As technology is increasingly becoming a big part of our younger generation’s life, it is important to acknowledge its damaging potential in the long run. Though it can be seen as a helpful tool to keep them entertained in the midst of a busy time for the parents, there has been shown to be more downsides to the screen time than good The use of screens at the early development stage has not only been shown to cause development and neurological impairment ( such as in autism), but it also hinders the recovery process. This has been shown to have a negative impact on the recovery from concussion.
(Kohl’s building blocks)
A study was conducted on 125 patients aged 12 to 25, to test the effects of 48hr deprivation of screen time on recovery after concussive symptoms. Control had a shorter duration of symptoms (3.5 days) than 8 days for those allowed screen time right after their concussion.
The Post-Concussive Symptom Scale on a score of 3 points was used to assess a 22-symptom scale for the subjects in the study. Each symptom is rated from 0 to 6 (severe).(Macnow & Curran, 2021)
(Middlebrook, 2016)
Dr. Mark Halsted, a pediatrician assistant at the University of Washington in St. Louis, has made remarks that ” It’s not just the prolonged sole exposure to screen time that can slow down recovery, but everything that involves high activity such as social events, school, etc.”
With exposure to video games, there is a high requirement for concentration and focus for prolonged time on cognitive expenditure.
Using screen has often shown to decrease in score for cognitive testing
Impairment in social and behavioral skills as seen in autism
Due to compromised white matter integrity, reduced cortical thickness as seen in different brain scans.
As you can’t keep straining an injured arm, a concussed brain should keep out of screens to avoid further injury
therefore, this information should not pass unnoticed because of how much screen time has become an intergrated part of our lifestyle. The same way you coulnd’t keep hitting a bruised arm, is the same way screen time and high demanding activities should be avoided for a concussed individual.
Works Cited
Kohl’s building blocks. (n.d.). Retrieved from Importance of Limiting Screen time: https://penfieldbuildingblocks.org/parenting-tips/importance-limiting-screen-time/
Macnow, T., & Curran, T. (2021). Effect of Screen Time on Recovery From Concussion. A randomized clinical trail. JAMA Pediatrics.
Middlebrook, H. (2016, October 21). New screen time rules for kids, by doctors . Retrieved from CNN: https://www.cnn.com/2016/10/21/health/screen-time-media-rules-children-aap/index.html
It is shown that the majority of activities one should limit are primarily ones that involve cognitive function and stress. This is due to the energy crisis the brain undergoes when experiencing such trauma as a concussion. When the brain experiences trauma, it begins rapid attempts at restoring balance, or homeostasis. While doing this, ATP (energy) becomes depleted in efforts to recover. This energy depletion creates a slew of issues regarding signaling, neurotransmitters, etc. that may be mitigated via cognitive rest (Giza and Hovda, 2014). Although, it is not recommended that one rest during their entire recovery process (as in lying in bed in a dark room for multiple days). There have been cases in which such rest has shown to be detrimental to one’s recovery process. Complete rest, in which one avoids all stimuli, may instigate further rumination on one’s injury, creating depressive or anxious symptoms. Also, studies have shown that those prescribed with 5 days of rest experienced worsened post-concussive symptoms than those only prescribed 2 days of rest. So, although rest is necessary, it is only useful in moderation.
Pharmacological Intervention
Medication currently used to treat concussion are primarily intended to relieve concussive symptoms an individual is experiencing at that time. There are no FDA-approved medications for the treatment of concussion. Although, there are many pharmacological options one may pursue to lessen symptoms. The primary headache relievers include acetaminophen and NSAIDs, and amitriptyline and nortriptyline. The former pain relievers have actually been shown to be overused in those with concussions, and have the possibility of worsening symptoms. The latter medications are tricyclic antidepressants that may be used for migraines. They have been shown to relieve headache symptoms in pediatric concussions. Stimulants, such as amantadine and methylphenidate, may both be used to mitigate cognitive fatigue. Amantadine is a dopamine agonist that may theoretically improve brain functioning, while methylphenidate has been shown to improve cognition and mental fatigue after TBI in adults. In order to improve sleep in those with concussions, melatonin and trazodone are both recommended sleep aids. Trazodone is a serotonin antagonist often used for insomnia. Lastly, hypertonic saline may be used in severe TBI to reduce intracranial pressure. Also intravenous migraine therapy, such as metoclopramide or prochlorperazine, have been shown to significantly reduce pain in 93% of patients (Halstead, 2016).
