This past week in class we discussed the various medications being used to treat bipolar disorder. In the article we were assigned to read for the week, it discusses what exactly bipolar disorder is, how the disorder is treated, and the most plausible explanation for what is occurring in the brains of those affected by bipolar disorder.
There are two different types of bipolar disorder, bipolar I which is characterized by alternating periods of mania and depression, or bipolar II which is characterized by alternating periods of hypomania and depression. The disorder itself is linked to multiple different genes within the human genome. There are 88 different risk alleles, or genetic sequences, that are present in those with bipolar disorder. If someone has fifteen of these sequences then they are at a significantly higher risk than the general population. Besides the alternating cycles of moods, bipolar disorder brings with it many other health problems. Bipolar sufferers often take up smoking or substance abuse in their manic phases. The treatments for this disorder can bring on obesity and diabetes in the patient. Perhaps one of the worst things facing a bipolar disorder sufferer however is the increased chance of suicide that they face which is 10 to 20 times the rate among the general population.
As for the treatment of Bipolar Disorder, doctors use a technique called rational polypharmacy, which pretty much amounts to treating new symptoms as they pop up with various mood stabilizers, antipsychotics, antidepressants, and hypnotic benzodiazepines.
And this really only gets to the heart of the matter in that researchers do not really know yet what the root causes of Bipolar Disorder is, but they think that it has something to do with arachidonic acid. The theory here lies in that the chemicals that are used to treat the symptoms of bipolar disorder are interfering with the actions of arachidonic acid in the cell. Therefore, the researchers believe that the chemicals are correcting a chemical imbalance with regards to arachidonic acid.
For our discussions this week we talked about treatment of bipolar disorder and what it means for society. We talked about what it would mean for society if we found a cure for Bipolar Disorder, or more to the point if we even needed to find a cure immediately. We had the good luck to have two people who have happened to know someone with bipolar disorder and they both agreed that the disorder does not really affect them that much as long as they stay on their medications. This kind of segued into our next discussion question about the affects on the body that mood stabilizers have, namely obesity and diabetes and if these could possibly be worse side effects than the others because they could contribute to the depression that is felt by sufferers. I think we agreed in the end that this is merely a matter of adaption the same as learning to take all of your medication, the sufferer needed to take into account the weight gain that they would experience in the course of their treatment. I think the most interesting conversation we had however was about mood itself, namely are we misdiagnosing bipolar disorder in people who are just emotional. Like could we possibly be medicating people who are not like bipolar disorder sufferers in that their mood swings are chemically induced, but that the mood swings that these people experience are the result of them being more open with their feelings than the rest of us. It made me for one wonder whether as a society we use drugs to help people, or to make them more like the rest of us. I mean you have to take into account people who suffer from some sort of mental problems, but contribute so much to the arts and sciences.
That’s all for this week, next week’s topic will be the relationship between leptin and obesity
Bipolar Disorder: What is causing this mysterious disorder?
One minute you are overly happy and outgoing believing you can do anything you put your mind to but the next you feel tired, worried, and unexcited about all of the activities you once enjoyed. These polar opposite feelings are commonly experienced by people with bipolar disorder. In my neurochemistry class this week we investigated a possible cause for the mood cycling associated with bipolar disorder. After better understanding bipolar disorder we addressed other issues surrounding the disease. Before I explain the new research regarding a possible cause, I would like to briefly expand on what bipolar disorder is.
Bipolar disorder is a disease characterized by mood cycling between periods of depression and excessive excitement called mania. Mania is commonly described as feeling overly happy or excited, having unrealistic beliefs in one’s own ability, experiencing racing thoughts, and being restless. Depression is when one feels sad, worried, helpless, and lonely for extended periods of time. Bipolar disorder can be diagnosed under two categories depending on the level of mania and depression. Bipolar 1 is characterized by having one or more manic episodes but a depression episode is not required. Bipolar 2 is diagnosed when someone has one or more depressed episodes, one or more hypomanic episodes, but no manic episodes. Hypomanic episodes are less severe manic episodes characterized by unexplained happiness.
