effects of reflexive cervical muscle ......muscle contraction likely has a significant affect on...

IRCOBI Conference – Graz (Austria) September 2004 269

EFFECTS OF REFLEXIVE CERVICAL MUSCLE CONTRACTION ON WHIPLASH

KINEMATICS AND INJURY

Brian D. Stemper, Narayan Yoganandan, Frank A. Pintar, Thomas A. Gennarelli

Department of Neurosurgery, Medical College of Wisconsin, and Zablocki VA Medical Center

Milwaukee, WI, USA

ABSTRACT

The ability of neck muscles to react in time to mitigate whiplash injury in unaware occupants

remains unclear. A validated head-neck computer model was implemented to determine the effect of

reflexive contraction on capsular ligament elongations in whiplash. Contraction parameters were

chosen for the maximum kinematic effect. Contraction decreased segmental angulations less than

10% during the retraction phase and decreased capsular ligament elongations in the middle while

slightly increasing elongations at the inferior and superior ends of the cervical spine. Due to inherent

reflexive contraction delays, it remains unlikely that reflexive contraction can significantly affect the

whiplash injury mechanism.

Key Words: Biomechanics, rear impacts, spine, computer model, facet joints

THE ABILITY OF NECK MUSCLES to mitigate whiplash injury in the unaware occupant continues

to be a topic of debate in biomechanics literature. By measuring electromyographical (EMG) signals

of superficial neck muscles, experimental investigators concluded that reflexive contraction of the

neck muscles (in particular the sternocleidomastoid) can affect spinal kinematics in whiplash

(Magnusson et al., 1999; Brault et al., 2000; Kumar et al., 2002). These assumptions are largely based

on the relative timing between EMG and head or thorax accelerations. However, a separate group of

researchers assert that whiplash injury in the unaware occupant occurs during the initial stages of

head-neck kinematics (retraction) prior to the generation of significant muscle forces (Geigl et al.,

1994; Ono et al., 1997; Deng et al., 2000; Stemper et al., 2003). The most important issue in the

present debate is the timing of the whiplash injury mechanism relative to the timing of reflexive

muscle contraction and force generation. To affect the whiplash injury mechanism, cervical muscles

must react and generate sufficient forces to decrease spinal kinematics prior to the time of injury

occurrence.

The present investigation exercised a validated head-neck computer model in whiplash to

measure region-dependent elongation of facet joint capsular ligaments. To test the effects of muscle

contraction in the unaware occupant, the model implemented reflexive muscle contraction with

parameters obtained from literature. Contraction parameters were chosen to provide the greatest

kinematic effect. The hypothesis was that reflexive muscle contraction would not markedly alter

ligament elongations during the retraction phase because of inherent physiological timing delays

associated with this type of contraction.

LITERATURE REVIEW

Experimental investigators implemented human volunteers, full-body cadavers, and intact

head-neck complexes to correlate neck motions to potential whiplash injury mechanisms (Geigl et al.,

1994; Ono et al., 1997; Deng et al., 2000; Cusick et al., 2001; Kumar et al., 2002). Three phases of

cervical spinal kinematics result from whiplash loading (Ono et al., 1997; Davidsson et al., 1998; Ono

et al., 1999). During the initial phase, the thorax is displaced anteriorly due to interaction with the

seatback, while the head remains stationary due to its inertia, resulting in retraction of the head relative


to the thorax. To compensate for head retraction, the cervical spine sustains non-physiologic S-

curvature, characterized by extension in lower and flexion in upper segments (Cusick et al., 2001). In

the second phase, loading is transferred up the cervical spine, and the entire head-neck complex moves

into extension and continues in that mode until the head contacts the head restraint. In the final phase,

the head rebounds from the head restraint, forcing the head-neck complex into flexion. Injury

mechanisms hypothesized to occur in each of these stages are discussed below.

