Manuscript Title:
Biomechanics of Subdural Hemorrhage in American Football
Names/Degrees of Coauthors:
Jonathan A. Forbes, M.D.1
Thomas J. Withrow, Ph.D.2
Erwin Yap, B.E1
Adib A. Abla, M.D.3
Joseph S. Cheng, M.D.1
Reid Thompson, M.D.1
Allen Sills, M.D.1
Department/Institution of Coauthors:
Department of Neurological Surgery1
Vanderbilt University Medical Center
Nashville, Tennessee, USA
Department of Mechanical Engineering2
Vanderbilt University
Nashville, Tennessee, USA
Department of Neurological Surgery3
Barrow Neurological Institute
Phoenix, Arizona, USA
Corresponding Author:
Jonathan A. Forbes
915 9th Avenue North
Nashville, TN 37208
Telephone: (615) 416.2801
Fax: (615) 343.8104
Email: jonathan.forbes@vanderbilt.edu
Reprint Requests:
Reid Thompson
Department of Neurological Surgery
1161 21st Avenue S., Rm. T4224 MCN
Vanderbilt University Medical Center
Nashville, TN 37232-2380
Key Words: biomechanics, subdural hemorrhage, American football, rotational,
translational, acceleration
Running Head: Biomechanics of SDH in American Football
Financial Support: N/A
Presentation Note: A portion of this work was presented on 21 August, 2010 at the
Annual Meeting of the Tennessee Neurosurgical Society in Memphis, TN
Conflict of Interest Statement: The authors have no conflict of interests to report.
Acknowledgements: The authors would like to thank Mark Kroenig B.E. for his
assistance with principles of engineering on this paper.
Disclosure: The authors report no conflicts of interest concerning the materials or
methods used in this study or the findings specified in this paper.
Abstract
BACKGROUND: Since 1945, over 350 American football players have died from
subdural hemorrhage (SDH) following helmeted collisions.
OBJECTIVE: To utilize a case illustration and discussion of the literature to
characterize the biomechanical factors associated with SDH following helmeted
collisions in American football.
METHODS: The English literature was reviewed in search of scholarly articles
describing the material properties of bridging veins (BVs), thresholds of
rotational/translational acceleration associated with BV rupture and SDH, and the
rotational/translational accelerations observed during peak impact conditions at all levels
of American football.
RESULTS: Cadaveric studies indicate that BV rupture occurs when the vessel is
stretched to approximately 150% of its resting length. Because accurate measurement of
tensile strain of BVs during helmeted impacts is not feasible, alternative parameters such
as head acceleration have been tracked. Previous studies have demonstrated rotational
acceleration (RA) to be a much greater risk factor for development of SDH than
translational acceleration (TA). Based on previous cadaveric studies, the threshold of RA
required to result in BV rupture for the average duration of a helmeted collision in the
NFL (15 ms) is thought to approximate 4,500-10,000 rad/s2. This figure overlaps with
RAs incurred during peak impact conditions in American football—in part, explaining
why approximately 6 catastrophic head injuries occur in high school and college level
football every year.
CONCLUSION: Modification of the current helmet quality assurance standard to
include limits on RA would be expected to decrease the present incidence of catastrophic
head injury at the high-school and collegiate levels in American football.
Introduction
Since the inception of the sport in 1869, American football players have suffered head
injuries related to the physical nature of the game. During the first 36 years American
football was played, 18 deaths were recorded1. In response to these injuries, President
Roosevelt called together members of academic institutions across the country to
reevaluate rules of the sport in 1905 and the American Football Rules Committee was
born2. Following this meeting and others like it, general knowledge about the state of
catastrophic injuries in the game of football has progressively advanced. Since 1931,
football-related deaths have been recorded annually3. Review of data collected from the
time period of 1945 to 1994 by Cantu et al. demonstrated subdural hemorrhage (SDH) to
be responsible for the majority of fatalities in American football. Specifically, 352 of 684
fatalities during this time period were secondary to SDH.
Equipment design in football has influenced the incidence of catastrophic injuries since
the sentinel years of the sport in the late 19th century. Helmet use became mandatory in
the NCAA in 1939 and the NFL in 19404. The introduction of plastic helmets in the late
1940s and the addition of the facemask in the 1950s afforded increased protection to the
head, but also led to unanticipated changes in behavior and/or technique—with initial
contact now more frequently being made with the helmet3. Consequently, the incidence
of brain-injury related fatalities peaked during the 5-year span from 1965 to 1969. In
response, the National Operating Committee on Standards for Athletic Equipment
(NOCSAE) was founded in 1969 and the first safety standards for helmets were
implemented in 1973. Under the auspices of NOCSAE, the NCAA set forth rules to
prevent the use of the crown of the helmet as the initial point of contact in 1975.
Standards regarding the energy attenuating properties of helmets were expanded to
college football in 1978 and to high school football in 1980. Certification of helmets by
NOCSAE soon after the new standards were implemented resulted in a 50% decrease in
the severity index (SI) score—a measure of translational acceleration of the head in
response to fixed impact parameters5—in comparison to the era prior to helmet
certification. As a result of these actions, the incidence of brain-injury related deaths
during the five-year period from 1985 to 1989 decreased approximately 79% when
compared to the period of time from 1965 to 19693. At the present time, all high school
and college football players wear helmets meeting NOCSAE standards.