One of the most difficult parts of treating bipolar disorder is that scientists don’t really know what is causing the disease. However, recent research seems to imply that a biological cascade, called the arachidonic acid cascade, might be a significant piece of the bipolar disorder puzzle. Arachidonic acid is a molecule cut out of lipids in the lipid bilayer membrane surrounding our cells. According to the research paper, arachidonic acid is important in the brain because it influences the release of neurotransmitters and gene transcription. However, when too much arachidonic acid is produced it can cause damage to neurons (brain cells). The researchers think that when too much arachidonic acid is produced the mania-like episodes are triggered. Unfortunately the relation between arachidonic acid and depression was not clearly identified. Additionally, I would like to note that the arachidonic acid hypothesis is not the only possible cause for bipolar disorder. There are two others called the GSK-3 inhibition hypothesis and the myo-inositol hypothesis but these were not focused on in the paper.
Finally, the arachidonic acid cascade hypothesis agrees with the present-day treatments for bipolar disorder. The most common type of drug used for the treatment of bipolar disorder is mood stabilizers. Common mood stabilizers include lithium, valproate, and carbamazepine. These mood stabilizers are thought to work by limiting the production of arachidonic acid either by inhibiting the neurotransmitter receptor or the enzymes associated arachidonic acid fabrication. Although these drugs have been relatively successful, bipolar disorder is still not completely understood. Therefore, additional research is needed to better understand what is truly going on in bipolar disorder and what the best ways to fix the problems are.
Source:
1) http://www.nimh.nih.gov/health/publications/bipolar-disorder/what-are-the-symptoms-of-bipolar-disorder.shtml
Mountains and Valleys: The Roller Coaster that is Bipolar Disorder.
Bipolar Disorder. What is it? You may have a preconceived notion, like I did, that it is when you can turn on a dime and change moods from hyperactive to depressed in the blink of an eye. Well that was what I thought before this weeks discussion. Bipolar is a disorder characterized by extreme mood swings that can last from a few days, to weeks, to even years. There are 4 main types of bipolar; I, II, cyclothymic and rapid cycling. Bipolar I is where you have 1 or more manic episodes with depressive moods not required for diagnosis. Bipolar II is having no manic, 1 or more hypomanic episodes and 1 or more major depressive episodes. Cyclothymic bipolar is classified as having 1 or more hypomanic with periods of depressive moods that do not fall into the category of major depression. Rapid cycling is applied to all the previous categories and refers to having 4 or more major mood swings in any given year. Bipolar is usually fairly hard to diagnose because of all the coinciding complications that can go along with bipolar, such as; social phobia, OCD, ADHD and anxiety disorder.
The first thing we discussed was the hypothesis we thought should be researched in order to find a way of treating bipolar. The one that I thought should be researched the most was the myo-inositol depletion pathway, which describes the mechanism that Lithium has on the inositol pathway in the brain. Lithium is the most widely used drug for the treatment of bipolar even though the exact mechanism is not entirely known at this time, which is why I think that this hypothesis should be researched the most. What is hypothesized is that Lithium inhibits a protein in the brain, inositol-monophosphotase, which converts the inositol-monophosphates into myo-inositol, thus the name myo-inositol depletion hypothesis.
The next thing we discussed was that in pregnant women, whether or not you treat the disorder, the mother has a higher likelihood of abusing drugs, smoking, and being overweight and the child has an increased risk of being born with complications that could be detrimental to its health. In untreated mothers, the children were also shown to be at risk of being born with small heads and low blood sugar. Now the question was do we treat the disorder and have the child live with the effects of the drug or do we not treat it and have the child deal with complications that arise from not treating. A saying from a mental health expert, Dr. Salvatore Gentile, says that the issue is not whether or not to treat the disorder, it is how to treat the disorder in respect to pregnant women with bipolar disorder. I agree with this statement because once we know how to treat bipolar without posing significant risk to pregnant women’s children, the question of whether or not to treat them becomes irrelevant. However, until research shows what the exact change is that occurs in people with bipolar, a cure will be hard to come by and the question of whether or not to treat it will stay relevant.
