Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the month “October, 2012”

The moment of Now:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

In my life, there is no next year.

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

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

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

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

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

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

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

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

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

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Brain injury and Alzheimer’s disease:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This too has happened to me on numerous occasions:

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

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

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

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

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

UPDATE:

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

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

Related articles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Vision

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

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

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

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

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

MUSCULOSKELETAL DYSFUNCTION

Muscular dysfunction

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

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

SUMMARY

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

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

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

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

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

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

 

Pertussis: antibiotic resistance and additional testing information:

If you’ve read my recent blog posts, you are more in the know than most of the doctors currently are in regards to Pertussis. However, there are a few points that I want to clarify.

I think one of the most important things you can do is get tested. Again, my local doctors did not see the necessity in doing this, and I have a feeling that they aren’t the only doctors that hold this belief. This means that you need to be able to voice your reasoning for having it done and have enough confidence to possibly argue for it with them. You also need to be able to demand the right kind of testing, and here is why:

When my daughter had a positive test, I went to my doctor. I had an appointment scheduled at that time anyway, so I decided that I needed to have myself tested and treated. I was not very sick at that time. I was just starting to get a slight cough. I had already had the cold like symptoms 12 to 14 days prior, so I was a bit surprised that I hadn’t developed the severe coughing like everyone else had. I had only started coughing the night before my appointment.

I had not started researching Pertussis at that point, so I was pretty uninformed. My doctor did feel that it was necessary to be tested. He ordered a blood test because our local lab did not perform the nasopharyngeal swabs. They treated the nasopharyngeal tests as a “procedure”, and their phlebotomists were not skilled in performing “procedures”. Because of this, my GP ordered the blood testing.

If you’ve read my previous posts, then you would realize that having blood testing during the first few days of developing the “whooping” cough, would not be accurate. Having a blood test during this period can lead to false negatives because your antibodies do not have the time to build in response to the infection.

I also had to take my son to get tested. We took him to the Children’s Hospital urgent care department last Saturday. Now, my son by this time had his “whooping” cough for more than 4 weeks. The nurse that was in charge of his care was very reluctant in getting him tested. She did not see the need. I explained that it wasn’t for his care but so that health department could record his case. When I finally convinced them to do it, they were going to do the nasopharyngeal testing. This was the incorrect procedure. At this point I had researched it and I knew it, so I voiced my concerns and stated that he needed to have the blood test performed.

I’m sure you can understand that my correcting the nurse was not met with the best attitude. Actually, she did not come back, but they did both the nasopharyngeal and blood testing, and I was satisfied.

I got the call back today. My son’s nasopharyngeal test was negative (which is what I was expecting because it was beyond the time frame for that test to work), but his lab work showed he had recently had the infection.

So, I was right. If I hadn’t stood my ground, he wouldn’t have had the confirmation that he had it. The hospital has now contacted the community health department and his high school, which was the whole point of having him tested.

What does this mean for you?

You need to know about Pertussis. You need to know about testing, treatment, symptoms, etc because your doctor may or may not know about it. They make mistakes, and because Pertussis is rare and is making a comeback, in order to get the best care you and your family deserves, you might need to stand your ground against them. It’s hard to do even when you know you are correct, so you have to be absolute and persistent. The most important reason for getting a test is to proactively prevent it from spreading. It can kill babies and toddlers, and right now there is a country wide misbelief that if you have your vaccinations that you won’t get it.

The following is the chart used by the CDC to describe when the tests should be done:

Optimal timing for diagnostic testing (weeks).

Culture is best done from nasopharyngeal (NP) specimens collected during the first 2 weeks of cough when viable bacteria are still present in the nasopharynx.  After the first 2 weeks, sensitivity is decreased and the risk of false-negatives increases rapidly.

PCR should be tested from nasopharyngeal specimens taken at 0-3 weeks following cough onset, but may provide accurate results for up to 4 weeks of cough in infants or unvaccinated persons. After the fourth week of cough, the amount of bacterial DNA rapidly diminishes, which increases the risk of obtaining falsely-negative results.

For the CDC single point serology, the optimal timing for specimen collection is 2 to 8 weeks following cough onset, when the antibody titters are at their highest; however, serology may be performed on specimens collected up to 12 weeks following cough onset.

(So again, from the above information, the reason my son had a negative nasopharyngeal test was because he had his cough for more than 4 weeks, but he had a positive blood test. If I hadn’t demanded the blood testing, they would not have diagnosed him properly as having it. In my case, because I had only started coughing within a 24 hour period before my blood test was done, I got a false negative. I has not researched Pertussis when I had my blood test done, or I would have requested the nasopharyngeal swab.)

