Underneath the Helmet: What Happens to the Brain After a Concussion and Why Athletes Should Care

Posted on February 12, 2025 by Meg / 0 Comment

Concussions are a common type of traumatic brain injury that results from physical trauma to the brain, usually a hit, blow, or sharp jolt (Mayo Clinic Staff, 2022). But concussions are more than just a bump on the head, they trigger a cascade of complex biological processes that can have both immediate and long-term effects on the brain. The article “The New Neurometabolic Cascade of Concussion” (Giza & Hovda, 2014) highlights the pathophysiology of concussions, connecting how various physiological defects disrupt brain function and manifest themselves as symptoms.

In the United States alone, over 3.8 million sport-related concussions occur per year (University of Michigan Health, 2019), and its prevalence coupled with the potential for long-term effects, makes it a necessary area for research. For athletes, parents, and coaches, understanding this science is crucial to understanding the importance of proper recovery. The more we understand about concussions, the better we can prevent, recognize, and treat them.

The Neurometabolic Cascade: A Blitz in the Brain

When a concussion occurs, the brain undergoes a series of physiological changes known as the neurometabolic cascade. This process involves disruptions in ion balance, energy and metabolism, and cellular structure, which can lead to both short-term and chronic symptoms.

Ionic Flux

The initial trauma causes stretching and distortion of neurons, leading to tears in cell membranes. This allows potassium ions to flood out of cells and calcium ions to rush in, creating an ionic imbalance. This sudden depolarization triggers a wave of spreading depression. This is thought to be the biological basis for migraines as well, which likely explains symptoms of headaches, dizziness, and nausea.

Why does it matter for athletes?
Spreading depression can cause migraine-like symptoms like headaches, light sensitivity, sound sensitivity, and nausea. These symptoms are not just uncomfortable, but they’re also a sign that the brain is struggling to restore homeostasis.

Energy Crisis and Metabolic Dysfunction

To restore ion balance, the brain’s cells activate energy-dependent pumps, which require large amounts of ATP. This leads to hyperglycolysis, where the brain uses more glucose, which further depletes the brain’s energy reserves. At the same time, blood flow to the brain may decrease, creating a mismatch between energy supply and demand. This metabolic crisis can last for days or even weeks, leaving the brain vulnerable to further injury.

Why does it matter for athletes?
During this period of metabolic dysfunction, the brain is less able to handle additional stress. A second concussion during this time can increase damage and prolong recovery. This is why rest and taking time away from practice and games is so important!

Mitochondrial Dysfunction and Oxidative Stress

The influx of calcium into cells is particularly harmful to mitochondria. Excess calcium disrupts mitochondrial function, impairing ATP generation. This exacerbates the energy crisis and causes oxidative stress, which can persist long after the concussion.

Structural Damage: Axons and Cytoskeleton on Injured Reserve

Besides metabolic changes, concussions can cause physical damage to the brain.

Axonal Injury

The mechanical forces of a concussion can stretch and damage axons’ neurofilaments and microtubules, which is known as traumatic axonal injury (TAI). This damages the white matter in the brain, leading to symptoms like slowed processing speed, memory problems, and impaired reaction time.

Cytoskeletal Collapse

The cytoskeleton also may suffer injury. Calcium influx phosphorylates the cytoskeleton’s neurofilament side-arms leading to structural collapse. Injury to both axons and the cytoskeleton may alter neurotransmission, the way cells communicate with each other.

Why does it matter for athletes?
Even mild axon and cytoskeleton damage can impair cognitive and motor function, making it harder for athletes to perform at their best. Repeated concussions can compound the damage, increasing the risk of prolonged recovery or long-term deficits.

Inflammation and Chronic Risks

While inflammation is a natural response to injury, chronic inflammation can harm the brain. After a concussion, microglia become activated, causing inflammation that can damage neurons and disrupt brain function.

Why does it matter for athletes?
Chronic inflammation may contribute to persistent concussion symptoms and increase the risk of long-term neurodegeneration. Researchers are working to better understand this link to develop treatments to protect athletes’ brains.

From Sprint to Marathon: Acute Injury to Chronic Disease

The acute changes triggered by a concussion, such as ionic flux, energy crisis, and axonal injury can cause long-term problems.

Altered Protein Degradation and Aggregation
Concussions can disrupt the brain’s ability to clear damaged proteins, leading to the accumulation of toxic molecules like tau proteins. Oxidative stress can lead to dysfunction of the ubiquitin-proteasome system, which is necessary for normal protein degradation. These protein aggregates are a hallmark of chronic traumatic encephalopathy (CTE) and other neurodegenerative diseases.

Chronic Axonal Degeneration
Even after the initial injury, axons may continue to degenerate, leading to progressive brain atrophy and cognitive decline.

Cumulative Effects of Repeat Injuries
Repeated concussions, especially without adequate recovery time, can amplify all of the previously mentioned pathologies, increasing the risk of chronic impairment.

The science of concussions reveals just how vulnerable the brain is to injury, and even more so to repeat injuries. Starting with the initial ionic flux and continuing through the neurometabolic cascade, every concussion leaves a mark. For athletes, this highlights the importance of stopping play if a concussion is suspected, taking enough time to rest and recover, and working to prevent future injuries. By understanding the complex pathophysiology of concussions, we can better protect and treat athletes, keeping sports safe and fun.

References

Giza, C. C., & Hovda, D. A. (2014). The New Neurometabolic Cascade of Concussion. Neurosurgery, 75(Supplement 4), S24–S33. https://doi.org/10.1227/neu.0000000000000505

Mayo Clinic Staff. (2022, February 17). Concussion – Symptoms and Causes. Mayo Clinic; Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/concussion/symptoms-causes/syc-20355594

University of Michigan Health. (2019). Concussion in Athletes | Michigan Medicine. Uofmhealth.org. https://www.uofmhealth.org/conditions-treatments/brain-neurological-conditions/concussion-athletes-neurosport

Community/Disease/Health

Insulin signaling and Alzheimer’s disease

Posted on February 12, 2025 by rhurley1 / 0 Comment

The article we have covered this week, “Insulin signaling pathway and related molecules: Role in neurodegeneration and Alzheimer’s disease,” was an article about the correlation between the reception of insulin and Alzheimer’s. Basically, it works as following; insulin has to bind to a receptor along a phospholipid bilayer, and various chemicals (such as Grb2, MAP, and Kinases) must take their respective places to fulfill their roles, and then regular expression and regulation takes place. However, must that process fail, various things can go wrong to cause Alzheimer’s disease such as insulin resistance.The topic today is why people should care about this topic and what the people must know, so without further ado let’s get reading!

