A Collection of Medical & Legal Information About Brain Injury

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Brain Trauma and Alzheimer’s

Historically, there has been an association between brain injury and the later development of Alzheimer’s. The research regarding persons who have suffered repetitive trauma (boxers or football players) is clear – that repetitive trauma gives rise to the devastating condition known as Chronic Traumatic Encephalopathy, which is in effect, ultra early Alzheimer’s (U. EAD). In recent autopsies of deceased football players, pathologists encountered brains which appeared to be the brains of elderly people, when in fact the individuals were in their 30’s or 40’s. The repetitive trauma creates an accumulation of amyloid plaque and later “tangles” known as intracellular neurofibrillary threads (NFT) which are the hallmarks of this condition.

 

It was speculated, but not proven by any study, that a similar development could occur in the brain after a single traumatic brain injury in humans. Now, a recent study (Johnson VE et al. 2012) has shown that in those with a history of a single traumatic brain injury, there is long term pathology, involving a greater density of amyloid plaques and widespread NFT, in a third of the patients followed with survival of a year or more. The authors noted “This suggests that a single TBI induces long term neuropathologic changes akin to those found in neuro-degenerative disease.” Another study published in Brain Pathology (Chen X et al., 2009) followed 23 cases of post TBI survival patients for three years and found that even years later there was continued neuronal swelling in the axonal bulbs and axons. Strangely, the degree of axonal pathology three years later in survivors was higher than the cases in which death occurred after a much shorter duration, showing that axons continued to swell and disconnect over a protracted period of time. They noted “that the” at persistent nature of this pathology suggests that TBI can induce a progressive neuro-degenerative process.” The final mystery was that in this study, unlike some others, they did not find accumulation of amyloid plaque years later, even in the face of ongoing degeneration of brain tissue.

This news adds the our already staggering burden of future Alzheimer’s victims. To add thousands of additional individuals a year, because of TBI, to the pool of likely or even possible Alzheimer’s victims is distressing. We can only hope that our politicians and leaders in healthcare are taking notice of this potential time bomb. Add in injured soldiers and those unknowingly injured by repetitive trauma in a lifetime of sports and the future need for an Alzheimer’s cure becomes almost imperative.

New Study Sheds Light on TBI and Loss of Consciousness

An excellent study in the Journal of Neurotrauma (Browne KD et al. 2011) has shed light on another aspect of symptom onset – unconsciousness. Many insurance companies and some unread doctors, will insist that no brain injury can have occurred in an accident whereby the victim did not lose consciousness. They would likewise suggest that the primary method of brain injury in trauma, diffuse axonal injury, can likewise not occur unless the victim has a loss of consciousness. However, Dr. Browne and his colleagues using pigs, very rapidly rotated their heads in different directions without striking an object. This motion alone was found to cause diffuse axonal injury at levels consistent with mild traumatic brain injury. Interestingly, they found that rotation in the axial plane (being hit in the rear or front of a vehicle moving forward to back) produced unconsciousness in the pigs, while forces in which the head rotated along the croronal plane did not produce a sustained loss of consciousness. A week after the trauma the brains of the pigs were looked at and it was shown that both types of rotation produced similar and significant amount of DAI in both pigs, while the axial plane pigs brain stem showed signs of injury.

 

Therefore, it can now be said that loss of consciousness during an accident is a feature of the direction of movement of the head more than it is about the seriousness of the eventual brain injury found. Damage to the neurons of the brain can occur and do occur in the context of a mild traumatic brain injury with or without the unconsciousness that arises from damage or pressure to the brain stem. Loss of consciousness is not a equirement for brain injury nor for the presence or absence of DAI damage in the brain.

 

This study sheds light on why certain car accidents tend to knock out the occupants, while others do not. It is well known that angular rotational forces (e.g. a car hit from the side and not the rear) can injure the brain more readily.

TBI and Symptom Onset: What is Real?