The primary action one can take to ensure full recovery from a concussion is avoidance of a repeat concussion. This is especially important considering that it has been shown individuals are more susceptible to secondary injury following a primary TBI. This risk for subsequent injury is highest within the first 10 days of the initial trauma. This is likely to biological vulnerability from the ongoing energy crisis in the brain, as discussed previously. Magnetic resonance spectroscopy has displayed that reductions in a specific metabolite, NAA, took 15 days longer to return to normal levels in those with a repeat concussion, versus those with only a primary injury. Studies have also shown that repeat mild TBI may result in white matter damage in the brain, as well as cognitive impairments. If one experiences a second concussion before full recovery from the initial one, it is likely that their symptoms will worsen and last much longer. Although, if one experiences a repeat concussion after full recovery, it has been seen that these act like two, separate injuries (Giza and Hovda, 2014).
References
Giza CC, Hovda DA. The New Neurometabolic Cascade of Concussion. Neurosurgery. 2014; 75. doi:10.1227/neu.0000000000000505
Halstead ME. Pharmacologic Therapies for Pediatric Concussions. Sports Health: A Multidisciplinary Approach. 2016; 8(1):50–52. doi:10.1177/1941738115622158
A concussion is a condition of neurological signs and symptoms that are caused by a biomechanical force to the brain. Symptoms of a concussion include headache, nausea or vomiting, dizziness, poor balance, light/noise sensitivity, fatigue, memory problems, confusion, etc. The cause of a concussion is a bump, blow, or jolt to the head or body that causes the head to move rapidly back and forth, as seen in Figure 1. The sudden movement of the head causes the brain to “bounce” around or twist in the skull causing injuries to the brain. The injuries to neural tissue caused by a concussion are predominantly functional or microstructural. Functional injuries include ionic shifts, metabolic changes, and impaired neurotransmission. Microstructural injuries include axonal stretch, axonal disconnection, inflammation, cell death, and cytoskeletal damage.
Between 1.7 to 3 million sport-related concussions happen each year with around 300,000 of those from American football. About 5 in 10 concussions gounreported or undetected. According to a study published in 2005, there are about 0.41 concussions per NFL game with 67.7% of concussions involving impact by another player’s helmet. 92% of players who sustain a concussion return to practice in less than 7 days. This data is shocking; however, it is from 16 years ago. The technology to prevent concussions in football and the concussion protocol have changed. Nevertheless, the deadly costs of repetitive hits to the brain are being revealed.
Chronic Traumatic Encephalopathy (CTE)
CTE develops gradually from an accumulation of blows to the head or repeated concussions. Symptoms vary between individuals but tend to resemble other degenerative brain conditions like Alzheimer’s disease: memory loss, depression, mood swings, personality change, fatigue, anxiety, frustration, etc. There is no diagnostic test for CTE, thus, a diagnosis cannot be confirmed until the post-mortem brain can be examined. Football players have a high risk of developing CTE as they are subjected to repetitive head injuries.
From a study of 202 brains from deceased players of American football, CTE was diagnosed in 177 players (87%), including 110 of 111 former NFL players (99%). The most common cause of death for participants with mild or severe CTE pathology was suicide, 27% vs. 47%. 86% of former NFL players hadsevere CTE, compared to 56% of former college players and 56% of semiprofessional players. The level of neurofibrillary tangles correlated positively with the severity of CTE. Neurofibrillary tangles (NFTs) are abnormal accumulations of the hyperphosphorylated (too activated) protein
tau. Normally, tau supports the structure of the neuron by stabilizing microtubules which help guide nutrients and molecules down the cell. Within tangles, hyperphosphorylated tau detaches from the microtubules and stick to each other, forming tangles that block the neuron’s transport system from inside the cell. In figure 2 you can see the mass amounts of NFTs in a region of Aaron Hernandez’s brain. Additionally, there were deposits of amyloid- in all stages of CTE. This protein forms plagues that disrupt communication between neurons.
NFTs and amyloid- plaques are key markers of Alzheimer’s disease and associated with symptoms of impulsivity, depression, apathy, anxiety, explosivity, aggression, memory loss, and confusion. Among those that showed CTE pathology, 42.3% presented with cognitive symptoms in life, 43.2% showed behavior/mood symptoms, and 14.4% presented with both cognitive symptoms and behavior/mood symptoms.