The article informs us that some of the distinguishable characteristics of Alzheimer’s disease are connected to both poor and abnormal insulin signaling. Though, the article specifically mentions neurofibrillary tangles and amyloid-beta plaques. As a result of this connection, we can now classify Alzheimer’s as the third type of diabetes by definition of diabetes.

Figure one from the article mentioned above^1 is specifically excellent at explaining insulin reception where it was needed (excellently timed, or in other words placed). This simultaneously is even a chart which shows what can go wrong, and spawn Alzheimer’s disease in the brain as a result. Although, it could feel scrambled if you’re not too familiar with the many acronyms in the Neuroscience field. This was an excellent piece to me for it is maximized simplicity, for clear reasons that kind of thing strongly helps. The figure may also benefit people uninvolved in Neuroscience as well because figure one works like a flowchart, and I find that effective myself in general because it’s easy on the eyes to track or logicate.

Now, at this point, one, such as yourself, may wonder why people really should care about all the above information. Well, let’s answer with essential basics to answer ourselves by quickly asking ourselves something simpler first; what really is a concussion? Well, concussion is not very nice at all and looks even worse when examined scientifically. According to Mayo Clinic, a concussion is defined as a, “mild traumatic brain injury that affects brain function….”^2 Considering that we know the brain to be the most vital organ of all in the body, it’s no shock that such a scenario is serious and even severe. This reminds me of something.

This human body response to direct brain trauma, a concussion, reminds me of my own concept of “alternative neurology.” Alternative neurology is a concept I have conceptualized in class just a couple weeks ago. Alternative neurology is the term, or in other words an unofficial term, for the brain’s ability to adapt to form after damages forces cell death and other happenstances. My term may sound much like neuroplasticity, a word used to reference the brain’s ability to adapt to stimulus in general, but rather alternative neurology adaptation refers to so-called “bad stimulus” solely whereas neuroplasticity instead includes any stimulus at all which is more general.

1. “Insulin signaling pathway and related molecules: Role in neurodegeneration and Alzheimer’s disease”

2. https://www.mayoclinic.org/diseases-conditions/concussion/symptoms-causes/syc-20355594

Uncategorized

The Ubiquitin-Proteasome System: A Key Player In Brain Health and Disease

Posted on February 12, 2025 by ealslebe / 0 Comment

About Mild TBI and Concussion | Traumatic Brain Injury & Concussion | CDC

Figure 1 [1]

Your brain is like a smartphone, dropping it, similar to a traumatic brain injury (TBI). It may look fine on the outside, but on the inside, the technology is malfunctioning and the systems are no longer syncing properly. After a concussion, the brain experiences an “energy crisis,” trying to fix itself while running low on battery. Key signals get scrambled, causing people to feel dizzy, slow, or sensitive to light and sound. Worse, if another concussion happens too soon after the first it causes the brain to become more vulnerable to long term injury. [2]

The human body has intricate mechanisms to maintain balance and keep cells functioning properly. One of these is the Ubiquitin-Proteasome System (UPS) – a crucial process responsible for breaking down damaged or misfiled proteins. When this system is disrupted, harmful proteins accumulate, leading to various neurodegenerative conditions.[3]

The Role of UPS in the Brain

The UPS is essentially the body’s “garbage disposal” for proteins. It ensures that faulty proteins are identified, tagged with ubiquitin molecules, and sent to the proteasome for degradation. This process helps maintain normal cell function and prevents toxic buildup. However, when UPS function is impaired – especially following a TBI – serious consequences can arise.[3]

Ubiquitin signalling in neurodegeneration: mechanisms and therapeutic opportunities | Cell Death & Differentiation

Figure 2 [4]

How UPS Dysfunction Contributes to Neurodegeneration

1. TBI and UPS Breakdown

TBI can significantly impair the proteasome’s efficiency, leading to the accumulation of damaged proteins. This can contribute to long-term neurodegenerative processes through several mechanisms:

Proteasome Impairment – TBI reduces proteasome activity, allowing harmful protein aggregates to build up. These aggregates are a hallmark of diseases like Alzheimer’s and Parkinson’s.
Oxidative Stress – The brain undergoes oxidative stress after a TBI, which damages the proteasome and diminishes its ability to clear out toxic proteins.
Neuroinflammation – Excess glutamate release after a TBI leads to increased calcium levels in neurons, disrupting the function of enzymes essential for UPS operation.

2. UPS Dysfunction and Neurodegenerative Diseases

When the UPS function is compromised, the brain struggles to clear out harmful proteins like tau, amyloid-beta, and alpha-synuclein – which are associated with Alzheimer’s, Parkinson’s, and other neurodegenerative diseases.

Chronic Traumatic Encephalopathy (CTE) – This condition, often found in athletes and military personnel exposed to repeated TBIs, is linked to an accumulation of abnormal tau proteins, partly due to UPS failure.
Mitochondrial Damage – The UPS plays a role in maintaining healthy mitochondria. When it fails, defective mitophagy (the removal of damaged mitochondria) can increase the risk of neuronal cell death.
Synaptic Dysfunction – The UPS regulates synaptic plasticity by degrading unnecessary synaptic proteins. When disrupted, memory deficits and cognitive decline – characteristic of Alzheimer’s – can occur.