For many years it has been medical gospel that symptoms of a tramatic brain injury will appear immediately after the impact and will thereafter decrease over the passage of time through recovery.  However, more research into the biological impact of TBI at the cellular level suggest that some of the damage to the brain tissue following trauma can continue for months and even years after the time of trauma.  There are also other factors which make this a formally “gospel” of symptom onset antiquated and untrue in many cases.

 

Canadian researchers (Doucher PA, et al. 2010) looked at how even initially mild axon damage tends to worsen in hours, days and even weeks after a head injury.  They found that within axon cells (white matter fibers that transmit information between lobes of the brain) trauma adversely affects the crucial pumping systems within the brain cell, throwing the healthy percentage of different chemicals in the cell out of whack, causing cell death.  In particular, the sodium, calcium, and potassium levels become excitotoxic, in which the electrical current in the cell is out of whack causing degeneration and death of the cell.

 

It is well known now that brain atrophy can appear even in the context of a mild traumatic brain injury.  Because of brain swelling, there are a few studies which indicate how much brain atrophy occurs within the first two months after injury, but one study suggest that most of the atrophy takes place during this time.  However, in cases of moderate and severe TBI, follow up studies have shown that the atrophy in the brain continues occurring at above normal aging rates, for a year and more.  Studies of the pathological chemical reactions following traumatic brain injury can continue to be found four years after the initial injury.  Using spectroscopy, which measures the exact correlation of chemical products within the brain, they have found that traumatized brains keep this adverse composition of brain matter and thus ongoing symptoms, for years following impact.

 

Finally, onset is often “delayed” because the victim, post injury, is doing nothing to tax the brain.  Two weeks in bed or off work or school, with no multi-tasking or complex social environment to deal with can give the illusion “that all is well.”  Even after returning to work or school, it can take months to fully realize or admit that “things are not right.”   Often friends and family gently point this out.

 

Victims should not be penalized by insurance companies for human nature – hoping they will be okay and going back to work.  When adverse psychological symptoms snowball and become worse.  This can also account for reports of significant impairment arising months after trauma

 

Overall, the research shows delayed biological events in the brain for months or a year post impact.  Treating doctors need to be aware of this.

THE BRAIN AS PREDICTION COMPUTER

In recent years a theory has been developed describing the brain as actively employing memory against incoming sensory data in order to avoid focusing on known factors and to try to predict instantaneously what is going to happen next. The brain has thus been called “a prediction computer.” It has also been called the “top-down prediction theory.” It rose through evolution and it allows our brains to function and not be overwhelmed by the amount of incoming sensory information.

 

A very interesting example of this can be shown on a YouTube clip (see Hollow Face Optical Illusion). There, we see something that is virtually never seen in the real world, namely a hollow face, which our brains “interpret” as a normal face, based upon 100% of our past experience. This shows how the “top-down” prediction model of how the brain works can actually alter our perceptions of what is really coming in through out sensory organs. Our brain is saying “this can’t possible be a hollow face” so it recreates what we see as a normal face. We have perception of an object, our brain’s instantaneous attempt to understand it, and to predict what it means. In the vast majority of instances, we sense things that we have previously sensed before. In that way, scientist have described the way the brain works as “saving band width” or not sending along sensory data that is or has been well predicted. Another example would be comparing your memories of a random day in the past thirty days with your memories of, say a vacation to Europe. Because your brain is less able to “predict” what is around the corner in a new and novel place, the experience is much better remembered than a day through the daily routine.

These theories and studies (Friston 2010; Bubic 2010; Keraga, 2007) also lead us into some interesting directions regarding rehabilitation of an injured brain and perhaps methods to utilize during our lives to strengthen the brain against the ravages of old age and dementia. Neuro-regeneration of brain cells is known to be enhanced by confronting “novelty.” It is obvious how this might occur – new connections and memories must be developed to accommodate confronting sensory data (visually, through sounds or taste) that is novel as unpredictable.

 

Thus, persons who are hardwired to seek novelty (neophilia) would tend to strengthen their brain over time when compared to individuals who stay within the confines of the very well known parameters of life. Likewise, it would seem that experiencing “avant garde” art and the added effort on the part of the brain, should be promotional of neuro-regeneration since, by its nature, it will confront the brain with new and unexpected sensory input, whether it be new modes of music, painting or even food. Studies have shown that the uncomfortable feeling people have when experiencing atonal or novel music is in part created by the brain sending out signals that it is confronting something unexpected. Further studies need to be done to confirm this connection.