Aaron Hernandez
A particular case study of CTE in a football player showed severe CTE pathology and the symptomology described with severe CTE. This case is of Aaron Hernandez.
Aaron Hernandez was a tight end for the New England Patriots until his career ended with his arrest for the murder of Odin Lloyd. Two years after his conviction for first degree murder, Hernandez committed suicide within his prison cell. Pre-mortem, professionals thought he had CTE, but this was confirmed after his death when
researchers were allowed to examine his brain. For a little bit of background Hernandez had been playing football since high school. He had many of the symptomology of CTE: changes in mood, aggression, depression, mood swings, personality changes, and memory loss. His brain: through Figure 3 you can see there is an atrophy of his brain specifically in the fornix and hippocampalregions. They also saw perforations of the septum pellucid and deposits of tau that you can see on this picture. Also, you can see that he had a lot of ventricular enlargements.
The researchers who examined Hernandez’s brain claim that it is the worst case of CTE they have ever seen in someone of his age of 27 years old.
After the death of Hernandez, his family filed a lawsuit against the New England Patriots and the NFL for being fully aware of the damage that could be inflicted from inflicted from repetitive impact injuries and not disclosing, treating, or protecting Hernandez from those dangers. They have since dropped this charge.
CTE makes a murderer?
I’m not sure that a neurodegenerative disease can make a murderer. In my opinion, neuronal dysfunction can be an aggravating trigger for homicidal tendencies. But this does not mean having CTE excuses such heinous acts. Instead, I believe CTE is a serious disease that is experienced by the many who experience repetitive traumatic brain injuries and shows itself as a change in key brain functions. CTE is something that should put fear in athletes, coaches, parents, and society. The development of CTE changes the brain and changes the person. And the truth is staring us in the face, if individuals continue to hit their head whether it be in combat, self-injury, accidents, or football they may see a change in themselves only explainable by CTE.
When addressing the role of the high fat diet and obesity, it is important to evaluate the types of fats in a given diet. While a high fat diet can lead to increase in obesity, a low fat diets as intervention for obesity is not supported. Rather, increasing the intake of unsaturated fatty acids over saturated fatty acids, carbohydrates, and proteins, can be beneficial for the obese population. Therefore, one must evaluate the types of fat intake that one is receiving, and aim to increase and supplement polyunsaturated fatty acids and some monounsaturated fatty acids when reversing obesity and insulin resistance.
So, what are the types of fat? Which types are “good?”
Trans fat is a byproduct of hydrogenation that is used to turn healthy oils into solids to prevent from becoming rancid. It has no known health benefits and is banned in the United States. It is known to increase the amount of LDL cholesterol in the bloodstream, while reducing the good, HDL, cholesterol. It also causes massive inflammation, and contribute to insulin resistance.
Saturated fats are solid at room temperature. They are found in red meats, whole milk, cheese, coconut oil, and baked goods, etc. A diet that is rich in saturated fats can increase total cholesterol.
Monounsaturated and polyunsaturated fats are good fats that come from vegetables, fish, nuts and seeds. In particular, monounsaturated fats have a single carbon to carbon double bond. Foods such as olive oil, avocados, nuts, and foods familiar to the “Mediterranean diet” are high in monounsaturated fats. Polyunsaturated fats are essential fats. They are required for normal body functions and humans need to obtain them from food sources. They have two or more double bonds. They are used for many different processes in the body, mainly for building cell membranes, cover our nerves, and are used in blood clotting, muscle movement, and controlling inflammation. Eating polyunsaturated fats instead of saturated fats or highly refined carbohydrates reduces LDL cholesterol and lowers triglycerides. The two main types of polyunsaturated fats are omega-3 and omega-6 fatty acids.
Omega-3 fatty acids can be found in salmon, flaxseeds, walnuts, and mackerel, shrimp, hemp and chia seeds, among others. Omega-3 fatty acids are known to prevent and treat heart disease and stroke, they reduce blood pressure, raise HDL, lower triglycerides, and restore leptin and insulin sensitivity, especially in the obese population. The figure below shows how omega-3 PUFAs protect cell membranes through exerting anti-inflammatory effects through modulating NF-kB signaling, NLRP3 inflammasome, PPARa/y, GPR120, and TGF-B signaling. Omega-6 food sources include vegetable and corn oils, sunflower seeds, peanut butter, eggs, and almonds, and they have been linked to protect against heart disease.