Reflexive contraction of the neck muscles can be modeled in a unique sequence that correlates

to experimental findings. The three specific stages of reflexive muscle contraction are reflex delay,

electromechanical delay (EMD), and build-up of muscle forces (Siegmund and Brault 2000). Reflex

delay is most commonly defined in human volunteer rear impact studies as the delay between the

stimulus (impact) and initiation of electrical muscle activity (Szabo and Welcher 1996; Ono et al.,

1997; Kaneoka et al., 1999; Magnusson et al., 1999; Brault et al., 2000; Kumar et al., 2002; Siegmund

et al., 2003). These investigations reported mean EMG reflex delays from the initiation of T1

acceleration to be 48 msec. The second phase, EMD, has received considerable attention in literature,

and is characterized by the conversion of electrical muscle activity into mechanical force (Table 1).

This time delay varies depending on type of contraction, velocity of movement, involved muscle,

fatigue, age, and gender (Norman and Komi 1979; Zhou et al., 1995). EMD values for reflexive

contractions are typically shorter than voluntary contractions (Table 1). The final phase involves the

build-up of tensile force to the maximum value for the neural activation level, characterized by muscle

force rise time. This value has been reported to be 81 msec for cervical muscles in canines subjected

to 3 to 5 g vertical accelerations (Tennyson et al., 1977). Although literature demonstrated a range of

values for the stages of muscle contraction, the earliest time of maximum muscle contraction is

approximately 140 msec. The ability of reflexive neck muscle contraction to mitigate whiplash injury

largely depends on the kinematic phase during which injury occurs. Muscle contraction likely has a

significant affect on kinematics occurring later than 140 msec. The effect of this contraction prior to

140 msec is however, unclear. This is an objective of the present study.

Table 1: Times of electromechanical delay reported in the literature.

Author Muscle Contraction Type EMD (ms)

(Cavanagh and Komi 1979) biceps and brachioradialis voluntary concentric 56

(Corcos et al., 1992) biceps voluntary isometric 13-31

(Granata et al., 2000) knee extensor reflex (isometric) 54 ± 15

(Granata et al., 2004) lumbar paraspinal reflex 29-34

(Nilsson et al., 1977) vastus lateralis voluntary concentric 95 ± 3

(Norman and Komi 1979) biceps and triceps voluntary eccentric 26-41

(Vint et al., 2001) biceps voluntary concentric 84 ± 13

(Vos et al., 1991) vastus lateralis voluntary concentric 82 ± 15

(Zhou et al., 1995) knee extensor reflex (isometric) 22-24

Soft tissue injuries to the cervical spine resulting from automotive rear impacts were first

recognized in 1928 (Crowe 1928). By 1995, 10,000 clinical and experimental articles were published

on the subject (Spitzer et al., 1995). During that time, research with clinical patients, human

volunteers, cadavers, animals, and crash test dummies led to a number of whiplash injury theories.

One of the first theories was injury to the anterior cervical structures as a result of hyperextension of

the head-neck complex (Macnab 1971). This theory was tested using human volunteers, monkeys,

and crash test dummies. To prevent hyperextension injuries in automotive rear impacts, in 1969 the

United States government mandated head restraints for all new passenger cars within its borders

(NHTSA 1969). However, these safety devices were only marginally successful at mitigating

whiplash injury, decreasing overall injury risk in rear impacts by 5 to 20% (O'Neill et al., 1972;

Kahane 1982). Other injury theories included neuronal degeneration due to pressure gradients in the

spinal canal resulting from differential motion between the head and thorax during the retraction phase

(Svensson et al., 1993; Schmitt et al., 2003), and injury to the anterior cervical muscles due to


eccentric contraction during the retraction phase (Brault et al., 2000). Both theories recognized the

significance of initial head retraction resulting in abnormal S-curvature in the cervical spine.

Recently, a number of clinical and experimental investigations focused on injury to cervical facet

joints as a likely mechanism of injury (Barnsley et al., 1995; Ono et al., 1997; Yang et al., 1997;

Kaneoka et al., 1999; Cusick et al., 2001; Yoganandan et al., 2001). Lower cervical facet joints

sustained tension in anterior regions and compression in posterior regions during the retraction phase

(Cusick et al., 2001). Excess tension in the joint capsular ligament can lead to subcatastrophic or

catastrophic tissue failure (Yoganandan et al., 1989; Winkelstein et al., 2000; Siegmund et al., 2001).

