The Curious Case of the Karius Concussion Conundrum

karius concussion
Credit – Fox Sports

Liverpool goalkeeper Loris Karius has been under the microscope of the world after two seemingly bone-headed mistakes during the Champions league Final against Real Madrid, yet it was revealed on June 4th that a Karius concussion occurred in the 48th minute when he was hit in the side of the head by a Sergio Ramos elbow.

Take a look at the incident:

And the moment of contact:

karius concussion
Credit – Fox Sports

For the record, Ramos was clearly pushed in the back as he tried to jump which threw him completely off balance.  I don’t think he shoulders any of the blame for the Karius concussion, unlike his tussle with Mohamed Salah earlier in the game that resulted in Salah leaving the game with a shoulder injury – I wrote about that injury here.

3 minutes after the concussion, Karius made this decision:

And in the 84th minute, this happened (goodnight and goodluck):

A handful of days later (on June 4th), medical providers with the permission of Karius released the following information on the Karius concussion:

On May 31, 2018 Mr. Karius underwent a comprehensive examination by Dr. Ross Zafonte and Dr. Lenore Herget, DPT in Boston at Massachusetts General Hospital and Spaulding Rehabilitation Hospital.

 

After carefully reviewing game film and integrating a detailed history – including his reported present and immediate post-contact subjective symptoms – physical examination and objective metrics, we have concluded that Mr. Karius sustained a concussion during the match May 26, 2018.

 

At the time of our evaluation, Mr. Karius’s principal residual symptoms and objective signs suggested that visual spatial dysfunction existed and likely occurred immediately following the event. Additional symptomatic and objectively noted areas of dysfunction also persisted. It could be possible that such deficits would affect performance.

Additionally, it was reported that 26/30 concussions tests came back positive for Karius.

To explore the Karius concussion and understand how it affected him, I detail the following questions:

  • What is a concussion and what caused the Karius concussion?
  • What happens to the brain after a concussion?
  • What are the potential symptoms of Karius concussion?
  • What is “visual spatial dysfunction” and how would that affect Karius in-game?
  • Is the Karius concussion just “an excuse” for his mistakes?
  • What is the concussion protocol in UEFA?
  • Why wasn’t Karius evaluated and taken out of the game?
  • The recovery timeline for the Karius concussion
  • Are there any long-term implications?

I. What is a concussion and what caused the Karius concussion

A concussion is considered a mild traumatic brain injury (MTBI).  In medical circles, concussion and MTBI are often used interchangeably.  If the term traumatic brain injury (TBI) had been used in lieu of concussion from the jump, maybe it would’ve been taken more seriously…but that’s a whole different conversation.

The moment of contact between Ramos’ elbow and Karius was the initial impetus for the Karius concussion. However, you might be surprised to learn that it’s not the initial contact (known as focal trauma) which is the main contributor to a concussion/MTBI.

In fact, the head hitting or getting hit by an external object isn’t a pre-requisite for concussion/MTBI.  Studies have shown that focal (confined to one area) brain injuries are largely absent in concussion/MTBI.  This means a concussion/MTBI can occur with either direct or indirect contact to the head.

The key contributors to concussion/MTBI are the linear and/or rotational inertial (acceleration/deceleration) forces imparted onto the brain from the start/stop movement of the head and neck.

Take a look:

karius concussion
Credit – WBUR

Since brain tissue one of the softest biological materials, it’s very vulnerable to these forces.  In particular, brain tissue is extremely susceptible to the shearing force caused by rotational forces.

If the shearing damage is widespread, it can result in a loss of consciousness. That’s why a loss of consciousness is a key indicator for higher severity of concussion/MTBI (a greater extent of damage in the brain).

Fortunately, the Karius concussion – or perhaps unfortunately because if he gets knocked out then he assuredly gets assessed and taken out of the game…and doesn’t have to suffer the plethora of worldwide hot takes – didn’t result in a loss of consciousness.