 

The unexpected, the new, the novel, the challenging – all of these should be part of a regular diet for a healthy brain. Try to fool the prediction computer, shake it up a little bit.

The Second Brain in the Gut

In the last ten years a series of discoveries has changed our ideas about our mind/body connection. The evidence is building that one cannot distinguish the mind from the body, as previously thought. For example, with humans there is a second brain, complete with one hundred million neurons, which exists embedded in our intestines, known as the enteric nervous system. A bit of a surprise!

 

There is even a new field known as “Neuorgastroenterology” which studies the function and effects of the enteric nervous system. Does this second brain “help” us think? The early answer was no, but further studies have clouded the issue. Scientist have found that 90% of the information passing between the second brain through the first brain through the vagus nerve is information from the gut to the brain not the other way around. The enteric nervous systems uses 30 neuro-transmitters, just as the brain does. This explains why we feel emotional moods in the gut. Irritable bowel syndrome actually arises from too much serotonin in the gut. To complicate matters even further – serotonin is the primary neuro-transmitter involved in mood regulation (think prozac).

 

A recent study (Cryan JF, 2011) shows that the microbiota (actually foreign microorganisms that work in symbiosis, helping us digest our food) actually communicate with the brain and affect our behavior. Stress response, anxiety and depression have all been modulated by using mice bred not to accept certain bacteria in their gut.

 

This is only the beginning. This field has just begun to look into the full effects of the enteric nervous system on our lives. The effects of these discoveries on how we think about traumatic brain injury rehabilitation, mental illness rehabilitation and the pharmacology of mental illness will be far reaching. It is strange and humbling to think that billions of non-human bacteria are having a say in how we feel and act. For more information see the Second Brain by Michael Gershon.

 

Glia Discoveries II

I just read Douglas Fields fascinating new book “The Other Brain” in which he brings together all of the recent findings which are now causing the overlooked glia in the brain to be studied and appreciated.

 

In the field of chronic pain, which costs billions of dollars in lost production and drug addiction, it has often been noted that many of these people do not show pain profiles on electrical studies indicating the presence of pain in their nerves.  This has been used to ridicule certain types of chronic pain sufferers such as those with fibromyalgia, chronic fatigue syndrome, complex regional pain syndrome (CRPS), and others.  The latest research suggests that chronic pain may have its source in the brain’s microglia, which is odd since glia have no involvement in transmitting normal pain.  They found that the microglia, which are activated as part of the immune response to injury and repair, secrete cytokines and chemokines causing neurons to become hyper excited.  Several drugs including Minocycline, have been successfully injected into animals to block the normal reaction of microglia to injury, resulting in relief of chronic pain.  Microglia has also been found to react to the presence of ATP, which is released by injured neurons, causing chronic spinal cord pain.

 

The study of the glia is also shedding light on possible connections between glia and addiction.  Rats in prolonged treatment with morphine showed increased amounts of inflammatory cytokines, produced by glia, in their blood stream.  Targeting glia can reduce or eliminate morphine and other drug tolerances from arising.

 

They also know that almost all brain cancers involve not neurons, but glia cells.  Therefore advances in determining what is formerly ignored cells are up to, will have a positive effect on fighting the horrors of brain cancer.

 

Part of the glia known as astrozytes are known to be two to ten times more plentiful than neurons in the brain.  Microglia are responsible for many of the positive immune responses in our brain and function as white blood cells do in other parts of our body.  However, we now know that microglia can cause collateral damage and create many neurological disorders when they are clean and attack missions get out of hand.

 

Researchers and writers are now speculating as to whether this vast part of the brain that has been ignored is the part of the brain that controls dreaming or the unconscious.  Even further out speculation tries to link the massive amounts of junk (DNA) in the human genome to glia cells. “Junk” DNA is DNA that has no known function and glia cells were a large part of the brain that was also thought to have little or no function.  Perhaps uncovering a relationship between these two now important features of the human body will result in discoveries that will help us understand the consciousness itself.