Chronic traumatic encephalopathy - Wikipedia

Figure 3[5]

Potential Therapeutic Strategies

Given the critical role of the UPS in preventing neurodegeneration, researchers are exploring ways to enhance its function. Some promising approaches include:

Proteasome Activators – These drugs aim to boost UPS activity, helping clear toxic proteins before they accumulate. Specifically, Benzamil.
Ubiquitin Ligase Modulation – Targeting E3 ligases, enzymes that tag proteins for degradation, may help enhance the clearance of harmful proteins and offer neuroprotection.
Antioxidant Therapy – Since oxidative stress can damage the UPS, using antioxidants to restore cellular redox balance may prevent neurodegeneration after TBI.

The Ubiquitin-Proteasome System is vital for brain health, but when disrupted – especially following a TBI – it can set the stage for serious neurodegenerative diseases like Alzheimer’s and Parkinson’s, scientists can develop targeted therapies to restore its function and protect the brain. Research into proteasome activators, ubiquitin ligase modulation, and antioxidant strategies offer hope for preventing and treating neurodegenerative diseases in the future.

References

[1]Centers for Disease Control and Prevention. (n.d.). About mild TBI and concussion. Centers for Disease Control and Prevention. https://www.cdc.gov/traumatic-brain-injury/about/index.html

[2]Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct;75 Suppl 4(0 4):S24-33. doi: 10.1227/NEU.0000000000000505. PMID: 25232881; PMCID: PMC4479139.

[3]Rao, G., Croft, B., Teng, C., & Awasthi, V. (2015). Ubiquitin-Proteasome System in neurodegenerative disorders. Journal of Drug Metabolism & Toxicology, 06(04):187. doi: 10.4172/2157-7609.1000187. PMID: 30761219; PMCID: PMC6370320.

[4]Schmidt, M. F., Gan, Z. Y., Komander, D., & Dewson, G. (2021, January 7). Ubiquitin signalling in neurodegeneration: Mechanisms and therapeutic opportunities. Nature News. https://www.nature.com/articles/s41418-020-00706-7

[5]Wikimedia Foundation. (2025, February 9). Chronic traumatic encephalopathy. Wikipedia. https://en.wikipedia.org/wiki/Chronic_traumatic_encephalopathy

Uncategorized

CTE: The Hidden Dangers of Repeated Head Trauma

Posted on February 12, 2025 by rlannin1 / 0 Comment

Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease caused by repeated head trauma [1]. This leads to the buildup of tau proteins in the brain. This condition can result in symptoms like memory loss, mood changes, and cognitive decline, often appearing years after the injuries occur. CTE is a common neurodegenerative disease, however, there are a lot of people who don’t even realize they have it. It is common with high impact sports, which many people partake in. CTE leads to cell death and other failures of basic human functions, as pictured in Picture 1.

Chronic traumatic encephalopathy - Wikipedia Picture 1 [2]

In “The New Neurometabolic Cascade of Concussion,” [3] by Giza and Hovda describes the updated understanding of the brain’s metabolic and functional response following a concussion. Traditional views of concussion mainly focused on mechanical damage, but more recent research brings forth the disruption of cellular and biochemical processes, like CTE.

The topic of Chronic Traumatic Encephalopathy has a lot of ongoing research for several reasons including a lack of a definitive diagnosis in living people. CTE can only be fully diagnosed through post-mortem brain tissue analysis. This limits our ability to study the it in living individuals and makes progress hard to understand in its early stages.

In addition, there is a long latency period. CTE often develops years or even decades after repeated head trauma. This makes it difficult to predict who might develop it and when. Researchers are still trying to identify early biomarkers that could predict its onset. There is also a lot of complexity in CTE. The exact mechanisms behind it are unclear. The accumulation of tau protein in the brain is a bit part of CTE, but the precise cause of CTE buildup, the role of repeated concussions, and genetic and environmental factors are still being studied.

Understanding CTE pathophysiology is a problem. Research has advanced our understanding of CTE, particularly the accumulation of tau proteins in the brain. Also linking CTE to repeated trauma and looking at the connection between repeated concussions and head impacts with the development of CTE, especially in contact sports is important [4]. See Table 1 for more information on 631 former football players and the supposed stages or lack there of of CTE they have. This has helped to shift focus on prevention and better concussion management. We should encourage sports to implement safer protocols to reduce the risk of long-term brain damage. Early detection and biomarkers are also a challenge. Although diagnosing CTE in living individuals is still not great, ongoing research is working to identify biomarkers or neuroimaging techniques that could detect early signs of CTE. Also, by identifying the diverse range of symptoms such as mood disorders, aggression, and cognitive decline associated with CTE, researchers are helping to distinguish it from other mental health or neurodegenerative conditions. This could lead to better strategies for affected people and improve the understanding of brain injury’s psychological and emotional impact.

What's Going On in This Graph? | Football and C.T.E. - The New York Times

Table 1 [5]

One of the interesting topics for future research is the development of biomarkers for early detection of CTE. If researchers can find reliable blood tests or imaging markers that mark the existence of tau protein or other things associated with CTE, it would be a major breakthrough. This could help identify individuals at risk and allow for earlier intervention.

The issue of CTE mostly affects athlete safety, especially in contact sports. It raises concerns for parents, coaches, and sports organizations about the long-term risks of head injuries. As awareness grows, there’s a push for stricter safety protocols, better concussion management, and safer sports practices. The topic also prompts cultural shifts in how we view and value contact sports.

What do you think? Should young athletes be allowed to play high-contact sports, given the risks of long-term brain damage? How can sports organizations better balance competitive play with player safety? What role does technology play in preventing and detecting concussions in real-time?

CTE is a serious, long-term consequence of repeated head injuries, and understanding its risks is crucial for protecting athletes or successive head injury at all levels. What changes can we make to protect future generations of athletes from the dangers of head trauma? How can we push for better detection and prevention?

