My Brain Hurts: The Ben Roethlisberger Story
In an October game against the Atlanta Falcons, Pittsburgh Steelers quarterback Ben Roethlisberger was sandwiched between two oncoming defenders and fell motionless to the turf. Ben was carted off to the locker room, where he was diagnosed with a concussion. He did not return, and the Steelers proceeded to lose the game in overtime. Against the Oakland Raiders the following week, Ben threw four interceptions in a Steelers loss, leading many chagrined fans to wonder if he had recovered fully from his concussion. Could there be any truth to the possibility that the embarrassing loss to the lowly Raiders was a result of the beating taken by Ben’s brain a full week earlier? And for that matter, what the hell is a concussion, anyway?
Concussion, clinically known by the oxymoronic name “mild traumatic brain injury” (MTBI), occurs following a robust blow to the head and is characterized by dizziness, confusion, headaches, visual disturbances and possible slight amnesia. Also, a brief loss of consciousness often occurs, as anyone who’s played Mike Tyson’s Punch-out knows. As Ben no doubt explains at his dinner parties,a concussion is the result of a sudden transfer of kinetic energy that elicits diffuse structural stress in the brain.1 All concussions require a rapid deceleration or acceleration of the head, which compels the skull and brain to absorb the bulk of the force.2 As such, had the Falcons lineman instead shot an arrow through Ben’s head, concussion would not have occurred (the 15-yard penalty notwithstanding). Or, if his head was already flush against the turf at the moment of impact, the force would have been largely transferred to the ground (Newton’s third law), again likely preventing concussion. Typically, Roethlisberger’s brain floats in a protective stew of cerebral spinal fluid (CSF), cushioning his brain from banging into the skull as it sloshes around with each head movement. However, the rapid movement of his head caused by the blow slammed his brain into his skull, and another MTBI was born.
Ben’s concussion may have bruised his ego, but not his brain. In fact, concussion is distinguished from other brain injuries by the lack of gross structural damage—only minor shearing of nerve fibers and some capillary damage may occur.3 The negative effects of a concussion are due primarily to the effects of structural stresses on the normal functioning of brain cells (neurons). In a healthy brain, neurons communicate with each other through impulses that travel down the ‘axon’ (a tube-like extension of the cell), and subsequently trigger the release of neurotransmitters onto other neurons. This nerve impulse is actually a traveling wave of ions (primarily positively-charged sodium and potassium atoms) flowing into and out of the axon through tiny channels in the cell wall. When Ben was tackled and his brain slammed into his skull, the mechanical impact triggered a rapid depolarization (inward flow of positive ions) in Ben’s neurons in the region of impact4 that was due to disruptions in the neuronal membrane and the opening of a huge number of ion channels.
For a single neuron, depolarization itself is not harmful: it is a necessary part of neuronal signaling. Positively-charged sodium ions flow into the cell, which increases the cell’s internal voltage potential, and this in turn triggers voltage-gated channels which let positively-charged potassium ions flow out, thus returning the voltage potential to baseline. But in a concussion, the synchronous release of potassium ions from a multitude of neurons is problematic. A massive simultaneous depolarization event is followed by a diffuse suppression in neuronal activity termed “spreading depression”5 that propagates through the brain and may be the cause of any temporary loss of consciousness.6 Excessive extracellular potassium is usually taken up by surrounding glial cells,7 the brain’s custodial staff. However, much like the Steelers’ blockers, the glial cells are overwhelmed. Sodium-potassium pumps try desperately to return neurons to their resting state, necessitating high levels of adenosine triphosphate (ATP), the primary fuel that cells burn. The drastic need for ATP initiates a state of intense energy consumption in the brain,6 a problem that is compounded by concurrent decreases in cerebral blood flow (CBF), the reasons for which are not certain.8
Like New York City in a brown-out, the initial demand for energy triggered by the acute ionic imbalance places demands on compensatory systems, and this cascade of events impedes normal brain function. Low CBF means less oxygen is available, so neurons must turn to glucose as a metabolic source of ATP.9 The overloading of glucose metabolism creates an excess of lactate and thus a more acidic intracellular environment as well as producing alterations in the neuronal membrane and the blood-brain barrier.10 The depolarization also increases intracellular calcium beyond normal levels, impairing the ATP-producing mitochondria,11 and further escalating the energy problem. CBF typically remains low and Ca2+ levels remain high for several days following MTBI,6 putting Ben’s neurons at an increased vulnerability for impaired function or cell death. It is this neuronal energy crisis and intracellular dysfunction that impair neuronal signaling and account for the neurological glitches that accompanied his concussion.