The final thing we discussed was the statistic that out of 7.7 million Americans that suffer from schizophrenia and bipolar, approximately 40% of schizophrenics and 51% of bipolar people are untreated in any given year. The question posed was why are so many people not getting treated? I think that one of the main reasons is that the medication that can be used has some serious side effects and that most people would rather suffer from the adverse effects of schizophrenia and bipolar disorder than risk having to deal with the side effects of the drugs. I think that until bipolar is “figured out” and a drug that targets the main cause of it has been developed, I think that the statistic will remain high and a lot of people will go on untreated.
That is all for the bipolar week of discussion. Next week is all about Obesity and all the details that entail.
Lithium as a Treatment for Bipolar Disorder
There are several mood disorders that affect people everywhere. One particularly debilitating disorder is bipolar disorder. This disorder is classified by changes of mood between depression and mania. What is particularly mind-boggling about this is that we do not know the exact cause of the swings, and therefore we do not have a particular target for a treatment. Scientists have isolated a few areas in which they believe to have an effect on this and have found a few antipsychotic drugs that although have severe side effects, have shown a slight improvement in patient health.
The most common of these drugs is lithium. Even though this drug is commonly prescribed for the disorder, the actual effect it has on the body is rather foggy. What scientists believe to be true is that lithium slows down the activity of IMPase in the body which in turn will slow down production of inositol and phosphate which are believed to have an effect on the chemical imbalances in bipolar patients.
When looking at this drug, it seems completely different than other drugs. It is a single element rather than some large branching molecule. The question we ask ourselves is how did scientists stumble upon lithium to treat bipolar disorder?
Originally lithium was believed to combine with uric acid and produce a solution that helped break down uric acid accumulation. This knowledge helped them treat diseases in the 19th century such as gout. Around the 1940s it was reasoned that a high sodium diet was responsible for hypertensive patients and that they would benefit from a salt free diet. This led to the production of lithium chloride as an alternative to table salt. This ended up being a failure causing several people to die and lithium salts were taken off the market. Lithium was then ignored until 1949 when a group of scientists hypothesized that mania was caused by a normal body product circulating the body in excess. They found this product to be urea. They then made a solution of lithium urate and injected it into guinea pigs to see how much uric acid increased the toxicity of the urea. Although it did not have an effect on urea concentration, it did seem to have a calming effect on the guinea pigs and was believed that this was cause by the lithium. Since then it has been used as an effective medication for bipolar.
As you can see, bipolar disorder is very confusing disorder in which we do not know a lot about. As stated, lithium is currently the most popular medication and was originally discovered on accident when trying to establish how much urea was toxic in the body. For more information on this topic, visit http://www.bphope.com/Item.aspx/162/through-the-ages-its-been-there
The Ups and Downs of Bipolar Disorder Treatments
Are the costs of bipolar disorder treatment outweighing the benefits? The current treatment methods involve Lithium drugs for these psychoactive treatments. They have been found to suppress the extreme swings in mood involved in bipolar disorder, and lessen the emotional suffering in patients as well. At the same time, scientists are not even completely sure what is the root cause of bipolar disorder and what is neurologically occurring in the brain. Lithium psychoactives activate a huge range of pathways in your brain, one of which involves treating bipolar disorder. The long-term deficits of these drugs involve extreme amounts of weight gain in a rapid timeframe, with other effects still being investigated. Do these effects outweigh their treatment benefits?