References

[1] Cho, H., Hyeon, S. J., Shin, J.-Y., Alvarez, V. E., Stein, T. D., Lee, J., Kowall, N. W., McKee, A. C., Ryu, H., & Seo, J.-S. (2020). Alterations of transcriptome signatures in head trauma-related neurodegenerative disorders. Scientific Reports, 10(1). https://doi.org/10.1038/s41598-020-65916-y

[2] “Chronic Traumatic Encephalopathy.” Wikipedia, Wikimedia Foundation, 9 Feb. 2025, en.wikipedia.org/wiki/Chronic_traumatic_encephalopathy.

[3] Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct;75 Suppl 4(0 4):S24-33. doi: 10.1227/NEU.0000000000000505. PMID: 25232881; PMCID: PMC4479139.

[4] Su, Y., Protas, H., Luo, J., Chen, K., Alosco, M. L., Adler, C. H., Balcer, L. J., Bernick, C., Au, R., Banks, S. J., Barr, W. B., Coleman, M. J., Dodick, D. W., Katz, D. I., Marek, K. L., McClean, M. D., McKee, A. C., Mez, J., Daneshvar, D. H., et al. (2023). Flortaucipir tau PET findings from former professional and college American football players in the DIAGNOSE CTE research project. Alzheimer’s & Dementia, 20(3), 1827–1838. https://doi.org/10.1002/alz.13602

[5] The Learning Network. “What’s Going on in This Graph? | Football and C.T.E.” The New York Times, The New York Times, 21 Sept. 2023, www.nytimes.com/2023/09/21/learning/whats-going-on-in-this-graph-oct-4-2023.html.

Health

TBI: An Ecosystem in Crisis

Posted on February 12, 2025 by ttiongso / 0 Comment

The brain is home to a multitude of different cell types that each occupy their own niche. Some of these cells are neurons, which relay information across the brain; astrocytes, which safely pull nutrients from the blood to fuel neurons; and oligodendrocytes, which form the fatty myelin sheath, which speeds up the propagation of electrical signals across an axon. There are many other cell types and processes that occupy the brain, making balance a very complicated ordeal, and this balance can be disturbed.

How TBI affects the brain

Traumatic brain injury or TBI occurs when violent acceleration causes the brain to crash into the skull. This injury is commonly associated with sports like football but can also happen as the result of a fall or car accident. When a TBI occurs, forceful contact between the brain and the skull results in physical damage, chemical dysregulation, and an energy crisis.[1]

In Figure 1 the following steps are described:

The force of impact disrupts the membrane walls causing the ions Potassium to leak out and Sodium/Calcium to rush into the cell faster than they can be pumped in/out.[1]
The cell begins to rapidly and indiscriminately release the excitatory neurotransmitter glutamate causing excitotoxicity.[1]
The unregulated Influx of Calcium is a significant problem because it is stored in and does damage to the mitochondria.[1]
The damage from Calcium alongside the rapid use of the sodium-potassium pumps means that the cell quickly depletes its ATP and enters an energy crisis.[1]

Symptoms

TBI is characterized by a wide array of symptoms and can be broken down into mild, moderate, and severe.

Mild TBI [2]

Physical symptoms

Headache
Nausea
labored speech
Dizziness

Cognitive and sensory symptoms

Depression
Anxiety
Confusion/disorientation
Light or sound sensitivity

Moderate/TBI [2]

Physical symptoms

Loss of consciousness for minutes
Persistent headache
Persistent nausea/vomiting
Uneven pupil dilation
Loss of coordination

Cognitive and sensory symptoms

Increased agitation
Confusion
Difficulties speaking

Severe TBI [2]

Physical symptoms

Loss of consciousness for hours
Severe long-lasting headache
Seizures
Clear fluid draining from the nose or ears
Weakness in toes and fingers

Cognitive and sensory symptoms

Increased agitation
Profound confusion
Slurred speech
Coma

Figure 2 [1] This image describes how the different mechanisms of TBIs are expressed as symptoms.

Prevalence

TBIs have become increasingly common among all age groups and genders. In the Study, “Recent Trends in Youth Concussions: A Brief Report“, Researchers found that from 2013-2018 rates of TBI increased. The researchers looked at the health records of 8,832,419 individuals (4,246,492 males, and 4,585,931 females). These individuals were broken up into 4 categories based on age: under 18, 18-37, 38-59, and 60+. Each of these groups demonstrated a steep increase in TBI cases between 2014 and 2018 [3]. Each group demonstrated a significant increase from 2016-2018 which could be taken as a strict increase but could also signal the development of better diagnostic tools and criteria.

Why Does This Matter?

From the study described above it is clear that TBIs are become a bigger issue for every demographic. Understanding how the mechanisms of TBIs impact the system at micro and macro levels is key for developing better treatments and guidelines

Footnotes

[1]Giza, C. c, & Hovda, D. A. (2014, July 1). The new neurometabolic cascade of concussion. Neurosurgery. https://pubmed.ncbi.nlm.nih.gov/25232881/

[2]Mayo Clinic. (2021, February 4). Traumatic brain injury. https://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/symptoms-causes/syc-20378557

[3]Askow, A. T., Erickson, J. L., & Jagim, A. R. (2020, December 29). Recent trends in youth concussions: A brief report. Journal of primary care & community health. https://pmc.ncbi.nlm.nih.gov/articles/PMC7780302/#table2-2150132720985058

Disease/Health

Football: The Epidemic Hidden Beneath the Helmet

Posted on February 12, 2025 by hdahlsei / 0 Comment

You dive for the ball, just barely have it in your hands, when you collide head-first with the player from the other team! You pick yourself up off the ground, shake off the blow, and keep going. You’re wearing a helmet, so you’re fine, right? Beyond your helmet, under your skull, zoom in on your brain, and now you have tiny pores in your lipid membranes. A rush of sodium and calcium enter your brain cells. The neurometabolic cascade has begun.