However, there’s still a huge crisis occurring in his brain…

II. The Karius concussion and his brain in crisis

The damaged brain tissue creates a series of bad events (domino affect) for the brain, termed a “neurometabolic cascade”, that leaves the brain very vulnerable.

Before we go any further, I’ve given you a choice…3 roads diverged in the wood and it’s up to you to pick one.

I’ve broken down the physiological events of a concussion/MTBI at 3 different levels of detail and complexity, each corresponding to a higher degree of detail and complexity (and I’ve done my best to simplify and translate even the most complex things, as I always try to).

Depending on your interest level in the details, you can choose either:

A. The general overview

B. Detailing the key deficit (the major domino to fall) that occurs during concussion/MTBI

C. Detailing the entire neurometabolic cascade
I leave that in your hands.  If you choose road A or road B, skip down to section III – Symptoms after you’re done.

A. The general overview

There’s a series of events and mechanisms that lead to a mismatch of supply and demand in the brain – it needs resources to repair but there aren’t enough available (in fact, the amount of resources is actually lower than normal).  This results in a short-term “energy crisis” and brain impairment.

You can see that mismatch in following graph, focus on the black line which shows cerebral blood flow (CBF, or blood flow to the brain):

karius concussion
Credit – Giza, “The new neurometabolic cascade of concussion”

As you can see, the black line (CBF) is below normal and that means reduced resources for the brain.

This short-term mismatch is why any concussion/MTBI recovery protocol has an initial 24-48 hour period of no stimulus – it’s giving the brain time to recover while reducing stress on it.

Continue to possible symptoms

B. The Major Domino to Fall

Micropores in cell membranes

A concussion/MTBI creates micropores (“holes”) in the membranes of brain cells (neurons) – it’s like puncturing holes into the walls of cells.

Due to those holes, the cells can’t regulate what’s going in and what’s going out.  This creates an influx and efflux of ions. Don’t worry about the specifics, in general just know that a lot of things are going in and out of the cells in quantities and ratios that aren’t normal.

This leads to a snowball effect (termed “diffuse depolarization”) in neighboring cells where those cell membranes are dysregulated as well.

This is how the brain’s energy crisis begins.

At this point, the brain attempts to restore it’s equilibrium.  This requires a huge amount of energy and the production of ATP (a major energy source for your body) shifts into over-drive.

However, during this early period of concussion/MTBI, there’s reduced cerebral (brain) blood flow caused by arterial vasoconstriction (narrowing of arteries). Here’s an illuminating table:

karius concussion
Credit – Giza, “The new neurometabolic cascade of concussion”

Focus on the bottom black line, which represents cerebral blood flow.  While a bunch of other ions and things are increasing, blood flow is below normal levels.

This means that the ATP (energy source) can’t get to the brain in the quantities required – resulting in a mismatch between energy supply and demand.  In other words, there aren’t enough immediate resources to repair the brain and bring it back to equilibrium

Adding to this problem, mitochondria (“the energy factories of the cells”) become dysfunctional – worsening the energy crisis.

Lastly, intra-cellular redox (this is a process that keeps cells in equilibrium and functioning) is altered.  This puts additional stress on the brain by creating damaging free radicals and shifting metabolic pathways.  The latter can trigger longer-lasting impairments and set the stage of increased vulnerability to repeated injury – especially pertinent in sports-related concussion/MTBI.

So I know that’s a whole lot to digest and no blame if you’re like “WTF mate” so here’s an analogy that might help:

Imagine a brain cell is a city with a giant wall around it. Like this one:

Karius concussion

During normal functioning, the city (cell) is able to regulate who gets in and out (ions) via its surrounding wall (membrane).  However, an earthquake (concussion/MTBI) occurs and the wall gets broken down in multiple spots.  Now there’s no regulation of who is coming in or out – this throws the city into a panic (disequilibrium).  Adding to the mess, neighboring cities (cells) also start to panic (diffuse depolarization).