This week we saw a great deal of discussion on the symptoms of bipolar disorder and what current treatments have to offer. Bipolar disorder is defined as a psychological disorder contrasting between periods of deep depression and manic excitement. While most manic episodes, patients deny having symptoms and experiencing problems, the suffering in depressive episodes is clear and more detrimental. Any treatment of depressive symptoms is typically viewed as a huge improvement and of extreme benefit. Patients experience fewer depressive episodes and they are less severe. This is also true of the manic episodes. Treatments involve therapy and psychoactives in combination or isolation. Therapy alone does not typically help enough so drugs are used additionally. Psychoactives drugs like Lithium have been fairly effective in treatment of the disorder itself, but scientists still don’t know what it is affecting in the brain, and this is where the trouble in treatments comes along.
The malefic of drug treatment options is disconcerting because, aside from suppressing swings, no one knows what else will go wrong in your brain and cause long-term side effects. The most well understood side effect of psychoactives is weight gain. I looked more specifically into it this week and found that psychoactive drugs activate a histamine receptor in your brain. This activation creates a lot more AMPK than normal, leading to a huge increase in desire to eat. As a result, patients are consuming much more food than normal; weight gain in young patients was as much as 18 pounds in 11 weeks worth of time. This is a shocking amount to consider when you realize that most patients will be on these drugs for the rest of their lives, and they will be gaining weight at these rates for their life. Effects of this weight gain include type II diabetes, high blood pressure, high cholesterol, etc associated with obesity. Now, the drugs that are supposed to improve your mood and overall quality of life are causing you to eat more than ever before and lead to a much shorter life span due to such huge, no pun intended, weight gains. The current question patients must ask themselves is whether or not they are willing to gain 50 pounds and shorten their life expectancy to lead a normal life, or suffer emotionally while maintaining a normal body weight. The answer is not clear or evident in the least. The tradeoffs of each are significant and raise the question of quantity of life or quality of life. If you were a patient, you must ask yourself, do the effects of treatment outweigh their benefits?
Concussions and Advances in safer Helmets
This past week in class we dis
cussed the neurological complications of concussions. The most common occurrences of concussions occur in sports, specifically football and soccer. In fact, last year during the preseason and regular season of the NFL a total number of 217 concussions occurred. Add into this fact the numerous concussions which arise in high school and college sports the number of concussions is drastically high. Concussions are caused by a blunt impact to the head. This blunt impact interrupts the brain’s “wiring” so to speak. A concussion disturbs the normal function of neurons.
First, it is important to note that in order for a signal to be sent from the brain there must be an action potential. Action potential is the sudden rise or fall of charge within the membrane of a neuron. Now it might sound odd to say that there is charge within our cells but this charge is not like static electricity. This charge is present in the form of metal ions such as calcium or potassium inside and outside the cell. A concussion causes a depolarization of the neurons, which means that the charge housed in the cell is higher than its natural state. This causes a massive influx of calcium into the neuron. The overabundance of calcium causes potassium to be pumped outside the neuron. Due to the exchange of these ions from the outside and inside of the neuron, signaling is interrupted by a concussion.
A major complication with concussion is the state of hypoglycolysis it induces. Hypoglycolysis is a state in which cells are deprived of sugar, glucose. Without an adequate supply of energy, glucose, cells begin to die. This apoptosis of neurons is the cause of permanent damage that can result from concussions. Another complication is restricted blood flow to the brain or specific parts of the brain. This is also known ischemia, which can result in unconsciousness, stroke, and cell death.
Because of the risks associated with concussions there has been numerous research studies on improving helmets for sports and recreation. I recall the 2010 NFL season when Aaron Rodgers received multiple concussions and he appeared games later with a new helmet. That got me thinking if helmet technology alone would be enough to prevent concussions. The only problem with improving the strengths of helmets is that they can become dangerous weapons for football players. Football players could obtain the notion that, because they have an impermeable helmet, they themselves are invincible and will have less regard for the safety of their heads. Therefore, I think alternatives to helmet research would be a viable options.