I found the following website is also a good reference on what tests should be ordered and why: http://labtestsonline.org/understanding/analytes/pertussis/tab/test

The other very important topic I wanted to discuss, is antibiotic resistant Pertussis.

Ok, Pertussis in and of itself isn’t a significant health issue compared to other communicable diseases, but the number of reports of people who have pertussis has been increasing every year. Again, this is for several factors mentioned in my previous posts. That said, there are also numerous reports of antibiotic resistant pertussis strains.

The general treatment for pertussis is the erythromycin family of drugs. However, since the 1940’s there have been cases of antibiotic resistant forms of pertussis. There have been additional cases reported from Arizona, California, Utah and Wyoming in the past 4 years. This year, there was a report in France.

In these cases, those treated with the erythromycin family of drugs did not recover as expected from pertussis. It seems that in these cases, the person continued to get worse even after receiving treatment. Now, as I reported previously, antibiotics do not stop the symptoms (generally) unless the treatment is started in the first few weeks of infection (before the cough begins or shortly after it begins). The symptoms from Pertussis are caused by the toxins that are  caused from the infection as well as the immune response our body has to the toxins. The reason a person is prescribed antibiotics is to kill the bacteria so that it does not continue to spread. So, I do not fully understand why having an antibiotic resistant form is significant. Unless, it is more contagious than its non mutated form. It also seems that with the antibiotic resistant form, the infection lasts longer and is more symptomatic.

The following provides the cases that were researched in France, as well as in the United States:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358168/

http://jmm.sgmjournals.org/content/57/12/1577.full

http://jac.oxfordjournals.org/content/early/2007/09/06/jac.dkm343.full.pdf

After further review of the above articles and others, I found that the importance of antibiotic resistant pertussis is that a person generally experiences an improvement with initial antibiotic treatment, but after a week or more, there is a sudden worsening of symptoms. This seems to be the alarm that indicates a person has an antibiotic resistant form of Pertussis.

I also find that it is important for medical evaluation and treatment if your symptoms do become worse. This is because Pertussis can cause pneumonia and other secondary infections to occur. So, if you are feeling better, but then start to run a fever or have trouble breathing, etc it is important to be re-evaluated.

I do not know with certainty if antibiotic resistant pertussis is contagious beyond the five days of antibiotic treatment. I would assume that it is. However, you would want to contact a specialist (I would suggest speaking with an infectious disease specialist).

I will try to update posts as I can with the most up to date information.

Pertussis the Basics:

So, I think this is some of the basic information that you should know regarding Pertussis.

1.) ~80% of reported cases for pertussis have happened in those who have been FULLY vaccinated. ~11% happened in those who were partially vaccinated. ~ 8% were in those not vaccinated at all. (That was from a study done in 2011 regarding all of the cases reported to the CDC.)
2.) 2012 is on course to have the most recorded (verified cases) since 1959. There is an expectation that more than 40,000 cases will be verified nation wide. So, far approximately 29,000 cases were reported to the CDC as of September 20, 2012. Please see the previous posts as to the possible reasons why.3.) This figure does not include the number of cases that go misdiagnosed or un-diagnosed. It is estimated that there are 2- 3 cases unreported for every case that is.

4.) Children under the age of 1 have the highest risk of death and serious complications. They usually have to be hospitalized. Their symptoms tend to be apnea. They may not have any indications that they are sick at all, except they tend to gasp for breath. They usually do not have the gasping or whooping cough that is present in children and adults.

5.) There are 3 phases to the illness:


Stage 1: Symptoms mimic the common cold and is contagious via sneezing. (In our case, we had nasal congestion, headache, fatigue, and all over body aches.) It generally lasts 7 to 10 days but can last from 4 to 21 days.

Stage 2: Severe coughing that can lead to vomiting (may or may not develop a “whooping” sound with the coughing). Generally, the coughing will go in “spells” and then resolve. These coughing fits will be worse at night. This stage lasts from 1-6 weeks but can last up to 10 weeks.

Stage 3: Recovery: coughing is less severe and finally resolves

6.) A person can develop the severe coughing spells with subsequent upper respiratory infections (ie, colds) after they are over the Pertussis bacterial infection.

7.) Teenagers and Adults are at a high risk for developing pertussis, but it is generally not life threatening, unless they have a compromised immune system or are over the age of 65.
8.) The coughing is not caused by the bacteria directly but by the body’s response to toxins that the bacteria and your immune system produce. These toxins cause inflammation of the respiratory tract and paralysis of the cilia in the respiratory tract. The infection has recently been discovered in deeper tissues of the lungs as well.9.) YOU MAY NOT HAVE A FEVER or might only have a low grade fever with the infection.

