Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the category “Central Pontine Myelinolysis/ Extrapontine Myelinolysis”

The Stages:

It’s been hard the past few months, and I think that shows in my “personal” posts. I’ve been told by some that I’ve been a bit negative about what I’m going through. I’ve been told by others that I’m depressed.

It is really hard to live through what I’ve lived through, and I found out that all of those things that I’ve experienced are normal.  For those of you who might now be used to going through difficult times in your life, having CPM/EPM might be a slap in the face. I’ve gone through really difficult times, and it was still a slap in the face for me. It seems that most people tend to not quite understand everything you are experiencing, so I thought this post would be dedicated to getting a better grasp on what to expect. It’s  not just what your significant other might live through, but it’s the steps or processes that you might live through too.

I think once you get on the other side of this process, then you can really start to live the rest of your life as it is now or prepare for the future. I want to stress that these steps do not have any specific order. They are NOT an exact science. You might experience one of these steps. You might experience all of these steps. You might live in a cycle of these steps. There’s no guarantee, but I hope it helps you understand what to expect and gives you a few resources on how to cope with it.

You are your own person, so don’t expect anyone to try to identify what you are living through. They can’t know what you are living through, but it’s important to understand that they are living with or around you and because they love you, seeing you in pain will give them pain of their own.

They aren’t trying to make your life miserable, so try to be patient. They are doing the best that they can to give you the support that you need, but it isn’t easy for them. You will find that they will go these same stages too because it is a trauma to their life just in a different way.

I hope that makes sense.

The stages are known as the five stages of death, but it’s actually a more accurate way to describe as the five stages of trauma. In other words, it’s classically known as the five stages of death and dying, but you will find that people live through these same stages when ever there is a major impact to their life…loss of a limb, brain injury, loss of a job, an end to a relationship, terminal illness, etc.

The five stages:

Denial.

Anger.

Bargaining.

Depression.

Acceptance.

For me, I don’t think I went through denial. I think I went into shock and fear. I didn’t understand fully what having CPM/EPM meant. I could recite the worst possible scenarios that could happen, and I felt lucky after I passed through the first 12 weeks without dying, but I was still scared because there is that unknown.

I really didn’t want to make adjustments to my routines because I really thought in time things would get better. Maybe that was denial, but my doctors gave me the hope that I would recover in a year or so, and that I would see major improvements in that time. I did experience huge improvements in the first 12 weeks, even in 6 to 9 months, but now things have leveled off, and I believe in things like memory they are getting worse. So, I don’t know if that’s denial.  I had different expectations.

I definitely experienced anger. I am still experiencing anger. I have to say there are days that I will get in the shower and cry. Yes, I know it’s strange to cry in the shower, but it is one of the few times where I can be alone..no kids, no puppy, no phone calls, and I have time to focus on what I am going through. And what I am going through sucks. It sucks. So, this morning, I was thinking about how this stupid doctor screwed up my treatment for something that EVERY doctor is supposed to know how to treat, and now I am going through SO much stress and anxiety. All I wanted to do was be a doctor, and there was no guarantee that it would happen, but I had made it so far through so much, and so I become extremely ANGRY. Yes, I am. I am hurt and because I am so hurt, I am angry. That doctor will go to sleep tonight and he may only think about what he is going to do this weekend. Is he going to fall asleep tonight and think about how I lost my life? No, probably not.

It’s stressful living this life. It’s hard right now, and I have no idea what I am going to do with my future or how much of a future I have. And so Anger is something that I am learning to live with but that anger comes from the pain and hurt over what has happened to me. I just want to go back to being normal and I can’t.

Bargaining, well I’ve begun to do that. I was in Chicago a few weeks ago, and I found an Irish vendor. It was basically Irish and Catholic trinkets of all kind. I went through the medals of all the saints, and I found the medal of St. Jude. St. Jude is the saint of lost causes, especially when dealing with health issues. So, I had to get the medal. I had to wear it daily. It didn’t take long for me to lose it. I have no idea what I did with it. But, it’s really sad because even though I haven’t stepped inside a church (except for a recent baptism and wedding) in YEARS, I had to buy this medal of St. Jude and wear it and pray with all my heart: Please let me get better. Please let my legal issues work out. Please let me get better. I will help the poor, post an article in the newspaper. Whatever, I can do to fix this I will do it.

I had no idea that this was all “normal” for what I was going through. I mean I think I went through something similar while I was in the hospital. It was a: please don’t let me die, kind of prayer.  It was a scary time, but the only thing I did was pray a bit. It wasn’t the same as when I bought and wore a St. Jude medal recently. It wasn’t until that point that I really started the bargaining: if you make me better, I will……

Heck, if you ask anyone, including me, you’ll understand that I’ve been dealing with depression. I think it goes hand in hand with the anger, hurt, and frustration. It’s a slap in the face when you’re told to just be patient that things can get better, but then you hit a stagnant point. This just haven’t moved, and I don’t have any patience. I really don’t.

It is depressing facing the fact that you are not like other people. Your life has changed, and it’s not for the better. You are facing so many bad circumstances and you have no control over it. How are you going to be able to live the rest of you life like this? Are you going to be able to watch your children get older? You might be facing unemployment or financial uncertainty or be dependent upon friends and family to just do the basic things in your life.

This is depressing.

Eventually, you will move to acceptance. This is one of the more peaceful stages of your trauma. You start to realize that your life has changed and that there isn’t much that you can do to control the situation. It isn’t right. It isn’t fair, but you can not move beyond the other steps until you reach this one. And it can’t just be a process of saying that you are hurt or listing the horrible way the injury has impacted your life. You have to get to a point where you actually feel and accept the injury.

Literally for the past year, I have been very vocal about my experience and how it has changed my life, but that didn’t mean that I accepted what was going on with me personally. I was in denial about how permanent these changes are. I still hold out hope that things will get better, but I’ve come to accept that I will NEVER be the same person. I have been changed, physically, mentally, emotionally by my experiences. I have come to accept that I will have to write things down to make sure I can track how much I’ve spent. I will have to label places around my house and make a conscious effort to keep placing things where they belong. I will have to trust my son when he tells me that he didn’t take money from my purse or the cashier when she tells me that I received the correct change.

IT IS EXTREMELY HARD FOR ME TO DO THIS. EXTREMELY. I’m an unbelievably independent person. I’ve always had an unbelievable memory that I took for granted. I’ve never had to label things, etc. But now I am accepting that those changes have to be made, and I will have to commit myself to doing them.

It’s hard. It’s not fair. It sucks. I shouldn’t have to do it. I’m still very angry about it. It’s depressing, but I am going to have to accept it, learn to live with it and adjust or I will never be able to move past it, and I’m ready to move past it.