Despite initial hope that regulatory changes and technological advances would eliminate
catastrophic head injury entirely, the decrease in brain-injury related fatalities in
American football realized after the creation of NOCSAE appears to have largely
plateaued. While the 5-year period from 1990 to 1994 was the safest in the 20th century
with a total of 9 brain-injury related deaths, this number increased to 25 brain-injury
related fatalities—all secondary to SDH—from 1994 to 1999. In a separate review of
high school and collegiate football players, the incidence of catastrophic head injury from
2000-2002 (6/year) was similar to the incidence from 1990-2000 (7.2/year)6. 94% of the
catastrophic head injuries between 1990 and 2002 involved subdural hematoma.
As evidenced by the curious observation that the incidence of catastrophic head injury
appears to be approximately 3.3 times higher in high school athletes than college
athletes6, the occurrence of subdural hematoma in football is a multifactorial
phenomenon that relates to more than just the mass and velocity of the players involved.
Recent advances in the characterization of brain motion and vessel strain required for
SDH formation have improved our knowledge of this pathophysiologic entity.
Additionally, incremental advances in helmet assessment7-8 allow for precise
characterization of the rotational and translational accelerations that are reached with
standard and elite high school and collegiate level impact parameters. While reports of
SDH related to helmeted collisions in American football have been described in the
past,9,10 to the authors’ knowledge this report is the first to discuss the biomechanics of
SDH formation specifically as the concept relates to American football. The literature
regarding the incidence and biomechanics of this injury is reviewed and future measures
for prevention are discussed.
Case Illustration
History and Examination. A 17 year-old male initially presented to the Vanderbilt
Children’s Hospital Emergency Department (ED) approximately 60 hours following a
helmet-to-helmet collision at football practice that was negative for loss of consciousness.
The collision described by the patient occurred during a tackling drill in which he was
struck just to the left of midline at mid-facemask level while carrying the ball. The initial
contact was reportedly made with the crown of the opposing player’s helmet. Witness
reports indicated the struck player’s head snapped back in extension immediately
following the impact. When asked about previous collisions, the player responded that he
had suffered another high-impact collision as the striking player in a similar tackling drill
approximately 4 days prior to the second collision (6.5 days prior to presentation).
However, the patient denied any significant associated symptoms following the first
collision. There was no other reported history of head trauma in the preceding weeks.
During the initial 48-hour time period following the second collision, the patient
complained of a moderate to severe headache. When he awoke on the second day
following the collision, the headache had progressed in severity and was associated with
significant nausea. The pain progressively worsened throughout the day and his father
took him to the ED that evening. In the ED, a non-contrast CT scan of the head was
accomplished and demonstrated a subacute left frontoparietal subdural hematoma,
slightly hyperdense to cortex, measuring approximately 11 mm in widest thickness. 6 mm
of left to right midline shift was visible on the scan (Figure 1a). No underlying fracture of
the calvarium was present. Of note, evaluation of the bony windows demonstrated a focal
calvarial irregularity overlying the side of SDH (Figure 1b). Physical examination in the
ED demonstrated a healthy, neurologically intact adolescent male in moderate distress.
The patient stood approximately 1.83 meters tall and weighed 76 kilograms (6’0”, 168
pounds).
Figure 1. (A) Pre-operative CT imaging with soft-tissue windowing demonstrates a left subacute
frontoparietal subdural hematoma slightly hyperdense to cortex, measuring approximately 11 mm in widest
thickness with 6 mm of left to right midline shift. Arrow indicates the interface between brain and
hematoma. (B) Pre-operative CT imaging with bone windowing reveals a small focal calvarial irregularity
overlying the SDH (indicated by arrow). (C) CT imaging of the head with soft-tissue windowing status post
craniotomy for evacuation.
Hospital Course. The patient was admitted to the Pediatric Intensive Care Unit (PICU),
where his headache and nausea initially improved with medication. The plan tentatively
set forth at that time was to attempt to await clot liquefication and proceed with burr hole
drainage in 10-14 days time to avoid the morbidity of a craniotomy. He was observed
overnight with serial neurological examinations. The patient’s headaches continued to
worsen on hospital day 1, however, and the decision was made to proceed with
craniotomy for evacuation of clot on hospital day 2.
Operation. The patient was taken to the neurosurgical operating room and, after induction
of general anesthesia, was placed in the Mayfield head holder with his head turned
approximately 20 degrees to the right. After reviewing clot morphology on CT imaging, a
reverse question mark flap was turned just beginning anterior to the tragus and then
sweeping around the temporal region, the parietal area, and forward toward the edge of
the hairline. The operation proceeded in standard fashion and an oval-shaped craniotomy
measuring approximately 15 cm in the A-P dimension was performed. Upon opening the
dura, a jet of subacute blood under significant pressure was encountered. The remaining
portion of the dura was then opened to expose the entire clot. While removing the
hematoma, an area of venous bleeding involving a bridging vessel along the parasagittal,
posterior frontal region was identified. This site was felt to represent the source of the
subdural and was cauterized with bipolar electrocautery. Of interest, the subdural
hematoma had tracked into the sylvian fissure, dissecting a portion of the fissure. The
remainder of the clot was evacuated, and the wound was irrigated and closed in the
standard fashion following replacement of the bone flap.