10.) An antibiotic kills the bacteria and makes it non-contagious, but it does not get rid of the coughing or other symptoms once the severe coughing begins (because that’s the body’s reaction to the toxins the bacteria produced).

11.) The general incubation period (period from when you were exposed till the time you develop your first symptom) is 7-10 days (BUT IT CAN TAKE UP TO 6 WEEKS!!!!). This means that if you have lunch with a friend who is sick with pertussis during the contagious period, you may not develop the first symptoms until 6 weeks later.

12.) If you have been exposed, at the first onset of sneezing, runny nose, headache, sore throat or mild cough, you need to be treated with an antibiotic, ESPECIALLY IF YOU HAVE CONTACT WITH INFANTS or Toddlers. Early treatment with antibiotics can prevent further symptoms from developing. (If you are treated in the first two weeks (before the coughing attacks begin, then you may not get as sick.)

13.) If you are not treated with antibiotics, you are contagious for approximately three weeks!!! After three weeks of illness, the bacteria is generally gone and your symptoms are being caused by the toxins.

14.) Once you begin taking antibiotics, you are contagious for FIVE days after you take it.

15.) Nasopharyngeal testing is most accurate within two weeks after the coughing fits develop. After that it is less accurate, and there is a higher chance of false NEGATIVES. Blood tests can be used from the 2 to 8 week point(after onset of severe coughing) but is not as accurate as the nasopharyngeal swab test. To indicate recent infections via blood testing, it is important to have your IGA antibodies tested. If those are above normal, it is because you have recently had the illness.

 16.) Unlike other bacterial infections, this infection produces generous amounts of CLEAR, stringy mucous. (This is another reason that it is commonly misdiagnosed as allergies, cold, etc).
So, what does all this mean?
It means, you have to be proactive. It’s important that if you’ve had it (especially in confirmed cases) that you let people you’ve been in close contact with (up to six weeks prior!) know that you were diagnosed. I also believe it is fundamentally important to get a confirmation of the illness. Because if your doctor just proactively treats you with an antibiotic, you may not have it, and you don’t want to panic people if you don’t. Also, you may have an antibiotic resistant form or a form different from pertussis that is causing the same symptoms, in which it is important to confirm and report any mutations so that these issues can be addressed through the CDC.
The testing for pertussis is not instantaneous, so I would highly recommend that if it is suspected that you have it, quarantine yourself and those you live with until you have a definitive answer.
Finally, there is no treatment for the symptoms, though early antibiotic might lessen the severity in your symptoms (because you kill the bacteria before it causes a maximal amount of toxins). So why take an antibiotic at all?  Because it kills the bacteria and prevents it from being spread. (and again early use of antibiotics will lessen the amount of toxins that build in your system.)
I’ve talked with many health professionals over the past week, as well as representatives from the CDC. There isn’t any medication that can be prescribed that will remove the toxins. You body just has to clear them naturally and this is why it can take up to 6 weeks for you to recover from the cough.
However, it is suggested that there are OTC remedies that might help relieve the coughing spells. I will provide both basic OTC remedies, as well as non traditional remedies that might help. None of these suggestions are proven, but when you are miserable or your children are miserable, you will find you are willing to do anything that might help.
Basic OTC remedies:
Delsym cough syrup (or other OTC cough syrup- didn’t work well for us)
Vicks vapor rub (applied generously at night)
Cold air vaporizer with Eucalyptus
Baking soda and salt baths
anti-inflammatory drugs: ibuprofen
Sleeping upright or as much as possible
Non-traditional:
Antibacterial or antimicrobial:
Silver Colloidal
garlic
Vitamin C
Vitamin A
Vitamin E
Echinacea
Golden Seal
Olive Leaf
Wellness Formula
Honey
To help eliminating the mucous:
Total Cleanse: respiratory
muellin
Oregano
Cell Food
Charcoal
Sonnie’s 7
There is no scientific proof that any of those remedies both natural and basic OTC medications work at all in relieving the symptoms, killing the bacteria, or preventing the spread of whooping cough or any other illness or infection. However, you will find that when you’re child is coughing so hard that they are vomiting that you will try anything.
If you do try the natural based products, in order for any relief at all, they need to be used on a consistent basis. Natural products do not have the potency that prescription medicines have, so they do not provide immediate relief.
Please feel free to ask questions or leave advice for what has worked for you.
Most of the information provided in this post has come from the CDC: http://www.cdc.gov/pertussis/index.html

Pertussis- Is there an increase and why?:

We are in the midst of an outbreak of Pertussis, and there is a lot of information pointing blame at those who have not been immunized or fully immunized. At first, that was what was widely believed to be the cause.