One example of this alternative helmet is the invisible bicycle helmet. This “helmet” was developed by a company called Hövding. There research developed an inflatable “helmet” which is hidden in a collar which looks like a scarf. Upon a bicycling accident, such as hitting a curb and flipping your bike, the collar would activate and releases the airbag like helmet. The helmet bursts out of the collar and balloons around your head creating a protective cocoon. Although they developed the invisible bike helmet for use with bicycles only, I’m confident that sometime in the future this technology can be expanded beyond bicycles and can be applied to contact sports.
Here is a link to the Hövding website:
http://www.hovding.com/en/how
Here are two videos: One explaining Hövding and their development of the Invisible Bike Helmet and the other shows a 
demonstration of the helmet on a crash test dummy:
http://www.youtube.com/watch?v=g3S62ZtyiRg
http://www.youtube.com/watch?v=Tn65Bows0Ws
References:
http://theconcussionblog.com/2012/01/10/2011-concussion-report-end-of-regular-season/
Pictures courtesy of Google Images
Concussions: a Silent Killer
In full contact sports around the world, there is one word that can strike fear into the minds of hopeful athletes, concussion. Having hearing the phrase “You have a concussion” the average athlete will probably be overcome with sadness as this means they should sit out for a game or two. When it comes to the science behind concussions, what really is happening?
Concussions first start with a blow to the head causing stretching of the brain cells. Once this happens, the neurons start a release of neurotransmitters which will signal for a release of potassium from the cell. In a normal cell, the potassium concentration is much greater on the inside, so after the concussion, the cell tries to reestablish this norm and consumes a great amount of energy bringing the potassium back into the cell. Because the cell uses so much energy, it tries to counter that by increasing metabolism in your body to replenish it which will eventually lead to lactate accumulation, calcium influx, and cell death.
As stated before, concussions are a large problem in sports. Athletes will often receive minor concussions and continue to play even though if they get injured again they could undergo even more serious side effects. The question then becomes, should we have federal regulations as to how long a player has to sit out after a concussion? Although this may seem like a harsh rule, I believe it should be followed, at least until we have developed a better treatment for concussions. Before you get mad, hear me out. Although professional football players may have a relatively short recovery time compared to a high school or college athlete, I feel they should still have to sit out the same amount of time. This is attributed to the fact that most lower level sports players idolize the professionals and will want to take after them in every way they can. This is not a good thing in this case as the younger players are still in a brain development state and if they return to play too early, there could be serious consequences. This regulation would also eliminate any “gray area” and require everyone to sit out the same amount of time. In my opinion, this would be the best solution to the problem. People don’t realize this severity of a concussion and I feel that this minor regulation would allow for more people to open their eyes to this problem.
Another possible solution to the concussion problem would be to have greater emphasis and training before the season starts to make people aware of concussions. One big problem is people don’t realize how severe these can be and just a little team meeting before the season with a “scare tactics” video may make players more aware of the problem and perhaps fix two things. One, they would be aware of the severity and perhaps be more willing to sit out after an injury and two, they would be more aware and perhaps play less violently and lower the number of cases around the nation.
As you can see, concussions are attributed to major blows to the head which can cause serious brain issues in your life. In sports, many players shrug off concussions and go right back to play. I feel that the enforcement of a minor regulation on sports leagues would help people open their eyes to concussions allowing them to play safer and if they do get a concussion, be more willing to sit out for a game or two.
Concussions Are Sort of a Big Deal. We Should Do Something About Those.
Concussions are fairly common and inexpensive with the treatments we currently use (some good old rest and relaxation); as a result, it is often hard to see them as a serious injury. A broken bone causes a lot of pain and hubbub, having to get a cast and waiting months for it to heal – it’s a very apparent injury with constant reminders that something’s damaged. Considering the attention it demands, most people would probably consider a broken bone much more severe than a concussion. Although brain damage via concussion is much less apparent, it is a very serious matter, possibly resulting in decreased cognitive capacity or, in extreme cases, death. The brain is the most sensitive and vital organ we have, so the importance of its health and protection makes all others pale in comparison, even though the bills for other injuries might suggest otherwise. The question then becomes: how do we best spend our efforts to deal with injuries like concussions – in prevention or treatment?