I really hope you find support in this post. I would have never realized that these steps are a process, and keep in mind that with any major change in your life just because you go through the cycle of these steps once doesn’t mean that you won’t go through them again.

Take care 🙂

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.

 

CPM: THE STATISTICS

So after months of trying to find out the answers to this question, I have found a beginning answer. Now, here’s the thing. This is the diagnosis code for CPM, but it doesn’t include a diagnosis code for those who develop EPM only…at least I don’t believe it does. But, it’s a start. 🙂

First the ICD-9 diagnosis code for CPM is

The way I found this is through my friend Jeffery Amitin. He left it in a message he posted in 2008. The ICD-10 code is G37.2:

2012 ICD-10-CM Diagnosis Code G37.2

Central pontine myelinolysis

  • G37.2 is a billable ICD-10-CM code that can be used to specify a diagnosis.
  • On October 1, 2013 ICD-10-CM will replace ICD-9-CM in the United States, therefore, G37.2 and all ICD-10-CM diagnosis codes should only be used for training or planning purposes until then.

Mortality Data

  • Between 1999-2007 there were 209 deaths in the United States where ICD-10 G37.2 was indicated as the underlying cause of death 
  • ICD-10 G37.2 as underlying cause of death data broken down by: gender, age, race, year

ICD-10-CM G37.2 is part of Diagnostic Related Group(s) (MS-DRG v28.0):

  • 058 Multiple sclerosis & cerebellar ataxia with mcc
  • 059 Multiple sclerosis & cerebellar ataxia with cc
  • 060 Multiple sclerosis & cerebellar ataxia without cc/mcc

Convert ICD-10-CM G37.2 to ICD-9-CM

The following ICD-10-CM Index entries contain back-references to ICD-10-CM G37.2:

  • Myelinolysis, pontine, central G37.2

Now, the above information states that the number of deaths related to CPM from 1999 to 2007 were 209 deaths. Now, I believe this is an EXTREMELY low number because it is believed that at least a 1/3 of patients who develop CPM die. The following information for 2010 ALONE, makes me doubt that the number of deaths related to CPM over an 8 year period is only 209.

2010 National statistics – principal diagnosis only

Outcomes by 341.8 Cns Demyelination Nec
341.8 Cns Demyelination Nec Standard errors
Total number of discharges 524 56
In-hospital deaths * *

The above information states that there were 524 DISCHARGES related to CPM…that doesn’t include the number of those who died from CPM.

The other interesting finding in the statistics above is that there WERE NOT ANY DEATHS related to CPM. Now, I really believe that’s not possible at all. Obviously, there’s information that is missing. 😦

Now this makes a little more sense. If you list the number of diagnosis of CPM that is diagnosed in combination with another disorder/disease, then the number of those who impacted jumps dramatically:

2010 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”
341.8 Cns Demyelination Nec
341.8 Cns Demyelination Nec Standard errors
Total number of discharges 2,490 190

The following chart is the number of those who have been diagnosed with CPM over the past 18 years. Considering that the number of cases of hyponatremia have increased over the past 10 years, it is a bit unusual not to see the same type of increase in the number of cases of CPM. Again, I have to wonder if the data reported on CPM, due to the nature that it is usually caused by malpractice, is in accurate. I will continue to try to find out information as it becomes available.

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

Number of discharges
ICD-9-CM all-listed diagnosis code and name 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
341.8 Cns Demyelination Nec 1,956 1,831 2,127 2,386 2,594 2,300 1,906 1,711 1,662 1,666 2,003 2,097 2,103 2,435 2,537 2,299 2,168 2,490

Keep in mind, that the above information is the number of people DISCHARGED. This is not a record of the number of deaths related to CPM.

Please use the following website to find out more information regarding CPM. You have to do research on all hospitals in the nation and use the ICD code 341.8 to locate these charts.

Also, please feel free to contact me with any questions.

 

Spasticity

This post is brought to you by my friend Deb. She has CPM/EPM too.  She’s had it for four years, and her story is one of determination and strength. She is truly amazing. I am going to start listing her story under the “Your Hyponatremia/CPM story” section, but this information on spasticity was gathered by her.

Thank You, Deb, for your help!! 🙂

Submitted on 2012/06/11 at 2:11 pm

Here is some info on spasticity and how it effects your body;
Spasticity is a muscle control disorder that is characterized by tight or stiff muscles and an inability to control those muscles. In addition, reflexes may persist for too long and may be too strong (hyperactive reflexes). For example, an infant with a hyperactive grasp reflex may keep his or her hand in a tight fist.

What Causes Spasticity?

Spasticity is caused by an imbalance of signals from the central nervous system (brain and spinal cord) to the muscles. This imbalance is often found in people with cerebral palsy, traumatic brain injury, stroke, multiple sclerosis, and spinal cord injury.

What Are the Symptoms of Spasticity?
Increased muscle tone
Overactive reflexes
Involuntary movements, which may include spasms (brisk and/or sustained involuntary muscle contraction) and clonus (series of fast involuntary contractions)
Pain
Decreased functional abilities and delayed motor development
Difficulty with care and hygiene
Abnormal posture
Contractures (permanent contraction of the muscle and tendon due to severe persistent stiffness and spasms)
Bone and joint deformities

How Is Spasticity Diagnosed?

Your doctor will evaluate your medical history in order to diagnose spasticity. He or she will look at what medications you have taken and whether you have a history of neurological or muscular disorders in your family.

Several tests can help confirm the diagnosis. These tests evaluate your arm and leg movements, muscular activity, passive and active range of motion, and ability to perform self-care activities.

How Is Spasticity Treated?

Treatment for spasticity may include medications like Lioresal, Zanaflex, Dantrium, Valium, or Klonopin. Occupational and physical therapy programs, involving muscle stretching and range of motion exercises, and sometimes the use of braces, may help prevent tendon shortening. Rehabilitation also may help to reduce or stabilize the severity of symptoms and to improve functional performance. Local injections of phenol or botulinum toxin may be used to relax specific muscles. Surgery may be recommended for tendon release, to cut the nerve-muscle pathway, or to implant a baclofen pump (intrathecal baclofen therapy).

Learn more about baclofen pump therapy.

How Painful Is Spasticity?

The pain associated with spasticity can be as mild as a feeling of tight muscles, or it can be severe enough to produce painful spasms of the extremities, usually the legs. Spasticity also can cause low back pain and result in feelings of pain or tightness in and around joints.

What Is the Outlook for People With Spasticity?

