Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Brain damage”

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.

 

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!

I can’t do it all:

 

I’ve been at a breaking point for weeks now. It seems like when you think you can’t handle one more thing, five more things are forced upon you.

All of the things that I’ve been going through over the past few weeks are related to having a brain injury, and it has made me SO angry, and so upset because there is nothing that I can do about it.

I’m stuck living with it, and there’s nothing more that I can do to fix it. Don’t get me wrong, I am trying to fix it still. I’ve just started taking several new medications to help with the things like pain in my hands, cramping, shaking, etc. I’m going to start taking medicines for ADHD to see if that will help with my focus, and I will start taking anti-depressants to see if that can help make me happy that I have a brain injury and have lost everything I was working so hard to achieve over the past few years.

You know, I’m just going to say this. I think people, doctors, therapists, all believe that when life hands you shit, you should smile about it and exclaim how fantastic it is and not feel horrible that you’ve been handed a whole load of shit.

If you lose the love of your life or a child, and spend the next few months crying over that, they believe that you need antidepressants. They believe you are depressed. I wonder what people did before they had antidepressants?

They mourned, and it was an expectation. They wore black. They stayed inside. They didn’t participate in normal social activities, but somewhere along the way, we began denying ourselves this process, and began to feel that if you were upset that the man/woman you lived with for 50 years died, that you should start taking antidepressants to help get you through it.

Now, I don’t have all the answers. I don’t. I could simply argue that people would have used anti-depressants if they had them available. We have advancements in medicine that make these wonderful new medicines available, so why shouldn’t we take advantage of them?

But, I think there is a need to find the middle.

For weeks, I’ve been struggling with the stress of dealing with lawyer stuff, family issues, work issues, health problems and then the disheartening realization that I am still unable (at this time) to return to studying for the MCAT. AND it really hit home this week that this totally SUCKS, and it’s completely unfair, and there is nothing that I can do about it.

I have SO much stress directly related to having a brain injury, and it could have been prevented. It SHOULDN’T have happened!!!

No matter what happens, I will never receive enough compensation to make up for what I have lost, and at this point, I don’t think I’ll receive any compensation for what I have lost.

So, I was at my cognitive therapist appointment and tearing up at the idea that they want me to do more there as well. I’m just so fried mentally, emotionally, etc that the idea of doing these worksheets that a 7 year old would have no problem doing about caused me to have a complete breakdown.

And then to make it even worse, my therapist looked over at me and told me that I would need to start taking antidepressants or I would need to give up things that I was already doing or wanted to do. She told me that I needed to stop doing things in order to get better because if I was so overwhelmed when I came in to work with her, then I would not be able to do anything that they needed me to do.

Of course this makes sense. If I’m so stressed out that the thought of doing mental tasks that they require me to do sends me into a tizzy, then they really can’t do anything for me.

This ramped up my anxiety and stress by 80. I mean, my therapist understands me, and she has helped me so greatly over the past several months. She KNOWS and UNDERSTANDS what I’m going through. She has the answers, and she’s a fantastic person and a wonderful friend, and if there is anyone who is going to help me get back to “normal” then it is her.

What am I going to do if I lose her too?

So, I’m left with the choice of going on antidepressants or stopping therapy. There really is no choice. I’ve already made the call to my doctor.

I have to say that even I don’t cotton to the idea of going on antidepressants, I understand why my cognitive therapist wants me to do it. I’m functioning on the edge of about completely losing it every day. She can’t work with that. And, I spend a good portion of my therapy time discussing how crazy my life is and how stressful it is, and that adds extra stress to her life.

As she put it, she sees a younger version of herself in me (sans the brain injury), and it is physically and mentally exhausting to see me make the same mistakes that she made.

In the end, she said, I can’t do it all, and I spent the night wondering what was I supposed to give up. How was I supposed to give something  up? I can’t very well go home, and say to my kids or Tom, well, I’m sorry. I’m unavailable for anything any longer, fend for yourselves. I can’t call the lawyer and say, sorry if you need answers to the questions that you want me to answer, figure it out on your own. I can’t call my disability insurance company and say, too bad if you need medical records, I have brain damage so screw you. I can’t walk into work and say, I’m just going to stare at a wall for the next 5 hours, don’t bother me.

So what am I supposed to stop doing? I have no flipping clue.

That night, I went to my psychologists office, and I’m going through all the same stressful things that I went over at my cognitive therapists office. I was overwhelmed. I am overwhelmed. What am I supposed to do?

Can you imagine my surprise when she told me that I needed to start taking medicines for ADD? She felt that I had a long standing issue with ADD, but that the brain damage has just pushed it over the edge. She believes that taking medicines for ADD would really help ground me and help keep me on task.

At this point, I will try anything. Truly, I think I will try anything. So, I added that to the list of things to see my doctor for. But, then she told me something else, she told me that I needed to give something up, that I can’t do it all. It was hard enough for someone who didn’t have a brain injury to try to accomplish what everyone wants or expects me to accomplish, so I shouldn’t put that extra pressure on myself to be perfect or to do everything that everyone wants me to do.

Here it was, two people, two extremely smart, extremely wise women telling me that I was going to have to stop trying to do everything. I have to accept that I can’t do the same things that I used to do, no matter how unfair it was. I have to stop telling myself, I used to be able to… Having that mentality, holding onto the past, will keep me from moving forward in the future. Wow, right?!

I have to learn to accept and be able to say: I can’t do it all.

 

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