Clinical studies correlated injury to lower cervical facet joints with the most commonly reported

whiplash symptoms (Barnsley et al., 1995). Because of these clinical and experimental investigations,

the injury mechanism examined in the present study was tensile injury to the facet joint capsular

ligaments during the retraction phase, the time of nonphysiologic cervical S-curvature, and as

described in the previous paragraph this study was focused on analyzing the effect of reflexive

contraction in the unaware occupant.

METHODS

A head-neck computer model was used to investigate the effects of reflexive muscle

contraction on kinematics of the cervical spine in whiplash. The model was exercised using

MADYMO software (TNO, the Netherlands) and consisted of the head, seven cervical vertebrae, first

thoracic vertebra, and soft tissues of the cervical spine incorporated as ligaments, intervertebral discs,

facet joints, and passive neck musculature. Bony components of the head-neck complex were

modeled as rigid bodies, including mass and inertial properties of bone and surrounding soft tissues

(de Jager 1996; van der Horst 2002). Bony geometry was incorporated using CT images of a single

male specimen (de Jager 1996). Level-dependent, nonlinear, viscoelastic soft tissue material

properties were based on literature (Table 2). Facet joints were modeled with high compressive

stiffness and zero shear and tensile stiffness, according to synovial joint mechanics. Resistance to

facet joint tension and shear motion was accomplished through elongation of the capsular ligaments.

Table 2: Material properties of the head-neck computer model.

Spinal component Spinal level Loading Material Property Reference

Upper cervical Anterior longitudinal ligament

Lower cervical Tension (Pintar 1986; Yoganandan et al., 1989)

Upper cervical Posterior longitudinal ligament


Upper cervical Ligamentum flavum


Upper cervical Interspinous ligament


Upper cervical Capsular ligament


Shear (Moroney et al., 1988)

Tension (Pintar et al., 1986) Intervertebral disc All levels

Compression (Eberlein et al., 1999)

Neck musculature was modeled using the MADYMO Hill-type muscle model (TNO

Automotive). The Hill model consists of parallel elastic and contractile elements in series with two

elastic elements. The contractile element controls the active force generation of the muscle, the elastic

elements account for stiffness of the muscle fibers, surrounding tissue, and the tendons and

aponeurosis. Muscles were attached to individual vertebrae according to local coordinates, creating

‘sliding’ interfaces that permitted localized muscle elongation and allowed muscles to ‘wrap’ around

the vertebral column and develop more realistic lines of muscle action. In most cases, attachment

points were defined at each cervical level between origin and insertion. Passive muscle resistance to


motion of the head-neck complex was approximated according to literature (Deng and Goldsmith

1987).

Muscles were divided into three activation groups by their kinematic effect: flexors, extensors,

and sternocleidomastoid. Because the sternocleidomastoid cannot be classified uniquely as a flexor or

extensor due to proximal attachment points anterior to the cervical spine and distal attachment points

posterior to the occipital condyles, this muscle was included in its own kinematic activation group.

Reflexive muscle contraction was divided into three phases consisting of the reflex delay, EMD, and

muscle rise time (Figure 1). Muscles sustained zero neural activation (force generation) during the

first two phases and linearly ramped up to maximum activation during the muscle rise time. Two

reflex delays, 45 and 54 msec, were implemented to represent the literature (Ono et al., 1997;

Magnusson et al., 1999). Electromechanical delay was 13 msec (Corcos et al., 1992). Muscle rise

time to maximum neural activation lasted 81 msec (Tennyson et al., 1977). Muscle activation was

accomplished according to synergistic assumptions, wherein all muscles of a specific group were

activated to the same level. The ratio of maximum activation levels between the three muscle groups

was determined prior to whiplash simulations in order to obtain a sagitally balanced contraction to

balance the flexion and extension moments applied to the head. It was determined that 90% activation

of the flexors, 45% of the sternocleidomastoid, and 30% of the extensors resulted in +1g vertical

acceleration of the head to counterbalance the acceleration of gravity, with minimal sagittal plane

rotation of the head. These activation levels were implemented during whiplash simulations.