Given time, and depending on the severity of the injury, the brain will recover on its own. Team physicians are responsible for determining this timing, based largely on signs of neuropsychological symptoms. Same-day return to play may occur if there is no loss of consciousness and all symptoms disappear within 15 minutes.12 Otherwise, assuming there is no apparent structural damage, at least several days of rest are required, allowing for a complete return to normal neurological and cognitive functioning. This period is highly variable--Chiefs quarterback Trent Green was sidelined for 8 games following concussion earlier this year. Roethlisberger was tested on a variety of reaction time cognitive tasks to ensure neurological recovery before receiving medical clearance to play against the Raiders.
There are conflicting reports on the extent of general long-term cognitive effects of concussion13,14 (remember, Big Ben’s pre-concussion intelligence must be taken into account). A small subset of individuals do suffer from post-concussion syndrome, which may include headaches, memory impairment, difficulty concentrating and depression– even 3 months and beyond after injury. A recent study has found an association between late-life memory trouble and the incidence of concussion as an athlete.15 Former NFL players that suffered from one or two concussions reported significantly more cognitive impairment than those that suffered none, and less than those who suffered three or more concussions. So we’ll see how well Ben is holding up in 30 years.
Are concussions in football preventable? Certainly not completely, but helmet improvements are an obvious start. You may remember a couple players in the mid-1980’s wearing the ProCap Eliminator, an extra cap that velcroed to the top of the usual helmet, which the manufacturer claimed would prevent concussions. These additions, however, were problematic for three reasons: (1) no scientific evidence that they actually worked, (2) outright ugliness, and (3) irony thicker than the padding (If you need to wear two helmets to do something, is it really a good idea to be doing it at all?). Practical solutions were instead put forward in the exciting conclusion of a 13-part report16 in Neurosurgery by the NFL’s MTBI Committee, formed in 1994 by commissioner Paul Tagliabue.17 Several improvements to helmet design resulted from this thorough assessment of concussive impacts18—namely, greater coverage of the head and more protective, energy-absorbing padding on the side and rear of the helmet. In addition, experiments with helmeted dummies prompted researchers to conclude that softer and thicker grades of vinyl nitrile could reduce concussions by 10-20% a year. Prohibitions on intentional helmet-to-helmet contact also came out of this study; the committee found that about 2/3 of concussions were caused by such blows,19 which now result in a 15-yard personal foul penalty. Other elements may play a role, such as the use of newer, softer turf.20 Mouthguards may be beneficial against upward blows to the head by decreasing acceleration and increasing effective distance between the mandible and the skull,21 though scientific evidence has yet to confirm this idea. No follow-up study is yet available to determine whether these changes have had any effect on the number of concussions in the NFL.
There is one other option that Roethlisberger might particularly like: alcohol. Research has shown that low doses of ethanol have neuroprotective characteristics with regards to minor brain trauma. Ethanol increases post-concussion CBF, diminishing the brain’s energy crisis that is so significant in concussive injuries.22 So maybe next time Big Ben should just down a couple of ice-cold Iron City beers before he takes the field. He might be less vulnerable to concussion, and he’ll have a ready-made excuse for throwing into triple coverage.
References
1. Cantu RC. 1992. Cerebral concussion in sport. Management and prevention. Sports Med. 14(1): 64-74.
2. Parkinson D. 1982. The biomechanics of concussion. Clin Neurosurg 29: 131-45.
3. Bailes JE, Cantu RC. 2001. Head injury in athletes. Neurosurgery. 48(1): 26-45.
4. Shaw NA. 2002. The neurophysiology of concussion. Prog Neurobiol. 67(4): 281-344.
6. Giza CC, Hovda DA. 2001. The neurometabolic cascade of concussion. J Athl Train. 36(3): 228-35.
12. Cantu RC. 1998. Return to play guidelines after a head injury. Clin Sports Med. 17(1): 45-60.
17. Tagliabue P. 2003. Tackling concussions in sports. Neurosurgery. 53(4): 796.
Sportsology
You probably didn’t learn about the scientific method in your junior high gym class, and not too many post-game interviews touch on quantum theory. But don’t be fooled: the athletic and scientific worlds are not such strange bedfellows. Boxing, for instance, is often called “the sweet science.” And no less an expert than Ted Williams, perhaps baseball’s greatest batter, described his craft in his book, The Science of Hitting. We turn our focus to this intriguing relationship here in Sportsology, where we endeavor to examine the world of sports with a scientific eye. Sportsology will explore athletic topics that you never knew you cared about, from the physics of the curveball to Olympic abstinence. We hope to arm you with knowledge to, at the very least, make you the most annoying person at the sports bar.