The city (cells) calls on all workers and possible resources (ATP) to repair the walls (membranes) and bring back those who belong while expelling those who don’t (specific ions).  However, the major power plants (mitochondria) are damaged (mitochondrial dysfunction)and roads to the city (arteries) are blocked off (arterial vasoconstriction).  Additionally, pollution safeguards (intra-cellular redox) have broken down, resulting in increased toxicity in the city overall.

In sum: you have a city that needs significant rebuilding and cleanup work asap but doesn’t have nearly enough resources.  That’s the crisis the Karius concussion caused in his brain.

Continue to possible symptoms

C. Detailing the full neurometabolic cascade

Let’s go through the events and domino affect that occurs during concussion/MTBI (if you’ve read my piece on Jaylen Brown’s concussion/MTBI, this section will be familiar with you and hopefully a good review):

1. Micropores in cell membranes

A concussion/MTBI creates micropores (“holes”) in the membranes of brain cells (neurons) – it’s like puncturing holes into the walls of cells.

Due to those holes, the cells can’t regulate what’s going in and what’s going out.  This creates an influx and efflux of ions. Don’t worry about the specifics, in general just know that a lot of things are going in and out of the cells in quantities and ratios that aren’t normal.

This leads to a snowball effect (termed “diffuse depolarization”) in neighboring cells where those cell membranes are dysregulated as well.

This is how the brain’s energy crisis begins.

At this point, the brain attempts to restore it’s equilibrium.  This requires a huge amount of energy and the production of ATP (a major energy source for your body) shifts into over-drive.

However, during this early period of concussion/MTBI, there’s reduced cerebral (brain) blood flow.  This is caused by arterial vasoconstriction (narrowing of arteries). Here’s an illuminating table:

karis concussion
Credit – Giza, “The new neurometabolic cascade of concussion”

Focus on the bottom black line, which represents cerebral blood flow.  While a bunch of other ions and things are increasing, blood flow is below normal levels.

This means that the ATP (energy source) can’t get to the brain in the quantities required – resulting in a mismatch between energy supply and demand.  In other words, there aren’t enough immediate resources to repair the brain and bring it back to equilibrium

Adding to this problem, mitochondria (“the energy factories of the cells”) become dysfunctional – worsening the energy crisis.

Lastly, intra-cellular redox (this is a process that keeps cells in equilibrium and functioning) is altered.  This puts additional stress on the brain by creating damaging free radicals and shifting metabolic pathways.  The latter can trigger longer-lasting impairments and set the stage of increased vulnerability to repeated injury – especially pertinent in sports-related concussion/MTBI.

So I know that’s a whole lot to digest and no blame if you’re like “WTF mate” so here’s an analogy that might help:

Imagine a brain cell is a city with a giant wall around it. Like this one:

Karius concussion

During normal functioning, the city (cell) is able to regulate who gets in and out (ions) via its surrounding wall (membrane).  However, an earthquake (concussion/MTBI) occurs and the wall gets broken down in multiple spots.  Now there’s no regulation of who is coming in or out – this throws the city into a panic (disequilibrium).  Adding to the mess, neighboring cities (cells) also start to panic (diffuse depolarization).

The city (cells) calls on all workers and possible resources (ATP) to repair the walls (membranes) and bring back those who belong while expelling those who don’t (specific ions).  However, the major power plants (mitochondria) are damaged (mitochondrial dysfunction)and roads to the city (arteries) are blocked off (arterial vasoconstriction).  Additionally, pollution safeguards (intra-cellular redox) have broken down, resulting in increased toxicity in the city overall.

In sum: you have a city that needs significant rebuilding and cleanup work asap but doesn’t have nearly enough resources.  That’s the crisis the Karius concussion caused in his brain.