The outlook varies per person. An individual’s outlook depends on the severity of his or her spasticity and any disorder associated with the spasticity

I am including a few additional videos of spasticity. Please understand that these are demonstrations of extreme spasticity, and there can be ranges from slight to extreme. Also, I am including links to articles that I think are interesting. I live in Ohio where medical uses of marijuana are not allowed, but considering the drugs that I’ve been on in the past year to try to treat my pain, cramping, etc. If it was available legally,  I think I would try it.

The following video shows extreme spasticity:

http://www.youtube.com/watch?feature=fvwp&v=wfYNgYgEUoQ&NR=1

The following video shows a person who is improving from spasticity after therapy and baclofen pump:

http://www.youtube.com/watch?v=V2_3lXMKT7Q

Explanation of spasticity due to central nervous system:

http://www.youtube.com/watch?v=lEtkIIoo-3c&feature=related

A large number of case reports regarding CPM/EPM:

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

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

11/105. immunoglobulins are effective in pontine myelinolysis.

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

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

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

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

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

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

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

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

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

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

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

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

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

18/105. Central pontine myelinolysis.

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

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

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

20/105. Decreased diffusion in central pontine myelinolysis.

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

Late onset symptoms:

It’s a two-for tonight 🙂

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

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

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

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

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

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

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

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

Here is the link:

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

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

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

 

What’s wrong with me: psychological impact of CPM/EPM:

A few days ago I posted regarding how CPM/EPM has impacted my emotional abilities as well as my cognitive abilities. At that time, I didn’t have a lot of information regarding if this is a typical symptom of CPM/EPM.

Now, I have to stress what I’m sure I’ve mentioned previously; CPM/EPM is RARE. Hyponatremia is not rare, but developing CPM/EPM after it does not happen very often.

It is because it is so rare, there is not very much information, especially detailed information or studies that diagnose the symptoms. So, if  you approach a doctor to get answers, you might very well be given a blank stare. Let’s face it, if we had heart disease or cancer, we would get more information as to what to expect, but CPM isn’t widely seen by the medical profession, and even more importantly there aren’t long term studies or follow up of these patients. You’ll also find a lot of discrepancy in the research articles that are written.

I’ve been to several doctors who have never seen a patient with it.

What does this mean for us?

Don’t set high expectations for doctors who treat you, and as I’ve said before with CPM/EPM, ANYTHING GOES. NO one can tell you with absolution what is happening to you or things that have changed after you developed CPM/EPM isn’t normal or typical, because they DON’T KNOW. They really don’t.

I hope that over time, more research will be done for us who suffer from it, but in the mean time, I hope you find that my blog provides the most detailed information on what to expect.

SO, here’s what I found:

There is a link to emotional issues after CPM/EPM. There’s also a very solid link to cognitive issues. I’m also still trying to find links to the impulsiveness.

The following two links provide brief descriptions in their abstracts about having behavioral changes as well as cognitive changes. Now, here’s the thing; these articles require you to pay for access. I am citing their links, but I will only be able to post them after I gain access to them when I go to my local university, which is what I recommend if you don’t want to pay for them. Simply write down the name of the article, the publication date, etc and go to your local or major university library to access them, usually for free.

http://www.ncbi.nlm.nih.gov/pubmed/10514953

The following link provides information on the cognitive deficits a person experienced after developing CPM/EPM (but again to access full article requires payment):

http://www.tandfonline.com/doi/abs/10.1080/13554799808410619#preview

The following research article gives a fantastic description of how the damage occurs, but I will post that under the information regarding hyponatremia and the CPM section that describes how the damage occurs. The following quotes, I’m including gives an example of why I believe articles are pretty vague, but does give a more detailed account of the cognitive symptoms that we may experience:

A more recent study examined 12 individuals with CPEPM related to a variety of medical causes. In this more diverse population, four patients died in the acute  phase, and two were lost to follow-up. The remaining six were reported to have “good motor and cerebellar recovery.” However, all five of the patients who received neuropsychological testing had evidence of subcortical/frontal dysfunction, and most of these (4/5) were unable to return to work.

The next quote also describes another study that was researched:

Almost half (12/25) died either during the acute phase (2) or after hospital discharge (10). One was lost to follow-up. At final follow-up (mean 2.2 years; median: 1 year; range: 0 – 8 years), 29% (7/24) were normal; 17% (4/24) had mild cognitive or extrapyramidal deficits; and 54% (13/24) had a poor outcome (died or were dependent).

To clarify the above study: 2 people died immediately, 10 died after hospital discharge (but it doesn’t say from what); one died but not sure from what; 7 were “normal”, but it doesn’t clarify what that means; and 4 had deficits. Now, if you do the math these numbers don’t add up to 25…so what does that mean? There must be a mistake or error somewhere, and I think that helps to emphasize my point. The research articles on CPM/EPM are vague.

The next quote provides information from this research article on some of the cognitive impairments experienced:

A patient with only EPM (lesions in
the basal ganglia) had severely impaired attention, verbal and visual memory, visuospatial function, frontal
executive function, recognition memory, free recall
memory, and naming, with preservation of other language-related functions.
29
All these deficits are consistent with previous reports in patients with basal ganglia
lesions. In the other case, the patient had CPEPM (lesions in the pons, caudate, lentiform nucleus, thalamus,
and internal capsules).
28
At 1 week, the patient had
prominent deficits in attention and concentration (e.g.,
high distractibility, slow visual scanning), memory (immediate verbal recall and memory for daily events),
visuomotor functioning, and fine motor speed.

The above information really defines what I’ve been experiencing. My lesions were in the basal ganglia, so I have to say it’s pretty accurate in my regards.

The study goes on to explain that there were additional cognitive dysfunctions that occurred after the initial damage occurred and resulted in “pathological crying and laughter at 6 months after symptom onset, all consistent with a brainstem process.”

Doesn’t that sound a bit familiar. I’m not sure exactly what the pathological crying means. I’m guessing they mean it was inappropriate.

THE ABOVE QUOTES COME FROM THIS ARTICLE: http://neuro.psychiatryonline.org/data/Journals/NP/4399/jnp00411000369.pdf

It is very insightful, but I recommend breaking it up into sections because it can become a bit overwhelming.

So this is the information that I have found up to this point, but I’m sure there will be further information to come. There’s so much to go through..dud links…search results that don’t have anything to do with what you want, etc. Consider this post, like all of mine, a work in progress.

I hope it helps, and if you find something, message me with the link so I can add it. I REALLY appreciate your feedback. Truly the only way we can find out what is happening with CPM/EPM is through your feedback of what’s happening to you, so LEAVE comments, and details, etc. You’ll be helping other people!!