I’ve always thought that a concussion was just bruising of the brain (which is actually a contusion), but there’s a lot more to it than some burst capillaries. Immediately following the hit to the head in a concussion, a number of things happen rapidly to offset homeostasis in the brain. Neuronal membranes are disrupted, causing the opening of K+ channels, depolarizing the neuron. Depolarization causes a random release of glutamate which binds to NMDA receptors that allow Ca2+ to flow into the cell and more K+ to flow out of the cell, depolarizing it even more. At this point there is a major imbalance in K+ concentration, which is far from homeostasis; to counter this, ion pumps in the membrane are activated to pump Na+ and K+ back into the cell. This requires energy, however, so glycolysis goes into overdrive to convert glucose to ATP to power the pumps. After brain trauma, oxidative metabolism performed by the mitochondria is also impaired, leading to reduced ATP production, calling for an increase in glycolysis. All of this glycolysis is producing a giant amount of lactate, which can induce increased cellular acidity, membrane damage, altered blood brain barrier permeability, and cerebral swelling, all leading to neuronal dysfunction and possible cell death, all characteristic of concussion.
Looking at the prospect of treatment, not only would the treatment have to be administered within minutes of occurrence, some very influential processes would have to be altered, which always worries me – either glycolysis would have to be shut off (and considering its importance to all life processes, this is likely not a great option) or the ion channels controlling K+ and Ca2+ flow would have to be blocked. Ion channel blockers have been identified and used, but they have produced mixed results and many, if not all, of them have a list of possible negative side effects as long as my arm, ranging from headaches to death. At that point, I’d rather take my chances with the concussion.
Prevention of concussion would solve the problem right then and there. Most of the concussion incidents in our society are due to sports, a setting that can be regulated to greatly control its occurrence. The issue here is that the game would be altered to such a degree that some would question whether it’s worth playing anymore. The point of competition is to give your all against the other team and whoever comes out on top had more to give and was therefore the better competitor. Forcing people to hold back would destroy the point, although the importance of health versus a game seems like an obvious choice. I guess the bottom line is, people still know the risks and put their health on the line anyway; who’s to tell them they can’t?
To choose sides, I tend toward treatment, but with a twist; I think researchers should focus on developing reliable methods for diagnosing concussions so people can know their risks with repeated injury, and any available treatment can be administered to an appropriate degree for the extent of the concussion. Overtreatment with ion channels can be an issue because homeostasis is usually the goal, so going too much in the opposite direction can swing one’s system into an equally problematic state. However, in the end, each option is complicated and has its positive and negative aspects – there may be no ideal answer. What do you think is the best route?
Head Shot: Football and Concussions
The paper we read for this week takes us down to the basic mechanism of concussions, and by investigating the neurometabolic changes the authors try to find the relationship between these changes and sports related issues. Since I have no personal experiences with concussions, I decided to seek help from the internet in order to find some Inspirations to write this blog. And luckily, one of my favorite TV programs, Sport Science by ESPN, did a sector on the topic, NFL Concussions and helmet to helmet collisions. Although this video was filmed over two years ago, I find it still fits perfectly with the recent controversial topic of sports and concussions, especially in the NFL.
Earlier in the year, some former NFL players filed lawsuits against the league for repeated traumatic injuries to their heads. As of today, the number of the total players (both recent and former) in these lawsuits has snowballed to nearly 3000. Although personally I do not believe they have a strong case, but since I am a science student not an expert in law, it is more appropriate for me to just dive into the science part of the issue.