Post-operative Course. Post-operative CT scan (Figure 1c) demonstrated evacuation of
the clot. The patient did well following the procedure and was discharged home on postoperative day 2. He was seen in follow-up 6 weeks following the procedure, where he
was noted to be neurologically intact and without complaint. The patient was counseled
not to return to the football field and stated his desire to take up the sport of tennis at this
time.
Discussion of Scientific Principles
1. Relative motion that develops between the brain and skull results in the
development of tensile stress on intervening bridging veins.
Helmeted collisions result in abrupt changes in the velocity of the head. The helmet itself
distributes the applied force over a surface area estimated to be approximately 10 times
greater than the surface area of contact in unhelmeted collisions11. A foam layer that rests
in between the hard outer shell and the player’s head absorbs energy during compression.
In addition to shock-absorption, the intervening layer of foam helps to prolong the
duration of the impulse of the collision. The energy-attenuating properties of modern
helmets are exemplified by one recent study of 50 low to mid-velocity (impact velocities
ranging from 2 to 5 m/s) helmet to helmet impacts in a laboratory setting; in this study,
linear acceleration of the helmet was approximately 16.6 times greater than linear
acceleration of the center of gravity of the head12. At higher impact velocities, the foam
padding bottoms out and head acceleration increases significantly7. Energy that is
transferred during helmeted collisions results in relative deceleration of the cranium and
its internal structures. Previous studies have noted CSF to be approximately 4% more
dense than brain tissue13. As the head decelerates in a helmeted collision, the denser CSF
gravitates towards the site of impact with concomitant displacement of the brain in the
opposite direction14. The relative motion that develops between the brain and skull results
in tensile stress on intervening veins that traverse the subarachnoid and subdural space to
drain in the intracranial venous sinuses. Stress on these tissues is defined as force divided
by the cross sectional area to which the force is applied.
These stresses often result in some degree of elongation of the vessels. The measured
deformation in the length of the bridging vein (BV) in response to the tensile stress
applied is termed strain.
At lower tensile stresses, the BVs deform elastically and return to their original
dimensions when the applied stress is removed. At higher tensile stresses, the BVs
undergo plastic deformation (e.g., deformation which becomes irreversible in nature).
Further increases in the amount of tensile stress applied eventuate in vessel rupture. The
stress/strain thresholds for plastic deformation are referred to as the yield stress/strain.
The stress/strain thresholds for vessel rupture are referred to as the ultimate stress/strain.
Individual anatomic characteristics, including the angle of the superior sagittal sinus
(SSS)-BV complex involved, and impact direction have been found to influence the
susceptibility of these vessels to rupture15. In a finite element analysis by Huang et al.,
BVs that drained forward into the SSS at 60 degrees from the sagittal plane were
subjected to the greatest strain during an occipital impact. In a cadaveric study by Oka et
al., the angles of SSS-BV intersections were found to vary with anteroposterior location;
specifically, veins arising within 5 mm of the frontal pole were directed posterior with an
average angle of intersection of 110 degrees from the sagittal plane—these BVs drained
in line with the direction of flow through the SSS16. Veins of the intermediate frontal lobe
drained into the SSS at approximately right angles and all veins posterior to this location
were found to drain anteriorly into the SSS (against direction of flow) with angles
ranging from 10 to 85 degrees from the sagittal plane. Thus, the specific location of BV
rupture appears to be related to the direction of impact. In traumatic settings, a proclivity
for BV rupture to occur in the subdural portion of the vein has been observed. This has
been hypothesized to occur because of a relative increased in the fragility of the BV wall
in the subdural region when compared to the subarachnoid portion17.
The material properties of BVs have been analyzed using cadaveric models (see Table 1).
In these studies, irreversible deformation of BVs was documented with yield strains of
18-29%. Vessel rupture occurred with ultimate strains of 25-53%18,19,20. It is worth noting
that phenomena such as postmortem proteolysis and preconditioning can affect the
clinical applicability of cadaveric data21. However, recent studies indicate the ultimate
strain of fresh small vessel cadaveric specimens to be only slightly lower than
comparable vessels obtained during surgical procedures19. Given that samples obtained
soon after death more closely mimic the material properties of in vivo vessels, it is likely
that the figures obtained by Monson et al. and Lee and Haut et al., which utilized fresh
cadavers less than 2 days post-mortem and indicated an ultimate strain of 50-53%, are
more accurate than the study by Delye et al.—which reported relatively higher stresses
and lower strains associated with vessel rupture in much older cadaver specimens than
the aforementioned two studies.
Model
Study
Cadaveric/Fresh
(<2d*)
Cadaveric/Fresh
(<2d*)
Lee and Haut et al.,
1989
Monson et al.,
2005
Cadaveric (5d^)
Delye, et al., 2006
Ultimate
Stress (MPa)
Ultimate
Strain
Yield Stress
(MPa)
Yield Strain
Young’s
Modulus
3.33
53%
NR
NR
NR
1.32
50%
1.15
29%
6.43
4.99
25%
4.13
18%
30.69
Table1: This table is a summary of previous studies attempting to define threshold of superior sagittal
sinus-BV failure in terms of stress and strain. NR: not recorded, MPa: megapascal. Young’s modulus is
equal to tensile stress divided by tensile strain (i.e., [force/area]/[change in length/length]).*Specimens
were obtained less than 2 days post-mortem. ^Published post-mortem interval was 5 days.