2. Cytoskeleton damage

The cytoskeleton, according to Science Direct, is an organized network of proteins that aides with cell function. It provides the cell with shape, structure, compartmentalization, and transport:

karius concussion
Credit – study.com

During a concussion/MTBI, this skeleton is damaged and further affects the function of brain cells.

3. Axonal dysfunction

Axons are the part of a neuron (nerve cell) that helps transmit signals to other cells. They’re often referred to as nerve fibers. Here’s what the basic neuron looks like:

karius concussion

Your brain is full of neurons and therefore axons.  These axons are very vulnerable to stretch and can be extensively damaged from high shear forces, like those that occur during a concussion/MTBI.

Here’s a picture of axonal shear:

karius concussion

This creates axon dysfunction and if the force is high enough, the axon will actually tear and disconnect. This hinders a basic component of brain function – brain cell communication.

4. Altered neurotransmission

At the end of each nerve (the terminal), tiny messenger chemicals (neurotransmitters) are transmitted from one nerve to the next. This is called neurotransmission.  Here’s a look:

karius concussion
Credit – wikispaces

A concussion/MTBI interferes with and alters this process.  This further messes with brain cell communication.

5. Inflammation

A concussion/MTBI up-regulates inflammatory markers and inflammation in the brain. This has been associated with damage to certain parts of the brain and is a risk factor for Parkinson’s disease.

6. Cell death

In the case of a concussion/MTBI, there isn’t much cell death in the acute (short-term) phase.  However, there is the possibility of long-term structural changes that appear over time, even after only one concussion.

Quick Review (great graphic but feel free to skip this)

I found a great graphic that organizes the neurometabolic cascade extremely well.  Check it out:

karius concussion
Credit – SPORTS HEALTH

III. The possible symptoms resulting from the Karius concussion

A concussion/MTBI can cause a variety of symptoms, lasting from minutes to hours to days to weeks.

Since we just went through some of the events that take place in a concussion/MTBI, lets first take a look at how those events may be linked to certain symptoms. This table is a great summary:

karius concussion
Credit – Giza “The new neurometabolic cascade”

Now, let’s take a more general approach.

A. Commonly reported concussion/MTBI symptoms, organized by general category:

  • Affective/emotional
    • commonly reported
      • anxiety/nervousness
      • irritability
      • depression
        • each of these can last days to weeks
  •  Cognitive
    • commonly reported
      • confusion
        • usually lasts minutes to hours
      • difficulty concentrating
      • difficulty remembering
      • disoriented
        • these 3 can last days to weeks
      • feeling foggy
      • feeling slowed down
  •  Sleep
    • generally, any sleep alteration can last days to weeks
    • commonly reported
      • drowsiness
      • increased sleep quantity
  •  Sensory/physical
    • commonly reported
      •  headache
        • can last from minutes to hours to days to weeks
      • dizziness
      • nausea
        • these 2 usually last minutes to hours
      • fatigue
      • light sensitivity
        • these 2 usually last days to weeks
      • double vision (diplopia)
      • poor eye tracking
      • difficulty focusing vision
      • eye strain
    • A few noteworthy symptoms
      •  Vomiting
        • can last minutes to hours
      • light-headedness
      • tinnitus (ringing of the ears)
        1. these 2 can last days to weeks

Here’s the full list if you’re interested.

In addition to the physiological changes and symptoms, we have to consider contextual factors as layers potentially compounding the Karius concussion….

B. Compounding Factors

Karius was a young 24 year old keeper playing in the biggest match of his life.  This can result in a huge amount of stress, anxiety, and overall pressure on him.  That stress ratchets up as the game moves along, and goes up about 10 notches after he lets in the Benzema goal.

“Ah crap, what just happened?  What did I do?  Have I let my team down…what will they think? Have I let all the fans down?”

I don’t even want to imagine his mental state after Bale’s shot deflected off his hands into the back of the net.

This in-game stress and cognitive load can exacerbate the ongoing crisis in his brain.  It’s like demanding more crops from a famine stricken region.