0

100

0 200time (msec)

{

EMD

Reflex

Time

Mu

scle

Forc

e R

ise T

ime

Maxim um Neura l

Act ivat ion

(45 to 54 msec)

(13 msec)

(81

mse

c)

0

100

0 200time (msec)

{

EMD

Reflex

Time

Mu

scle

Forc

e R

ise T

ime

Maxim um Neura l

Act ivat ion

(45 to 54 msec)

(13 msec)

(81

mse

c)

Figure 1: Neural activation (percentage of maximum activation) of the flexor muscle group.

Whiplash loading was imparted to the model by accelerating the T1 vertebra anteriorly. The

acceleration pulse was integrated to compute T1 change in velocity. Rear impact velocity of 2.6 m/sec

was imparted for all simulations. Prior to initiation of T1 acceleration, the occipital condyles were

positioned directly superior to the T1 vertebral body, and the Frankfort plane was maintained

horizontal. The cervical spine demonstrated normal lordotic posture, and the T1 vertebra was given an

anterior orientation of 25 deg to simulate normal driving alignment. During the entire whiplash

simulation, the T1 vertebra was constrained against rotation and superior and lateral translation.

Overall, level-by-level segmental, and facet joint kinematic responses without muscle contraction had

been previously validated with respect to experimental head-neck cadaver specimens subjected to

similar rear impact loading magnitudes (Stemper et al., 2004). The validation process is discussed in

further detail below.

To quantify the effects of reflexive muscle contraction on kinematics of the head-neck

complex, facet joint capsular ligament elongations at the C2-C3 through C6-C7 levels were compared

between the two muscle contraction simulations (54 and 45 msec reflex delays) and the simulation

without muscle contraction. Ligament elongation was defined as the increase in length from the

original ligament length at the initiation of T1 acceleration. In particular, facet joint capsular ligament

elongations were computed in four anatomic regions of the joint (ventral, lateral, dorsal, and medial)

during the time of maximum cervical S-curvature. This time was determined as the time of maximum

segmental flexion at the C2-C3 level during the retraction phase.


RESULTS

The model demonstrated retraction and extension phases of whiplash kinematics for the

simulations with and without reflexive muscle contraction (Figure 2). Rebound did not occur due to

the absence of a head rest. Maximum S-curvature during the retraction phase occurred earlier with

decreasing reflex delays: 76 msec for the simulation without contraction, and 75 and 71 msec for the

54- and 45-msec reflex delay simulations, respectively. Reflexive muscle contraction also resulted in

a more timely transition from retraction to extension phases, occurring at 99 msec for the 54-msec

reflex delay and 94 msec for the 45-msec reflex delay, compared to 114 msec for the simulation

without contraction. Reflexive muscle contraction decreased the overall head extension angle relative

to T1 at the time of maximum S-curvature by 5.1% for the 54-msec delay and 24.9% for the 45-msec

delay.

Retraction Extension Figure 2: Initial position, retraction, and extension phases.

Neural activation of neck muscles initiated at 67 and 58 msec for the 54- and 45-msec reflex

delays. Muscle groups attained sub-maximal activation levels during the time of maximum S-

curvature (Table 3). Maximum activation, which coincided with maximum tensile force generation,

occurred at 148 and 139 msec.

Table 3: Percent of maximum neural activation during maximum S-curvature.

Flexors Extensors SCM

45-msec delay 16.0 16.0 16.0

54-msec delay 9.9 9.9 9.9

No contraction 0.0 0.0 0.0

During maximum S-curvature, flexion at the C2-C3 segmental level and extension at the C3-

C4 through C6-C7 levels was evident (Figure 3). Reflexive muscle contraction decreased segmental

angulations at all cervical levels, with the 45-msec reflex delay having a greater kinematic effect. The

54-msec reflex delay had a minimal effect on segmental angulations at the time of maximum S-

curvature (<1%). At the C2-C3, C4-C5, C5-C6, and C6-C7 levels, the 45-msec reflex delay

contraction decreased segmental angulations by less than 10%.