2. Subdural hemorrhage at impact conditions in American football relates to
dangerous levels of rotational acceleration.
Because accurate measurement of vessel strain is difficult to obtain in in vivo models of
helmeted collisions, related input variables (e.g., translational and rotational acceleration)
have been used as surrogate parameters to describe the pattern of energy transfer in these
settings. Head motion in any helmeted collision can be broken down into elements of
translational and rotational acceleration. In seeking to determine whether a force will
result in rotational acceleration, translational acceleration, or both, it is useful to consider
where the force is applied and how the object subjected to the force is confined. If an
object is not confined and the force is applied through the center of gravity, the object
then experiences pure translational acceleration. If the object is confined to a point or
“pivot”, the object experiences pure rotational acceleration when subjected to a force
orthogonal to the axis of rotation. If the object is not confined and a force is applied at
some distance from the center of gravity, the object experiences translational acceleration
in addition to rotational acceleration about the center of gravity.
Relatively speaking, a much greater degree of translational acceleration (TA) is required
to produce BV rupture and SDH than rotational acceleration (RA)15. The risk of subdural
hematoma formation has been found to be proportional to both the amount of RA
incurred and the duration of the collision22. Cadaveric studies indicate that the critical
threshold of RA, above which risk of BV rupture and SDH formation becomes
appreciable, approximates 4,500-10,000 rad/s2 (see Table 2) 15,22-25. It is also worth noting
that the duration of the collision appears to affect the amount of RA that can be tolerated.
In the study by Lowenhielm et al., 4,500 rad/s2 was proposed as the critical RA for BV
rupture in collisions ranging from 15-44 msec. In contrast, the study by Depreitere et al.
described a critical value of 10,000 rad/s2 for collisions lasting under 10 msec. The
average duration of high-impact NFL collisions approximates 15 msec26, placing the
theoretical critical threshold for RA somewhere in between these two figures. It does not
escape attention that cadaveric specimens used in these studies are much older (average
age of 79.2 in Depreitere’s study) than subjects playing high school, collegiate, and
professional football. The advanced age of these specimens would indicate a much
greater degree of underlying cerebral atrophy. This, in turn, would be expected to lead to
a hypothetical increase in the relative motion between brain and skull14. Thus, the
threshold for RA obtained from the available cadaveric data might be expected to be
lower than the true RA threshold for BV rupture in American football players. In addition
to the direction, duration, and relative acceleration of the collision, many other
underlying factors specific to the patient—including intracranial anatomy (e.g., degree of
cerebral atrophy, presence/absence of arachnoid cyst, orientation of SSS-BV complex),
relative fragility of the vessel wall, and coagulation status—can influence the risk of
SDH22.
Model
Human
Animal
Study
Proposed
Critical RA for
SDH (rad/s2 )
Proposed
Critical TA
for SDH (g)
Impulse
Duration
(msec)
Finite element analysis
vs. Cadaver Study vs.
Animal Study
Site of Impact
Lowenhielm
et. al, 1974
Huang et. al,
1999
Depreitere et.
al, 2006
4,500
n/a
15-44
Cadaver study
Occipital
71,200
3,913
3.5
Finite element analysis
(humans)
Occipital
10,000
n/a
<10
Cadaver study
Occipital
Gennarelli et.
al, 1982
100,000
*
4
Animal study
Frontal
Table 2: This table is a summary of previous studies attempting to define the threshold of rotational
acceleration for development of subdural hematoma. g: gravity, msec: milliseconds. * = paper stated that
purely translational motions cannot induce acute SDHs. Cadaveric human studies are shaded white, finite
elment analysis and animal study are shaded grey.
3. The lower effective mass of the struck player in comparison to the striking
player leads to greater rotational acceleration of intracranial structures and an
increased risk of subdural hemorrhage.
When discussing the biomechanics of helmeted collisions in American football, the
concept of effective masses of the struck and striking players warrants discussion.
Immediately prior to the collision, the striking player anticipates the blow and aligns his
head, neck, and torso to maximize effective mass for impact. In contrast, the struck player
is often at a disadvantage in his ability to anticipate the collision. This disadvantage
translates to a lower effective mass, on average, than the striking player; in a
reconstruction of 25 NFL impacts that resulted in concussion by Viano et al., the striking
player had, on average, an effective mass 67% greater than that of the struck player.
Recalling Newton’s 3rd law, the players involved in the collision exert forces on one
another that are equal and opposite direction. Applying Newton’s 2nd law (force = mass ∙
acceleration), the lower effective mass of the struck player results in greater values of
rotational and translational acceleration27.
In any collision, momentum of a body is characterized by mass of that body multiplied by
velocity. The change in momentum of a body in a collision is a quantity known as
impulse and is equal to the mass of a body multiplied by the change in velocity. Impulse
is also equivalent to impact force integrated over time. In an example where a player runs
down the field, is struck, and falls to the ground with a final velocity of zero, the change
of momentum that player experiences is a negative quantity equal to mass multiplied by
his initial velocity. Simplifying this scenario to involve a standard force that does not
change throughout the collision, this quantity is equivalent to the incident force applied
times the duration of time in which it is applied.
Another way of interpreting this equation is that by increasing the duration of the
collision, the incident force that is applied to the player in question can be decreased.