Now that we’ve touched on potential symptoms and compounding factors, lets talk about the one symptom that we know was immediately caused by the Karius concussion and how it affected him in-game….

IV. Visual-Spatial dysfunction from the Karius concussion

As I noted at the start of the piece, an examination revealed that the Karius concussion likely led to immediate visual spatial dysfunction.  Here’s the official quote once more:

At the time of our evaluation, Mr. Karius’s principal residual symptoms and objective signs suggested that visual spatial dysfunction existed and likely occurred immediately following the event.

To understand what visual-spatial dysfunction is, we have to first understand what visual-spatial processing is.

Generally, visual-spatial processing is involved in things like focusing on a single object (termed “binocularity”), being able to tell where your body and things are in space (known as “spatial orientation”), posture, and balance.

Every day tasks like merging in traffic, navigating through your neighborhood, judging the distance between your body and laptop for proper hand placement, imagining object movements and motion, and reading require visual-spatial processing.  It’s intimately involved in our second to second lives and incredibly important.

During sports, visual-spatial processing takes on another level of importance due to the constant movement, balance, tracking of objects (ball, players), constant judgement of space, and so on.

For Karius, as a goal keeper, his visual-spatial system is constantly stressed –  tracking his teammates and opponents, judging distances and spaces, tracking the ball at distance and as it comes toward him, and coordinating his own movements, balance, and posture.  And that’s just the tip of the iceberg.

After the Karius concussion, visual-spatial dysfunction can affect all of those things to varying degrees.

With that in mind, lets take a closer look at the two mistakes he made (my apologies to the Liverpool fans):

1 – The Benzema Goal

The opener of the Liverpool – Real Madrid match came when Benzema deflected in a Karius pass:

In this scenario, Karius had to locate and track the positioning of his potential targets and Benzema, making visual-spatial inferences the entire time:

Karius Concussion
Credit – Fox Sports

When Karius opts to not throw the initial pass, and brings the ball back in , he has to relocate his teammate on the right while tracking Benzema’s movement and proximity:

karius concussion
credit – Fox Sports

Clearly that didn’t go well.  He seems to have misjudged his initial passing lane, didn’t track Benzema well, and then clearly misjudged how close Benzema was to him.

Moving onto the 84th minute…

2 – The Bale Goal

In the 84th, Bale took a speculative shot from outside the box that deflected off Karius’ hands into the net and put the nail in the coffin:

Karius concussion
Credit – Fox Sports

To catch a ball, Karius’ visual-spatial system must first locate the ball, and then gauge the speed and distance of the ball in flight. In this case, he’s also dealing with initial visual interference from the Liverpool defender trying to body block the shot:

karius concussion
Credit – Fox Sports

With the ball hurling towards him and a late clear view, the visual-spatial system kicked into over-drive to adjust Karius’ movements and put him in the best position for the catch.  In this case, that would be a slight movement to his left to keep his body, chest, and hands centered to the ball:

karius concussion
Credit – Fox Sports

Karius’ body position was still off-center when the ball arrived, forcing him to reach across his body with his right arm rather having both arms and hands in a symmetrical position. This resulted in the ball hitting the top of his left hand rather than the middle inner aspect of both hands, and the ball caromed to the left and into the net:

karius concussion
Credit – Fox Sports

With the blistering pace and movement on Bale’s shots, even the slightest visual-spatial deficit would affect the catch.

____

In both cases, we’ll never know what Karius was seeing or feeling but his visual-spatial processing is being challenged in both cases.  Immediate dysfunction could have played a huge factor in both mistakes and that’s bolstered by the fact both plays came after the Karius concussion, with Benzema’s just mere minutes after.

Unfortunately, and what often seems to be the case after “invisible” injuries like a concussion/MTBI, I’ve heard some talk that Karius concussion is being used as an excuse….

V. Is the Karius Concussion a 20/20 hindsight excuse?

Absolutely not.