The Science: The New Neurometabolic Cascade of Concussion

Traumatic brain injuries, like a head-first collision during football, cause abnormal ion flux, the moving of ions across the cell membrane. Specifically, large amounts of calcium go into the cell, leading to phosphorylation and structural issues in the axons and cytoskeleton of neurons. The large amounts of calcium, as well as sodium entering the cell, cause rapid depolarization, leading to repeated glutamate release, the main excitatory neurotransmitter. This cascade of signaling disrupts the ionic balance of the cells, and in an attempt for the ionic pumps to restore homeostasis, they use too much ATP. This puts your brain cells into an energy crisis, which is further exacerbated by the excess calcium being sequestered to the cell’s mitochondria to try and help the ionic balance. Now the mitochondria are dysfunctional, and that definitely doesn’t help the energy crisis. This entire cascade of events leads to the activation of your brain’s microglia, cells of your immune system that respond to the injury. This leads to brain inflammation [1].

The events during the neurometabolic cascade [1].

So the ions in your brain are currently out of balance, causing you to have a migraine, along with sensitivity to light and sound. The injuries to your axons are leaving you with impaired cognition, slowed processing speed, and slow reaction time. So much for that game-winning maneuver you were planning. You are in an energy crisis, which is leaving you vulnerable to a second injury, and you’re right back out on the field.

Long-Term Impacts: Chronic Traumatic Encephalopathy

Let’s say you get through this game with minimal effects from your earlier collision, but in the next game, when you score the winning touchdown, you crash into the end zone head-first. Then a couple of games later, you get tacked to the ground, and your head feels like it’s vibrating from how hard it smashed against your helmet. This time, when your mitochondria are zapped of energy, your axons are injured, and your microglia are mad at you for making them work overtime, the neurometabolic cascade leads to more harrowing long-term impacts. The metabolic changes last longer, and trigger intracellular proteases, which can cause the cascade to lead to apoptotic cell death [1].

Chronic Traumatic Encephalopathy is a neurodegenerative disorder caused by repeated injury to the brain. Symptoms include cognitive impairment, behavioral changes, mood disorders, and motor symptoms [2]. CTE has been linked to contact sports such as football [3], and studies are showing that more than one-third of football players believe that they are impacted [4].

Chronic Traumatic Encephalopathy, as seen on the top images, compared to normal brain physiology as seen on the bottom images [5].

These acute and chronic dangers of traumatic brain injuries are even more frightening in kids before their brains have finished developing. When the brain is injured during critical periods of development, it can impact the brain’s ability to function normally [6]. This means it’s even more crucial for return to play and other guidelines to take into consideration the science behind repeated head injury. Or even better, the guidelines around protecting our brains during contact sports, biking, riding in vehicles, and other activities need to be stricter. Should kids with delicate, developing brains really be playing brutal contact sports like football, soccer, or boxing? Why can’t society modify these activities to prevent head collisions, and make safer helmets? We need to continue research into the long-term impacts of traumatic brain injuries and use that science to make informed decisions regarding contact sports, especially in developing brains.

References

[1] Giza, C. C., & Hovda, D. A. (2014). The new neurometabolic cascade of concussion. Neurosurgery, 75(Supplement 4), 24–33. https://doi.org/10.1227/neu.0000000000000505

[2] Mayo Foundation for Medical Education and Research. (2023, November 18). Chronic traumatic encephalopathy. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921

[3] U.S. Department of Health and Human Services. (2023, August 28). CTE identified in brain donations from young amateur athletes. National Institutes of Health. https://www.nih.gov/news-events/news-releases/cte-identified-brain-donations-young-amateur-athletes

[4] Study of Former NFL Players Finds 1 in 3 Believe They Have CTE. Mass General Brigham. (2024, September 23). https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/study-finds-1-in-3-former-nfl-players-believe-they-have-cte#:~:text=A%20new%20study%20of%20nearly,mortem%20exam%20of%20the%20brain.

[5] U.S. Department of Health and Human Services. (2023b, September 19). Chronic traumatic encephalopathy in young athletes. National Institutes of Health. https://www.nih.gov/news-events/nih-research-matters/chronic-traumatic-encephalopathy-young-athletes

[6] Blackwell, L. S., & Grell, R. (2023a). Pediatric traumatic brain injury: Impact on the developing brain. Pediatric Neurology, 148, 215–222. https://doi.org/10.1016/j.pediatrneurol.2023.06.019

Health

The Brain’s Breaking Point: What Really Happens After a Concussion

Posted on February 12, 2025 by jdeitz1 / 0 Comment

Imagine an athlete taking a hard hit during a game. They seem fine—no visible injury on a brain scan—but beneath the surface, a silent storm is unfolding. The impact triggers a neurometabolic cascade, a chain reaction that disrupts the brain’s delicate balance. Ions flood in and out of neurons, and a surge of glutamate—a key neurotransmitter—fires indiscriminately, setting off a wave of cellular chaos. To restore order, the brain scrambles to pump ions back into place, demanding enormous amounts of energy. But here’s the problem: blood flow remains restricted, creating a metabolic crisis where the brain is starving for fuel just when it needs it most.

In the following hours and days, this energy imbalance lingers, leaving the brain in a fragile state. The axons—the brain’s communication highways—are stretched and damaged, slowing down thought and reaction time. Neurotransmitters misfire, affecting mood, memory, and cognitive function. Meanwhile, inflammation and oxidative stress take their toll, making the brain more vulnerable to further injury. If a second concussion happens before the brain fully recovers, the damage can be exponentially worse, with a higher risk of long-term impairment. [1]

The Role of Age in Concussion Recovery

Recovery from a concussion isn’t the same for everyone. Age plays a significant role in how the brain responds to injury. There’s ongoing debate about whether younger or older individuals are more vulnerable. Children’s brains are still developing, which may make them more susceptible to injury—but also more resilient in terms of recovery. Some studies suggest that children aged 10-14 have the highest rates of emergency visits for sports-related concussions (SRCs), yet their long-term outcomes may not necessarily be worse than adults. However, repeated concussions during this critical developmental stage can lead to longer recovery times and exacerbate symptoms. [2]

On the other hand, older adults face unique challenges in concussion recovery. Research suggests that multiple concussions can accelerate cognitive decline and increase the risk of mild cognitive impairment (MCI) and Alzheimer’s disease. Former athletes who have suffered repeated concussions often show subtle deficits in attention and motor control—effects that may not be immediately noticeable but can surface later in life. A study comparing high school and college athletes found no major difference in concussion severity, although younger athletes took slightly longer to return to baseline. [2]

[3]

The Search for Biomarkers

With concussions being difficult to diagnose through traditional imaging, researchers are turning to biomarkers—biological indicators that can help detect and track brain injury. Several key biomarkers have been identified:

Astroglial Injury: Elevated levels of S100β and glial fibrillary acidic protein (GFAP) indicate astrocyte activation due to brain trauma. [4]

Neuronal Injury: Neuron-specific enolase (NSE) and ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) are released when neurons are damaged, with UCH-L1 levels being linked to intracranial lesions seen on CT scans.

