hypoglycaemia
Hyperglycaemia
Hypernatraemia
Hyponatraemia
Hypomagnesaemia
Osmotic demyelination syndrome (central pontine myelinolysis)
Splenorenal shunt

 

Literature also seems to suggest that these reasons that these choreic movements occur is because of injury the putanem or basal ganglia. It suggests that there is a decreased amount of GABA, and there there are issues with Dopamine and glutamate.

Frankly, folks, I simply can’t read through this very detailed information from the following journal link, but it goes into great explanation why both dystonia and chorea are found in a variety of brain damage injuries, including CPM/EPM, Huntington’s disease, and many others.

Here is the quote:

As discussed earlier, dystonia and chorea most commonly result from striatal dysfunction, and hypoxia-ischaemia has been shown to alter several neurotransmitter systems in the striatum. Glutamate is the main neurotransmitter in cortical neurons projecting to the striatum and may contribute excitotoxic injury. Hypoxia-ischaemia has been shown to increase striatal extracellular glutamate, and decrease glutamate transporter concentrations. Direct lesioning of the globus pallidus with excitatory amino acids in monkeys produces cocontraction of opposing muscle groups on reaching, as in dystonia.9Extracellular dopamine concentrations rise and concentrations of dopamine metabolites fall after hypoxia-ischaemia.710Dopamine may also potentiate the excitotoxic properties of glutamate, and depleting the striatum of dopamine before hypoxia-ischaemia decreases the degree of striatal injury. In the neonatal rat model of cerebral hypoxia-ischaemia, striatal D1 and D2 dopamine receptor numbers fluctuate until 9 to 11 weeks after injury, at which time the D1 receptor number has returned to normal but the reduction in D2 receptors persists.11 Hypoxia-ischaemia also results in areas of complete loss of preproenkephalin mRNA in the dorsal striatum of the rat brain.12 Enkephalin, together with GABA, is an inhibitory neurotransmitter in the projections from the putamen to the external pallidum. Hypoxic-ischaemic necrosis of medium sized spiny striatal neurons may be responsible for decreased concentrations of the inhibitory neurotransmitter, GABA. By contrast, the striatal cholinergic system remains relatively preserved or even upregulated after hypoxia-ischaemia, as evidenced by an increase in cholinergic fibres and cell bodies, and an increase in acetylcholine release.13This is interesting in that anticholinergic medications often ameliorate dystonic movements.

http://jnnp.bmj.com/content/65/4/436.full

J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

I will try to add more to this post in the future if I can, but right now, I can’t. Please feel free to leave questions or suggestions as you like.

 

Have a great night 🙂

 

CPM/EPM- Locked-In Syndrome:

I am sorry that I have not reported on this critical symptom of CPM/EPM previously. I thought I had covered it previously, but I’m not finding any previous posts about it. Please forgive me if I have posted about it, but this should be a much more informative post.

Locked in syndrome is an issue that occurs with brain injury, so it is not just a symptom related to CPM/EPM alone. It can happen with stroke and also with head trauma. It is characterized by the inability to move ANYTHING, except for the eyes. Generally, a person is able to open and close their eyelids and look vertically up. However, they are unable to speak. Sometimes, they are unable to make any sounds at all. Even though they have significant paralysis, their cognitive functions seem to be close to normal or near normal.

It is difficult to determine how many people are actually impacted by locked in syndrome because most of those impacted die before it can be definitively diagnosed. It is also suspected that a number of patients might not be diagnosed because they make an astounding recovery.

Now, again, locked in syndrome is not solely caused by CPM, but it is generally related to an injury to the pontine area of the brain. It is believed that strokes are the primary cause of locked in syndrome. It can also be caused by infection and other demyelination causes.

I found this to be extremely interesting. Firstly, a person may not be able to move even their eyes, so it is believed that a number of persons who are impacted by locked in syndrome might be misdiagnosed as being in a vegetative state, ie that they have little or no cognitive function. It is also sometimes confused with coma.

Due to the complex nature of locked in syndrome, it makes it difficult to determine the true number of people that are impacted. That’s pretty scary, especially when you take into consideration cases like Terry Schiavo.

It was never clearly determined if Terry Schiavo was in a vegetative, completely brain damaged state or if she had some cognitive function and had significant paralysis. It has been determined that she had an electrolyte imbalance, possibly related to an eating disorder, but there is also concern that her injuries were caused by an attack from her husband. It truly is a mystery, but that’s the scary part with people being in an locked in state. It is extremely difficult to determine the extent to their injuries.

For more on Terry Schiavo, I found this website to be very informative: http://www.wnd.com/2005/03/29516/

Now there are different levels of paralysis with locked in syndrome. A person can be completely paralyzed in which there is no ability for movement, even their eyes are paralyzed. There is classic which a person retains the ability to move their eyes (vertically or blink), and then there is incomplete locked in syndrome. In this version, a person has very limited movement.

A person who has more movement has a better chance of recovery.

I found the following website extremely detailed in describing locked in syndrome and what to expect: http://cirrie.buffalo.edu/encyclopedia/en/article/303/

I found this paragraph interesting:

Alertness often fluctuates, especially during the acute phase (Gutling et al., 1996). Several authors reported that cognitive functions were generally preserved although cognitive impairment may be present (Smith et al., 2008; Smith and Delargy, 2005; Ruff et al., 1987). Attention and memory disorders are observed in nearly half the cases, especially in individuals with a post-traumatic LIS (León-Carrión et al., 2002; Ruff et al., 1987; Garrard et al., 2002). Emotional lability is a common symptom (Garrard et al., 2002). Apathy is sometimes observed and may persist in some cases (Beaudoin and De Serres, 2008). Recovery of cognitive functions is often observed in individuals during the first year (Brunoet al., 2008).

I think the above is true for most brain injuries. There seems to be cognitive issues with memory, attention and learning. There is also that psychological factor that is involved in brain injury as well. These are issues that I have experienced but have had difficulty locating in the literature describing CPM/EPM…not the cognitive issues but the psychological aspects, so I found this to be “proof” that this behavior isn’t unlikely with CPM/EPM.

I found this video EXTREMELY relevant. I really think that this is what happened to Terry Schiavo. I have been told by a friend recently that a similar situation is happening NOW to their family member.

This is a similar story to Terry’s.

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

The following video is also heartbreaking:

http://www.youtube.com/watch?v=6gqSYIDsKjs

The following is a story of a women who has locked in syndrome, and how she finds that her life is still important and worth living. It’s very inspiring.

http://www.youtube.com/watch?v=A3uEMyVnThI&feature=related

I found this story also inspiring:

http://www.youtube.com/watch?v=ZR2GQikB7I4

http://www.youtube.com/watch?v=3IO6i0syM8Q

I really think it’s important for people to realize that if you or someone you love develops this condition, it does not mean that you life is over, and it is important to WAIT before pulling feeding tubes or other life supportive measures.

I pray that any of you reading this are just looking for information, and are not experiencing this personally. It is an extremely difficult condition to live with and to watch your loved ones experience, especially in the beginning, but as technology becomes more advanced, I believe there will be more hope and further recovery for even the most devastating cases of locked in syndrome.

In closing, I believe the most important thing for a significant recovery is early recognition and an immediate start to rehabilitation. It is also important to get all senses involved through the use of bitter liquids, sounds, movements, etc.

Please feel free to comment regarding your personal experiences with locked in syndrome or questions.

 

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