Firstly, if there’s anyone who needs to make an “excuse”, it’s the officials and Liverpool medical staff for not recognizing/assessing the Karius concussion and removing him from the game. It’s their responsibility to see the play, recognize there might be a head injury involved, and then objectively rule a player in or out.

Anyways, one of the arguments I’ve heard to support the “excuse” assertion is that Karius made some great saves after the concussion/MTBI, and therefore he couldn’t have been concussed.

Frankly, that’s a really silly argument and shows a lack of understanding of concussion/MTBI.  Concussion/MTBI isn’t a binary injury where once you suffer it, you can’t do anything.

I honestly wish it was that simple.

If that was the case, it wouldn’t have taken this long and all these instances of post-death CTE autopsies, diagnoses, and examples of players being debilitated to bring concussion/MTBI to the forefront and public eye.

The reality is concussion/MTBI creates deficits on a spectrum, it’s not all or nothing.

The other argument I heard was from prominent Chelsea goalkeeper Thibaut Courtois who used his anecdotal experience to contrast it with the Karius concussion and throw shade at him:

“I guess he got a blow on his head but it happened to me with Alexis Sanchez. I had a concussion and I couldn’t see the ball so after 20 minutes I went out of the game.

 

“I feel sorry for what happened to him but to blame it on concussion now… in that space, that he made those mistakes he also made two amazing saves. Was that luck then, because he couldn’t see the ball? I don’t know.

Firstly, anecdotal experiences mean nothing when it comes to someone else’s injury, especially in the case of concussion/MTBI – as I said before, concussion symptoms are so variable.  Just because Courtois had trouble seeing the ball has no bearing on whether Karius had it or not.

This is where I wish individuals would just keep quiet rather than reinforcing the norms and stereotypes that already exist with concussion/MTBI.

Lastly, Courtois also said:

“If you have concussion you will leave the game or the doctors will tell you: ‘Look, you cannot see clearly anymore, you must leave the game’.”

This is just patently false.  We saw it in the case of the Karius concussion, we see it way too often in the NFL (with teams like the Seahawks getting fined for not concussion testing Russel Wilson), and another prominent example that comes to mind is Germany’s Kristoff Kramer.

During the 2014 World Final against Argentina, Kramer took a heavy blow to the head, and moments later had this exchange with an official:

Kramer (to referee Nicola Rizzoli): “Ref, is this the final?”

 

Rizzoli thinks he’s joking and makes him repeat the question: “I need to know if this is really the final”

 

Rizzoli: “Yes”

 

Kramer: “Thanks, it was important to know that”

You can’t make that up.

Rizzoli let Germany midfielder Bastian Schweinsteiger know about the exchange (and I don’t blame Bastian, it’s not his role or expertise to be aware of concussion/MTBI symptoms), and Kramer continued to play for 14 more minutes until he slumped to the ground.

But Karius didn’t have a concussion/MTBI because the team medical staff will always pull a player from the game, right Thibaut?

Cmon.

So no a concussion/MTBI is absolutely not an “excuse” – it’s a completely valid reason and Karius’ mistakes line-up very well with his immediate symptom of visual-spatial dysfunction.

Now that we’ve put that to bed, what exactly is UEFA concussion/MTBI protocol?

VI. UEFA concussion/MTBI protocol and the Karius concussion

In Article 47 of the UEFA Champions League Regulations Handbook for 2015-2018 (you can find the full handbook here), the concussion/MTBI protocol states:

In the event of a suspected concussion the referee stops the game to allow the injured player to be assessed by the team doctor, in accordance with Law 5 of the IFAB Laws of the Game. In principle this should take no more than three minutes, unless a serious incident requires the player to be treated on the field of play or immobilized on the field for immediate transfer to hospital (e.g. spinal injury).