However, recently, it has become accepted that the pertussis vaccine is not as effective as an earlier version. There are a few theories as to why, but the medically accepted reason right now is the new formula that was introduced in the late 1990’s is not as effective as the original vaccine. The original vaccine contained whole cells of the bacteria. The new vaccine contains acellular components of the bacteria.

They changed the formula because there were serious side effects ranging from fever and malaise to meningitis. Frankly, there have been significantly more claims of reactions to the original (whole cell) vaccine, but those are the widely accepted reasons behind changing it.

Unfortunately, about 20% of the children that receive the whole cell vaccine experience mild side effects. About 0.1% of infants experience convulsions soon after receiving the vaccine and in a very small number of cases (1 in 150,000?) severe or irreversible brain damage may occur. In the absence of the disease in an immune population, parents have begun to wonder if the risk of vaccinating children outweighs the risk of the disease, and the value of the whole cell vaccine has been questioned. (http://textbookofbacteriology.net/themicrobialworld/pertussis.html)

From ABCnews.com: http://abcnews.go.com/Health/Wellness/whooping-cough-vaccine-effective-early-form-study-finds/story?id=16898211#.UHsvmMXA-8A

The original vaccine, which contained a small amount of inactivated whole bacteria, was a crude form that brought with it side effects like fever and swelling at the injection site, but it was considered lifelong lasting at preventing the disease. In the late 1990s, it was substituted for a so-called cleaner vaccine that only used small particles of the bacteria and was considered safer but might not be as effective long term.

According to an article published in JAMA– (http://jama.jamanetwork.com/article.aspx?articleid=1362036), the vaccination for pertussis is not effective:

To assess clinical, epidemiologic, and laboratory factors associated with this increase, all pertussis cases reported during January 1–June 16, 2012, were reviewed. Consistent with national trends, high rates of pertussis were observed among infants aged <1 year and children aged 10 years. However, the incidence in adolescents aged 13–14 years also was increased, despite high rates of vaccination with tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine, suggesting early waning of immunity.

The following article is in accordance to the belief of the vaccine not being as effective, according to an article in the Oxford Journals, Clinical Infectious Disease: (http://cid.oxfordjournals.org/content/early/2012/03/13/cid.cis287.short).

We identified 171 cases of clinical pertussis; 132 in pediatric patients. There was a notable increase in cases in patients aged 8-12. The rate of testing peaked in infants, but remained relatively constant until age 12. The rate of positive tests was low for ages zero to six, and increased in preadolescents, peaking at age 12. Vaccination rates of PCR positive preadolescents were approximately equal to that of controls. Vaccine Effectiveness was 41%, 24%, 79%, for ages 2-7, 8-12, 13-18, respectively.

Conclusions: Our data suggests that the current schedule of acellular pertussis vaccine doses is insufficient to prevent outbreaks of pertussis. We noted a markedly increased rate of disease from age 8 through 12, proportionate to the interval since the last scheduled vaccine. Stable rates of testing ruled out selection bias. The possibility of earlier or more numerous booster doses of acellular pertussis vaccine either as part of routine immunization or for outbreak control should be entertained.

So the question starts with, does the vaccine really work? And it is not certain if it does. If we use the data from above Oxford Journal article, the effectiveness of the vaccine in ages 2-7 was 41%, ages 8-12 only 24%, and ages 13-18 it was 79%.

Frankly, I don’t think any of those statistics are promising considering the severity of the infection.

According to the National Vaccine Information Center, there is also evidence that the vaccine has caused pertussis to mutate so that the vaccine does not work effectively:

There is also some evidence that B. pertussis bacteria may have evolved to become vaccine resistant. (http://www.nvic.org/vaccines-and-diseases/Whooping-Cough.aspx)

The idea that there was a mutation in reaction to the vaccine was published in a research article by Dr. Fritz Mooi. Dr. Mooi has studied Bordetella Pertussis for over 15 years and is world renowned as an expert on Pertussis: (http://www.ncbi.nlm.nih.gov/pubmed/19879977):

The etiologic agent of pertussis, Bordetella pertussis, is extremely monomorphic and its ability to persist in the face of intensive vaccination is intriguing. Numerous studies have shown that B. pertussis populations changed after the introduction of vaccination suggesting adaptation. These adaptations did not involve the acquisition of novel genes but small genetic changes, mainly SNPs, and occurred in successive steps in a period of 40 years. The earliest adaptations resulted in antigenic divergence with vaccine strains. More recently, strains emerged with increased pertussis toxin (Ptx) production. Here I argue that the resurgence of pertussis is the compound effect of pathogen adaptation and waning immunity.