UPDATED: 04/20/12….Ok, so folks, so I have been trying to find more references to the psychological impacts of CPM/EPM.  The following link is in reference to a man who developed CPM/EPM after quitting drinking. They performed an MRI that showed lesions in his brain correlating to CPM. His behavior and symptoms progressed, and he began to develop angry outbursts, etc. They performed another MRI that showed demeylination was spreading further in the basal ganglia and the pons.

Two days after the admission, he showed violent behavior, agitation and irritability, getting angry on the slightest provocation without any mental changes or Parkinson symptoms or aggravation of his dysarthria. At first, we considered his symptoms to be alcohol withdrawal psychosis and started antipsychotics to control him, but his symptoms worsened. We performed MRI again 5 days after he developed psychiatric symptoms. The second MRI showed extended lesions in the bilateral basal ganglia and pons, as compared with the previous MRI.

The previous quote and information comes from: http://alcalc.oxfordjournals.org/content/43/6/647.full

This research article states that damage specifically associated with the basal ganglia areas are documented to cause behavioral and cognitive changes:

Abnormality of the basal ganglia is known to cause various cognitive dysfunctions and abnormal behavior via the involvement of the corticostriatothalamic or cortical–subcortical circuit through the basal ganglia (Carlsson,1988), while the role of pontine pathology for cognitive function and personality remains unclear.

UPDATE: 11/14/12

I have found this great research article that sites long term effects of brain injuries. In subsequent posts, I have decided that is safe to draw correlations between all brain injuries, so the following article describes what may happen psychologically after developing a brain injury. I have found that I have experienced a number of these issues, especially with distancing myself emotionally from people. There seems to be an emotional disconnect on a personal level, but I have the ability to cry over anything I experience regarding my brain injury. I don’t have all the answers for what is happening on a psychological level, but the following article does describe a lot:

http://apt.rcpsych.org/content/5/4/250.full.pdf —Psychiatric Sequelae of Acquired Brain Injury-Ken Barrett, APT 1999, 5:250-258

 

I am adding this quote from another research article that I found:

A patient with central pontine myelinolysis (CPM) underwent neurological and mental status examination, as well as neuropsychological testing, during the acute stage of the disease. After correction of the hyponatremia, a gross change in his neuropsychiatric status was observed. The patient underwent extensive neurological, psychiatric, and neuropsychological testing during the acute phase of the disease and at follow-up 4 months later. All major neurological and neuropsychiatric symptoms present at onset were fully reversible. Neuropsychological examination revealed deficits in the domains of attention and concentration, short-term memory and memory consolidation, visual motor and fine motor speeds, and learning ability. Although improved, neuropsychological testing still revealed remarkable deficits at follow-up. We conclude that neuropsychological deficits can accompany CPM, and that these deficits do not necessarily diminish simultaneously with the radiological or clinical neurological findings but may persist for a longer period of time, or even become permanent. In his recovery the patient started to manifest new neurological symptoms consisting of a mild resting tremor of both hands and slow choreoathetotic movements of the trunk and the head, which we considered to be late neurological sequelae of CPM. The significance of CPM in the differential diagnosis of acute behavioral changes after correction of hyponatremia is stressed, even if correction is achieved slowly and carefully.

This really explains the problems that I’ve experienced, and even mentions that you can have late onset symptoms related to CPM/EPM. The above quote comes from http://www.ncbi.nlm.nih.gov/pubmed/10514953

 

A new MRI for identifying brain injuries:

Did you know that in it wasn’t until 1843 that a physician linked having dirty hands to passing infections?

Click the following link to learn more regarding the history of hand washing: http://www.accessexcellence.org/AE/AEC/CC/hand_background.php

Originally, hysteria was categorized as an ailment that inflicted women after having babies. It apparently caused a host of symptoms such as, “anxiety, nervousness, fullness in the lower abdomen, erotic fantasies, paralytic states and fainting…”

Until the mid 1800’s to early 1900’s, it was believed that a woman experienced these issues because her uterus was “floating” around her body and choking her. Doctors treated it by causing orgasms in women. This was an actual selling point for vibrators. They “cured” hysteria. Use the following link to learn more, http://ije.oxfordjournals.org/content/30/4/904.full

So, what’s my point? Modern medicine and treatments are NEW. We know more about the human body and health than what our ancestors did, but there is still so much we need to learn, discover and understand.

This post is dedicated to a new technology that is in process to help those with minor and major brain injuries. This new advancement is promising as it is supposed to detect actual damage in neuro fibers in the brain. In my earlier blog posts, I mentioned how the injuries related to CPM/EPM are like having a short circuit in an electrical wire. This new type of MRI(High Definition Fiber Tracking) actually detects those short circuits! Where normal MRI’s and CT scans will show inflammation and bleeds, this MRI scan actual shows the neuron damage and can potentially predict how successful recovery will be.

This is exciting news for us!!! This might give us a definitive proof for the cognitive issues that we experience. It might show us how likely we will be to recover and to what extent. YEAH!!

For additional information on the upcoming information regarding this new MRI(High Definition Fiber Tracking) use the following links:

http://abcnews.go.com/Health/wireStory/finding-unseen-damage-traumatic-brain-injury-15830461

The following is a research article written about the MRI:

Click to access Pittsburgh%20HDFT%20TBI%20Diagnosis%20report.pdf

I had to copy the image (below)  from the above link, just because it is that freaking awesome!!

New MRI

I really believe that this technology could greatly benefit those of us who are suffering from the “unseen injury”. Be patient friends, because this new scan will probably not be covered by insurance companies nor will it be offered in the next few months. I’m guessing it won’t be available for another year or more. (If you are interested in possibly getting it earlier, there are research studies being done at the University of Pittsburgh now.)

 

Brain Injury:

This might seem utterly ridiculous, but up to this point, I did not realize I HAVE a brain injury. EPM and CPM causes a BRAIN INJURY. Maybe it would be more appropriate to state, that I didn’t realize what it meant to have this injury.

Of course, I’ve known that I have had damage to my brain, but that already happened, and for whatever reason, I did not consider that injury along the same line of having an injury caused in a car crash or stroke, etc.

The injury was in the past. It happened. It’s over.

This is the reaction that I’ve had from all of my doctors up to this point. Every doctor that’s treated me for issues related to EPM has stressed to me that the injury has happened. It will not happen again. The damage has been done and from that point forward I will only get better.

Many of my doctors have stressed that because my MRI has shown improvements, healing, then it’s just a matter of time before I’m 100% normal again.

Let me stress, this is NOT true. As, I’ve mentioned on numerous occasions, the MRI detects inflammation in the brain and even though the inflammation does dissipate in the months after CPM/EPM, it does not mean that you are going to be 100% back to normal. You may or you may not. The MRI images do NOT correlate to the symptoms you experience with this injury.

