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 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 . 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.
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:
- Is a brain injury an acute incident or a chronic disease: (whatishyponatremia.org)
- Study Links Single Occurrence of Traumatic Brain Injury to Alzheimer’s (prweb.com)
- Top Signs You are at Risk for Alzheimer’s (belmarrahealth.com)
- Traumatic brain injury may lead to Alzheimer’s (cleveland.legalexaminer.com)
- Fish Oil: Experimental Treatment For Traumatic Brain Injuries (fox2now.com)
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