The other consideration is that there are different types of pertussis, and the vaccine is only targeting one type of Bordetella bacteria, Bordetella pertussis.  According to an article published in JAMA: (http://jama.jamanetwork.com/article.aspx?articleid=1150090)

An unusual 2010 outbreak of whooping cough in Ohio that disproportionately affected adolescents led disease hunters from the US Centers for Disease Control and Prevention (CDC) to the surprising discovery that about a third of the cases were caused by infection with Bordetella holmesii and not Bordetella pertussis, the usual isolate among individuals with the characteristic symptoms of whooping cough.

There are other forms of Bordetella that cause whooping cough beside Bordetella holmesii. According to the National Vaccine Information Center (http://www.nvic.org/vaccines-and-diseases/Whooping-Cough.aspx):

There is another Bordetella pertussis whooping cough disease called B. parapertussis. Symptoms of B. parapertussis whooping cough can look identical to B, pertussis whooping cough but they are usually milder. B, parapertussis is increasing in the U.S. and other countries, which have had high pertussis vaccination rates for few decades. There are estimates that perhaps up to 30 percent of whooping cough disease in highly vaccinated populations may be  caused by B. parapertussis organisms.

It is possible to have both B. pertussis and B. parapertussis infections at the same time. Parapertussis is often milder than B. pertussis but can also involve serious complications which lead to pneumonia and death.

Pertussis vaccines widely used around the world do not protect against parapertussis. There is no vaccine for parapertussis.

Finally, is there an actual increase at all?

Right now, there is a LOT of publicity decreeing an outbreak, and you have people taking sides of who is to blame. You have people saying that it is being caused by the vaccine itself. You have people stating it’s from vaccinations not working or that it’s because some people aren’t getting vaccinations. Some people believe that the vaccines have caused mutations in the bacteria, and others believe that the vaccinations aren’t working because of the mutations in the bacteria. The most intriguing idea that I found is a belief that there hasn’t been any increase at ALL.

This final group that I’m researching believes that the number of people getting pertussis hasn’t increased, but the methods and standards for “classifying” a person as having pertussis has changed.

Previously, in order to be diagnosed with pertussis, a person had to have a persistent cough for more than 3 weeks AND a positive test for pertussis in order to have a “confirmed” case of pertussis. The CDC changed their definition and now states that a person only has to have the cough for 2 weeks AND a positive test for pertussis.

There have also been more defined symptoms for having pertussis. This makes it more likely for a physician who might not have considered it as being pertussis to now consider and test for it.

Regardless of these changes, it is also firmly accepted that for every reported and confirmed case of pertussis there are two or three cases that still go unreported.

I found this to be true in the case of my family.

When the test was positive, I thought, boy they’re going to want to notify EVERYONE (my son was sick first, and he went to school the entire time), but when the community health department called, I was told that even though my daughter had the positive test, they would not consider her as to having it because she has only had the cough for 10 days. Further, they were not going to “confirm” my son as having it even though he’s had his cough for 4 weeks because he did not have the positive test.

I was shocked! There weren’t going to be any notifications at all. I found this to be incredulous. The community health representative told me that if I took my son back to get tested, and he had a positive test than they would submit the confirmation, and if I called them back to report that my daughter still had her cough after 14 days, they would confirm her case too.

Why should this matter?

My children exposed a significant number of people while they were unknowingly contagious, so I approached their doctor to get the lab work done, but found out that she did not feel that it was necessary. AND it is not necessary for them. They don’t need the confirmation. They are being treated, but it is going unreported and therefore no one else will get the notice. The people that they exposed will not know to watch out for the illness.

I tried to address those concerns with their doctor, and she said it didn’t matter because as long as the people that they’ve had contact with have had their vaccinations, they won’t get it. I tried to express that I had found information to the contrary and even representatives from the CDC were stating that the vaccination is not as effective as it had been previously.  She felt I was wrong.

Frankly, it doesn’t matter to me what she thinks of me, it’s the fact that she is treating other people and if she doesn’t understand the importance of having the illness reported, then I’m at a loss. She  felt that we should just contact everyone that we’ve been in contact with over the past few weeks, but it simply isn’t as simple as that. My son plays for both JV and Varsity football. He is in contact with 100’s of people each week. We went to a MAJOR amusement park for two weekends while they were sick. There is no way to contact everyone that they’ve exposed, especially without the help of the community health department.

