Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Alzheimer’s disease”

10 Aug 2013

Exciting new developments in Electro-stimulation and brain disorders and diseases:

Yes, I am still alive. 😉 However, I am still struggling. I am working at getting help for the vision issues that have become significant over the past few months.

Someone sent me this report. It is something you listen to, like a radio show. I am REALLY excited at what this might mean for us. Could this be a cure to issues we experience after a brain injury? I will attempt to contact Dr. Lozano to see if he thinks this could help those like us.

My only concern would be that because there is damage to the circuitry in the brain that stimulation might not be as effective. Really, I believe there is no way to know for sure until you try it–a potential cure to our problems. Can’t help but feel excited and hopeful 🙂

Can Hacking The Brain Make You Healthier?
by NPR/TED STAFF
August 09, 201310:01 AM
http://www.npr.org/player/v2/mediaPlayer.html?action=1&t=1&islist=false&id=209618161&m=209620407

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged , , , , , , , ,
31 Jan 2013

Identifying Brain Injury:

There has been a lot of attention focused on brain injuries recently. We are finding out more and more every day that minor hits to the head can lead to ongoing issues with cognitive abilities.

It’s been over 18 months since I experienced my brain injury due to extra pontine myelinolysis. It was very shortly after the injury occurred that the MRI images stopped showing the lesions that were originally there, but I continued to experience deficits.

Initially, I had an abnormal EEG, but subsequent EEG’s done 8 to 12 weeks later showed normal.

What does it mean when your images show everything has returned to normal, but you are still experiencing issues? Trust me, I had a doctor tell me that because my tests were now normal that my symptoms were not being caused by the brain injury.

This leaves you in a position of not knowing, and this lack of evidence in  current medical imaging/testing is what so many people with brain injuries face. Whether you were injured after a roadside bomb in Iraq, had minor or major concussions after playing in sports, hit your head after falling off your bike, or suffered from an internal injury like stroke or CPM/EPM, you may experience symptoms long after your injury. In some cases, your symptoms may become progressively worse, but the images don’t show any injury at all. Doctors rely so heavily on what the tests say vs what the patient says that you may face a doctor telling you that there is nothing wrong with you, and that is beyond frustrating and depressing.

This is what has caught headlines as more NFL players are ending their lives over their ongoing decline in cognitive abilities. They have gone through testing, MRI, neuropsychological exams, EEG’s, CT’s, etc and the tests showed that they were normal.

It is the frustration that millions of people face each year as they struggle to find answers and more importantly find help.

The most fantastic news that I have is that technology is starting to advance to the point that doctors can finally start to identify injuries that weren’t detectable by any other methods. This is such a relief to those of us who live with the consequences of brain injury. It is so unfortunate that so many doctors need to have this “physical” evidence instead of trying to help a person deal with the outcome of their injury. In other words, would some of those NFL players that took their lives still be alive today if a doctor told them, “no matter what the tests say, you have an injury and let’s work to fix it” ?  If they got treatment based on the symptoms that they experienced instead of being prescribed anti-depressants and anti anxiety medications, would they be here now? It’s a tough question to answer, but the loss of their lives had a purpose. It has brought awareness and funding to support brain injury research.

The purpose of this post is to bring to light some of the most current research on brain injuries. What are the new tests being done? Where are they being done? Will they help you?

One type of injury that we tend to not discuss often is “chemo brain”. Chemo brain is a term used to describe people who have undergone chemotherapy and experienced cognitive issues, especially with concentration and memory. Doctors have dismissed those symptoms as being depression, anxiety, fatigue, etc. They did not believe that they were caused by a physical condition. However, in December of 2012, several research studies using fMRI, PET and other scans, showed evidence that chemo brain is real.

Often, cognitive complaints were associated with persistent fatigue and depressive symptoms, making it challenging to sort out whether or not the complaints of poor memory, attention, and difficulties with multitasking were related to brain dysfunction or were merely a manifestation of an uncontrolled mood disorder.4–6 Many who complained were younger patients with breast cancer who had become menopausal prematurely with chemotherapy, and their experiences of vasomotor symptoms, nighttime awakening, and poor sleep might have explained some of their cognitive complaints.7

http://jco.ascopubs.org/content/30/3/229.short

The study goes on to explain the reasons behind why chemo brain (and in my opinion other brain injuries tend to progress). As I have mentioned prior in my blog and this research paper goes on to suggest, there seems to be an autoimmune response that causes ongoing inflammation and injury to the brain.