-5

0

5

10

C2-C3 C3-C4 C4-C5 C5-C6 C6-C7

Seg

men

tal

angle

(deg

)

No con t ract ion

54-msec delay

45-msec delay

Figure 3: Segmental angulations at the time of maximum S-curvature.

Facet joint capsular ligaments demonstrated region- and level-dependent elongations during

the whiplash simulation without muscle contraction (Figure 4). Elongation magnitudes were below

2.0 mm in all anatomic regions. At the C2-C3 level, the dorsal anatomic region of the capsular

ligament sustained maximum elongation. At the C3-C4 through C6-C7 levels, lateral anatomic

regions of the capsular ligament sustained maximum elongations. Ligament elongations in the lateral

joint regions increased inferiorly, with maximum elongation at the C6-C7 level.

0

0.5

1

1.5

2

2.5

C2-C3 C3-C4 C4-C5 C5-C6 C6-C7

Lig

am

ent

elo

ng

ati

on

(m

m)

Ventral

Lateral

Dorsal

Medial

D L L L L

Figure 4: Capsular ligament elongations for the simulation without muscle contraction.

Simulations with reflexive muscle contraction demonstrated maximum elongations in the

same joint regions as the simulation without muscle contraction (C2-C3: dorsal, C3-C4 to C6-C7:

lateral). Facet joint capsular ligament elongations in those regions were compared to the simulation

without contraction (Figure 5). Muscle contraction decreased capsular ligament elongations at the C3-

C4 and C4-C5 levels by less than 16 percent for the 54-msec delay, and 16.4 percent at the C4-C5

level and 32.7 percent at the C3-C4 levels for the 45-msec delay. However, reflexive contraction

increased elongations at the C2-C3, C5-C6, and C6-C7 levels by a maximum of 21 percent.


0.0

0.5

1.0

1.5

2.0

2.5

3.0

C2-C3 C3-C4 C4-C5 C5-C6 C6-C7

Lig

amen

t el

ongat

ion (

mm

)

No con t ract ion

54-msec delay

45-msec delay

DORSAL LATERAL LATERAL LATERAL LATERAL

Figure 5: Capsular ligament elongations at the time of maximum S-curvature.

DISCUSSION

Stabilization of the head-neck complex in an unaware occupant is accomplished in three

stages: passive structures (spinal soft tissues, passive musculature) act first, followed by reflexive

muscle contraction, and finally, voluntary muscle contraction (Simoneau et al., 2003). In a whiplash

event, wherein the injury mechanism likely occurs prior to head restraint contact, kinematics are

dominated by the first two stages. The ability of the occupant to mitigate injurious loading largely

depends on the mechanical properties of the passive structures and the timing of the reflexive muscle

contraction. Low-velocity whiplash loading has been experimentally shown to exceed the mechanical

thresholds of the passive neck structures, resulting in soft tissue spinal injury in human cadavers

subjected to whiplash (Deng et al., 2000; Yoganandan et al., 2000; Yoganandan et al., 2001).

However, the debate over the ability of reflexive neck muscle contraction in the unaware occupant to

mitigate whiplash injury is unresolved. Human cadaver studies cannot resolve this issue, and

awareness effects limit the applicability of human volunteer studies. The purpose of the present

investigation was to quantify the timing of reflexive neck muscle contraction relative to kinematics of

the facet joint capsular ligaments, structures clinically and experimentally linked to whiplash injury.

The present investigation focused on the time of injury as the non-physiologic S-curvature that occurs

during the retraction phase of whiplash kinematics, prior to head restraint contact.