 

Any player suffering a head injury that requires assessment for potential concussion will only be allowed to continue playing after the assessment, on specific confirmation by the team doctor to the referee of the player’s fitness to do so.

UEFA, to their credit, implemented this 3-minute rule and return to play eligibility for the 2015-2018 cycle.  However, why wasn’t it applied to the Karius concussion?

According to league officials and the medical staff, they didn’t see the collision between Ramos and Karius take place.  We can speculate on the veracity of that statement considering big games can skew the idea of risk/reward for all parties involved (like with Kristoff Kramer) but I’ll have to take those comments at face value – they were unaware and therefore the UEFA concussion/MTBI assessment wasn’t initiated.

That being said, what is UEFA doing to mitigate the chances that this doesn’t happen in the future and injuries like the Karius concussion aren’t missed?

VII.  New UEFA concussion/MTBI protocol

From my understanding, UEFA had already been considering updating the protocol to allow for medical staff on the sidelines or in the stands to review incidents with video playback, such as with tablets.

This video rewind and playback of concerning incidents was implemented by the EPL in 2016 and mirrors the head injury assessment process in the Rugby Union.

The Karius concussion has brought increased scrutiny and pressure for that change to take place.  Additionally, there are increasing calls to give more time for the concussion/MTBI assessment and allow for a temporary sub.

Here’s what Dr. Willie Stewart, a British neurosurgeon who has been a champion for improving head injury assessment in soccer and rugby, told BBC Sport:

“Football doesn’t allow an interchange for a player to be assessed to see if he has a brain injury; doesn’t allow significant time for the medics to assess the player; doesn’t have a video review of events to be able to say if there was a glancing blow on my goalkeeper’s head which I didn’t notice.

 

“It’s unacceptable in 2018 that it should be this way.”

100% agreed.

Additionally, Premier League docs are currently at the forefront of demanding change in concussion/MTBI protocol and assessment, asking for the following:

  • If a player is suspecting of having a concussion/MTBI, they are allotted 10 minutes off the field for further assessment
  • In those 10 minutes, a temporary substitute is allowed.  If a concussion/MTBI is confirmed, the temporary sub becomes permanent
  • The addition of a 4th substitute in cases where a player has to be taken off due to concussion/MTBI

The overall point of these is, first and foremost, to increase player safety.  Additionally, these changes would decrease the pressure on medical staffs to rush to judgement regarding a concussion/MTBI diagnosis and decrease the pressure on players, especially goal keepers, to stay in the game after head injury.

Personally I’m all for it.  A slight upset in the flow of the game is worth exponentially improving player safety and head injury assessment. Of course there will be the “traditionalist” detractors but there always are.  Remember when people were complaining that goal-line technology would upset the flow and beauty of the game?

Oh brother.

So now that we’ve talked in-depth about the Karius concussion and UEFA protocol, what does his recovery timeline look like?

VIII. Karius concussion recovery timeline & rehab

A. Timeline

Concussion/MTBI recovery is variable and will depend on the extent and type of symptoms.  However, there are general concussion/MTBI recovery timelines:

  • 85-90% of the time, all symptoms are gone within 7-10 days.  It’s no surprise that this 7-10 day timeline parallels the 7-10 days that it takes for the brain to get out of its energy crisis
  • Less commonly, it takes 2-4 weeks for symptoms to resolve
  • Least commonly, it can take over 4+ weeks.  This is termed “post concussion syndrome” (PCS).  Having treated it multiple times, PCS is really difficult to rehab and BRUTAL to deal with. Wish this only on your worst enemies (I wrote more about it here).

The old paradigm on concussion/MTBI management was to grade it as “mild, moderate, or severe” and have that individual simply set out for a set number of weeks (mild = 1-2 weeks, moderate = 2+ weeks, etc).

The current paradigm and recovery is not based on a pre-ordained amount of time but rather dictated by symptom resolution and introducing incremental activity, without exacerbating symptoms.