The ratio of omega-3 to omega-6 fats is important, especially in regards to inflammation and it is recommended that rather than decreasing the amount of omega-6s in your diet, which can be anti-inflammatory, it is better to increase your omega-3 intake.
It’s estimated that 1 in 54 children in the United States will be diagnosed with autism today.[1] Early signs of autism may be detected as early as 18 months, but they typically appear around the age of 2 or 3.1 Autism spectrum disorder (ASD) is a neurodevelopmental disorder that stems from problems with the central nervous system (CNS).[2] We will explore what some of these CNS issues are later in the post.
According to Mayo Clinic, there are several important risk factors that increase the likelihood of developing autism. The most important risk factor is biological sex—boys are 4X more likely to develop ASD compared to girls.[3] Other risk factors include family history, being a preterm baby born before 26 weeks of gestation, being a child of older parents, and having other comorbidities like X syndrome.3 For more in-depth information on risk factors, Mayo Clinic has a great resource here.
Symptoms of Autism
Now that we know ASD is a relatively common disease, as well as some of its risk factors, what are some symptoms to look out for when suspecting someone of having ASD? As previously mentioned, these symptoms can be detected during early infancy and if caught earlier, there is a better prognosis.1 Many of the
symptoms are related to impairments in social communication and interaction. Some examples are failing to respond to their name, resisting holding, lack of facial expression, has delayed speech, doesn’t understand simple questions or directions, and has difficulty reading nonverbal cues.3 Another class of symptoms include behavioral abnormalities, these symptoms are easier to recognize compared to the more nuanced social impairments. Common behavioral patterns found in children with ASD are performing repetitive movements (hand flapping, rocking, spinning), causing self-harm, sensitive to stimuli, and having hyper-specific food preferences.3
It should be noted that autism is expressed differently in girls than boys. Some of the symptoms are different. To help tell the difference, a handy “signs of autism” sheet can be seen just below this text.
Signs of autism in boys and girls. Reproduced from Avozapp.com
mTORC1 Overview and Relationship to ASD
To understand one of the fundamental causes of ASD, we first must understand a key complex in the underlying neurochemistry. Mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) plays a critical role in ASDs pathogenesis via modulating the rate of autophagy.2 Autophagy can by thought of as the breakdown of useless cellular molecules to be repurposed into something useful. In ASD, mTORC1 is hyperactive and causes a decrease in autophagy.2 As you can see in the figure below, when mTORC1 is activated, it inhibits ULK1.
Artstract created by B.Badenoch through addition of activators and inhibitors based on original pathway. Modified from MDPI.com
When ULK1 is activated, it promotes autophagy and keeps the cell free of excess debris.2 This process is not functioning well in those with ASD. Because of this, the cells swell leading to the increased brain and head size associated with ASD.2 This ultimately leads to neuronal dysfunction and can possibly explain why lower IQ is associated with many on the ASD spectrum.2
What useful information can we glean from this pathway? Understanding this pathway gives researchers yet another tool to try and reduce the symptoms associated with ASD while a cure. Particularly, I find it interesting that insulin is an activator of mTORC1, and that maybe by reducing insulin levels mTORC1 could be more inhibited. What ideas do you have for reducing mTORC1 signaling?
Concluding Remarks
Autism spectrum disorder affects many people in the modern United States. Luckily, there are good resources, like Mayo Clinic, who have listed different symptoms of ASD to be aware of. This information is especially salient to parents of young children because the sooner ASD is caught, the better the outcome for the child can be.3 One of the most visible symptoms of ASD is the enlarged head/brain size. By understanding that mTORC1 hyperactivation leads to decreased autophagy, we can begin to understand why this symptom occurs. Furthermore, by understanding the activators of mTORC1, we can hypothesize ways of reducing mTORC1 activation and find ways to reduce the negative symptoms of ASD.
[1] “What Is Autism?” What Is Autism?, Autism Speaks, 2021, https://www.autismspeaks.org/what-autism#:~:text=Autism%2C%20or%20autism%20spectrum%20disorder,in%20the%20United%20States%20today.