HEAD RESTRAINTS

The effectiveness of head restraints in mitigating whiplash injury was reported to be minimal

(O'Neill et al., 1972; Kahane 1982). This finding implies that whiplash injury likely occurs prior to

the time that the head contacts the head restraint, for conventional restraints positioned with a finite

backset. A survey of the experimental rear impact literature revealed that the average time of head

restraint contact after initiation of T1 acceleration is 77.9 msec (Table 4). In the present study,

maximum S-curvature of the cervical spine occurred just prior to the mean time of head restraint

contact. During the cervical S-curvature, reflexive muscle contraction activation levels were less than

20% of maximum levels (Table 3). The kinematic effect of reflexive muscle contraction was also

minimal during this time, decreasing the overall head to T1 angulation by less than 25% and level-by-

level segmental angulations by less than 10% at the shortest reflex delay. Present results lead to the

conclusion that reflexive muscle contraction is unlikely to mitigate whiplash injuries occurring during

the retraction phase due to inherent delays involved in the initiation and buildup of these contractions.


Table 4: Experimental times of head restraint contact.

Investigator Impact velocity

(m/sec)

T1 acceleration

(msec)

HR contact

(msec)

T1 acc to HR contact

(msec)

(Davidsson et al., 1998) 1.9 50 98 48

(Deng et al., 2000) 2.0 120 230 110

(Deng et al., 2000) 2.2 140 266 126

(Hell and Langwieder 1998) 2.6 50 130 80

(Hell and Langwieder 1998) 2.6 40 110 70

(McConnell et al., 1993) 2.2 100 140 40

(Siegmund et al., 1997) 1.1 30 118 88

(Siegmund et al., 1997) 2.2 30 94 64

(Kroonenberg et al., 1998) 1.8 - 2.6 0 75 75

Mean 77.9

CAPSULAR LIGAMENT ELONGATIONS

Reflexive muscle contraction had a marginal effect on capsular ligament elongations.

Maximum ligament elongations occurred in the same anatomic facet joint regions during both

simulations with reflexive muscle contraction and the simulation without muscle contraction. Muscle

contraction had an inconsistent effect on the magnitude of capsular ligament elongations. In the

middle cervical spine, contraction decreased elongations by only 16.4 percent at the C4-C5 level.

However, reflexive contraction increased elongations at the inferior and superior ends of the cervical

spine up to 21 percent. Because experimental whiplash studies produced injuries in the cervical facet

joints (Deng et al., 2000; Yoganandan et al., 2000) and due to clinical findings linking facet joint

injury with common whiplash symptoms (Barnsley et al., 1995), cervical facet joints are strongly

implicated in whiplash injury. Although the effect of reflexive contraction on capsular ligament

elongations was relatively small, present results suggest that reflexive muscle contraction may slightly

decrease the likelihood of whiplash injury at specific cervical levels, while slightly increasing the

likelihood of injury at other levels. The dependence of these results on reflex delay, with a greater

kinematic effect for shorter delays, indicates that shorter reflex delays than those used in the present

study would have a larger effect on spinal kinematics. However, shorter contraction delays are

unlikely in vivo as the present study maximized the kinematic effect of reflexive contraction according

to literature.

REFLEXIVE CONTRACTION PARAMETERS

Reflexive muscle contraction parameters were chosen to provide the maximum effect on

whiplash kinematics. The 45-msec reflex delay, although not the minimum value reported in

literature, was the shortest reflex delay obtained for human volunteers subjected to similar magnitudes

of rear impact loading (Ono et al., 1997). Because of a reported correlation between impact severity

and reflex delay (Kumar et al., 2002), the 54- and 45-msec delays were chosen to represent literature.

Likewise, the 13-msec EMD was chosen to minimize this delay and maximize the effect of reflexive

contraction on spinal kinematics. EMD values were reported as high as 95 msec for voluntary

contractions (Nilsson et al., 1977), and 54 msec for reflexive contractions (Granata et al., 2000).