Timelines are far more individualized, variable, and based on objective testing.  They can be shorter, they can be longer – it all depends on how the individual responds.

Additionally, there is an emerging paradigm when it comes to concussion/MTBI & activity. The latest research on active recovery in concussion/MTBI shows that having some symptoms during incremental activity doesn’t negatively affect recovery.

What this means is that the brain may parallel other parts of the body in how it responds to progressive loading. For example, when rehabbing achilles tendonitis, there’s an acceptable range of pain (symptoms) during stepwise increases in activity and loading.  The brain may be similar.

This could result in return to play guidelines changing from “must stop if any symptoms appear” to “stopping is indicated by severity of symptoms”.

However, this research is relatively fresh and there are a lot of questions to be answered, such as:

  • Is this modified rest and activity beneficial for only certain patient profiles?
  • Which type of activity is best?
  • What is the acceptable level of of symptom provocation?
  • What is optimal timing and ratio of rest vs activity?

B. Concussion/MTBI Rehab

The good folks at the UPMC Sports Medicine Concussion Program have created 6 different categories/trajectories for sports-related concussion/MTBI.

These 6 categories are:

  1. cognitive/fatigue
  2. vestibular
  3. ocular
  4. post-traumatic migraine
  5. cervical
  6. anxiety/mood

This is a great infographic from their site:

karius concussion
Credit – UPMC

The point of these categories is to help identify the specific Karius concussion problems and symptoms which then informs treatment and recovery timelines.  If you can address the major contributing factors, then it may unlock and make treating everything else easier and more effective.

Once the Karius concussion has resolved and he has no symptoms, does he face any long-term risks?

VIII. Long-term implications

Generally, the brain’s greatest window of vulnerability is for the first 10-15 days after concussion/MTBI.

Based on what we talked about earlier with the brain’s initial energy crisis, that makes sense.  It’s like hurricane hitting a city while it’s still trying to recover from the last hurricane – naturally, there are exponential consequences.

Additionally, there’s something called “second impact syndrome”.  This is more theory than proof at this point, but it’s a situation in which the brain swells after experiencing a second concussion/MTBI while still recovering from the first one. This can lead to death within minutes.

All in all, the long-term consequences after one concussion/MTBI are unclear.  It continues to be an emerging sphere in research.  One study did find that a single incident of concussion/MTBI is present in 20-30% of people with Alzheimers/Parkinsons disease, compared to 8-10% of the normal group. However, there’s a lot more work to be done.

However, the effect of multiple concussions/MTBIs is becoming quite clear – crystal even. It’s been linked to the development of chronic traumatic encephalopathy (CTE) which can result in confusion, memory loss, aggression, depression, impulsiveness, and progressive dementia. CTE has come to light in the public eye in recent years due to high publicity NFL cases.

So for Karius, one concussion/MTBI may or may not lead to any long-term issues.  The key is treating his major symptoms right now, getting him back to full activity, continuing to check-in, and hoping he doesn’t suffer another concussion/MTBI like he did in the CL Final.

IX. All in All

All in all, the Karius concussion absolutely sucks and concussions/MTBIs in general suck.  His was made even worse by the timing of it and the events that took place afterwards – not just in-game but more so how he was skewered unfairly in the media and by fans alike.

The good news is that Loris Karius should make a 100% recovery and this high profile incident could be the final catalyst and impetus needed for UEFA and domestic leagues to implement better concussion/MTBI protocols.

Thanks for reading and until next time.

______________________________________________________________________

If you want the latest articles delivered straight to you, subscribe to the email list on the sidebar.

If you want to chat more with me and join the community, we have a facebook group and a Youtube channel.

If you’re interested in details on injury prevention and rehab, sports performance, stress management or want to set-up a free consult & injury screening, check out my clinical site – 3CB Performance.

If you’re interested in the latest NBA and NFL updates, check out ClutchPoints.

______________________________________________________________________

Please follow and like us:

Leave a Reply