With the new rules change being discussed, catchers will not be allowed to block home plate off from oncoming runners, and runners no longer allowed to target catchers, inspiring contact and a collision. If such events were to occur, they will be subject to disciplinary action; umpires will be able to review calls when there are questions of how a collision was provoked and whom by, the catcher or runner.
A source of contention for several years already, many have taken to the internet and other media sources to vocalize their displeasure with the vanquishing of home plate collisions and its effect on the tradition and culture of baseball. In spite of these few dissenters of the proposed changes, the change has been welcome by most, in particular, catchers, with the 'safety first' approach being taken lauded. A recent article by Amanda Rykoff, which includes quotes from a number of managers who were catchers, goes far in feeling the pulse of how the rule changes are being received, in particular with its role in prevent future injuries, especially concussions. While each of the managers expresses an understanding that not every injury at the plate can be prevented, they do all feel that the rule change can do more good than bad in preventing injuries and potentially prolonging careers.
Here at Camden Depot, we have already taken a cursory look at concussions, both in understanding its pathophysiology, as well as what steps are taken to treat concussions; we also have had a brief look at the player performances pre and post concussion for those who suffered one in 2013, with the results being inconclusive.
Let's now go back to those 20 concussions and look at how they happened. How many happened at the plate, if any? Of those suffering concussions, were they all catchers, or was it a mix of other positions and situations?
From the above chart, we have exactly half of the 2013 concussions happening via a foul tip to the catcher's mask, with the next most common cause of injury coming from being hit by a pitch during an at bat. For collisions you would expect at the plate during a close play -- a player-player collision -- only ten percent, or two in total, arose from this cause. Digging deeper and we find that neither of these two player-player collisions occurred at the plate; one came from outfielders colliding, while the other occurred when the baserunner hit his head on a middle infielder's knee trying to break up a play at second base.
Here is a further breakdown of 2013 concussions by position and course of injury:
| Position | N = | Concussion Source (N) |
|---|---|---|
| Catcher | 11 | Foul tip (10), Hit by pitch (1) |
| Infield | 5 | Hit by pitch (3), player-player collision (1), player-turf collision (1) |
| Outfield | 3 | Player-turf collision (2), Player-player collision (1) |
| Pitcher | 1 | Batted ball |
Focusing on catchers, we see those aforementioned foul tip inspired concussions, along with one hit by pitch during an at bat -- for those curious, that is Max Stassi of the Houston Astros. Looking across all positions, we only see two player-player collisions, none occurring at the plate.
Overall, we see an interesting disconnect in the 2013 data -- while preventing home plate collisions should absolutely be pursued from the catcher's health perspective, we don't see any tangible instances that could have been prevented were the rules change in place last season. In fact, a vast number of the concussions we see are simply unfortunate happenstance -- the foul tip, a pitch that gets away from a pitcher, even a slight misstep, causing a loss of balance -- and not the result of a premeditated, hard nosed play. That being said, safety is of the utmost importance and any way that injuries can be minimized must be pursued, neurological injury or otherwise, even if our selection biased laden retrospection shows us that concussions at home plate are perhaps better minimized by the improved safety of catcher's equipment. As such, any effort made to improve player health should be pursued, even if for some, the damage is already done.
In a similar vein and a similarly morbid conversation, the Winter Meetings also brought news pertaining to concussions and baseball neuroscience when it was reported that former outfielder Ryan Freel, who took his own life last December due to what many believed was a result of the effects of multiple collisions and concussions sustained, had suffered from chronic traumatic encephalopathy (CTE). Commonly diagnosed in football players post-mortem, it is believed that Freel is the first baseball player to be diagnosed with the still poorly understood disorder; the Boston University Center for the Study of Traumatic Encephalopathy and Sports Legacy Institute released their report that Freel was suffering from Stage II CTE the same day the MLB approved the rule changes regarding home plate collisions. While his Baseball Prospectus player card only reflects two concussions and 65 games lost due to these injuries, it is widely felt that Freel had sustained many more concussions, but had not sought treatment for them, which potentially prompted the cognitive, behavioral, and mood impairments that define CTE.
Briefly, CTE is a progressive neurodegenerative disorder marked by widespread accumulation of hyperphosphorylated tau (p-tau). p-tau is a specialized protein that helps provide structure to the brain; when it becomes hyperphosphorylated, its structure changes, causing neurofibrillary tangles. While most frequently seen in contact sports and in occupations exposed to explosive blast, CTE can occur when exposed to any form of repetitive brain trauma. While concussions are common in CTE, they do not fully explain or bear full responsibility for one developing CTE; being such a 'new' disorder with research only now beginning to be undertaken regarding its pathology, any causal interpretations of CTE should be done cautiously. In short, those with CTE have had a history concussions or other head trauma, but not everyone who has had a concussion will be diagnosed with CTE.
Caveats of correlation implying causation aside, symptomatically, CTE can cause concentration and memory problems as well as disorientation and confusion, dizziness, and headache. Erratic emotions can also transpire, with aggression and psychosis common with CTE. As CTE progresses, behavior issues increase in intensity and erraticism, with aggression and symptoms similar to those of Parkinson's disease. Cognitive abilities decrease, leading to a dementia with more Parkinson's symptoms, including speech and walking abnormalities. There is no cure for CTE and the symptoms cannot be stopped.
With respect to CTE staging, symptoms in stage I chronic traumatic encephalopathy include headache and loss of attention and concentration. Additional symptoms in stage II include depression, explosivity and short-term memory loss, as discussed regarding Freel. For stage III, executive dysfunction and cognitive impairment are present, with dementia, word-finding difficulty and aggression hallmarks of Stage IV CTE.
There is still much research needed to be performed, analyzed, and understood before we can truly understand the extent and long term issues at play in concussive injuries and CTE, in general, and as it relates to baseball injuries. As discussed, the new rules related to home plate collisions are a step in the right direction, but might take years to show any real results in regards to a drop in injuries, concussion or otherwise. If causes for concussion in 2013 are to be used as an example, concussions may not appreciably drop, given many of the concussions arising from unintentional and freak plays. However, with the news of Freel's CTE diagnosis and the knowledge of the man and his style of play potentially leading to his premature demise, anything that the game can do to take better care of their players on the field and 50 years from now should be pursued, given the severity of the symptoms seen in concussions and CTE.
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