Again, she also believes that other people won’t need to worry about it because they’ve been vaccinated (I shared this belief prior to a week ago), but now I know that might not be 100% true.

She wasn’t the only local doctor who feels this way. I took my children back to the local children’s hospital yesterday, and the nurse that was taking care of them didn’t understand the need for testing and agreed with my doctor. As long as they were being treated, what’s it matter?

Our babysitter has been exposed over the past few weeks, and she started getting sick this week. Her father wasn’t going to do anything about it. Since she is 18 (and fully vaccinated), we took her to her doctor, and he treated her but did not run the testing to see if she had it. The doctor felt that she probably did have it, but he felt that testing or reporting of it was unnecessary.

Granted, the information in this post is new. It just gained major media attention in September that there are more reported cases since the 1950’s AND that those who have been vaccinated are getting ill too, but it is mind BLOWING to think that the local medical community does not understand why testing and reporting it is necessary.

That is the reason, I am writing about it now. I feel it fundamentally important that if you believe you have pertussis, than you need to get treated ASAP. You need to quarantine yourself until you’ve been on antibiotics for at least 5 days. You need to push for getting the testing done and have it reported to your local health department, and PLEASE do not think that just because you’ve been vaccinated (even fully vaccinated) that you don’t have it. Especially get tested if you find out that someone you know has been diagnosed with it and then you start to develop symptoms.

Our story:

Can  you believe that my family has been diagnosed with Pertussis? Me neither.

Frankly, folks, I have always stayed away from vaccinations. I have this belief that the reason I developed autoimmune issues was because I had a booster series of immunizations in 2000. I started gaining weight and getting sick shortly after, and the rest is history.

I have no physical proof that the immunizations led to my autoimmune issues, but I got sick from them. I ran a fever within 24 hours after the booster. I felt horrible. I spent an entire day unable to leave my couch.

Ok, so I chose not to get my kids fully vaccinated. I got my daughter her first two series when she was a baby, and she got sick hours later. It was at that point, I thought, “Why am I making her sick? It can’t be good for her.”

She was preemie. She was tiny, and up to that point, I had spent all of my time trying to prevent her from getting sick, and then I allowed them to give her something that made her sick. It just didn’t feel right, and I believed that as long as they weren’t being exposed to people who had illnesses, then they wouldn’t need the vaccinations.

When they got older or if we traveled or if the threat of getting something became more risky than the vaccination itself, then I would proceed to get them vaccinated.

There is a fear of having your children get ill, and there is guilt if you get them vaccinated and they get sick. And there is fear and guilt if you don’t vaccinate them and  they get sick.

It’s a roll of the dice. There is danger in either choice, and it’s a matter of which is a bigger risk.

Not only is there a fear that your child might get sick from the immunizations, but there is a belief that if the disease is so rare and everyone else is vaccinated then what is the chance of your child coming into contact with one of these illnesses? That mentality, pushed my decision to not get further vaccinations.

Until last week, I have never hesitated at all in my decision. My children have been remarkably healthy. They haven’t even had any ear infections. My son has had issues with croup (viral) and strep throat (bacterial), but has never had any other ongoing medical issues. My daughter has had a cold twice in her life. She’s never had an ear infection, and I think she’s needed antibiotics once or twice in her life.

So, when my son started to get sick in the middle of September, I thought great, “it’s going to be an early cold season.” Sure enough, a few days later, we all had the sniffles. We each in turn had a headache, sneezing, stuffy noses, but what made this a different type of cold, we all had body aches.

Within a few days, we all started to recover from the cold, but my son instead of getting over it completely, developed a cough. It was no big deal at first. It was a dry cough. We kept him out of school for a few days and gave him OTC cold medicines. He seemed fine, but the cough was persistent.

After a week of coughing, we took him to the doctor, who said, he had allergies that has progressed into a bronchitis. She didn’t feel the need for antibiotics which was fine with us. Your immune system will fight off bacterial infections within a week or two on its own (in most cases).

He was producing a lot of mucous with his coughing spells, but it was clear mucous, so I figured it wasn’t necessary to have antibiotics anyway. (In most cases, bacterial infections cause thick yellow or green phlegm.)

A few days later, my daughter started to get sick. It was at this time that I realized this wasn’t from allergies or bronchitis because that night she sat upright in bed, while asleep, and coughed. It was hard for her to breathe because the coughing was so intense. I wanted to avoid having her go through what my son was going through, and I thought it would be best to get her on an antibiotic, so the next day I took her to the doctor.