Axonal Injury: Structural proteins like Alpha-II-spectrin, tau, and neurofilament light protein (NFL) provide insight into axonal damage, with tau deposits being particularly concerning due to their association with Alzheimer’s disease. [4]

[5]

The Long-Term Impact

For many, the symptoms of concussion—headaches, dizziness, and light sensitivity—feel eerily similar to migraines. This overlap isn’t a coincidence; research suggests that the same metabolic dysfunction seen in concussion may also underlie migraines. [6] More concerning is the potential for repeated concussions to contribute to chronic neurodegeneration, with evidence linking multiple head injuries to conditions like chronic traumatic encephalopathy (CTE).

Scientists are now using advanced imaging and biomarkers to track these changes in real-time, searching for ways to better diagnose, treat, and prevent long-term damage. As we learn more, one thing is clear: the effects of a concussion don’t end when the symptoms fade—what happens in those critical early days may set the stage for brain health years down the line.

Learn more about the science behind concussions at The New Neurometabolic Cascade of Concussion

[1]

C. Giza and D. A. Hovda, “The New Neurometabolic Cascade of Concussion,” Neurosurgery, vol. 75, no. Supplement 4, pp. S24–S33, Oct. 2014, doi: 10.1227/NEU.0000000000000505.

[2]

A. Hoge, J. Vanderploeg, M. Paris, J. M. Lang, and C. Olezeski, “Emergency Department Use by Children and Youth with Mental Health Conditions: A Health Equity Agenda,” Community Ment Health J, vol. 58, no. 7, pp. 1225–1239, Oct. 2022, doi: 10.1007/s10597-022-00937-7.

[3]

Concussion Infographics & Fact Sheets. [Online]. Available: https://biausa.org/public-affairs/media/concussion-awareness-infographics

[4]

Papa, “Potential Blood-based Biomarkers for Concussion,” Sports Medicine and Arthroscopy Review, vol. 24, no. 3, pp. 108–115, Sep. 2016, doi: 10.1097/JSA.0000000000000117.

[5]

S. Ghaith et al., “A Literature Review of Traumatic Brain Injury Biomarkers,” Mol Neurobiol, vol. 59, no. 7, pp. 4141–4158, Jul. 2022, doi: 10.1007/s12035-022-02822-6.

[6]

Sachdev and M. J. Marmura, “Metabolic Syndrome and Migraine,” Front. Neur., vol. 3, 2012, doi: 10.3389/fneur.2012.00161.

Health

Rethinking Concussion Protocols: Are We Doing Enough to Protect Athletes?

Posted on February 11, 2025 by gsparks1 / 0 Comment

Concussion protocols in sports are designed to protect athletes and prevent long-term brain damage. However, many athletes are still returning to play before they are fully recovered. Current protocols rely heavily on self-reported symptoms and subjective assessments, which can lead to players downplaying their injuries in order to compete.¹ As research determines the long-term risks of concussions, it’s time to reevaluate how we assess and manage these injuries.

The Limitations of Current Concussion Protocols

Concussion protocols vary across sports and organizations, often including sideline assessments, symptom checklists, cognitive testing, and gradual return-to-play (RTP) guidelines.¹ However, key problems remain:

Self-reported symptoms are unreliable – Studies show that symptoms alone do not accurately identify all concussed athletes or determine full recovery.¹ Athletes may underreport symptoms to avoid being sidelined.
Subjective assessments create inconsistencies – Tests like the Sport Concussion Assessment Tool (SCAT) rely on athlete-reported symptoms, which can be influenced by external pressures and personal motivation to compete.

Because of these limitations, athletes may unknowingly return before their brain has fully healed, increasing the risk of repeat concussions and long-term consequences.

The Effects of a Concussion

Concussions can trigger a wide range of effects within the brain. Figure 1 illustrates the complex cascade of events that follow this type of injury.² The process begins with an influx of cations, such as sodium and calcium. This forces neurons to increase energy production in the form of ATP. This increased activity quickly reduces the neuron’s resources, leading to an energy crisis.

As the cell works to restore this cation balance, more issues occur. The excessive production of ATP generates oxidative stress, which compromises the integrity of the cell membrane.³ The influx of calcium activates proteases enzymes that break down proteins which can result in protein loss within the cell. These disruptions can lead to axonal injury and cell death.²

Figure 1. Neurometabolic cascade of events that can occur after a concussion.²

This cascade of events within the neuron can lead to a variety of symptoms. Table 1 provides a detailed overview of these symptoms and their connection to the affected pathophysiological processes.

Table 1. Symptoms related to their affected pathophysiological process.²

A more detailed explanation of the cascade of effects caused by concussions can be found in this article.

The Science of Recovery and the Impact of Repeat Injuries

While it may seem that the symptoms are gone, the brain remains vulnerable. Returning too soon can lead to:

Second-impact syndrome – A condition where a second concussion occurs before the first has healed.
Chronic traumatic encephalopathy (CTE) – A degenerative brain disease linked to repeated head trauma.
Long-term cognitive impairment – Problems such as memory and behavioral issues.