[2] Sharma, A., & Mehan, S. (2021). Targeting pi3k-akt/mtor signaling in the prevention of autism. Neurochemistry International, 147, 105067–105067. https://doi.org/10.1016/j.neuint.2021.105067
[3] “Autism Spectrum Disorder.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 6 Jan. 2018, https://www.mayoclinic.org/diseases-conditions/autism-spectrum-disorder/symptoms-causes/syc-20352928.
10-20% of the population develops a stress disorder after exposed to traumatic, life-threatening events.[1] PTSD is a big problem in America, and it affects roughly 3.5% of U.S. adults yearly. It’s estimated that one in eleven people will be diagnosed with PTSD at some point in their life.[2] Many people know someone who is affected by PTSD. Luckily, Dr. Reul wrote a wonderful review paper on the subject. I will try and distill some of the most salient parts of his research and explain the cellular mechanism of PTSD and the role exercise has in PTSD treatment.
Cellular Cause of PTSD
The following description of the neurochemistry of PTSD can be confusing, so be sure to follow along with figure 1 below.
Bretton’s Artstract of how stress activates c-Fos amd Egr-1.
PTSD begins when a psychological stress is noticed. This causes markers of stress in the brain (like corticosterone and glutamate) to increase in concentration. These two signaling molecules act on different parts of a cell due to the nature of their atomic makeup. Because corticosterone is non-polar, it is able to go through the cell membrane and bind to a glucocorticoid receptor (GR). Conversely, glutamate is polar and can’t cross through the cell membrane.
Figure 1. PTSD Pathway
Luckily for glutamate, it’s receptor (NMDAR) is located on the outside of the membrane so it can bind without any issue. Once glutamate binds to NMDAR, NMDAR goes through a change in shape that allows for Calcium ions to travel into the cell. This causes a signaling cascade resulting in the activation of an enzyme called ERK. ERK is then able to bind to the activated GR. This ERK-GR complex then moves into the nucleus (where DNA is stored) and activates two final enzymes MSK1 and Elk-1. These final enzymes cause gene transcription that results in consolidation of memories associated with the stressful trigger.
Application of the cellular mechanism to the real world
Whew! Now that we have the basics understood, we can begin to understand why PTSD occurs. The current hypothesis is that the previously described pathway is sent into overdrive by the stressful event. In short, there is too much activation of GR and NMDAR leading to consolidated memories that are too salient. This explains why something as innocuous as an alarm clock can trigger someone’s symptoms of PTSD.
For example, pretend someone has witnessed a horrible, loud car crash. This causes immense psychological stress, and their brain is bathed in a neurochemical slurry of corticosterone and glutamate. This is going to lead to extreme memory consolidation of the car crash. One of the theories on how memories are stored is called the hierarchical model. You can learn more about it here. Basically, the theory posits that thinking of one attribute of something will prime the memory of it (e.g., thinking of wings, flight, and feathers makes one think of a bird).[3] Say one of the things you associate with the car crash is loud noise. Now when you are primed to think of a loud noise by your alarm clock, this triggers the memory of the car crash causing you to re-live that painful moment.[4]
That makes sense! How about treatment? Is there anything we can do to prevent or treat PTSD?
There are a few things one can do to prevent PTSD. The review paper found that rats who voluntarily exercised had increased neurogenesis and had part of the intracellular cascade of PTSD inhibited.1 Several other studies found that increased cytokines (a marker of stress) in the blood of soldiers before they went off to war led to an increased risk of their developing PTSD.[5] This suggests that finding ways to destress and lower cytokines in the body may be neuroprotective for PTSD.
Closing Remarks
PTSD is a widespread issue, but it’s not an insurmountable problem to overcome. As more people learn the underlying cellular mechanism, the more innovative treatments and preventative measures will be discovered. Until then, exercise and reducing stress in our lives seems to be the best way to prevent PTSD.
Sources
[1] Johannes, M. H. M. eR. (2014). Making memories of stressful events: a journey along epigenetic, gene transcription and signaling pathways. Frontiers in Psychiatry, 5. https://doi.org/10.3389/fpsyt.2014.00005
[2] “What Is Posttraumatic Stress Disorder?” What Is PTSD?, American Psychiatrics Association, 2020, https://www.psychiatry.org/patients-families/ptsd/what-is-ptsd#:~:text=PTSD%20affects%20approximately%203.5%20percent,as%20men%20to%20have%20PTSD.