My MRI images have shown improvements. My doctors have told me that I am certain to get better, and I have been left struggling with wondering; Why am I not back to my normal self? It’s almost 9 months post injury, why am I not normal yet?

Further, NONE of my doctors touched upon the issues that have been most concerning to me, deficits in my cognitive abilities. It is extremely difficult for me to stay on task. I have short term memory problems. I have problems with reading and writing. I have difficulty thinking of words. I have attention deficits. The list goes on.

I recently was in training for work, and after 30 minutes, I couldn’t retain any more information.

Have you ever made manicotti? If you aren’t familiar with it, is a large cylindrical shell. In most cases, you stuff the shell with a cheesy filling.  The shell is hollow and open on both ends. My ability to retain information is like a stuffing a manicotti shell. You can keep adding filling, but it’s just going to leak out the other side.

I might have retained some of the information from our recent training, but at this point, I’d say 70 to 80% is gone. I might remember parts of what I learned at points in time, but I almost guarantee that I couldn’t sit down and recall everything.

Here’s something that I don’t think I’ve discussed previously; I have found that my past memories have become extremely vivid and are constantly at the forefront of my mind. It’s so frustrating. I don’t know why these things are so blaring and concrete. I have no control over when they occur. I have no idea why they occur. They aren’t even significant events, but just random memories that are mundane and non influential.

Not all of them are mundane, and I have to say that’s even worse. Events that I would rather not think about come to my mind as well, bringing with me emotional turmoil and grief.

So why is it that I can remember sitting in the backseat of our beat up brown SAAB, as a kid, in the middle of the summer and arguing with my brother’s about Garbage Pail Kid cards, as we waited for our mother to come out of the grocery store around the age of 8, but I couldn’t remember to call my doctor’s office to schedule an appointment for the 4th day in row?

Folks, the stuff that filters through my mind on a daily basis in such GREAT detail about my past..from the weather and temperatures to clothes that I was wearing. It’s mind numbing. Why am I remembering these things constantly, but can’t retain 1/10th of events happening now?

After doing the research on my last post, Cognitive Therapy, I realized why. I HAVE A BRAIN INJURY!

CPM and EPM did more than just cause a temporary damage. I am utterly clueless why my current doctors who are treating me for this have been so adamant about not acknowledging this! I’ve spent the past 8 and a half months struggling to come to terms and prove that this isn’t something I’m making up. I’M NOT FAKING THIS, and now I understand why these things are happening to me.

I’ve had doctors tell me it was stress. It was from fatigue.  I’m faking these issues. It’s test anxiety. It’s not related to EPM. It’s long term ADHD. It’s from having high cortisol.

I’ve struggled to understand why these issues became a problem after I developed EPM. I’ve questioned my sanity. I’ve questioned the severity of these issues. I’ve wondered if I was exaggerating these problems.

I’ve had people try to tell me it’s normal. It’s what happens when you get older.

If you are reading this, then I’m here to tell you, those people are FULL of it.

Let me stress, the reason you have the issues that you do is because you have had a trauma to your brain!! The damage is not necessarily ongoing (though that is also questionable), but the cognitive issues ARE or at least can be.

I now have answers and understanding to why these issues are occurring AND I can share with you, hope.

I had no idea as to how much support there is for brain injuries. There is actually a tremendous wealth of information regarding what might be considered “minor” brain injury.

Now, I’m not going to classify EPM and/or CPM as a minor brain injury. There are people who are living their lives completely incapacitated, requiring 24 hour support. That’s not minor. On the other end of the spectrum, you have people like me, who have are “functionally disabled”. You can live your daily life with little or no assistance, but you have not returned to your former self.

The following information I found online from Dr. Thomas Kay a renowned neuropsychologist who has specialized in minor brain injuries:

There is a known natural course of recovery for concussion, and the vast majority of persons appear to recover completely. (“Appear” is italicized because there is increasing evidence that there may be sub-clinical residual damage that can become manifest under certain circumstances, or can accumulate and cross a threshold after a series of presumably fully recovered concussions.)

There are predictable clinical deficits that occur immediately after most concussions: problems with attention, concentration, and short term memory; irritability; headaches; dizziness and balance problems; sensory sensitivity). These are often referred to as the “post-concussion syndrome.” However, because only some of these symptoms come from an injury to the brain, while others come from non-brain body systems, I prefer to avoid the phrase “post-concussion syndrome,” and try to refer to “post-concussive symptoms.”

A subset of persons who suffer concussions, or mild traumatic brain injuries, have long term residual symptoms, and a smaller subset remains highly dysfunctional. There is a long standing, often bitter, debate about why some people do not recover completely from concussion or mild traumatic brain injury. At one extreme, some advocates maintain that all problems are due to permanent brain injury. At the other extreme, skeptics maintain that anyone who fails to recover from a concussion/MTBI either has psychological problems or is malingering, and maintain that it is not possible to sustain permanent neurological damage from a concussion.

He goes on to state:

It is important to realize that multiple factors other than neurological ones can contribute to the appearance of brain injury, or exacerbate the apparent severity of brain injury. These include pain, sleep deprivation, depression (which is extremely common), anxiety, PTSD, and the results of medication (especially narcotic analgesics).

The evaluation of MTBI is complex, and needs to sort out the various contributing factors. Comprehensive evaluation should be delayed until the natural course of recovery has been completed (often up to a year), and major psychological complications have receded. Briefer screenings can track cognitive recovery. Patients who are depressed will often perform much lower on cognitive tests, than when they are not depressed.

Tests of effort are also an essential part of neuropsychological testing. Multiple studies have shown a tendency for a high percentage of persons with MTBI to fail tests of effort, and underperform on cognitive tests. In my opinion, tests of effort may be failed for a variety of reasons having to do with motivation. In order for neuropsychological test data to be interpreted as valid, tests of effort must be passed. (Failure of tests of effort does NOT necessarily mean a person does not have a brain injury.)

Clinical treatment of persons with MTBI will depend on the relative contribution of neurological, physical, and psychological factors. The neuropsychological approach I take is determined entirely by the presentation, dynamics, and needs of each individual person. I conceptualize treatment of MTBI as the restoration of an effective sense of self. Limits on this restoration may or may not be set by neurological injury. Each individual is different.

I am going to elaborate on this post in the near future, but before I end tonight, I just wanted to share this exciting news. Yes, folks, we have a brain injury, and if you are experiencing these issues than you are not alone and there are people who will believe you and your issues. Most importantly, now you have a source for help. 🙂

Keep checking back on this post for the next few days because when time and energy allow, I will be updating with more detailed information for support and direction.