Concurrently, an increased understanding of immunology and mind-body interactions (psychoneuroimmunology) has made us more aware that events in the body (tissue trauma and inflammation from surgery, radiation, chemotherapy, and biologic and targeted therapies) can trigger systemic inflammation with secondary effects on the CNS.21,22In parallel, stress and cognitive threats can have direct effects on the hypothalamic pituitary adrenal axis and the sympathetic nervous system, leading to systemic responses that can affect the immune system.23 In addition, immune cells, responding to inflammation can traverse the blood-brain barrier and increase local inflammation in the brain, affecting emotional and cognitive function without the need for direct diffusion of chemotherapy into the brain substance.23–25

http://jco.ascopubs.org/content/30/3/229.short

The technology used to determine differences in the white matter between the control group and those treated with chemotherapy was called magnetic resonance imaging diffusion tensor imaging (DTI). The women that they tested showed decreased testing ability in memory, concentration/ attention.

Finally, the DTI detected decreased white matter integrity in tracts involved in cognition in the women treated with chemotherapy with no changes observed in the two control groups; this suggests a causal relationship between the chemotherapy exposure, cognitive complaints, NP test abnormalities, and white matter changes.

http://jco.ascopubs.org/content/30/3/229.short

PET scans are also being used to detect chem brain. When I hear accounts of chemo brain, the symptoms they mention are identical to those that I experience. It is so frustrating to have doctors tell me that this is not real, and I know that this is the same frustration experienced by so many of us who are suffering from brain injuries of all varieties. It brings me some relief to know that more research is being done, and technology is starting to show the causes of what we experience. I recommend the following link to learn about PET scans in the use of diagnosing chemo brain: http://www.npr.org/blogs/health/2012/12/28/168141465/another-side-effect-of-chemotherapy-chemo-brain

A friend posted these links about newer imaging used to diagnose brain injuries. I haven’t researched all of these as it takes a significant time for me to read through information, but I really want to get this information out there.

MEG Scan – detects errant electrical activity in the brain. Used in conjunction with FMRI and EEG.
http://www.research.va.gov/news/research_highlights/brain-injury-090808.cfm 

Diffusion Tensor Imaging (used above to diagnose chemo brain):
Problems in the white matter—for example, nerve fibers that are not bundled together coherently or that have lost their fatty “myelin” coating—show up in DTI scans but not in regular MRI scans.
Huang says he hopes to eventually incorporate a third imaging technique, chemical shift imaging (CSI), also called MR spectroscopy imaging. This method reveals the distribution of certain chemicals in the brain—another potential marker for subtle brain injury. http://www.research.va.gov/news/research_highlights/brain-injury-090808.cfm

MRI Neurography – Shows nerves. http://en.wikipedia.org/wiki/Magnetic_resonance_neurography
Magnetic resonance neurography (MRN) is the direct imaging of nerves in the body by optimizing selectivity for unique MRI water properties of nerves. It is a modification of magnetic resonance imaging. This technique yields a detailed image of a nerve from the resonance signal that arises from in the nerve itself rather than from surrounding tissues or from fat in the nerve lining. Because of the intraneural source of the image signal, the image provides a medically useful set of information about the internal state of the nerve such as the presence of irritation, nerve swelling (edema), compression, pinch or injury. Standard magnetic resonance images can show the outline of some nerves in portions of their courses but do not show the intrinsic signal from nerve water. Magnetic resonance neurography is used to evaluate major nerve compressions such as those affecting the sciatic nerve (e.g. piriformis syndrome), the brachial plexus nerves (e.g. thoracic outlet syndrome), the pudendal nerve, or virtually any named nerve in the body.

There is also a new one called high definition fiber tracking. http://schneiderlab.lrdc.pitt.edu/projects/hdft

Finally, there is Tau imaging: http://www.sbir.gov/sbirsearch/detail/102432

I will try to add and complete more of this post as I research further and learn more about the different types of imaging, but it is exciting work for those of us suffering from brain injury. Hope is on the horizon for getting answers and evidence for why we continue to experience the symptoms that we do.

 

 

Related articles

 

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged , , , , , , , , , , , , , , , ,
29 Jan 2013
3 Comments

Alternative Treatments for CPM/EPM and Brain Injury:

Hi, there.  I hope all is well, and moving forward for you.