She reassured me that it was allergies and the drainage was causing her to cough, and that she didn’t need antibiotics. She said, if she wasn’t better at the end of the week, we should call her back and get an antibiotic. That sounded great to us, so we went about our regular activities.

That weekend, she wasn’t better, but she wasn’t running a fever. She wasn’t coughing up green or yellow phlegm, so we called to get the antibiotics and went to a major amusement park for the day.

When she was there, the cough progressively got worse. She was coughing constantly, and I was becoming more concerned. This wasn’t right. She was really sick.

I thought, this might be whooping cough, but she doesn’t have a fever and she isn’t making a “whooping” sound when she coughs. It is just this persistent dry cough that makes it hard for her to breathe.

So, I started to do research. My stomach sank when I read that a person may not run a fever with whooping cough! And a person may not make the whooping sound with the cough. And a person does not produce green or yellow mucous but significant amounts of clear, stringy mucous.

At that point, I was 90% sure that she had it.

The next morning, I contacted her doctor through the emergency line, and explained my concerns. They felt it was not whooping cough, but if I was concerned, I should take her to the urgent care. Frankly, they made it seem like I was being paranoid and over reacting. Everyone thought I was over reacting, my friends, my family.

Despite the criticism, I took her to the local Children’s urgent care department. They started her on the correct type of antibiotics to error on the side of caution, and did a nasopharyngeal swab to determine if she did have pertussis.

The next day, we found out that she did have it.

I felt vindicated and guilty at the same time. I should have gotten the vaccinations. It was my fault. Where did my kids get this from?

My son is very social and athletic. He attends our local high school, and he said that a friend from a nearby city had been sick.

So, was there an outbreak in our state? That’s when I started to research this further, and what I cover in the next few blogs is what I found out.

Frankly, folks, what I found out is STARTLING, and I believe we are on the verge of something significant regarding re-emerging diseases.

Further, I really think it important for everyone to know the signs and symptoms because if you have a doctor like ours, you will find that either they don’t know enough about the infection or they don’t find it very concerning..or both.

Drawing a connection between general brain injuries and CPM/EPM:

A diagram of the forces on the brain in concussion

A diagram of the forces on the brain in concussion (Photo credit: Wikipedia)

I’ve said it before, but I believe it needs to be addressed further. Doctors do not know that much about CPM/EPM. Because there are only 2,000 to 2500 cases that are definitively diagnosed as CPM/EPM each year, there aren’t any “experts” that we can turn to. Because of this, it is necessary to draw understanding from what we know about brain injuries in general.

The brain is the most complex part of a human body, and the most interesting thing to remember is that we do not know that much about it.

Previously, it was believed that if you did not pass out from an injury (hit, fall, car accident) then a brain injury did not occur. Now, we know that is not always the case.

You can have short term to long term cognitive, physical or emotional issues from a simple bump on the head or even from whiplash.

So, let’s investigate brain injuries further:

The first type of more common and less recognized form of brain injury is a concussion. Concussion occurs when your brain is jostled, which results in impaired functioning. It can occur from a fall, a hit, a car accident, even from shaking (shaken baby syndrome). Generally, a concussion is determined from the symptoms that a person experiences. In other words, you may or may not have any outward physical signs of trauma, like bumps, bruising or bleeding. You may not even have a direct hit to the head. You may experience an impact to the body that leads to a jolt to the head that causes injury to the brain.

Concussions cause microscopic injuries that are generally not detectable by CT scans and do not cause pronounced bleeding of the brain. It is believed that the damage in the brain is from cellular damage. It is also believed that the damage to the brain is widespread. This is why if there is bleeding, it will not typically show on a CT scan because it is not significant enough to pool in one area to be detectable.

So, concussions result from injuries to the way the brain cell (neuron) functions vs having damage to the blood vessels in the brain that causes more significant bleeding. This type of injury is similar to the cellular type of injury that those with central pontine myelinolysis or EPM. You will also find this type of physiological type of injury with MS too.

The brain cells (neurons) may be severed completely in concussions or there may be physiological damage that is done that impacts the way the cell functions. So, the brain cell itself may be damaged or the way it works may be damaged.

What do I mean by that? I would compare it to when you have a neck injury that causes paralysis or a neck injury that just causes numbness and tingling to an extremity. If you have paralysis, the damage is complete and there’s little or no function to the impacted sites, and it can not be repaired. The wiring is cut and the signals can’t get through. If you have an injury that causes numbness and tingling, there is some information being processed, but it is not being processed correctly. This would be comparable to having a short circuit in an electrical wire. Sometimes, the information will get from point A to point B, sometimes it won’t. In these instances, sometimes your body can repair the damage.