 

The Updates:

This is I believe an amazing quote:

Brain injury is not an event or an outcome. It is the start of a misdiagnosed, misunderstood, under-funded neurological disease.

This quote is from the Brain Injury Association of America:

http://www.biausa.org/

I really believe it is absolutely true. I’m hoping it is not true for you, but it describes me to a T.

Update:  This person found my site and after reviewing it, I really found the information extremely beneficial. I recommend checking it out: http://brainhealthresources.wordpress.com/2012/05/09/there-is-help-for-battered-athletes-and-tbi-patients/

Cognitive Therapy:

Yesterday  (this was actually March 9 but I’m still writing this post :), I met with a cognitive therapist. I had done this earlier in my rehabilitation, but I found it to be a waste of time. My previous therapist worked with people who had major damage. If you read to them three to seven words, then asked them to repeat it, they weren’t able to do it.

I can repeat things back initially, but in five minutes, I can’t remember half of what you said. In ten minutes, I can’t remember 70% of what you said. The extent of this issue varies dramatically by how stressed I am, how much sleep I’ve had, how focused I am, if there are distractions,etc.

This is so stressful to me.

My first therapist didn’t seem to understand my frustration or the variability of in my symptoms.

Because my previous therapist recommended it, several months ago, I bought this really nice journal that I could fit in my purse and carry around with me so that I could keep notes. I did awesome with it the first week to 10 days, after that I have no idea where it went. NO CLUE!

I’ve looked for it. I’ve forgotten about it. Then I remember it and look for it again.

It’s so frustrating because I have no idea where it is, and I wrote down several things that I needed to remember, but now that I can’t find it, I don’t know if those things were really that important or not.

I had expressed to my original therapist that I had no problems with writing things down, but remembering where I wrote those things or what I did with the list or paper is the issue. She suggested the notebook, and as I mentioned above, this was a huge failure for me, and a continuing source of frustration and anxiety.

I wonder what the freak happened to it. Did it enter the Twilight Zone? Did my kid take it to school? Did Tom put it away somewhere? Is it shoved in a dark crevice of my car? (Notice, I how I’ve mentioned every other person as being responsible for it except myself. Despite the fact that I’m the one with brain injury, it is EXTREMELY difficult for me to accept that I am the one who has a deficit.)

You have no idea how much this eats at me. Thank God, by the end of the night, I will forget about it completely until the next time I remember it.

It’s frustrating for me that these things are happening. It’s not just not being able to remember but the frustration of being constantly distracted. I’m at a public library right now, and there’s SO much noise. There’s the ding of the elevator doors. There’s people coughing, talking, flipping through books, even the sound of my own typing is driving me crazy and causing me to lose focus.

I used to be able to study in the extremely busy passageway in the basement of a major university, and I could shut out everything without issue. I could go into my own little world in my mind, close the doors, and concentrate on physics or organic chemistry for HOURS. Literally, I would be able to do this for 8 to 12 hour stretches with just brief breaks. I was like a meditating Buddhist Monk. Now, I have the attention span of a fish, and that might be an unfair correlation on behalf of the fish.

I really thought when I started to see this new cognitive therapist that it would be useless. What could this person do to help me? How could she possibly know what I’m going through? I was very on guard prepared to argue my case on how EPM works and about how reading back simple lists probably wouldn’t help me get to my goal. I felt absolutely certain that because I’ve run into so many doctors who have raised their eyebrows and have doubted my sincerity, this would be just one more person that I would have to convince or teach about my condition.

Yesterday (03/09), I was having a bad day, and I certainly wasn’t at my best.  After my appointment, I left feeling relieved. Yes, relieved! This person gets it. She pulled out a sheet of paper that described what I’ve been experiencing to a T. This made me feel so relieved. I mean she knows what I’m going through. She understands what problems I have, and she’s going to try to help me get back on track.

More excitingly, she understands that I was a very capable, intelligent person before the injury, and she knows what I want to accomplish in the future. She’s looking at me as if I have a chance at still achieving my goals!!

Not only is she looking at me as if taking and passing the MCAT is absolutely achievable, but she worked with someone who was an ER doctor who had a brain injury and granted he’s no longer an ER doctor, but he’s a successful GP. This gave me a huge sense of hope.

I have not had any doctor at this point be able to do that. TRULY!! and I’ve seen dozens of them for this problem, but what she did for me in the two hours that I was there was give me a sense of hope. THIS MIGHT WORK!!

Let me try to explain a bit more about this. I’m not saying the doctors that I’ve seen previously to this point were just a waste of my time or were uncaring(some were, some are absolutely awesome). Some have really tried to assist me, but they didn’t have any plans. They didn’t pull out diagrams and wall maps with a step by step solution on how to get me back to where I was previously.

From almost every doctor, I’ve  gotten a response of: we think you’re going to be just fine. Just give it time.

I’m going to try to give you an idea of how this is such a screwed up way to handle an injury. If someone had a broken leg and you knew it was broken, would you tell them; you have a broken leg. If you wait about 6 to 12 weeks, it’ll heal. Then send him down the road?

NO! They’re right. The leg will heal, but will it heal correctly? No doctor would treat a patient like this. Once they determine the injury, the make plans. They either do surgery, put it in a cast, give the person crutches, and steps on what to expect and how to help it heal. Further, they asses the person over time to determine if they need physical therapy or additional steps to make the best recovery possible. They don’t simply state, well your leg is broken; have a great day.

When I left the hospital, I was walking into the unknown. Up to this point, I did not have anybody who said, this is what you need to do or I can help you get to where you want to go AND she knows where I’m going. She knows what I want to accomplish. She understands that I’m not just wanting to be able to sit down and read a book without forgetting what I read the day before; she understands that I want to be a doctor and that I need to have the ability to think on my feet.

So, what does this mean. This means my friends, Don’t Give Up!!! It’s been 9 months since I received this injury, and it’s been extremely difficult, but you don’t know what lies ahead, and you don’t know what’s going to happen next. Or if the next doctor’s appointment, is going to give you the person you need in your life who will reach out their hand and help you get to where you need to go. HAVE HOPE 🙂

Finally, I want to leave you with the information that my new therapist has given me because if it doesn’t hit the nail on the head, I don’t know what will.

Ok, folks, I spent over an hour trying to find a link to this doctor’s book, but I couldn’t find it, so I’m going to list some of the information from the pages that my therapist gave to me:

Excerpted from: “The Unseen Injury”, by Thomas Kay, Ph.D-neuropsychologist:

Statement of the Problem- We (a group of rehabilitation specialists in NY University Medical center) discovered that these patients appeared fine until they attempted to resume their responsibilities at home or at school. When they did so a significant number experienced great difficulty. They complained of inability to remember, concentrate, organize, handle a number of tasks at once, and get as much work done as efficiently as they used to. Their relationships with family, peers, and bosses often suffered and they developed psychological problems. their doctors were unable to find anything wrong with them and they were thought to be having psychiatric problems-or worse yet, to be faking.