I wanted to include this information from my friend, Adam. I have not researched this product or group myself, so I can’t account for what it says, but it seems like if it does everything that they promote it does, this could be a HUGE step in Brain Injury recovery and prevention of degeneration.

This is from the information that he sent me. It really sounds promising:

I am having a little trouble posting on your blog. Tried to post this
Actually the product I am referring to is at GNC Anatabloc. It has anatabine in it.

See also www.anatabloc.com You can see testimonials all over the internet.
www.gnc.com for one

My sister with lupus and diabetes, my neice with thyroid problems, a friend with MS and 100 other people I know are taking.

Controls and attacks inflammation. See brain studies.

TBI is traumatic brain injury
TBI

According to the Centers for Disease Control, 80,000 people in the United States suffer long-term disability from a traumatic brain injury (TBI) annually. Roskamp Institute scientists conducted a research study of TBI and control mice by administering a-natabine to measure its effectiveness for recovery from injury using scientific accepted methods. TBI mice treated with a placebo and the sham (untreated) mice recovered at a similar rate with deteriorated motor and cognitive functions. The a-natabine treated mice however had a significant recovery the researchers believe, by inhibiting inflation and reducing amyloid production. To quote the published research paper; “A-natabine treatment appeared to completely prevent the loss of spatial memory retention following severe TBI. Further study of this promising treatment is warranted and will include treatment in a mild closed head injury model as well as long term outcome from injury. Dietary supplementation for reducing secondary injury after TBI offers an easy path to clinical application and simplifies the administration of the therapeutic.” This pathological information warrant further studies with ongoing research in exploring other models of TBI using anatabine.

Alzheimer’s disease

Research study findings by Roskamp Institute were presented at Neuroscience 2012 about the impact of a-natabine in treating Alzheimer’s disease (AD). AD is a neurodegenerative disorder that causes problems with memory and behavior due to the increasing death of nerve cells in the brain. Most scientists, supported by research done at Roskamp Institute, agree that excessive amyloid plaque buildup (Abeta peptides) and neurofibrillary tangles (twisted protein fibers named tau) are directly related to the brain nerve cell loss. Data from the study using a well-known mouse model of AD shows that a-natabine treated mice have a significant reduction in the accumulation of plaque in the brain as compared to the control population. Scientists believe this occurs because a-natabine reduces or regulates human neuronal like protein BACE-1 (the rate limiting enzyme responsible for Abeta production). Cognitive tests of an ongoing investigation of a-natabine treated mice show greater cerebral functions and improved abilities as compared to the non-treated sample. Data from the study also show a-natabine’s anti-inflammatory results. A-natabine reduces neuroinflammation and STAT3 phosphorylation in the brain of transgenic AD mice. Additional research is warranted based upon results of this study regarding the potential benefit of a-natabine in the treatment of Alzheimer’s disease

http://www.rfdn.org/inflammaging.html

Here is a summary of the important research done at the Roskamp Institute.

http://www.mullanalzheimer.com/livesite/

http://www.rfdn.org/ms_anatabine.html

A quote re the peer reviewed study from Dr. Michael Mullan, the CEO and President of the Roskamp Institute, “Anatabine continues to demonstrate widespread anti-inflammatory properties in a broad array of pre-clinical models. Given the commonality of inflammatory systems in rodents and humans, there’s much reason to expect that anatabine will demonstrate similar properties in humans. In fact, the team went on to demonstrate that in human blood inflamed with LPS, the presence of anatabine dramatically dampened the inflammatory response, a result also included in the paper.”

After consulting with my cousin, the product that they recommend for inflammation is Neprinol. The difference between the product that Adam is recommending and Neprinol, is that Neprinol actually eats away at scar tissue. It dissolves it. The product that Adam is discussing, prevents inflammation. It makes me think that these two products combined could be a super healing combo for everything from arthritis to brain injury.

I will try to research these products more to find out what validity that they have or what the current research is describing, but these natural remedies tend to hit the market decades before mainstream medicine begins to manufacture information. For instance, my Aunt has been promoting the benefits of probiotics since the early 1980’s. Now, almost every doctor recommends probiotics after you finish an antibiotic. It is key in recovering a good GI system.