 

The Evolution of Neuroplasticity

The notion of “neuroplasticity,” that is the ability of the human brain to repair and rewire after injury or change in function, has undergone dramatic changes in the last 120 years. As early as the late 1800’s the father of modern psychology, William James, wrote extensively on the notion of neuroplasticity of the brain and quite accurately for his time. Starting in the earlier 20th century, scientist looked even closer at the brain and this notion, oddly, changed. The work of Ramon y. Cajal and others began to show structural areas of the brain that have never been described before. Further research was able to tie these newly discovered brain structures to specific functions in the human body. From this point, the 1920’s to almost the late 1990’s, the idea that the brain could significantly alter itself after injury or produce new brain cells was a lost idea. We all grew up with the idea that “You are born with a number of brain cells and then they begin dying.”

 

In the last twenty years amazing findings regarding the neuroplasticity of the brain have been published, including:

 

Taxi cab drivers after being forced to learn thousands of addresses in London, for purposes of training, developed larger areas of the brain known as the hippocampus, which is associated with memory;

The hippocampus in the olfactory areas of the brain were constantly producing new neurons though out our lives;

Children under six who undergo, unfortunately, a hemiectomy, whereby one half of their brain is taken out, are able to regain almost normal function because of the brain’s ability to rewire and literally take over the functions of the missing other half of the brain. There are limitations to this, for example, in a child who’s brain had managed to move control of a function to a new part of the brain because of the surgery, it was found that he was almost unable to learn any mathematics because the area of the brain where mathematics was learned had been occupied by another function after the surgery;

There are two types of stem cells in the human brain that can be activated for a number of reasons including injury, and can take the form and function of the missing brain matter and make repairs known as neuroregeneration. It is likely that neuroregeneration will be found to occur in all areas of the brain in the next ten years. However, it obviously does not occur at a scale where miraculous recovery from catastrophic injury can occur. Therapies and future modalities might be able to tease these cells into doing more repairs in the future.

 

So at the present time the brain science neuroplasticity is back in and is being talked about in thousands of studies a year. We now know that some of the plasticity, for example, in learning languages, ends at a very early age. Dr. Jeffery Schwartz in his fascinating recent book “The Mind and The Brain: Neuroplasticity and the Power of Mental Force” describes many interesting examples of neuroplasticity. It has been shown for example, that very young children of the age of two can understand and hear all of the many sounds in every language in the world. That is why language acquisition is spectacularly easy if it is done at a young age and is significantly harder as we age. Studies in Japanese adults, whereby they were asked to listen to certain English language sound, were literally unable to hear some of those sounds at all, as if they did not exists.

 

The young brain also responds quite adversely to lack of use. It has been shown that there is a crucial three month period in many mammals whereby if they are kept in a dark room or otherwise unable to use their eyes, that proper connections between the brain and the eye simply do not form and permanent blindness is a result. However, when there are areas in the brain that are under utilized or not utilized at all because of the lack of hearing, vision or other sensory input, that area is taken over by nearby parts of the brain and recruited to do work for them. Thus, nothing is wasted.

 

In a recent Wall Street Journal article, they described 2011 findings that show teenagers intellects and IQ can rise or fall as many as 20 points in just a few years. This is certainly contrary to the thinking of the last hundred years. These changes are consistent with other findings, where scientists have determined that experience can easily alter the brain and its networks of billions of neural synapses. This is consistent with some of the tenets of the relatively new concept of “Cognitive Reserve” whereby persons going through life with more active and stimulating everyday lives are more able to fend off the ravages of old age dementia and Alzheimer’s. All of these new findings but a ball squarely in each person’s court – you can alter your brain for the better and as the past President of the American Psychological Association noted “Those who are mentally active will likely benefit. The couch potatoes among us, who do not exercise themselves intellectually, will pay a price.”