[3] “Top 3 Models of Semantic Memory: Models: Memory: Psychology.” Psychology Discussion – Discuss Anything About Psychology, 11 Mar. 2017, https://www.psychologydiscussion.net/memory/models/top-3-models-of-semantic-memory-models-memory-psychology/3095#:~:text=Hierarchical%20Network%20Model%20of%20Semantic%20Memory%3A&text=are%20organised%20into%20a%20hierarchy,logically%20related%20and%20hierarchically%20organised.
Addiction has been a pervasive problem that has plagued human history since we began recording it. Addiction is an issue we are still grappling with, even in developed nations. In the United States, nearly 21 million people have one or more addictions but only 10% of them receive treatment. [1] This costs the US economy north of $600 billion annually and has resulted in 700,000 deaths from overdose between 1999 and 2017.1 These are abysmal numbers. I will try to shed some light on what some of the causes of addiction are, as well as a brief overview of the neurochemistry of addiction.
Neurochemistry of Addiction
Before we try tackling the chemistry, lets introduce the key brain structure in addiction. Arguably, the most important part of the brain in addiction is the nucleus accumbens (NAc). This is the area of the brain that all drugs of abuse act on in some way.[2] All addictive drugs cause an burst of dopamine (DA) release in the NAc. 4 While this is the structure that will be referenced in this article, it should be known that many more areas of the brain play a role in addiction. A comprehensive review can be found here.[3]
Dopaminergic-system-and-reward-processing-in-brain reproduced from PsyPost.
Now to introduce one of the chemical messengers in addiction: FosB. FosB has been found to be expressed after exposure to nearly all drugs of abuse. 4 After repeated drug exposure, the levels of FosB only increase in the brain. As the levels continue to climb, a person’s sensitivity to natural rewards and drugs increases (as does the likely hood of voluntarily consuming more drugs). 4 FosB causes epigenetic changes in the brain, which increase the likelihood that someone will do drugs. This is one of the causes for the vicious cycle of drug abuse.
Causes of Addiction—Epigenetics
I will not try and explain every cause of addiction in this post for two reasons:
It will be a very long list
We don’t know what all of the causes are
However, I will provide a brief overview so we can better understand the causes of addiction, both social and molecular. A recent literature review finds 50% of variance in addiction is dues to genetic variation, while the other 50% is due to environmental variance[4] First, lets explore the genetic variation, but to do this we have to understand some basic epigenetics.
One of the most fundamental aspects of epigenetics, is the ability of a histone protein to become acetylated (i.e. stick a acetyl group onto a histone). Normally, the histone protein tightly binds DNA and prevents it’s transcription into mRNA. However, when the histone protein is acetylated, it loosens up and allows the DNA to be transcribed (see the following image for a visual).[5]
Epigenetic Modifications. Reproduced from Wikimedia Commons
In addiction, histone acetylation occurs after acute exposure to stimulants like cocaine or amphetamine (meth). [6] Interestingly, these acetylations occur near promoters of c-fos and fosB in the nucleus accumbens (NAc). Earlier in this article, we mentioned how fosB is one of the molecular causes of promoting addiction. Now we know where it is coming from and why.
Conclusion
Drug addiction is still a problem in modern society. We have seen that epigenetic changes occur in the brain after exposure to drugs of abuse. This causes mental and physical changes to the person that increases their likelihood of continuing to consume drugs. Hopefully through studying the science behind what causes addiction, we can develop new treatments and improve on prevention strategies.
[2] Scofield, M. D., Heinsbroek, J. A., Gipson, C. D., Kupchik, Y. M., Spencer, S., Smith, A. C., Roberts-Wolfe, D., & Kalivas, P. W. (2016). The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis. Pharmacological reviews, 68(3), 816–871. https://doi.org/10.1124/pr.116.012484
[4] Reul, J. M. (2014). Making memories of stressful events: A journey along epigenetic, gene transcription, and signaling pathways. Frontiers in Psychiatry, 5. https://doi.org/10.3389/fpsyt.2014.00005
[6] Renthal, W., & Nestler, E. J. (2009). Histone acetylation in drug addiction. Seminars in cell & developmental biology, 20(4), 387–394. https://doi.org/10.1016/j.semcdb.2009.01.005
Concussions are a risk that most contact sports pose to athletes; however, concussions can occur from being in combat and unusual accidents. A concussion can be classified as a traumatic brain injury due to physical impact or force on the skull causing damage to the brain. The total impact/force to the brain can stimulate neuronal dysfunction. Some of the symptoms associated with concussion include: migraines, headaches, impaired cognition, and delayed reaction time.