Research confirms that even after successful completion of a graduated RTP protocol, athletes may still be at a higher risk of neurological and musculoskeletal injuries.¹ More measures are needed to track recovery.

Improving Concussion Protocols

Advancements in brain imaging and neurocognitive research can offer promising ways to enhance concussion management. Key improvements for concussion protocols could include:

Objective diagnostic tools – Tests like biomarker analysis, diffusion tensor imaging (DTI), and functional MRI (fMRI) can provide more accurate assessments of brain recovery.²
Stronger return-to-play goals – Rather than relying solely on self-reports, RTP should incorporate standardized neurocognitive assessments that detect lingering impairments.
Education – Athletes, coaches, and medical professionals should prioritize brain health over competition. RTP decisions should be made with long-term well-being in mind.

Beyond Sports: Why Better Concussion Protocols Matter for Everyone

Concussion management isn’t just a concern for professional athletes. It affects youth sports, military personnel, and everyday individuals. Improved protocols could:

Protect young athletes from long-term cognitive issues.
Help military veterans reduce the risk of neurodegenerative diseases.
Improve workplace and recreational injury management to prevent lasting damage.

If we continue relying on outdated or lenient concussion protocols, are we prioritizing competition over health? With advancements in science and technology, we have an opportunity to develop more accurate, evidence based concussion management strategies. It’s time to rethink our approach and ensure we are truly protecting those at risk.

Footnotes:

(1) Wellm, D.; Zentgraf, K. Diagnostic Tools for Return-to-Play Decisions in Sports-Related Concussion. J Concussion 2023, 7. https://doi.org/10.1177/20597002231183234.

(2) Giza, C. C.; Hovda, D. A. The New Neurometabolic Cascade of Concussion. Neurosurgery 2014, 75, S24–S33. https://doi.org/10.1227/NEU.0000000000000505.

(3) Hong, Y.; Boiti, A.; Vallone, D.; Foulkes, N. S. Reactive Oxygen Species Signaling and Oxidative Stress: Transcriptional Regulation and Evolution. Antioxidants. Multidisciplinary Digital Publishing Institute (MDPI) March 1, 2024. https://doi.org/10.3390/antiox13030312.

Uncategorized

AI: The Game Changer in Concussion Diagnosis

Posted on February 11, 2025 by Nessa Angau / 0 Comment

The Hidden Danger of Concussions in the NFL – The Cherokee Scout

Concussions are one of the most common yet misunderstood brain injuries. And they don’t just affect professional athletes—students, military personnel, and everyday people suffer concussions from falls, car accidents, and sports injuries. And while many assume concussions are easy to diagnose, their symptoms can be subtle, delayed, or mistaken for other conditions.

But here’s the problem: traditional concussion diagnosis relies heavily on subjective symptom reporting and outdated tests, leading to misdiagnoses and long-term health risks. Many people go undiagnosed, putting them at risk for chronic traumatic encephalopathy (CTE), memory loss, and cognitive decline. [1]

Therefore, AI is stepping in as a game-changer, offering faster, more accurate concussion detection that could revolutionize brain health. But, in what ways? Let’s read more!

1. Faster And More Accurate Diagnosis

Unlike traditional methods that rely on a doctor’s judgment, AI can analyze large amounts of brain data quickly, improving accuracy. AI models can scan MRI and CT images, detecting patterns that even trained professionals might miss! This means fewer misdiagnoses and faster treatment.

Figure 1. This scan demonstrates the use of fMRI and AI to decode language signals in the brain [2]

2. Tracking Recovery in Real-Time

Concussions don’t just disappear overnight—they require careful monitoring. AI-powered apps and wearables can track symptoms over time, alerting doctors when a patient isn’t healing properly. This is especially useful for athletes and soldiers, helping them avoid returning to activity too soon. [3]

3. Reducing Long-Term Brain Damage

Early detection is crucial. AI can identify subtle signs of brain trauma long before they become serious, helping doctors intervene early and prevent lasting damage. This could mean fewer cases of CTE and a better quality of life for concussion patients.

The Bigger Picture: AI and The Future of Brain Health

Future in Mental Health: How AI is Personalizing Treatment Plans — Figure 2. This diagram demonstrates the different advancements AI can be expanded towards. [4]

AI’s impact goes beyond concussions. The same technology used to diagnose brain injuries could be applied to mental health, neurodegenerative diseases, and stroke detection. Cool, right? But with these advancements come ethical concerns—how do we ensure AI diagnoses are reliable? Who is responsible if AI makes a mistake?

As AI continues to shape the future of medicine, it’s important to ask: How can we use this technology responsibly while maximizing its benefits?

AI is changing the way we detect and treat concussions, making diagnosis faster, monitoring more precise, and recovery safer. And as technology evolves, it has the potential to protect millions from long-term brain damage. But responsibility and accountability is absolutely critical—we need to ensure AI is accurate, accessible, and ethically used.

Therefore, the future of concussion care isn’t just about better technology—it’s about how we use it to improve lives. Will AI redefine brain health as we know it? Will AI be the next ultimate game changer in the future of medicine? The answer is closer in time than we think!

Resources

[1] Mayo Clinic. (2023, November 18). Chronic traumatic encephalopathy – Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921

[2] Hamilton, J. (2023, May). A decoder that uses brain scans to know what you mean — mostly. NPR. https://www.npr.org/sections/health-shots/2023/05/01/1173045261/a-decoder-that-uses-brain-scans-to-know-what-you-mean-mostly

[3] Haffeman, D. (2015). New ResearchKit App to Track Concussions in NYU Langone Study. NYU Langone News. https://nyulangone.org/news/new-researchkit-app-track-concussions-nyu-langone-study

[4] Singh, G. (2024, December 9). Future in Mental Health: How AI is Personalizing Treatment Plans. Resources. https://www.knowledge-sourcing.com/resources/thought-articles/future-in-mental-health-how-ai-is-personalizing-treatment-plans/

Uncategorized

Photophobia: The Fear of Light After TBI’s

Posted on February 11, 2025 by jcopiske / 0 Comment

PHOTOPHOBIA

Although photophobia literally means to have a ‘fear of light’, it actually refers to pain or discomfort caused by light exposure.