After calculation of the average incident force using the knowledge of the change in
momentum and duration of the collision, one is able to estimate the average amount of
TA experienced during the collision.
If there is rotation about an axis in a collision, it is then possible to calculate the
instantaneous RA with knowledge of the tangential TA and the distance from force
application to axis of rotation (e.g., lever arm).
4. The following variables increase rotational acceleration in a collision:
increases in impact force, decreases in rotational stiffness of the neck, and
increases in length of the lever arm.
To help understand rotational acceleration, it is helpful to review the additional concepts
of moment and rotational stiffness. Moment is a term synonymous with torque that is
equivalent to the applied force multiplied by the length of the lever arm. In a helmeted
collision, the moment is equal to the orthogonal component of the impact force exerted
by one player on the other multiplied by the distance from the site of impact to the axis of
rotation. Greater impact forces and larger moment arms lead to greater moments. As the
moment increases, so does the rotational acceleration of an object about a given axis.
Rotational stiffness is defined as the resistance of an object to deformation and varies
with material composition and structure. Alternatively, rotational stiffness can be thought
of the relationship in a particular setting between change in torque and change in angle.
In the setting of a helmeted collision with a fixed moment, as rotational stiffness of the
neck increases, angular displacement and rotational acceleration decrease.
The previous cadaveric studies listed in Table 2 analyzed the risk of BV rupture
following cranial rotation about the y-axis (e.g., flexion or extension of the cervical
spine). Moreover, witness reports indicate that the player described in the aforementioned
case illustration suffered significant rotational acceleration injury in extension of the
cervical spine. Thus, rotational acceleration about the y-axis is chosen for further
discussion. The standard published values for range of motion of the cervical spine
include approximately 70 degrees of extension starting from neutral position28. Some
proportion of this motion involves the atlanto-occipital junction—which is able to
accommodate approximately 15 to 20 degrees from flexion to maximal extension29. The
degree of sagittal motion increases from approximately 10 to 15 degrees per level from
C1-C3 to 15-25 degrees per level in the subaxial cervical spine30. Previous biomechanical
studies have demonstrated that extension is often initiated in the subaxial cervical spine
before progressing to involve the occiput-C1 and C1-2 articulations. This pattern of
extension may relate to the greater rotational stiffness ascribed to the O-C1 and C1-C2
articulations in comparison to the C2-C7 segments31. While an intricate discussion of the
biomechanics of extension of the cervical spine and calculation of the moment arm in
helmeted collisions is beyond the scope of this report, it is notable that the increased
moment arm and decreased rotational stiffness associated with extension about the
articulations of the subaxial cervical spine contributes disproportionately more to moment
and rotational acceleration than extension at the craniocervical junction. An increase in
the rotational stiffness at these levels (e.g., possibly achieved with strengthening
exercises targeting cervical musculature limiting extension) would be expected to result
in significant decreases in rotational acceleration secondary to impact.
The aforementioned concepts are depicted in the middle panel in a simulated collision in
Figure 2. Two points of rotation about the y-axis, involving extension at the O-C1 and
C5-6 articulations, are chosen to illustrate the relatively larger contribution of subaxial
cervical extension to RA. While previous considerations of the average effective mass of
the struck player have involved the mass of the head (4.38 kg), helmet (1.92 kg), neck
(1.06 kg) and a portion of the torso (1.04 kg)26, the center of gravity of the head itself—
previously reported to be approximately 20 mm above the center of the ears, just above
the eyes32—was chosen as the center of gravity of the effective mass of the struck player
in this example. The distance from this center of gravity to the assumed centers of
rotation at O-C1 and C5-C6 can be approximated at 7 cm and 17 cm, respectively33.
Reflexive muscular contraction often occurs approximately 60 milliseconds following
impact34. Consequently, without anticipation of the collision, the struck player exhibits a
compromised degree of muscular tone of the neck with concomitant decreased rotational
stiffness at time of impact. Rapid extension of the struck player’s cervical spine is
depicted by still photographs of another collision in high-school football in the top panel
of Figure 2. These photographs, taken from video footage at approximately 0, 10, 20, and
30 milliseconds following impact, illustrate rotational acceleration of the struck player’s
helmet about the y-axis in cervical extension. Elongation of the bridging vessels as a
consequence of relative motion between the brain and skull secondary to rotational
acceleration is depicted in the bottom panel of Figure 2.
Figure 2: (Top panel) Rapid extension of the struck player’s cervical spine is depicted by still photographs
of a collision in high-school football illustrated (note: no video of the collision described in this case report
was available; still photos are courtesy of Magnolia High School, New Martinsville, WV). These
photographs, taken from video footage at approximately 0, 10, 20, and 30 milliseconds following impact,
illustrate rotational acceleration of the struck player’s helmet about the y-axis in cervical extension.
(Middle panel) The impact force of the collision, the moment arm of rotation, the moment itself, and
rotational stiffness are illustrated in the middle panel. (Lower panel) The relationship between skull, brain,
and intervening bridging vein is illustrated. Elongation of the bridging vein with rupture as a consequence
of relative motion between the brain and skull secondary to rotational acceleration is depicted.
5. Values of rotational acceleration reached in peak impact conditions in
American football overlap with values of rotational acceleration potentially able
to result in BV rupture and SDH in cadaveric studies.
Referring to Table 2, the hypothetical values of TA required for BV rupture and SDH
formation are exceptionally high24 and have not been encountered even in elite level
impacts in the NFL. Accordingly, SDH formation in helmeted collisions is hypothesized
to relate to dangerous levels of RA. Review of the literature32,35,36 (Table 3) indicates that
RAs reached in peak impact conditions in professional football games result in significant
overlap with values of RA (4,500-10,000 rad/s2) previously discussed as able to result in
BV rupture and SDH formation in cadaveric studies (Table 2). In laboratory experiments
meant to simulate elite level impact conditions in the NFL, rotational accelerations
greater than 15,000 rad/s2 have been observed7.While the parameter of RA has not been
specifically assessed in high school and college impacts, comparable linear accelerations
reached in high-energy impacts at these levels indicate that overlap with the critical RA
of BV rupture may also present. This consideration explains, in part, why a significant
number of subdural hematomas occur as a result of helmeted collisions in high-school
football every year.
Level
Measurement
Study
Translational
Acceleration (g)
Rotational
Acceleration
(rad/s2 )
High School
Top 1% of Impacts
Schnebel et al., 2007
114.5g
NA
College
Top 1% of Impacts
Schnebel et al., 2007
127.8g
NA
Average Impact
Duma et al., 2005
32g
2,213
Average Concussion
Pellman et. al, part II
97.8g
6,432
Average Concussion + 1
standard deviation
Pellman et. al, part II
125.5g
8,245
Professional
Table 3: This table is a summary of the peak rotational and translational accelerations commonly
encountered by football player at the high school, collegiate, and professional levels. Accelerations for the
top 1% of measured collisions and average collisions are listed for high-school and collegiate levels.
Accelerations for average concussion of average concussion plus one standard deviation are listed for
professional football players.
6. The incidence of catastrophic head injury in American football should not be
expected to decrease without quality safeguards in limiting dangerous levels of
rotational acceleration.
Recent studies have done much to elucidate the important role of translational
acceleration in risk of concussion26,37. Pellman et al. has suggested that translational
acceleration should be the primary measure for assessment of performance of helmets
and that the added complexity of measuring RA may not be justified37. The authors feel
that this approach, while appropriate for reduction of concussive brain injury, fails to take
into consideration the strong association between RA and BV rupture with SDH
formation in helmeted collisions. Furthermore, as helmet manufactures continue to
increase the thickness of helmets in attempts to increase energy attenuation, there is a real
possibility that resultant increases in the moment arm in attempts to decrease TA8 might
unintentionally stabilize or possibly even worsen RA. A concerted effort to characterize
the true threshold of RA involved in SDH formation in young athletes and collaborate
with the helmet industry to lower impact RAs below this threshold would be
hypothesized to drastically lower and possibly even eradicate the incidence of
catastrophic head injuries in high school and collegiate football players.
Practical Considerations
As was previously mentioned, despite lower mass, lower impact velocity, and lower
impact acceleration, high-school football players have an incidence of catastrophic head
injury that is 3.3 times of college football players. Possibly etiologies for this disparity
are hypothetical. To the authors’ knowledge, peak-impact RAs have not been
systematically studied in a cohort of high-school football players. RAs in this population
might be higher than expected for a number of reasons. In laboratory reconstructions of
NFL collisions performed by Viano et al., decreased neck rotational stiffness resulted in
increases in peak head acceleration and changes in velocity. This has been thought to
translate to a relatively higher risk of helmeted injury in women and young athletes26—
populations shown to have weaker neck muscles than adult males38. However, studies
contrasting TAs experienced by high-school and collegiate athletes35 have noted that
mean linear accelerations of peak impacts were significantly higher in collegiate athletes
than with high-school athletes. Relatively weaker neck musculature would be expected to
yield proportional increases in both TA, as well as RA—thus indicating that this variable
may be less of a factor. Regardless, neck strengthening exercises would be expected to
help increase rotational stiffness, decrease impact acceleration, and lessen the risk of
helmeted injury.
Other possible causes behind the increased incidence of catastrophic head injury in highschool athletes include the increased raw number of impacts observed per player per
game at the high-school level35. This is thought to relate to larger percentage of highschool players that play “both ways”—on both offense and defense. An increase in the
number of high-energy collisions would been hypothesized to alter the material
properties of BVs subjected to tensile strain with associated alteration of the stress-strain
curve and possibly predispose to BV rupture with future high-level impacts22. This would
help explain an increased incidence of SDH formation despite lower overall average head
accelerations. In addition to possible alterations in the material properties of BVs, an
increased number of blows to the head can also result in a state of “grogginess” in which
neck muscle tone is reduced and ongoing collisions are often not anticipated properly26.
In a subgroup of athletes with this injury complex, head acceleration in response to future
collisions would be expected to increase.
One final proposed root cause of the increased incidence of catastrophic head injuries in
high-school athletes relates to the decreased funding available at this level. The ability of
helmets to attenuate energy is central to prevention of underlying injury to intracranial
structures. Increased helmet wear can lead to a phenomenon of “pre-compression” in the
foam layer and a decrease in the properties of energy-attenuation39. A greater amount of
funding at the collegiate and professional levels allows for high-standards in the quality
of the equipment used. Recent investigations have brought the practice of equipment
certification at youth and high-school levels into the national spotlight40. A 2008 article in
the New York Times discussed one company responsible for helmet certification who
faced legal ramifications for improperly returning approximately 4,000 helmets to the be
used in play during the 2005-2006 season. Companies who are in appropriate compliance
with NOCSAE certification visually inspect all helmets for cracks and other evidence of
dysfunction. However, even these companies only test a minority of helmets examined
for the ability of the helmet and suspension to achieve appropriate energy attenuation.
Specifically, NOCSAE requirements mandate that approximately 2% of helmets be
subjected to direct assessment with standard drop testing to ensure that dangerous
translational accelerations are not realized40. Presently, there are no guidelines with
regards to limitation of rotational acceleration. Improvements in this real-world process
of helmet quality assurance represent another possible avenue to decreasing the risk of
catastrophic head injury in young American football players.
Conclusion
The authors report a case involving a 17 year-old male who presented with progressive
headache, nausea and vomiting 2.5 days after a severe helmeted football collision that
occurred during practice. CT scan revealed a subacute SDH with shift and the patient
required an open craniotomy for evacuation. Details of this case are used to highlight
many of the scientific and real-world principles associated with the risk of SDH
following helmeted collisions. Moreover, the strong association between rotational
acceleration and SDH formation in helmeted injury is emphasized. Modification of the
current NOCSAE helmet standard to include limits on rotational acceleration would be
expected to decrease the present incidence of catastrophic head injury at the high-school
and collegiate levels in American football.
References:
1.
Levy ML, Ozgur BM, Berry C, Aryan HE, Apuzzo ML: Analysis and evolution of head
injury in football. Neurosurgery 55(3): 649-655, 2004.
2.
Mendez CV, Hurley RA, Lassonde M, Zhang L, Taber KH: Mild traumatic brain injury:
neuroimaging of sports-related concussion. J Neuropsychiatry Clin Neurosci 17(3): 297303, 2005.
3.
Cantu RC, Mueller FO: Brain injury-related fatalities in American football, 1945-1999.
Neurosurgery 52(4): 846-852; discussion 852-853, 2003.
4.
Levy ML, Ozgur BM, Berry C, Aryan HE, Apuzzo ML: Birth and evolution of the football
helmet. Neurosurgery 55(3): 656-661; discussion 661-662, 2004.
5.
Pellman EJ, Viano DC: Concussion in Professional Football: Summary of the Research
Conducted by the National Football League's Committee on Mild Traumatic Brain Injury.
Neurosurg Focus 21(4), 2006.
6.
Boden BP, Tacchetti RL, Cantu RC, Knowles SB, Mueller FO: Catastrophic head injuries in
high school and college football players. Am J Sports Med 35(7):1075-81, 2007.
7.
Pellman EJ, Viano DC, Withnall C, Shewchenko N, Bir CA, Halstead PD: Concussion in
professional football: helmet testing to assess impact performance--part 11. Neurosurgery
58(1): 78-96; discussion 78-96, 2006.
8.
Viano DC, Pellman EJ, Withnall C, Shewchenko N. Concussion in professional football:
performance of newer helmets in reconstructed game impacts--Part 13. Neurosurgery
59(3):591-606; discussion 591-6062006.
9.
Kersey RD: Acute subdural hematoma after a reported mild concussion: a case report. J Athl
Train 33(3): 264-268, 1998.
10. Logan SM, Bell GW, Leonard JC: Acute Subdural Hematoma in a High School Football
Player After 2 Unreported Episodes of Head Trauma: A Case Report. J Athl Train 36(4):
433-436, 2001.
11. Gay, T. The physics of football.
12. Manoogian S, McNeely D, Duma S, Brolinson G, Greenwald R: Head acceleration is less
than 10 percent of helmet acceleration in football impacts. Biomed Sci Instrum 42: 383-388,
2006.
13. Gurdjian ES, Gurdjian ES: Cerebral contusions: reappraisal of the mechanism of their
development. J Trauma 1976; 16:35–51.
14. Drew LB, Drew WE: The contrecoup-coup phenomenon: a new understanding of the
mechanism of closed head injury. Neurocrit Care 1(3): 385-90, 2004.
15. Huang HM, Lee MC, Chiu WT, Chen CT, Lee SY: Three-dimensional finite element analysis
for subdural hematoma. J Trauma 47: 538–544, 1999.
16. Oka k, Rhoton AL, Barry M, Rodriguez R: Microsurgical anatomy of the superficial veins of
the cerebrum. Neurosurgery 17: 711-748, 1985.
17. Yamashima T, Friede RL: Why do BVs rupture into the virtual subdural space? J Neurol
Neurosurg Psych 47: 121–127, 1984.
18. Lee MC, Haut RC: Insensitivity of tensile failure properties of human BVs to strain rate:
implications in biomechanics of subdural hematoma. J Biomech 22(6-7): 537-42, 1989.
19. Monson KL, Goldsmith W, Barbaro NM, Manley GT: Significance of source and size in the
mechanical response of human cerebral blood vessels. J Biomech 38: 737–744, 2005.
20. Delye H, Goffin J, Verschueren P, Vander Sloten J, Van der Perre G, Alaerts H et al.:
Biomechanical properties of the superior sagittal sinus-BV complex. Stapp Car Crash J 50:
625-36, 2006.
21. Gefen A, Margulies SS: Are in vivo and in situ brain tissues mechanically similar? J
Biomech 37(9): 1339-52, 2004.
22. Depreitere B, Van Lierde C, Vander Sloten J, Van Audekercke R, Van Der Perre G, Plets C et
al.: Mechanics of acute subdural hematomas resulting from BV rupture. Journal of
Neurosurgery 104(6): 950-956, 2006.
23. Löwenhielm P: Strain tolerance of the vv. cerebri sup. (BVs) calculated from head-on
collision tests with cadavers. Z Rechtsmedizin 75:131–144, 1974.
24. Gennarelli TA, Thibault LE: Biomechanics of acute subdural hematoma. J Trauma 22:680–
686, 1982.
25. Lee MC, Ueno K, Melvin JW: Finite element analysis of traumatic subdural hematoma, in
Proceedings of the 31st Stapp Car Crash Conference. New York, NY, Society of Automotive
Engineers, 1987, pp 67-77.
26. Viano DC, Casson IR, Pellman EJ: Concussion in professional football: biomechanics of the
struck player--part 14. Neurosurgery 61(2): 313-27; discussion 327-8, 2007.
27. Viano DC, Pellman EJ: Concussion in professional football: biomechanics of the striking
player--part 8. Neurosurgery 56(2):266-80; discussion 266-80, 2005.
28. Windle WF: The Spinal Cord and Its Reaction to Traumatic Injury: Anatomy, Physiology,
Pharmacology, Therapeutics. New York: M Dekker; 1980; xi, 384.
29. Bogduk N, Mercer S: Biomechanics of the cervical spine, I: normal kinematics. Clin
Biomech 15:633–648, 2000.
30. Dvorak J, Panjabi MM, Novotny JE, Antinnes JA: In vivo flexion/extension of the normal
cervical spine. J Orthop Res 9(6):828-34, 1991.
31. Nightingale RW, Chancey VC, Ottaviano D, Luck JF, Tran L, Prange M et al.: Flexion and
extension structural properties and strengths for male cervical spine segments. J Biomech 40:
535-542, 2007.
32. Pellman EJ, Viano DC, Tucker AM, Casson IR: Concussion in professional football: location
and direction of helmet impacts—part 2. Neurosurgery 53: 1328–1341, 2003.
33. Kantelhardt SR, Oberle J, Derakhshani S, Kast E: The cervical spine and its relation to
anterior plate-screw fixation: a quantitative study. Neurosurg Rev 28(4):308-12, 2005.
34. Foust DR, Chaffin DB, Snyder RG, Baum JK: Cervical range of motion and dynamic
responses and strength of cervical muscles, in Proceedings of the 17th Stapp Car Crash
Conference. Warrendale, PA, Society of Automotive Engineers, 1971, pp 285.
35. Schnebel B, Gwin JT, Anderson S, Gatlin R: In vivo study of head impacts in football: a
comparison of National Collegiate Athletic Association Division I versus high school
impacts. Neurosurgery 60(3): 490-5; discussion 495-6, 2007.
36. Duma SM, Manoogian SJ, Bussone WR, Brolinson PG, Goforth MW, Donnenwerth JJ,
Greenwald RM, Chu JJ, Crisco JJ. Analysis of real-time head accelerations in collegiate
football players. Clin J Sport Med 15(1):3-8, 2005.
37. Pellman EJ, Viano DC, Tucker AM, Casson IR, Waeckerle JF. Concussion in professional
football: reconstruction of game impacts and injuries. Neurosurgery 53:799–814, 2003.
38. Hilker CE, Yoganandan N, Pintar F: Experimental determination of adult and pediatric neck
scale factors. Stapp Car Crash J 46:417–429, 2002.
39. Liu D, Chang CY, Fan CM, Hsu SL. Influence of environmental factors on energy absorption
degradation of polystyrene foam in protective helmets. Engineering Failure Analysis 10:
581–591, 2003.
40. Schwarz, Alan. A Guilty Plea for Failing to Test Youth Helmets Properly. NY Times. Dec 22,
2008.
Figure 1. (A) Pre-operative CT imaging with soft-tissue windowing demonstrates a left subacute
frontoparietal subdural hematoma slightly hyperdense to cortex, measuring approximately 11 mm in widest
thickness with 6 mm of left to right midline shift. Arrow indicates the interface between brain and
hematoma. (B) Pre-operative CT imaging with bone windowing reveals a small focal calvarial irregularity
overlying the SDH (indicated by arrow). (C) CT imaging of the head with soft-tissue windowing status post
craniotomy for evacuation.
Figure 2: (Top panel) Rapid extension of the struck player’s cervical spine is depicted by still photographs
of a collision in high-school football illustrated (note: no video of the collision described in this case report
was available; still photos are courtesy of Magnolia High School, New Martinsville, WV). These
photographs, taken from video footage at approximately 0, 10, 20, and 30 milliseconds following impact,
illustrate rotational acceleration of the struck player’s helmet about the y-axis in cervical extension.
(Middle panel) The impact force of the collision, the moment arm of rotation, the moment itself, and
rotational stiffness are illustrated in the middle panel. (Lower panel) The relationship between skull, brain,
and intervening bridging vein is illustrated. Elongation of the bridging vein with rupture as a consequence
of relative motion between the brain and skull secondary to rotational acceleration is depicted.