However, the 13-msec delay, although obtained in voluntary contraction, was reported to be a more

accurate measurement (Siegmund and Brault 2000) and was, therefore, chosen to maximize the

kinematic effect. Muscle rise time to maximum neural activation (81 msec) was also consistent with

literature (Tennyson et al., 1977; Szabo and Welcher 1996; Magnusson et al., 1999; Kumar et al.,

2002). In the present study, maximum neural activation corresponded to maximum muscle force

generation. For all neck muscles, mean muscle force rise times obtained in human volunteer and

animal studies were reported between 63 msec (Szabo and Welcher 1996) and 253 msec (Kumar et al.,

2002). An investigation into the sensitivity of spinal kinematics to muscle rise time conducted prior to

this study revealed that segmental angulations changed by less than 1.3 percent at the C2-C3 and C4-

C5 through C6-C7 levels and by 10.4 percent at the C3-C4 level with variation of the muscle rise time


between 63 and 81 msec. The most sensitive contraction parameter, as indicated by the results of the

present study, was reflex delay. Minimizing the time to initiation of neural activation through reflex

delay and electromechanical delay resulted in the maximum effect of reflexive muscle contraction on

spinal kinematics.

MODEL VALIDATION

The present computer model was validated with respect to the overall head to T1 angulations,

level-by-level segmental angulations (C2-C3 through C6-C7 levels), and region-dependent facet joint

motions (C4-C5 through C6-C7 levels) obtained from ten intact head-neck cadaver specimens

subjected to 1.8 and 2.6 m/sec rear impacts (Stemper et al., 2004). Experimental specimens were

subject to identical boundary conditions as the computer model (e.g., initial head and spinal

orientations and T1 constraints). Validation corridors were developed from experimental specimens

consisting of the mean plus and minus one standard deviation kinematic responses. Corridors were

mass-scaled to account for biological variation in specimen anthropometry according to accepted

procedures (Maltese et al., 2002). Computer model response falling within the corridors was

considered valid. Validation plots for overall motion, segmental angulations from C2-C3 through C6-

C7 levels, and facet joint motions in the anterior and posterior joint regions from C4-C5 through C6-

C7 levels are presented in appendix A. While previous models used in the study of whiplash have

focused validation efforts primarily on head and thoracic accelerations, the present model is the first to

incorporate overall motions, level-by-level segmental angulations, and region-dependent facet joint

motions in the validation process.

INITIAL OCCUPANT POSITIONING

Initial positioning of the model in the present study focused on the “normal” automotive

occupant characteristics; lordotic posture, horizontal Frankfort plane, physiologic occipital condyle

positioning. This assumption was made for the sake of consistency and to simplify the analysis.

However, soft tissue injuries resulting from rear impacts can also occur under separate mechanisms

and with different factors. For example, the absence of an automotive head restraint may lead to

hyperextension injuries in the anterior cervical spine (i.e., anterior longitudinal ligament and endplate

failures). Out of position occupants may also exhibit separate pathologies. Axial rotation of the head

prior to impact places an additional pre-strain on the contralateral spinal components that may lower

the threshold of injury or alter the injury mechanism. For the sake of consistency and to model the

most typical whiplash event, occupant position was strictly controlled in the “normal” position prior to

impact in all simulations.

LIMITATIONS

A limitation of the present study was that of synergistic muscle contractions, wherein all

muscles of each kinematic group were activated to identical levels. Reflexive contraction of the neck

muscles in vivo likely occurs in a more complex sequence involving unique contraction levels, rates,

and timing for individual muscles (Winters and Stark 1988). While some of these parameters were

defined for the superficial muscles using EMG analysis of volunteers subjected to rear impacts (Szabo

and Welcher 1996; Ono et al., 1997; Kaneoka et al., 1999; Magnusson et al., 1999; Brault et al., 2000;

Kumar et al., 2002; Siegmund et al., 2003), data is clearly lacking for deep muscles. Because of this

inconsistency, it was necessary to assume equal contraction levels, rates, and timing for muscles with

similar kinematic effects.