This is a neuro-ophthalmological disorder, which means the optic nerves are affected along with the brain. So, even though eye disorders commonly involve light sensitivity, photophobia can be caused by a variety of things.

Photophobia is one of the most common ocular conditions that occur with tension headaches, migraines, or TBI’s (Traumatic brain injury’s).

TBI’s (Traumatic Brain Injury)

Photophobia is one of the most common symptoms of concussions and TBI’s. TBI produces cognitive symptoms such as dizziness, vertigo, nausea, irritability, cognitive delays, and vision related symptoms to light-sensitivity. About 40% of individuals with brain injuries experience sensitivity to light. But, Light sensitivity can show up post-concussion or 6 months to even years after the concussion occurred.

Cranial Nerve 5- trigeminal CN V

The star of the show in pain processing within the head and eyes is cranial nerve five (the trigeminal nerve), the largest cranial nerve. The trigeminal nuclei and nerves play a crucial role in moderating pain, particularly in the eyes and head.

The trigeminal ganglion houses the ophthalmic branch (V1), which is primarily responsible for transmitting pain signals from the cornea, conjunctiva, sclera, and uvea–these structures are extremely sensitive to pain.The trigeminal nerve is an essential player in processing sensory information from the face and head.

When pain is experienced, it is often linked to the release of (CGRP) Calcitonin gene-related peptide. This peptide is released in response to stimulation from the trigeminal nerve and plays a critical role in the pain signal transmission to the brain. CGRP is located in the trigeminals ganglion, which is triggered by stress, brain vessels, and or inflammation.

Figure 2, The CGRP pathway in response to migraines within CN V

What Causes Photophobia in TBI’s?

With TBIs, photophobia (light sensitivity is usually caused by injury to the thalamus, preventing it from getting oxygen. This disruption impairs its function, leading to heightened sensitivity to light. But, in a TBI light sensitivity could mean dysregulation in one or multiple areas of the brain. The problem isn’t always isolated.

This creates a symptom cascade, where an issue in one area can trigger problems in others area. Dysfunction in the visual process could possibly affect focus, balance, or overall symptoms which creates a harder recovery process.

Thalamus

The thalamus is in charge of relaying sensory information to the brain. It is crucial for directing sensory signals, when a TBI occurs the process is disrupted.

The dysregulated mechanism that occurs is neurovascular coupling, which happens in the brain and retina. When communication pathways are faulty, neurons and blood vessels start malfunctioning and there isn’t always enough oxygen to be used.

As a result, patients experience light sensitivity in order to minimize their sensory overload and are recommended to stay in dark rooms. This reduces the amount of visual input letting the brain rest and recover

Autonomic Nervous System

The autonomic nervous system (ANS) is in charge of involuntary system, which involves functions like heart rate, breathing, and digestion Within light sensitivity, pupils dilate more than needed in a post concussion scenario causing exposure to light causing sensitivity. The dysregulation in the ANS causes abnormal pupil responses.

Vestibular System

The vestibular system involves the inner ear, sight, and touch. Dysfunction in this area causes the body to become off balance, leading to dizziness and vertigo. When the Vestibular system and visual system disagree, this increases optic sensitivity–which in turn creates an overload of sensory information.

Superior Colliculus

The superior colliculus is in charge of visual mapping and coordination, aiding in detecting and locating visual and audio stimuli. This contributes motor functions to orient the head and eyes toward or away from a stimulus. This is described as a looming stimulus which can be perceived as a threat from an object moving towards you and initiates a response from fear. For example a snake would be processed in the superior colliculi and initiate a motor response which would orient an individual away from the snake, as the brain perceives it as dangerous. This can occur without eye movements as an instinct response.

Photophobia in TBI’s

Therefore, Photophobia in TBI’s is involved in several structures including thalamus, ANS, vestibular system, and superior colliculus. Light sensitivity is commonly found as a system of ocular disorders, in TBI’s it is a neurological dysfunction. This dysfunction occurs by dysregulation in sensory processing, such as lack of oxygen supplied to the brain or the miscommunication between sensory and visual pathways which increase light sensitivity.

CN V, The trigeminal nerve is responsible for transmitting these pain signals after TBI occurs. With the involvement of the CGRP pathway, the trigeminal nerve is responsible for a cascade of symptoms depending on the brain structure that is affected. Understanding photophobia in TBI’s in important for deciding treatment, limiting sensory input, and understanding multi-system dysfunction.

Footnotes:

Abusamak, Mohammad, and Hamzeh Mohammad Alrawashdeh. “Post-Concussion Syndrome Light Sensitivity: A Case Report and Review of the Literature.” Neuro-Ophthalmology 46, no. 2 (n.d.): 85–90. https://doi.org/10.1080/01658107.2021.1983612.

Grossman, Elan J., and Matilde Inglese. “The Role of Thalamic Damage in Mild Traumatic Brain Injury.” Journal of Neurotrauma 33, no. 2 (January 15, 2016): 163–67. https://doi.org/10.1089/neu.2015.3965.

Grossman, Ela

n J., and Matilde Inglese. “The Role of Thalamic Damage in Mild Traumatic Brain Injury.” Journal of Neurotrauma 33, no. 2 (January 15, 2016): 163–67. https://doi.org/10.1089/neu.2015.3965.

russ. “Light Sensitivity After a Brain Injury.” Optometrists.Org (blog). Accessed February 8, 2025. https://www.optometrists.org/vision-therapy/neuro-optometry/vision-and-brain-injuries/traumatic-brain-injury-and-neuro-optometry/light-sensitivity-after-a-brain-injury/.

Staff, By. “Neuroimaging Shines Light on Chronic Ocular Surface Pain, Photophobia.” Accessed February 10, 2025. https://www.reviewofoptometry.com/article/neuroimaging-shines-light-on-chronic-ocular-surface-pain-photophobia.