What happens during a concussion?
The total impact/force to the brain can stimulate neuronal dysfunction. Neuronal dysfunction includes increasing the concentration of sodium and calcium entering the cell, as well as increasing the concentration of potassium exiting the cell causing changes in neuronal signaling cascades and neurotransmission. In essence, the cell cannot maintain a typical state of functioning.
In order to compensate for the ionic imbalance, some additional calcium can be stored in the mitochondria. However, this increases metabolism so much that the production of free-radicals can cause even more damage to the neuron over time. The increased calcium concentration in the neuron can also stimulate neurofilament collapse. Neurofilaments are essential to transmit electrochemical impulses down the axon of a neuron and damage results in the diminished ability to transmit messages. Some examples of this include delayed reaction time and memory impairments, which are essential in sports.
Testing:
Many schools require athletes to conduct an ImPACT test online before sports are played to access normal brain function to create a baseline. Having the baseline is important to determine the extent of the damage, such as decreased visual memory and reaction time after a concussion. The online program can also indicate if someone is trying to hide their symptoms in order to return to sports, being handy for a medical professional to access return protocols. However, even if this tool is used to determine if a concussed athlete is ready to play again is debatable. Some studies demonstrate that BOLD (blood oxygen level dependent) increase after a concussion, improving overall cognition, to skew ImPACT testing results to put an athlete who still needs to rest at risk for a re-injury, resulting in even greater symptoms.
Concussions and sports:
The two sports with the highest practice-related concussion rates are football with 5.0 per 10,000 athletic exposures and cheerleading with 3.6 per 10,000 athletic exposures. Football helmets have gotten significantly better to reduce the amount of impact received by players, meanwhile cheerleading does not provide much in terms of safety equipment to protect the heads of athletes. Approximately 70% of concussions in cheerleading come from stunting, many occur from simple mistakes. Not all sports can completely avoid the risk of concussions, but safety and prevention techniques can always and should be improved.
Treatments for concussions:
Treatments for concussions are typically based on supportive services, such reducing screen time and working with a physical and occupational therapists. New research has indicated that the supplementation of DHA, which is an omega-3 fatty acid, which could decrease the recovery time associated with concussions. DHA has neuroprotective effects to help decrease oxidative stress, decrease inflammation, decrease calcium influx within the cell, and improve the integrity of ion pumps and channels as seen in Figure 1. However, the amount of DHA that needs to be supplemented to people with concussions is debatable, which could be due to prolonged poor nutrition, especially in athletes, or actually needing more DHA in the body after an injury. Therefore, having an adequate amount of DHA mitigate neuronal dysfunction as seen in typical concussions.
Despite so many individuals suffering from concussions every year, treatment options remain limited and very little can be done besides treat the symptoms of concussions.
Concussions extend beyond a simple hit to the head. Concussions can decrease cognitive function and reaction time, as well as needing to reduce normal activities (using any screens) and increasing the likelihood of developing neurodegenerative diseases later in life. Concussions can cause major distress in athletes who are students, which can impact their education by not being able to catch up on homework in an online capacity. Currently, treatment options are extremely limited and need more work to get people back to their normal functioning after experiencing a concussion.
The NFL is among the most watched sports league in the United States, it is also among the leading sports in diagnosed concussions. In 2019, the NFL had 224 diagnosed concussions over their 17-week season (Battista et al 2020). The NFL has been working to implement changes in the game and equipment to help decrease the number of head injuries each year.
Improvements in evaluation
The improvements in the protocol made since 2018 include, defining impact seizure and fencing responses as independent signs of potential loss of consciousness, representing “No-Go” criteria, requiring an evaluation for all players demonstrating gross motor instability to determine the cause of the instability, and requiring all players who undergo any concussion evaluation on game day to have a follow-up evaluation conducted the following day by a member of the medical staff (NFL players health and safety et al., 2021).