(The following is a picture of a neuron…the cells that compose your brain tissue. )

English: Complete neuron cell diagram. Neurons...

I would recommend checking out the following link for a little more information regarding the physiology of concussions (http://www.cordingleyneurology.com/contuseconcuss.html)

Based on what type of injury occurs, concussions can be mild (a person does not lose consciousness) or severe (a person can lose consciousness or even slip into a coma).

So how do you know if a concussion is mild or severe?

Generally, hospitals will look at the person’s symptoms to determine how severe a concussion is and also on if the person lost consciousness and for how long. That said, symptoms may or may not develop right when the injury takes place, and because of typical limitations on insurance plans, hospital staffing, and resources, most emergency rooms will dismiss the person to the care of family or friends within a few hours if the did not lose consciousness from the injury.

It is suspected that there are 1.6 to 3.8 million sports related concussions each year. Each year approximately 1.4 million people seek care for brain injuries. It’s obvious from the numbers I just mentioned that a significant number of people, especially those who participate in sports, do not seek medical treatment for the injuries that they have.

It can mean that a person does not suspect that their injury is significant enough to require treatment, or it might be that people do not realize a connection between their symptoms to the injury that they experience. I believe it is the latter.

This means it is important to recognize the symptoms of a concussion. Typical indicators of a concussion:

Physical Issues:                   Cognitive Issues:  

• Headache                            • Feeling mentally
• Nausea                                  “foggy”
• Vomiting                             • Feeling slowed  down
Balance problems             • Difficulty Concentrating
• Dizziness                              • Difficulty Remembering

• Visual problems                • Forgetful of recent information or conversations

• Fatigue                                • Confused about recent events

Sensitivity to light           • Answers questions slowly

• Sensitivity to noise          • Repeats questions

• Numbness/ Tingling

• Dazed or stunned

•Seizures may also occur immediately or even up to a year or more later.

Emotional Issues:                           Sleep Issues:

• Irritability                                        • Drowsiness

• Sadness                                            • Sleeping less

• More emotional than usual             • Sleeping more

• Nervousness                                      • Trouble falling asleep

I HIGHLY, HIGHLY recommend checking out the following link to learn more about the effects of concussion and other brain injuries (this is a great tool for those who have a brain injury as well as those who live with them)— http://www.brainline.org/landing_pages/TBI.html

Check out the following on how scientists are determining the function of how the brain works : http://connectedsocialmedia.com/5697/future-lab-mapping-the-network-in-the-brain/

It is also important to understand that you may not develop all of these symptoms, and the symptoms may not appear immediately after the injury. It may take days or weeks before the symptoms appear. It may happen a few hours after the injury. And unlike other brain injuries, these injuries do not typically appear on CT scans or MRI scans.

You may experience the following longer lasting issues in your daily life:

• Increased problems paying attention/concentrating
• Increased problems remembering/learning new information
• Longer time required to complete tasks
• Increased symptoms (e.g., headache, fatigue) during school/work
• Greater irritability, less tolerance for stressors
Until a full recovery is achieved, you may need the following supports:

• Time off from school/ work
• Shortened day
• Shortened classes (i.e., more frequent breaks)
• Rest breaks during the day
• Allowances for extended time to complete work/assignments/tests
• Reduced homework/work load
• No signiicant classroom or standardized testing at this time
Physicians and school personnel should monitor the student’s symptoms
with cognitive exertion (mental effort such as concentration, studying) to
evaluate the need and length of time supports should be provided.

The information above is from the CDC: http://www.cdc.gov/concussion/HeadsUp/physicians_tool_kit.html

Generally, a person will recover from mild concussions in a few weeks, but it is also important to remember that concussions can “build”. If a person, experiences a concussion and it is mild, and then experiences an additional injury, days,weeks or even months later, the injury can be catastrophic. It can actually lead to death. For this reason, there are new policies being implemented in schools and college athletic programs throughout the country that bench players for weeks or months following minor concussions.

Until concussions are understood more fully, I believe this should be a mandatory step for the protection of the individual.

Ok, so how does this relate to CPM/EPM? Concussions can impact any area of the brain, but as mentioned above the type of injury found in a concussion is believed to impact the physiology of the brain cells. It impacts how brain cells relay chemical signals, and this is true for CPM/EPM too. This is why there are similarities in the emotional, behavioral, cognitive and sleep symptoms of CPM/EPM and concussions.

I plan to research brain injuries further to hopefully discover answers as to why our experiences are so vast and different, and hopefully to determine what we can anticipate in how the injury responds to treatments.

Have a great night!

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