Diffuse Brain Injury- there is evidence that the subjective complaints and cognitive problem encountered by some persons after MBI, may have an organic basis. This microscopic stretching and tearing occurs because of mechanical forces. (In toxic and hypoxic injury, nerve impulse transmission maybe interrupted/damaged).

Because of the very nature of diffuse MBI, the resulting deficits are not specific to particular domains of cognition (such as language, perception, etc.) Rather, it is the overall speed, efficiency, execution and integration of mental processes that are disrupted in a general way.

Nature of the Deficits- A.) Speed and capacity of information Processing persons with diffuse MBI process information less quickly. They react less quickly, especially when faced with a choice, and simply take longer to mentally process most tasks. This goes hand-in hand with a reduced capacity to process large amounts of information at any one time as fewer details can be handled simultaneously. The threeshold for becoming overloaded with amount or speed is significantly lowered.

B.) Complex Attention Most persons with MBI have great difficulty splitting or shifting their attention among tasks, and can not efficiently execute complex operations that require multiple simultaneous in temporary abeyance. Similarly, flexibility of thinking may be reduced. there is a failure to shift to a new strategy or grasp alternative solutions, when the one presently being employed is unsuccessful. As a result of the above difficulties, there is often a decrease in complex problem solving.

C.) Learning and Memory: Additionally, failure to effectively sort out, organize and quickly store complex incoming information often leads to “missing” obvious details, or the inability to recall accurately and becomes experienced as a problem with “memory.” As a result, it is much more difficult to learn new routines, or large complex amounts of new information. There is great difficulty storing and retrieving NEW information. This may be auditory information, visual information, or both. Old information is intact. Most commonly, there is also a deficit in the spontaneous recall of newly learned information.

D.) Integrative and Abstract Thinking   Because of its highly intergrative nature, there may be deficits in the quality of abstract thinking. The ability to spontaneously make connections between ideas may be impaired and interpretation of the statemetns of others may be either overgeneralized or too concrete. There may be difficulty expressing thoughts concisely and accurately. Ideas may be expressed in an imprecise, roundabout, wordy manner. It may be difficult to find the right word resulting in deliberate speech with numerous pauses, at times, “talking around the word”.

E.) Executive Function  The process by which we plan, organize, initiate, monitor and adjust our thinking and behavior. The person with deficits in executive functioning may have difficulty setting realistic goals. They may be unable to efficiently plan and organize their thinking or behavior and this may manifest itself most dramatically in new and unstructured situations. they may be deficient in initiating new activities, once they are planned, and may be misperceived to be unmotivated. They may fail to notice when their performance is off. They may act impulsively or erratically, having difficulty modulating their behavior. Finally, executive deficits may take the form of failing to complete tasks as things are abandoned and never brought to completion.

F.) Emotional and Behavioral Control    Damage to the orbital under sided portions of the frontal lobes, and basilar and medial aspects of the temporal lobes, can result in the disruption of emotions and behavior. There is a disruption in the balance between lower emotional impulses and higher rational cortical control due to the disruption of nerve connections between these two areas. Emotions may suddenly erupt. The person may seem irritable.

There you have it folks. This describes me almost perfectly. I really would recommend that if you are suffering from a brain injury to print out this post and take it with you to your doctors appointments, give it to your friends and family, etc. I think it helps for them to realize, you aren’t making these things up. It’s coming from an outside source, a legitimate neuropsychologist.

I also want to stress that this does not mean that you will have all of these issues or that you will develop them in the future if you haven’t developed them as of yet. Keep in mind this is to give you an idea as to what has been seen in brain injuries.

Hope this helps!

 

Update:  This person found my site and after reviewing it, I really found the information extremely beneficial. I recommend checking it out: http://brainhealthresources.wordpress.com/2012/05/09/there-is-help-for-battered-athletes-and-tbi-patients/

Dystonia (cramping):

I’m struggling with what to approach or how to approach it.

I’ve covered in some detail how CPM/EPM is caused and what parts of the brain are effected. I could discuss in more detail what areas of the brain are known to be associated with certain symptoms. However, there is a lot of mystery still surrounding how damage to the brain will cause a specific symptom.

I could discuss in more detail how the damage occurs (pathogenesis).

I could discuss who are some doctors to reach out to (right now this list is rather short). I could discuss prognosis or go into more detail on symptoms.

There’s also the social support. For instance, if you are like me, you might not have returned to work full time or may be facing ongoing disability.

How do you get started with SSI or social security disability?

There’s the legal ramifications.

One of the problems I’ve had with this injury is making decisions, so my attention becomes fragmented.

I guess there’s no wrong way to scramble an egg, so I’ll just choose something.

Dystonia.

I don’t think I’ve gone into great detail regarding this issue, and if you’re reading this you’re in for a treat. 🙂

Dystonia is painful involuntary muscle contractions caused by a neurological (brain/spinal cord) issues.

There’s two types of classifications for dystonia: focal and generalized.

Focal dystonia generally effects a smaller, single area. For instance, you may have focal dystonia of your hand. Most of the time it is in one hand at a time. So, it’s not like both of your hands will cramp at the exact same time. It generally effects smaller muscles, like those of your face or neck.

Now, something, I did not know is that something like writer’s cramp is considered a focal dystonia.

(That said, guess what I’ve developed since having EPM. I’m getting it in my hands and feet.I know, really another symptom, but yes. It hurts when I type or write, especially for extended periods. Of course, I used to have this before I had EPM too (who hasn’t experienced writer’s cramp at some point in their life), but I never had it daily like since I’ve had EPM.)

I think the following video shows how minor these focal dystonic neurological issues might seem. In a lot of videos that you see online, dystonia seems to be extreme cramping, but that’s only in severe cases. It is in most cases, especially early on without treatment not as noticeable except for to those who are living with it. Please don’t take that to mean that this issue is not painful or abnormal.

http://www.youtube.com/watch?v=T7OpC9-Gd9g

Like everything, stress and fatigue tend to make these movement based issues worse.

I think what’s unusual with dystonia that’s caused by EPM, it tends to effect more than one area, not at a single time, but you can experience radiating cramping through out your body. So from the first week that I developed this, I would experience a pain in my hand, 30 seconds later I would have it in my foot, 30 seconds later it would be in my thumb, then my back. It was just constant circulating pain. It’s now become the cramping and stiffness as described in the video above.