After a traumatic head impact, the excitatory amino acids (EAAs) are accidentally released from the pre-synaptic neurons, which then bind to the NMDA receptors located on the post- synaptic neurons. Upon the activation of the NMDA receptors, the efflux of potassium and influx of calcium leads to neuronal depolarization. And since our body would like to restore the normal cell potential, the ATP requiring sodium potassium pumps in the cell will work overtime causing the “hypermetabolism” and eventually an energy crisis. The researchers suggest that the energy crisis is a likely mechanism for postconcussive vulnerability, making the brain less able to respond sufficiently to a second injury and potentially leading to longer-lasting deficits such as impaired coordination, attention, memory, and cognition. According to the Sport Science video, over 100,000 concussions occur at all levels of football field alone every year, and 60% of these results from head to head collisions. In the NFL, the average speed of the collision is 20 miles per hour, and a player’s head could experience nearly 190Gs of force in just 0.015 seconds. Even with improved technology, helmets could only reduce an 80G collision in half, which is still more than enough to cause a concussion.
All these facts only suggest that concussions and physical sports such as football go hand in hand. With proper care, most concussive patients are able to fully recover from mild concussions. But most people (including the players) sometimes underestimate the damages of repeated concussions and therefore result in permanent damages. After all, no matter what the outcomes of the lawsuits turn out to be, I believe the lawsuits themselves are positive. Because they have successfully raised the awareness of the importance of concussion care of the general public, and more importantly, the youth and adolescent players who see the NFL players as idols.
Concussions: What are they and why are they so dangerous?
Crash! Bang! “What a hit!” On Sunday every weekend during the fall, football catches our attentions with big, powerful hits between opposing teams. On occasion, players are assisted off the field under suspicion of suffering a head injury from such a hit. More often than not, the announcer informs you that the player will not be returning to the game due to concussion-like symptoms. In the case of my grandpa, this generally prompts an angry outburst followed by a comment about how “in the old days” men use to play through such injuries. I do agree with my grandpa that it does seem like there was less concern about concussions in the past than today. So why are concussions such a hot topic in football today? Why are players not allowed to return to finish the game?
Before I begin to answer these questions, it is best to understand what a concussion is. Concussions are a type of traumatic injury caused by a hit to the head or body, a fall, or another injury which results in jarring or shaking of the brain inside the skull.1Some common symptoms include confusion, disorientation, dizziness, headaches, unsteadiness, and vision problems.2 Concussions are generally associated with sports, but they can occur in daily activities as well. You are probably saying, “but why are they so dangerous?”
First, we need to understand what happens to the brain immediately following a concussion. After receiving a concussion, there is an increased concentration of calcium ions due to increased signaling in the brain, leading to stress on the neurons. Increased calcium concentrations can lead to stress on neurons as a result of calcium accumulation. One downside of calcium accumulation is that it slows down energy production by interfering with mitochondria in the cells. Additionally, when a concussion occurs, there is a disruption in the brain’s ability to regulate potassium ions inside and outside the cell. Normally potassium ions have a high concentration in the nerve cells so after a concussion the brain tries to restore this concentration gradient by causing the ion pumps in the brain to work overtime. Therefore, the brain requires extra energy (ATP) to run these pumps longer, leading to an energy shortage. The increased potassium and calcium ion concentrations greatly limit the body’s ability to produce enough energy to support the brain cells. It takes many days until these ions return to their normal concentrations.
If enough time is given for the brain to return to normal, there seems to be little or no lasting neurological conditions from concussions. However, the lasting effects from concussions appear to occur when someone gets another concussion before the first one is fully healed. According to the research paper, the brain is most vulnerable to lasting damage when it is working overtime producing energy to recover from the first injury. When there is a second concussion, the brain may not be able to produce enough energy to support the repair process for both the first and second concussions. The result is irreversible damage to the brain. Therefore, the injured NFL players are not allowed to return to the game because the NFL is trying to protect the players from a second concussion and thus permanent brain damage.
Sources:
1) http://www.webmd.com/brain/tc/traumatic-brain-injury-concussion-overview
2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155411/pdf/attr_36_03_0228.pdf