 

While many of these findings are good news for those who have suffered brain injury, a widespread or diffuse brain injury caused by a high speed collision, for example, is currently resistant to full recovery. “Focal” or specifically located injuries are much easier for the brain to readapt and deal with. Also, unfortunately for the moderate to severely brain injured, the likelihood of becoming a couch potato because of their injury, will likely have the effect of decreasing the likelihood of positive brain restructuring through life and will result in the injured falling further and further behind their peers.

 

Glial Cells: The “Dark Matter” of the Brain

By the time a patient gets to the emergency room, unconscious from a trauma, the primary injury to the brain – that is the structural damage to the brain tissue, neurons and blood vessels of the brain has already occurred. However, we know that this acute injury also sets into motions a complex cascade of molecular events known to create “secondary damage” to the brain. While this very complex puzzle has not been completely unraveled, we do know that one of the chemical events that occur after trauma to the brain is “oxidative stress”. The human body generally stays in balance by producing reactive oxygen species (ROS) and using them as part of our immune system. These molecules are highly reactive and destructive and are essential for keeping our immune system intact. However, after a trauma the balance is thrown out of wack and far too many ROS molecules are thrown into the blood stream. This condition of oxidating stress is also thought to be important in many neuro-regenerative diseases such as Lou Gehrig’s disease, Parkinson, Huntington’s Disease and Alzheimers. Key structures of the brain in all of this are the glial cells, a long ignored part of our brains.

 

In the early 1900’s there was a battle that raged over the make-up of the human brain between brilliant Spanish scientist Raymond Cajal and Italian Camillo Golgi. Cajal proposed that brain function was a rising from neurons in the brain, which was correct, but his theory reduced another important part of the brain structure, the glial cells, to an insignificant structural role only. However, in the past fifteen years it has been discovered that the glial cells are active in the brain and involved in many parts of cognition and memory. This is exciting because the glial cells make up a huge part of the brain structure and are currently almost like the “dark matter” of the universe. They are there but no one pays attention to them and no one knows all of what they do quite yet. There are several type of glial cells present in the human nervous system:

 

Astrocytes- These cells outnumber neurons five to one and are also found in the brain capillaries that form the “blood/brain barrier” that restricts what substances and molecules can enter the brain. The BBB as it is called, is very important in regards to a traumatic brain injury. It is thought that one of the injuries in trauma is a tearing or weakening of the BBB. Once that occurs the destructive ROS type molecules that the BBB generally keeps away from the brain are let in. This causes inflammation and destruction of brain tissue. It is thought that epilepsy can arise from a tear in the BBB as well as alzheimers and other neuro-degenerative diseases. Every month brings more research about additional fucntions of astrocytes in the brain.

Microglia- These are small cells that remove waste from central nervous system cells and offer protection as part of the immune system.

Oligodendrocytes – These are central nervous system structures that wrap around axons (the telegraph wire long branch of a neuron) and its insulating coat known as the myelin sheath. The destruction of this material can occur in high speed accidents or blast injuries. When the axons are stretched the coating can fall off or be damaged. This disables or adversely affects the neuron because of its electrical signal is then impaired. The new technology of MR/DTI can visualize this type of injury in the white matter of the human brain very sensitively. Water molecules that are suppose to run along the inside of the myelin in a straight line are shown on MR/DTI to be moving almost randomly in all directions. This is how damage is visualized on an MR/DTI.

Schwann Cells- These cells are also involved in the myelin sheath of a neuron and assist in the conduction of impulses.

A Study published in January 2010, in Nature showed that astrocytes, which comprise 90% of all human brain cells, are indeed involved in the electrical process that constitute thinking. The astrocyte needs to give a burst of electricity during the process, and thus is intimately related with neurons and the creation of cognition, contrary to 60 years of prior wisdom.

 

Not until the glial system further studies will we know enough about the chemical cascade following traumatic brain injury to prevent it. Current animal studies have shown great promise as an anti-oxidative neuro-protective medicine for the compound edaravone (Wang GH, et al., 2011) which has been shown to inhibit oxidative stress and inflammatory response as well as reducing glial activation. These compounds will not be available, unfortunately, for several years.

 

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