In most neurological cases of dystonia, you will have a primary problem and over time you will develop the cramping in other parts of your body.

I believe dystonia also causes the swallowing issues that are associated with EPM/CPM.

Possible causes for Dystonia:

Sometimes dystonia is but one symptom of a more pervasive disorder that affects the basal ganglia, such as:

  • Parkinson’s disease
  • Huntington’s disease
  • Traumatic brain injury (ie, CPM/EPM)
  • Stroke
  • Brain tumor
  • Oxygen deprivation
  • Infections, such as tuberculosis or encephalitis
  • Reactions to certain drugs
  • Heavy metal or carbon monoxide poisoning

The above information comes from: http://www.mayoclinic.com/health/dystonia/DS00684/DSECTION=causes

Now, generalized dystonia impacts Larger muscle groups in the body, such as those of your back and abdominal wall.

Check out this video for a woman who is living with generalized dystonia:

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

Again, please note, that not all cases of dystonia are that extreme, and they may not be permanent distortions but like with seizures, you can have cycles to it. It does become worse with activity and movement of an afflicted part of the body.

I do recommend the Mayoclinic website that I cited above to get additional information on dystonia.

I hope this gives you an understanding as to something you might experience with CPM/EPM. Hopefully, it brings you peace. If you are experiencing what I’m experiencing with the medical profession, you might feel a little less crazy by reading this. 😉

God Bless!

 

Tremors:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Doctors:

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

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

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

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

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

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

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

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

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

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

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

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

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

Is it too much to expect?

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

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

Yes, life is not black or white.

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

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

Dr. Noor Pirzada, University of Toledo Medical Center,

3120 Glendale Ave
Ruppert Health Center
Suite 1500 Door F
Toledo Ohio 43614
Phone: 419-383-3760
Fax: 419-383-3364
The following names come from GARD. They may or may not treat patients, but they have at least heard of it.
  • Dr. Richard Sterns: University of Rochester School of Medicine, Rochester, NY. (He is an expert in the treatment of hyponatremia and knows a lot about CPM/EPM.
  • Dr. Amyn Rojiani: University of South Florida, Tampa, FL.
  • Dr. Yeong-Hau Lien: University of Arizona, Tucson, AX

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

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

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

 

Discharged:

I think one of the hardest moments I faced after developing CPM/EPM was being discharged from the hospital. I literally had a bit of a break down. I don’t think my reaction was abnormal.

I was already beginning to see some improvements during the week I was hospitalized for CPM/EPM. At the same time, I was still really screwed up. I was NOT anywhere close back to my formal self.

I had only had the injury for about 10 days. I was aware from the very little access to information online that I would not be considered out of danger for at least 3 weeks from the date of injury. Some research suggests that you can be at risk for dying for up to 12 weeks. There’s just not enough research and answers fluctuate.

Everyday I woke up in the hospital I felt a sense of relief, but every time I went to sleep I felt anxiety. Would this be the time that I would not wake up or wake up and not be able to move?

At the same time, the doctors were monitoring my symptoms intently, but they were truly unable to do anything but watch me.

They were afraid to give me things like pain medications or even something as benign as glucose IV fluids because they were concerned with how they would impact my neurological functions.

Despite their not doing much of anything but observing, I felt a comfort in knowing I was there. If something bad happened, I knew that something could be done immediately.

I was also extremely dismayed at leaving because I was NOT normal. At that point in time, my list of neurological issues was extensive. I had problems losing my balance, walking into walls, developing hypotension when I was standing and hypertension when I was sitting. How was I going to get back to a “normal” life if I couldn’t even stand up for long periods of time without getting super sick?

One of my biggest issues at that time was my speech problems. It was extremely obvious, and I have a phone sales position. How could I perform my job if I couldn’t speak properly?

I’m sure if you are reading this, you are experiencing something similar to this or deficits that may be greater. It is terrifying. There aren’t any “real” answers. There is a lot of unknown.

This will probably lead to anxiety and depression when you are released from your hospital or hospice. It’s like losing an anchor in the middle of a hurricane.

What should you expect?

First, make a list of your questions. Is the hospital or rehabilitation center setting up ongoing occupational, speech, and physical therapy at home? Who will be in charge of your ongoing treatment? Will it be your general practitioner? Will it be a neurologist from the hospital who was treating you? Who should you consult regarding your work notes, disability claims, insurance questions? What will your insurance company cover? What will your co-pays be? Will you need 24 hour support, live in aid or daily assisted living? What type of medications will you need and those side effects? Is there any doctor associated with the hospital that has experience with CPM/EPM? Can you drive? Are there any specific physical limitations that should be avoided? Is there a support group they know of (you probably won’t find one for cpm/epm, but you might find one for neurological disorders or brain injuries?

Is there a source for your care givers? For instance, you may experience things like paranoia, dementia, irritability. These are normal psychological effects of it. If you become unstable, who should they call? If your symptoms become worse, what should they do?

If you were employed before your injury, you need to get in touch with your human resources department. If you are a caregiver of someone who has CPM/EPM, you will need to contact their employer to let them know what the situation is and find out about their disability policies. In most cases, you can fill out FMLA forms to help protect their/your job. If you are a caregiver, you will want to find out about becoming power of attorney.

In most cases, you were not anticipating this to occur, and it is a huge surprise. You might have been perfectly healthy previous to this injury, but now you’re facing the chance of having life long injuries. You probably did not have things like your living will, durable power of attorney, health care power of attorney.

IF you are reading this as a precaution, and you’ve never developed hyponatremia or your CPM/EPM, then I recommend taking the initiative and getting these basic legal affairs taken care of. Let’s look at the facts, you may never develop CPM or EPM, but you do have a fair risk of developing hyponatremia.

Further, you are going to die at some point, whether it’s a car accident in 3 weeks or a heart attack tomorrow. It’s inevitable. You need to be certain that you have everything ready for your family and your friends.

At the very least, you need to discuss your plans with your family and friends. It’s never a comfortable subject. No one wants to face the reality of losing someone they love, but it’s worse to leave the heavy burden to your family and friends when they are suffering from the pain of not having you in their life.

If you need help, most lawyers will consult with you free. There are legal forms that are available online. At the very least, you can create a document at home, typed or written that express your wishes.  You simply take that letter to a notary (usually a bank will have a notary) and sign and date it in front of them. It has to be signed and dated in front of the notary to be valid.

This is just a stepping stone on what to do. I hope this helps, and if you think of any additional advice to add, please feel free to do so.

Take care!

 

Getting a diagnosis:

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

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

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

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

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

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

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

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

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

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

So, what do you do?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Figure 1

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

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

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

Many blessings!

 

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

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

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