 

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged , , , , , , , , ,
02 Nov 2012

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

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

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

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

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

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

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

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

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

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

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

Those who have MS experience movement issues:

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

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

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

Stroke symptoms:

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

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

Effects of a right hemisphere stroke:

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

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

Effects of a left hemisphere stroke:

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

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

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

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

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

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

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

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

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

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

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

Issues that are attributed to brain damage:

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

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

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

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

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

 

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

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

Cognitive and neuropsychiatric sequelae

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

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

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

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Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis and tagged , , , , , , ,
27 Oct 2012
1 Comment

Brain injury and Alzheimer’s disease:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This too has happened to me on numerous occasions:

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

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

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

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

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

UPDATE:

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

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

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07 Aug 2012

Fate:

 

You are not supposed to talk about it. You aren’t supposed to ask, but I am. Why?

I truly don’t understand, and I don’t have an answer, but I find myself asking more and more, WHY?

Was I on the wrong path in life? Is there a reason behind what I’ve gone through in the past year? Was there something I was supposed to do or something that I was doing that made a higher power intervene?

I do not understand, and it eats at me each day. Why?

I finally had an answer to 8 years of ill health. The door had opened to me. I had an answer AND a solution.

I was going to have to live with endometriosis for the next 10-12 years, but I could do that, and by removing the pituitary microadenoma, I was going to stop the deterioration in my health. I couldn’t reverse the autoimmune issues, but they were mild compared to most with the same problems. It was truly an aspirin a day that would prevent major complications to Anti-phospolipid syndrome, as well as monitoring.

I am not exaggerating when I say the door was opening. Even my scleroderma antibody elevations had returned to normal. This lifted the fear that my health would continue to deteriorate from that.

I was ready and seated to take the MCAT after spending over 12 months of long hours of preparation, sometimes studying up to 12 to 14 hours a day on my days off. After finally having answers for my health issues, with having the knowledge that everything would be fixed, I KNEW I could do it. I KNEW I could reach the goal, and I was ready.

So, WHY? Why did this happen? Why was it when things finally looked their brightest did I develop brain damage?

Why have all of the doors not only slammed shut, but I have become trapped in this freaking cage. Not only is the vision of becoming a doctor fading and the reality of each day brings the realization that I have very little chance of ever meeting it, but even working my current job and living every day life has become a struggle. From the fights that I have with my family, from the loss of being able to enjoy simple things like Sudoku or crossword puzzles, each day holds challenges that I NEVER expected to face in my life. I never thought this would be me? I don’t think I could ever imagine such a horrible fate.

And so now, I am asking, WHY? I know, I shouldn’t. I know I should be so very grateful for what I have. I should be counting my blessings that I am not paralyzed, that I can do the things that I can do. I KNOW I should be thankful, but I am not. I am and I am not.

I have to say truly that my heart aches from it each day, the battle of knowing I should be grateful and the heart wrenching fact that I am not the same person I was 14 months ago, and I am depressed about it. I am so horribly, horribly depressed about it.

I haven’t stepped inside a church for years. But yesterday, I stepped inside the church I attended from infancy through graduation from high school in order to attend my niece’s baptism. I faced my parish priest that I hadn’t seen in over 5 years. He looked at me with his piercing blue eyes and asked, How are you? My eyes immediately started welling with tears, and I could not choke out a response. He asked, Are you doing okay, and I semi-shrugged and shook my head, No, but it could be worse. I am very lucky.

How could I explain to this person in a few words that everything I’ve struggled to live for in the past 8 years has evaporated, and that I have no idea as to why, and I don’t know how I can accept this new me. How could I explain that I am terrified from the realization that I am only 35, and I have the memory of a 60 year old person with Alzheimer’s? What is going to happen to me when I am 60?

How can I explain it kills me with embarrassment to face people that I have worked with for five to ten years, and I can’t remember their name? Or that people constantly make comments about or question my integrity? How there is nothing more that I would rather do than forget that this has ever happened to me and just get back to normal?

To look in his clear blue eyes and know that being back home is a safe zone, to stand in front of this man, and know without question that he BELIEVES everything I say because he knows who I am and what I stand for…period. The relief that I got from that moment gave me strength and walking away from it gave me the realization that I MISS that safety, the safe zone. I spent two hours around people that know and love me unconditionally and that make me feel normal even when I’m not. It made me realize how much I need that and crave that.

Is that why? Is that why this happened to me? To get a better understanding of what my family means to me?

Was it to put into perspective how I am missing so many important things in my life?

Was it a way to show that I am not on the right path in life? That I should be doing something else with my life? Is this Fate intervening?

I don’t know. I really don’t know, why.

 

 

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