Rule changes
Rules implemented on kickoffs
Since 2019, the NFL has implemented 3 new rules to help reduce the number of concussions. The blindside block is eliminated, expanding protection of defenseless players. It is now prohibited for a blocker to initiate forcible contact with his head, shoulder or forearm when his path is toward or parallel to his own end line. This is more of a technique change since concussions tend to be a bigger issue in the inexperienced NFL players. Another rule change was it is now a foul for running forward and leaping across the line of scrimmage in an obvious attempt to block a field goal. This just means you cannot get a running start in order to block a kick which results in less impact. Their last change wasn’t as much of a change, but they decided to keep the kickoff changes made in 2018 as there was a 35% decrease in concussions on kickoffs as a result (NFL Football Operations et al., 2021).
Equipment changes
The NFL uses Radio Frequency Identification (RFID) tags inside of the equipment which detects impact. These RFID tags help the league to collect more information than ever before about the duration and direction of head impacts players experience based on their positions, both during practices and games. The NFL then breaks down the concussion causing impacts and collects information on the players position, acceleration, and forces. This data has helped the NFL develop position specific helmets to help reduce the number of concussions suffered (NFL et al., 2021).
Conclusion
The NFL is continuing to collect impact data, implement new rules, and creating new equipment standards to help reduce the number of concussions each season. The goal of the NFL is to ultimately eliminate concussions from football; there is still a long way to go.
Health & Safety Rules Changes. NFL Football Operations. (2021, August). Retrieved from https://operations.nfl.com/the-rules/rules-changes/health-safety-rules-changes/.
Nfl. (2021, October 14). Built by data: NFL Helmet Innovation. NFL.com. Retrieved from https://www.nfl.com/playerhealthandsafety/equipment-and-innovation/engineering-technology/built-by-data-nfl-helmet-innovation.
Migraines are likely to occur following a concussion for a number of reasons. Whether the concussion was due to an impact or non-impact injury, there has been damage to the brain. Following a traumatic brain injury, the brain is hypersensitive due to the ionic flux and glutamate release. Immediately after an injury to the brain, there is a large release of neurotransmitters and ions. Glutamate binds to NMDA receptors and an increased amount of it will lead to more depolarization in the neurons. Potassium efflux and calcium influx occur which shifts membrane potential. These changes in physiology cause issues for various other cell functions. Figure 1 describes the different types of headaches that can occur following a concussion. The type of headache someone is experiencing can help physicians determine what areas of the brain have been damaged.
Figure 1: A few of the different types of headaches someone could experience following a concussion.
Vulnerability to Further Injury
The sodium-potassium pump must now work harder in order to restore membrane potentials. The Na+/K+ requires ATP, so the body will divert more energy to the damaged brain areas. An increased amount of ATP triggers an increase in glucose metabolism. This increased glucose metabolism will not last for long; there is often a state of impaired metabolism following hyperglycolysis.
Cerebral blood flow is often reduced following a concussion. The increased demand for ATP along with the decreased blood flow causes further issues in the brain. Energy reserves in the brain are depleted because of the overall lack of energy, oxygen, and mitochondrial function. Metabolic pathways are altered after a concussion and take time to recover. It is unknown how much time is needed for the brain to fully recover following a TBI, but there is a period of vulnerability after it occurs. The altered state of the brain takes time to recover. It is possible for another injury to happen after a concussion and has the potential to cause even worse damage. Figure 2 shows some common areas that are affected after a TBI and what their primary functions are.
Figure 2: Areas of the brain often damaged during a TBI and what processes they are responsible for.
Slowed/Altered Cognition
Damage to the brain following a concussion can lead to a wide variety of symptoms. During a TBI, there is damage to axons. This can occur on a microscale and cause disruption of action potential transport, disconnection, and microhemorrhages. MRI has been used to measure how white matter changes following a concussion. Researchers are able to gain insight into how much axonal damage has occurred by observing white matter. Studies have shown that decreased or damaged white matter after a TBI can lead to a myriad of symptoms such as depression, PTSD, impaired memory, and behavioral changes.
The parts of the brain responsible for judgment, problem-solving, and arousal are often damaged during a concussion. These physiological changes help explain why many people experience cognitive alterations. People can have increased fear responses and higher levels of depression following a TBI. This video provides a good explanation of common emotional symptoms after a concussion and how to help someone experiencing these changes.
(Kohl’s building blocks)
should include the avoidance of:
