Concussions and depression: Yes, Virginia, there IS a connection.

Wade Belak, 1976-2011


It’s been a rough summer for hockey. The deaths of Derek Boogaard, Rick Rypien and Wade Belak have raised questions about the role of fighting in the NHL, and whether the NHL/NHLPA are doing enough to support players with mental health issues. I was astounded to find I was consistently finding people questioning the link between head injury and depression in the numerous news stories and blog posts on the subject.

The CBC recently published an interview with Dr. Robert Cantu, co-director of the Centre for the Study of Traumatic Encepholopathy at Boston University. Dr. Cantu (a neurosurgeon) explains that depression, anxiety and substance abuse are all common in athletes with CTE (chronic traumatic encephalopathy). He goes on to state something any rational person could have guessed – that NHL players have admitted to him that they’ve had concussive-type injuries far more frequently than they’ve actually reported to their coach or trainers.


In a truly spectacular show of idiocy, the CBC’s story received comments like these, questioning the head injury/depression link:


IMHO, hockey players kids are raised as prima donnas who are encouraged to win at atl costs. I find a lot of them to be incredibly immature. Scientists should be looking at their lifestyle first. I would think the depression came from excesses in lifestyle, and an immaturity with which they cannot cope with the stress related to that lifestyle.

– GordonRobertson

Nice try.
These tragedies likely have more to do with the moral conflict one would have to deal with after having been paid a large sum of money to inflict violence on others.
Once again nice try Dr. Cantu.
Obviously the NHL did a good shopping job. 

– Hihohum


Wow. So here we have the (apparently not uncommon) opinions that depression comes from lifestyle excess, immaturity, and moral conflict. No doubt GordonRobertson and Hihohum’s opinions are based on their extensive reading on traumatic brain injury.




Hell no, because they’re completely wrong. There are literally thousands of studies linking traumatic brain injury to depression, and not just in CTE (a condition so dramatic that it actually changes the gross appearance of the brain), but also in mild concussive injuries. Something that keeps coming up is the argument that correlation does not imply causation. Do the concussions actually result in depression, or do people who’ve had concussions just happen to also be depressed?


Yes, concussions can cause depression. 


Researchers at McGill’s Montreal Neurological Institute did a study using fMRI (functional MRI), a technology which looks at blood flow to specific areas of the brain as related to neural activity. Put simply, the more neural activity in an area, the more blood flow to that area. The McGill team examined athletes suffering from post-concussive syndrome both with and without depression, and compared them to athletes who had never been head injured.  None of the athletes studied had been diagnosed with depression prior to their injury.  The team found that the fMRI results on the depressed post-concussion athletes were very similar to those seen in people with major depressive disorder. Let’s make this crystal clear – after a concussion, athletes with no history of depression became depressed. Fancy brain imaging on these athletes looked like fancy brain imaging done on people with regular (non-head injury-related) depression. What’s truly scary is that the concussed athletes (both depressed and not depressed) were also found to have areas of grey matter loss in their brains. Let me say that again another way. The actual anatomy of their brains had changed.


Not convinced?


How about the 3rd International Conference on Concussion in Sport? In 2008 a group of neurologists, neurosurgeons and representatives from various hockey organizations sat down in Zurich and spent a long time discussing nothing but concussions. The idea was to produce a list of recommendations for the management of head-injured athletes that could be used by doctors, trainers, and other people involved in their care. The group encouraged evaluating head injured athletes for depression, as “Mental health issues (such as depression) have been reported as a long-term consequence of traumatic brain injury, including sports related concussion.” They also provide about 11 references for that statement, which you’re more than welcome to look up on your own.


The implications


It’s difficult to pin down an exact percentage of people with concussions who end up with depression as well. A review article published in 2001 suggests the number could be as high as 42%. Dr. Cantu’s experience, as well as that of anyone who is an athlete, who’s been around an athlete, or who’s ever spoken to an athlete tells us that a lot of concussions go unreported. The implication is also that there are a lot of athletes (in the NHL and elsewhere) who could be suffering from depression and other mental health problems.

The NHL/NHLPA Substance Abuse and Behavioural Health Program has come under fire in the wake of Boogaard, Rypien and Belak’s deaths. The suggestion is that not enough is being done to protect the well-being of NHL players and alumni. The NHL and NHLPA released a joint statement on September 1st addressing the deaths.



While the circumstances of each case are unique, these tragic events cannot be ignored. We are committed to examining, in detail, the factors that may have contributed to these events, and to determining whether concrete steps can be taken to enhance player welfare and minimize the likelihood of such events taking place. Our organizations are committed to a thorough evaluation of our existing assistance programs and practices and will make immediate modifications and improvements to the extent they are deemed warranted.

It is important to ensure that every reasonable step and precaution is taken to make NHL Players, and all members of the NHL family, aware of the vast resources available to them when they are in need of assistance. We want individuals to feel comfortable seeking help when they need help.


Obviously NHL players are either not “aware of the vast resources” or not “comfortable seeking help”. Whatever is currently being done can’t be enough if three players have (directly or indirectly, intentionally or not) killed themselves in under 5 months. Were Rypien and Belak’s depression issues linked to head injuries? Does it matter? Whether their depression was pre-existing or the result of an injury, it was real, and it killed them.

Having said that, knowing that depression is found in as many as 42% of people suffering head injuries, it behooves the NHL to find a way to reduce those injuries. Fighting has been named as a culprit, as has contact with the head, hits from behind, and I’d add poorly fitted helmets to the list. The NHL has made efforts to reduce injury with Rule 43 (checking from behind), but remains miles behind other hockey organizations. One of the few sane commenters on the CBC article noted that the most exciting hockey game they’d watched in recent memory was the 2010 USA-Canada Olympic gold medal game – a game played under IIHF rules, where hits to the head and fighting aren’t permitted.


Take-home points


Some concussions cause depression. Period. No, no, we don’t need to talk about it. The science is there.

Fighting for the sake of fighting (I’m looking at you, Matt Carkner and Colton Orr) has no place in an NHL interested in the well-being of its players. Rule changes need to be made to reduce the incidence of head injuries. Obviously the very nature of the game dictates that you can’t eliminate every injury. The point is to eliminate what you can. The IIHF, NCAA and Olympics all have more protective rules, and all have exciting hockey.

The NHL/NHLPA need to do more to ensure their players and alumni’s mental health and substance abuse needs are taken care of. Three deaths in less than five months should be an enormous wake up call – one that never should have happened.


The folks at puckscene are hosting the Wade Belak Memorial Charity Drive to benefit the Tourette Syndrome Clinic at Toronto Western Hospital, the charity he’d chosen to skate for on Battle of the Blades.

September 4-10 is National Suicide Prevention Week in the US. Your contribution can be as simple as educating yourself on the warning signs of depression and suicidality. Extensive resources can also be found at The Canadian Association for Suicide Prevention.



Jen-Kai Chen; Karen M. Johnston; Michael Petrides; Alain Ptito
Neural Substrates of Symptoms of Depression Following Concussion in Male Athletes With Persisting Postconcussion Symptoms
Arch Gen Psychiatry. 2008;65(1):81-89.

M Aubry; R Cantu; J Dvorak; K Johnston; P McCrory; W Meeuwisse; M Molloy
Consensus Statement on Concussion in Sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008
Br J Sports Med 2009;43:i76-i84.

Eugene Gourley; Jeffrey S. Kreutzer; Ronald T. Seel
The prevalence and symptom rates of depression after traumatic brain injury: a comprehensive examination
Brain Injury 2001; 15(7):563-576.

Is it October yet? Part 1: Ace Bailey

This is the first in a series of posts looking at historic hockey injuries, intended to keep me busy and you interested while we wait for October to get here.

The history was provided by Jen aka @NHLhistorygirl. Jen is a librarian and graduate student at the University of North Dakota in the last stage of her MA in history: writing her thesis on the 1972 Summit Series, media, and notions of national identity. 

The first all-star game: A benefit for Ace Bailey

The night of December 12, 1933 was just like any other game night at Boston Gardens. The Bruins had a two-man advantage. The Leafs sent Ace Bailey and Red Horner out as part of the penalty kill. Red checked Bruin Eddie Shore into the boards, picked up the puck, and headed for the Bruins net. Bailey moved into Horner’s defensive position near the blueline. It’s the last thing Bailey would remember about that night.

Shore mistook Bailey for Horner, and took Bailey’s feet out from under him.  In an era without helmets, this was a dangerous move on Shore’s part. Bailey hit the ice head first, and began convulsing.

While Bailey’s teammates gathered around and the Boston trainers frantically tended to him, Horner punched Shore, who also hit the ice, bleeding. In the stands, a fan taunted Bailey, calling him a diver. Leafs owner Conn Smythe punched the fan, knocking teeth loose.

Bailey was awake when they took him to the dressing room, where Shore asked his forgiveness.  Bailey replied, “It’s all part of the game,” before losing consciousness and falling into convulsions again.  He was transported to Audubon Hospital, where he was diagnosed with a fractured skull. By morning, his condition was critical due to cerebral hemorrhaging.

He was moved to City Hospital, where neurosurgeon Dr. Donald Munro operated to relieve the cranial pressure on two different occasions. After the second surgery, the doctor pronounced Bailey’s chances as “very slim” and a priest was called to give Bailey last rites.  His pulse was 160 and he had a fever of 106. Newspapers had an obituary written and waiting. Reportedly, Bailey’s nurses would slap his hand or his cheek if it appeared he was slipping away. They kept telling him his team was down two men and needed him.

His condition finally improved, though Bailey says he did not regain full consciousness for fifteen days. With his playing days over and a plate in his head, Bailey asked the league’s permission to suit up as a linesman. Worried that any hit may cause Bailey further serious damage, his request was denied and he served many years as an off-ice official for the Leafs.

Bailey and Shore

Ace Bailey suffered what’s obviously best described as a devastating head injury. It’s amazing that he lived, even more so when you consider this happened in 1933. Penicillin had just been discovered (but wasn’t in widespread clinical use yet), and the concepts of tracheal intubation (breathing tubes) and IV anesthesia for surgery were brand new.

It’s hard to say exactly what Bailey’s specific head injury was. As such, this can really only be a look at a condition he may have had. There’s really no way to know what actually happened. We know his head hit the ice, he seized, was briefly awake and lucid, seized again, then stayed unconscious for a long time. During that period he had intracranial bleeding requiring surgical intervention, and developed an extremely high temperature.

The description of Bailey’s lucid interval could suggest he suffered an epidural bleed, which is the result of torn arteries between the skull and the dura mater (the tough covering around the brain and spinal cord). This is an uncommon type of traumatic head bleed, but made headlines in 2009 when actress Natasha Richardson died two days after a head injury sustained while skiing. She initially refused EMS care, then after a few hours was rushed to hospital with head injury symptoms and later died.

The stereotypical textbook progression of loss of consciousness-lucid interval-loss of consciousness actually doesn’t happen in most epidural bleeds. Patients can lose consciousness (or not), and may wake up (or not). The thing about the lucid interval is that’s the classic wording healthcare providers associate with the injury (and it’s extraordinarily unlikely to see it in other head bleeds).

A theory on why this happens is that the impact of the initial injury causes a loss of consciousness (from which the patient awakes), and the lucid interval represents the bleeding taking time to affect the brain as it happens between the hard skull and the relatively unyielding dura. Of course it’s important to note that this is just a theory, and the lucid interval can be of varying duration – anywhere from seconds to hours.

Why did Ace seize?

Seizures happen when the neurons in your brain aren’t firing in the nice, orderly pattern they’re used to. Seizures can be the result of a seizure disorder (like epilepsy), or an insult to the brain (like trauma, stroke, lack of oxygen, etc). In Bailey’s case, the impact of his head on the ice would have caused a cascade of events that set him up for seizure.

When his skull hit the ice, it stopped. His brain stopped when it hit the inside of the skull. The brain is a delicate thing, and it doesn’t like sudden changes. Not only would an impact with the skull likely cause a contusion (bruise) on the brain, it could potentially cause another on the other side thanks to something called a coup-contrecoup injury (French for blow-counterblow). The brain hits the skull on the side of the impact, and then in essence bounces back and hits the skull on the opposite side, causing a second contusion. Now you’ve got two areas of pissed-off brain that could misfire and cause a seizure.



Current treatment for a head injury of this type would start with transport to a trauma center. Obviously the treatment would also include the basics of pre-hospital trauma care (which I’ll grossly oversimplify here): Management of the airway with intubation if necessary, spinal immobilization, and IV fluids to replace volume loss from bleeding.

On arrival at the ER, head injured patients are often placed into the ominous-sounding medically-induced coma, which is to say they’re sedated and intubated. There are a lot of reasons this is done – for the patient’s comfort (they’re in pain, and probably scared to death), to have complete control of the airway (there’s no better airway control than having a tube stuffed into it), and for the now-controversial practice of reducing their intracranial pressure (ICP) by hyperventilating them. As we learned in this post, carbon dioxide (CO2) causes the vessels in your head to dilate, which would increase the amount of blood in there, and thus increase pressure. If you force hyperventilation, more CO2 is exhaled, reducing blood flow and therefore ICP. Hyperventilation of head injuries is falling out of favour now, as studies have shown that it doesn’t improve outcomes, and in fact can lower brain perfusion (which is bad for obvious reasons). CT scans and x-rays determine the extent of the injuries, and the patient is given IV steroids to reduce brain swelling. The patient may receive anti-seizure medications whether they’re seizing or not (to stop or prevent a seizure).

At this point the smart kids take over (that would be the neurosurgeons) and decide what sort of surgical intervention is needed. In rare cases epidural bleeds can be managed non-surgically with just steroids and observation. More often, however, the blood that’s filling the space between the skull and dura has to be taken out.

Epidural hematoma - Big red arrow provided for those who are immune to the obvious

Assuming you’re in a trauma center with neurosurgery on staff (as opposed to asleep in their golf course home with a pager on the nightstand) the treatment is craniotomy, evacuation of the blood, and ligation of the artery that’s bleeding. Translation: Take off part of the skull, suck out the blood, find what’s bleeding and tie it off. The piece of the skull may go back on at this point, or it may get stored in a fridge in the hospital basement until they’re sure the brain is done swelling and they can put it back on. If you’re in some outlying hospital with no hope of a neurosurgeon for a while, studies have shown that drilling a burr hole in the skull at the injury site is a good bridge to definitive care (yes, I saw that episode of Medical Incredible too).

As far as Bailey goes, it’s hard (impossible) to say what the two surgical procedures that he had actually were.  He’s said to have had a plate in his head, which suggests fragments of his fractured skull were removed (hello, craniotomy) and replaced. Why did he have two surgeries? Good question. It’s possible the bleeding wasn’t controlled the first time, and it’s possible it was done as a staged procedure – the first surgery to take the skull fragments out, and the second to put in the plate.

Post-Surgical Complications

After his two procedures, Bailey developed a pulse of 160 and a fever of 106, neither of which is part of a healthy recovery. There are two possible reasons for these symptoms, both of which have catchy acronyms – SIRS and PAID.

SIRS – Systemic Inflammatory Response Syndrome

SIRS is basically whole-body inflammation. It can be a result of infection (as one might get from brain surgery in 1933), or non-infectious events (trauma, burns, severe allergic reactions, etc). In Bailey’s case it could have been either. SIRS manifests as a high heart rate, a very high or very low body temperature, rapid breathing, and a very high or very low white blood cell count (those are the ones that fight infection). SIRS is pretty common in both the medical/surgical and trauma ICUs. Generally it’s treated with symptomatic management and control (where possible) of the cause (i.e. antibiotics). In 1933 it would have been treated by cooling Bailey, and having nurses slap him to keep him from dying. Super hi tech, and apparently pretty effective.

PAID – Paroxysmal Autonomic Instability with Dystonia

PAID is a scary complication of severe head injuries where the body loses its ability to control the autonomic nervous system – that’s the one that does all the automatic things you don’t pay attention to. Things like controlling your body temperature, your heart rate, digestion, and sweating. Patients with PAID have episodes of elevations in pulse, respiratory rate, blood pressure and body temperature. They also have dystonia – episodes of rigidity or posturing (abnormal body movements in response to brain injury).

Decerebrate posturing - A very distinctive response to head injury

PAID is generally seen in low-functioning head-injured patients in the ICU and rehab setting. It’s treated with medications to manage the symptoms, including muscle relaxants, beta blockers to lower heart rate, anti-hypertensive medications, and more. PAID can persist for months in these patients, and those who have it generally have head injuries so severe that they rarely return to full function. PAID seems like the less likely of the two possibilities, mostly because Bailey was awake within about two weeks of the injury, and went on to lead an essentially normal life.

Ace Bailey suffered a significant head injury by 21st century standards. The fact that he did it in 1933, had serious complications, and lived a full life afterwards is frankly amazing. An injury like this is unlikely now given the mandated use of helmets, but as we’ve seen in all the players whose lives and careers have been permanently affected by concussion, it doesn’t take a broken skull to change things forever.

Of OxyContin and Alcohol

I was boredly scrolling through my Twitter feed this afternoon when this caught my eye:

The part about not mixing OxyContin and alcohol is absolutely right.  The part about how people with head injuries should never use it?  Not quite.  First of all, there’s a difference between an acute head injury and a concussion five months ago.  But I’m getting ahead of myself.  This was next:

What’s that link?  Why, it’s the oh-so-reputable drug fact sheet!  And here’s what the renowned world experts at had to say that apparently caught Steve’s eye:

Oxycodone should not be taken by anyone who:

– blah blah blah

– has a head injury

– blah blah blah

And then I think he stopped reading.  Yes, Derek Boogaard sustained a concussion on December 9th of last year.  No, the mix of taking oxycodone after having had a concussion five months ago didn’t cause his death.  What caused his death was a mixture of oxycodone and alcohol.

What is OxyContin?

OxyContin is the trade name for oxycodone, which is a synthetic opiate.

What are opiates?

You’ll often hear the terms opiate and opioid used interchangeably.  Technically opiates are natural derivatives of a certain type of poppy, and opioids are the class of drug that binds the opioid receptors in the body.  So opioids as a whole include the opiates (morphine, opium) and the synthetic and semi-synthetic derivatives (oxycodone, fentanyl, methadone, heroin).

What do they do?

Opioids bind to the opioid receptors, which are found in the nervous and GI systems.  These drugs are used for pain relief, cough suppression, diarrhea, sedation and to ease withdrawal from other drugs in the same class.

What’s the big deal?

Opioids have a lot of side effects – sedation, constipation, itching, etc.  Unfortunately, they also have a nasty habit of causing respiratory depression in larger doses or extremely potent forms.  Also unfortunately, someone who has been using opioids for a long time will establish a tolerance, meaning they require higher and higher doses to achieve the same effects.

Where do head injuries fit into this?

In Derek Boogaard’s case, they don’t.  He had a concussion five months ago – he was not dealing with an acute head injury.  The reason “head injured” people shouldn’t have opioids has to do with intracranial pressure (ICP), the potential for respiratory depression with these drugs, and the nasty connection between the two.  The reason I have “head injured” in quotes?  Because we’re talking about people with acute injuries.  Those are the people that will have increased ICP.  Remember there’s a finite amount of space in your head.  If your brain is injured it swells, and since there’s not much of anywhere to go, you get an increase in the pressure inside your skull.

Now remember back to middle school science.  When you breathe, you exchange carbon dioxide for oxygen.  So if you’re taking opioids to the point that you’ve depressed your respiratory drive, you won’t be exchanging gases adequately and you’ll have increased levels of carbon dioxide.

Still with me?

We’re moving on to bigger and badasser science.  Carbon dioxide causes vasodilation in the cerebral vasculature.  Put simply – too much CO2 causes the blood vessels in your brain to dilate.  If you’re head injured and already have or are at risk for increased ICP, the last thing you need is increased CO2.  You’ll have bigger vessels, which means more blood, which means more space occupied, which means even higher pressure.  You’ll be making a bad situation worse and risking your brain trying to find a pressure release, which involves trying to squeeze its way out of the bottom of your skull.  That’s called herniation, and that’s generally deadly.


– Head injury = increased pressure in your head (from bleeding or swelling).

– Lots of opioids = respiratory depression (shallow/slow breathing, or no breathing).

– Respiratory depression = too much CO2

– Too much CO2 = more pressure in your head.

– Not good.

The Boogaard connection

Derek Boogaard’s cause of death was said to be a mixture of alcohol and oxycodone.  There’s not a huge amount of research on the pharmacology/pathophysiology of mixing alcohol and opioids, but they’re both depressant medications and together they’re dangerous.  Some studies suggest that alcohol alters opioid metabolism, resulting in an effectively higher serum concentration, and thus greater effects.  Common sense suggests that if you take two substances that can knock you out, one of which can make you stop breathing, that you’ve got all the ingredients for a terrible outcome.

From a paramedic’s perspective:

Over the years I’ve seen a lot of overdoses that resulted in death.  Most of them were opioid overdoses, and very, very few of them were on purpose.  Heroin addicts with the needle still in their arm,  college kids that got hammered and took too many pills, chronic pain patients with a huge opioid tolerance that fell asleep and never woke up.  People on the street, people in million dollar houses, and people just like you and me.

Before we start judging Derek, we need to stop and realize just how easy (and common) this situation is.  We know he was trying to get help.  We also know from his family’s statement that he’d been dealing with pain for a very long time.  The suggestion that taking oxycodone five months after his concussion was what caused his death minimizes his struggle, and isn’t scientifically based in reality.

Derek Boogaard’s family has asked that donations be made to Defending The Blue Line, a Minnesota charity that helps military kids stay involved in hockey with equipment donations, camps, and grants to cover fees.  Donations may be made online or by mail:

Defending the Blue Line,

c/o Boogaard’s Booguardians Memorial Fund,

1206 N. Frontage Road Suite B, Hastings, MN 55033.

My heart aches for the Boogaard family.  All the best to them.

– Jo

Helmets: The NHL vs. Everyone Else (Part 2)

Part 1 of the helmet series dealt with rules in various hockey organizations.  Part 2 will deal with the equipment itself – How it works, and why it works best when worn properly.  I’m not just talking about helmets, but about all the equipment currently in use in the NHL that protects the head and face – the helmet, visor, and mouth guard.  Let’s begin with…

The Helmet

What’s its job?

The helmet’s job is to protect the head.  Although that’s obvious, it’s not immediately obvious that there are things the helmet is good at, and things it sucks at.  Helmets are good at preventing direct injuries  – things like pucks, sticks, skate blades or the ice causing an injury to the surface of the head.  Helmets are not good at preventing indirect injuries, i.e. concussions.  The reason is the science behind how a concussion happens.

A quick trip into concussions…

A concussion refers to a brain injury causing a change in brain function.  Concussions vary in severity from very mild (feeling momentarily dazed) to severe (career ending – intractable vomiting, vision changes, permanent changes in balance, etc).  Concussions can result from a direct blow to the head, or a sudden head movement due to forces acting elsewhere (like a bodycheck on a player who doesn’t see it coming).

The brain essentially “floats” (snugly) inside the skull in cerebrospinal fluid (aka CSF, the stuff that surrounds your brain and spinal cord).  When the skull suddenly changes direction/stops/starts, the brain has to do the same.  In normal day-to-day life there’s no problem – the brain rides happily around in your skull changing direction as you do.  When there’s a sudden force applied that’s strong enough to move the head, the brain is inclined to stay where it is – remember Newton’s laws of motion? An object in motion tends to stay in motion until an external force is applied to it.

Translation: The brain wants to keep going in its original direction until something stops it.

During a hit, that inclination to keep going puts traction on the so-called “anchor point” of the brain – the midbrain – home to a lot of very important stuff, including the nucleus of the oculomotor nerve (the op center of the nerve that controls most of your eye movements).  This is where the term “rotational force” that you’ve been hearing tossed around with relation to concussions comes in.  Basically the brain is rotating on a somewhat fixed point, and when that happens you get an interruption in normal function.  The brain isn’t fond of stretching, moving, rotating, or really doing much of anything but happily riding in your skull.  Honestly, the brain is a bit of a jerk that doesn’t like to be touched, has its feelings hurt easily, and doesn’t like to be consistent about recovery.

The brain hates rotating.

It should be fairly clear now why helmets aren’t great at protecting against concussions.  They aren’t completely useless – they spread the impact across a larger area and the foam liner absorbs some of the energy, but the fact is if you hit your head hard enough your brain will move in a way that isn’t good for it.

So what’s the solution?

First, wear the helmet properly.  As we learned in part 1 of this series, the IIHF, Hockey Canada and USA Hockey require that equipment be worn “…in the manner for which it is designed”.  In fact, the IIHF goes so far as to specify how the helmet should fit: “A helmet shall be worn so that the lower edge of the helmet is not more than one finger-width above the eyebrows, and there shall only be enough room between the strap and the chin to insert one finger.” Failure to wear equipment properly results in a misconduct.

Toews, seriously?

A helmet will do a player absolutely no good against any injury if it doesn’t stay on his head.  Shane Prince of the Ottawa 67s found that out the hard way March 11th after a hit from the Niagara Ice Dogs’ Tim Billingsley resulted in his helmet flying off and the back of his head hitting the ice.

Prince got off relatively easily with a mild concussion, and is expected to return to the ice for the OHL playoffs this weekend.

Second, wear a better helmet.  Until the mid/late 90s there were still a few players in the NHL wearing the practically useless Jofa 235 (Gretzky, I’m looking at you), a helmet that was about as protective as a toque with a chinstrap.  NHL rules now vaguely state players must wear an “approved” helmet, but unlike the rest of the world, don’t specify who has to do the approval.  Regardless, sanity prevails and NHL players are keeping the fine people at Reebok, Easton and Bauer in business.

The Messier Project, which is Mark Messier in association with Cascade Sports, have come out with the M11 helmet, which they state has been proven to distribute impact forces better than traditional helmets.  In addition, they’ve shown that the M11 helmets protect better in successive impacts than traditional helmets.  The helmet also has what they call the Pro-Fit System, a ratchet at the back of the helmet that snugs it under the occiput (that big bump on the back of your head) for a more accurate fit.  What truly sets the M11 apart is the so-called Seven Technology.

Seven Technology

Instead of being padded only with foam, the helmet has several plastic units each made up of seven small interconnected plastic tubes.  These units deform under force – they flatten out and then rebound to their original form.  This absorbs and displaces the energy of the impact, meaning it’s that much less the brain has to take care of.  The Messier Project offers a great animation of how the technology works that does a far better job of explaining it than I can.

I would totally wear this.

Early iterations of this helmet were poorly reviewed because it was considered bulky, unattractive, and was poorly vented, but the M11 in its current form reviews well.  The Messier Project is currently gathering data from teams using their helmet.  They claim to have nine NHL players currently wearing their helmet, interestingly mostly Anaheim Ducks.

Third, rule changes and/or better enforcement.  Ideally the best way to avoid a concussion is to avoid getting hit in the head, or getting hit elsewhere in a way that results in sudden acceleration/deceleration of the head.  Since this is NHL hockey and I’m not stupid, I know that’s not going to happen.  Don’t get me wrong – I love hockey and I’d hate to see it diluted down to something unrecognizable.  I don’t, however, love head injuries, and I get particularly bent out of shape at avoidable head injuries.  So from a medical point of view I think it’s fair to say that wearing good equipment properly is a positive step towards at the very least reducing concussion incidence (and hopefully severity).


– Jo

New NHL Concussion Guidelines: Let’s Get the Doctor Involved!

There can’t be a hockey discussion without a head injury discussion.  It’s no surprise that day one of NHL GM meetings in Boca Raton has already produced policy changes that aim to increase player safety and reduce injury.  Some of the changes will go into effect almost immediately, some will be implemented at the beginning of next season.  Commissioner Gary Bettman laid it out in five steps:

  1. Equipment changes – reduce the size without reducing the safety.
  2. Revise concussion management protocols – have a doctor (not a trainer) make immediate return to play decisions.
  3. Hold club and coach responsible for players with repeated offenses leading to supplemental discipline.
  4. Study changes to rinks that can improve player safety – implement short-term fixes now, get rid of seamless glass for next season.
  5. Establish a committee dedicated to continued study of the issue.

Can we talk about step 2?

Currently, players with suspected concussions are evaluated by the trainer, generally on the bench.  The trainer’s evaluation has two possible outcomes – no concussion suspected and the player returns to the game immediately, or there is a suspected concussion and the player is removed to the dressing room and evaluated by the team physician.  If the physician’s evaluation is suspicious for concussion, the NHL Protocol for Concussion Evaluation and Management kicks in and the player is kept out of play pending certain testing.  The length of time is determined by the patient’s performance on neuropsychological tests (be patient, we’ll get into what those are), and the team physician makes the ultimate decision as to when the player can return.

The current NHL protocols are stringent with regards to keeping players off the ice once they’ve had a concussion, but don’t go far enough to get them off the ice in the first place – a determined player could insist to the trainer that he’s fine and end up back on the next shift.

The new protocol requires that the player be evaluated by a physician if he exhibits any of the following:

  • Loss of consciousness
  • Motor incoordination/balance problems
  • Slow to get up following a hit to the head
  • Blank or vacant look
  • Disorientation
  • Clutching the head after a hit
  • Visible facial injury in combination with any of the above

The physician will perform the evaluation in “…a quiet place free from distraction” (i.e. not the bench), and will use a standardized assessment tool – the NHL SCAT 2 (sports concussion assessment tool).  After training the trainers and doctors in the specifics of the new concussion policy, Bettman stated he expects it to go into effect by the end of the week.

Neuropsychological testing?  What?

Neuropsychological testing is a way of determining if someone’s brain is working properly by testing their ability to answer questions and perform simple memory and physical tasks.  The roadside sobriety tests that cops perform are a great example of simple neuropsychological testing.

The big deal here is that players are going to be evaluated immediately using the SCAT 2, and not by being asked “Are you okay?  You good to go back out?”.  The SCAT 2 is a series of (neuropsychological) tests that was developed in 2008 at the 3rd International Conference on Concussion in Sport, and represents revisions to previous concussion assessment protocols.  The SCAT 2 was designed for use by physicians, athletic trainers and other medical professionals.  If you’d like to have a copy of your own, it’s available for free download.

The NHL is already using the SCAT 2 (as are the IIHF, FIFA, and several other big name sports organizations), but the bench is absolutely the wrong place to do it, and it likely wasn’t happening unless the trainer made the decision to pull the player for physician assessment.

What exactly is the SCAT 2?

SCAT 2 Explained

Symptom evaluation: The patient is asked if he has any of 22 different symptoms that you’d normally associate with a concussion (nausea, dizziness, headache, etc), and grades them on a scale of 0-6 (none to severe).  This assigns him a symptom severity score.

Cognitive and physical evaluation:

  • Number of symptoms (out of 22)
  • Physical signs: loss of consciousness or balance problem.
  • Glasgow coma scale: Measures the ability to properly verbalize, follow motor commands, and open one’s eyes.  This is a test commonly used on trauma patients to get a quick assessment of their overall level of consciousness.  This is also a gross simplification on my part.  Want to know more?
  • Maddocks’ questions: A set of questions related to the game at hand and recent sport-related events (Where are we playing? What period is it? What team did we play last?”) that provides another gross overview of orientation and mental status.
  • Cognitive evaluation: Includes orientation (Day, Date, Year, etc), immediate memory (give the player a list of words and ask him to repeat them back to you), concentration (give the player a list of numbers, have him repeat them back in reverse order; have the player say the months of the year in reverse order).

Balance testing:  The player is asked to close his eyes and is given three 20-second standing trials –  feet together, on one foot, and heel to toe.

Coordination testing:  The player is asked to sit with one arm outstretched to the side.  He’s then asked to bend at the elbow and touch his nose five times in quick succession.

More cognitive testing:  The player is asked to recall the list of words from earlier in the test.

On my best day I’m not convinced this is a test I could ace.  It should be pretty clear now why it’s essential that this be performed in a quiet area with no distractions.  The SCAT 2 assigns the player a score, which is actually not used to determine if he can return to play.  What it does do is provide a great way to keep track of the player’s deficits over serial tests (i.e. give the same test multiple times and track the scores over time).

Return to Play

The SCAT 2 gives a great outline of a protocol that could be used to determine when a player could get back on the ice.  First and foremost, it suggests that a player suspected of having a concussion should not return to play that same day (I’m looking at you, Crosby).  It goes on to recommend that the player gradually resumes activity over a period of days (weeks, months, never) based on what he’s capable of doing – any limitation by symptoms means activity levels don’t progress upwards.  The progression of activity would be:

  • Complete rest until symptom-free
  • Light aerobic exercise
  • Sport-specific exercise
  • Non-contact drills
  • Full-contact drills after medical clearance
  • Return to competition

The SCAT 2 and the NHL Protocol for Concussion Evaluation and Management leave plenty of room for the team physician to decide if the player is ready to get back in action.  That, of course is the art of medicine.  That’s also fodder for another huge debate – whether team doctors are looking out for the athlete’s best interests, the team’s interest in getting their player back on the ice, or the athlete’s insistence that he’s fine, Coach.  Just fine.

Feel free to have that discussion amongst yourselves. Until I’m a team doctor I won’t be making assumptions.

– Jo


Helmets: The NHL vs. Everyone Else (Part 1)

Part 1: Helmet Rules

Since 1979, NHL players have had to wear helmets.  Frankly, there hasn’t been much progression in their equipment policy since then.  The only thing the NHL has to say about helmets is the vaguely worded rule 9.5:

“All players of both teams shall wear a helmet of design, material and construction approved by the League at all times while participating in a game, either on the playing surface or the players’ or penalty benches.”

Okay, so what exactly is a League-approved helmet?  It’s not specified in the publicly-available NHL rules.  A very scientific process involving googling pictures of NHL players has determined that it’s basically anything CSA/ASTM certified.

Dude, seriously.  Speak English.  What’s CSA/ASTM?

The CSA (Canadian Standards Association) and the ASTM (American Society for Testing and Materials) are organizations that set standards for and do testing of hockey protective gear (among several thousand other things).  The helmet standards these organizations set cover the actual construction of the helmet (ie. it can’t be leather, although that would be an interesting look), shock absorption (sorry, Wayne — the Jofa won’t cut it), penetration (can a puck or stick get through it?), retention systems (straps), field of vision, and the markings required on the helmets (the stickers on the back that prove it’s an approved helmet).

Clearly the NHL specifies that players must wear helmets that are adequately safety tested.  The kicker is that they don’t specify how the helmets must be worn, like just about every other major hockey organization does.  When a helmet flies off, it’s likely because the player wasn’t wearing it correctly.  Properly adjusted helmet straps should keep your lid in place.

Let’s Compare Head and Face Protection Rules…

For the sake of ease, I’m going to compare the NHL, the IIHF, Hockey Canada and USA Hockey.  I won’t go into goalie requirements – that’s a different animal altogether.  I also won’t discuss adult rec leagues, as some may choose to follow Hockey Canada or USA Hockey rules, and some may not.  The collection of garbage equipment that hits the ice every Sunday in my league tells you everything you need to know.


  • Helmet: You have to wear an approved helmet while on the ice or on the bench.  No helmet required during warmups.
  • Visor:  Permitted but not mandatory.
  • Cage: Rule 9.6 actually prohibits “…pads or protectors made of metal.” but goes on to specify that “A mask or protector of a design approved by the League may be worn by a player who has sustained a facial injury”, like the visor combo Brad Stuart of the Red Wings has been wearing after suffering a broken jaw earlier this year.
  • Mouth guard: Not required, although many players wear one.  Many players also gross me (and Johan Franzen) out by chewing on them instead of wearing them properly.


  • Helmet: Required in the game and in warmups.  Fit is specified: “A helmet shall be worn so that the lower edge of the helmet is not more than one finger-width above the eyebrows, and there shall only be enough room between the strap and the chin to insert one finger.”
  • Visor/cage: Full face masks or visors are recommended for all players.  Women and players under 18 are required to wear a full face mask.  Players born after 1974 must wear a visor at minimum.
  • Mouth guard: Mandatory for players under age 20.

Hockey Canada:

  • Helmet: Required in the game and in warmups, with strap securely fastened.
  • Visor/cage: Under 18 and women — Full-face protection.  Over 18 — Visor.
  • Mouth guard:  Compulsory if you’re wearing a visor.

USA Hockey:

This warms my heart: “USA Hockey strongly recommends that all players and goalkeepers in all age classifications properly wear an internal mouthpiece, a HECC approved helmet and a HECC approved full facemask for all games and practices.”  FYI, HECC is another standards organization.

  • Helmet: Required in games, warmups and practices, with strap securely fastened.
  • Visor/cage: Full-face protection is required for all players below adult level.
  • Mouth guard: Required for females 19 and under, and in all players through midget level (including high school).

This is a good time to stop and point out that the IIHF, Hockey Canada and USA Hockey require that equipment be worn “…in the manner for which is is designed” (IIHF) or the player can be given a misconduct.

The wrong way to wear a helmet. (photo: Andre Ringuette)

College Hockey (bonus section):

  • The NCAA requires full face masks and mouth guards (and helmets, obviously).
  • The CIS (Canadian Interuniversity Sport) requires a helmet and at minimum a half visor.  Mouthguards are mandatory with visors.

Obviously everyone is stricter than the NHL when it comes to face protection and equipment fit.  To an extent, head and facial protection is self-policed, in the sense that the players decide if they want to wear a visor, a mouth guard, etc.  There is absolutely no question that more protection leads to fewer injuries, and plenty of excellent research to prove it.  The question is why players who grew up in systems that require facial protection and properly-fitted equipment decide to take a step back once they’ve gone pro.  There are complaints of visibility problems, discomfort, etc., but if that’s what you grew up wearing, one would think you’d be used to it.  I’ll spare you the discussion of the visibility problems and discomfort caused by a stick or skate to the eye (see: Berard, Brian).

Next time I’ll get into the medical reasoning behind a properly-fitted, properly-worn helmet, facial protection, and mouth guards.  I’ll also discuss arguments for and against them, both reasonable and stupid.

– Jo