A second limitation was the T1 constraint preventing rotation and superior and lateral

translation. This constraint was included because the model was validated with respect to an intact

head-neck cadaver model subject to the same constraints (Stemper et al., 2004) and because the

literature on thoracic ramping is not consistent. While it is well acknowledged that the upper thorax

sustains ramping motion in whiplash due to the interaction with the seatback, the magnitude and

timing of this motion as reported in full-body cadaver and human volunteer experiments is


inconsistent (McConnell et al., 1993; Davidsson et al., 1998; Deng et al., 2000; Yoganandan et al.,

2000). This ramping motion is likely dependent upon a number of factors, including stiffness of the

seatback, curvature of the thoracic spine, angle of the seatback, magnitude of rear impact, occupant

awareness, and occupant posture. Experimental results quantify this variability, wherein mean T1

rotation at 100 ms for a seatback angle of 20 deg was twice the magnitude of that for a seatback angle

of 0 deg (Deng et al., 2000). To eliminate this variability, T1 was constrained in all degrees of

freedom except anterior displacement in the present analysis.

CONCLUSIONS

This study quantified the effects of reflexive muscle contraction on cervical spine kinematics

during the retraction phase. Kinematics of the cervical spine during this phase are such that abnormal

loading patterns are placed on the cervical facet joints that may result in catastrophic or

subcatastrophic injury to the capsular ligaments. A validated head-neck computer model was exposed

to 2.6 m/sec rear impacts and reflexive contraction was modeled using parameters obtained from

literature to produce the maximum kinematic effect. Results demonstrated that muscle contraction in

the unaware occupant has a minimal affect on segmental angulations during the retraction phase.

Kinematic response demonstrated a dependence upon reflex delay, with the shorter delay resulting in a

larger effect on capsular ligament elongations. However, the change in ligament elongation between

the shortest reflex delay and the simulation without contraction was less than 21 percent at the C2-C3,

C4-C5, C5-C6, and C6-C7 levels. Results for the present study demonstrated the importance of the

retraction phase of whiplash kinematics and indicated that reflexive muscle contraction in the unaware

occupant may play a secondary role in minimizing the likelihood of capsular ligament injury during

whiplash.

ACKNOWLEDGMENTS

This study was supported in part by PHS CDC Grant R49CCR-515433 and the Department of

Veterans Affairs Medical Research.

REFERENCES

Barnsley, L., Lord, S. M., Wallis, B. J. and Bogduk, N. “The prevalence of chronic cervical zygapophyseal joint

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APPENDIX A: VALIDATION OF THE HEAD-NECK COMPUTER MODEL

Overall head to T1 angulation: experimentally obtained validation corridors are shaded, computer

model response is provided.

-15

0

15

30

45

60

75

50 100 150

He

ad

to

T1

an

gle

(d

eg

)

Time (msec)-15

0

15

30

45

60

75

50 100 150

-15

0

15

30

45

60

75

50 100 150

He

ad

to

T1

an

gle

(d

eg

)

Time (msec)

Segmental angulation: experimentally obtained validation corridors are shaded, computer model

response is provided.

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ng

le (

de

g)

Time (msec)

C2-C3

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ng

le (

de

g)

Time (msec)

C2-C3

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ng

le (

de

g)

Time (msec)

C3-C4

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ng

le (

de

g)

Time (msec)

C3-C4

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ngle

(d

eg

)

Time (msec)

C4-C5

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal a

ngle

(d

eg

)

Time (msec)

C4-C5

-5

0

5

10

15

20

25

50 100 150

Segm

en

tal a

ng

le (

de

g)

Time (msec)

C5-C6

-5

0

5

10

15

20

25

50 100 150

Segm

en

tal a

ng

le (

de

g)

Time (msec)

C5-C6

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal an

gle

(d

eg)

Time (msec)

C6-C7

-5

0

5

10

15

20

25

50 100 150

Se

gm

en

tal an

gle

(d

eg)

Time (msec)

C6-C7


Facet joint motion: experimentally obtained validation corridors are shaded, computer model response

is provided.

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C4-C5, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C4-C5, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C4-C5, Anterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C4-C5, Anterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C5-C6, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C5-C6, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C5-C6, Anterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C5-C6, Anterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C6-C7, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C6-C7, Posterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C6-C7, Anterior

-1

0

1

2

3

4

5

50 100 150

Fa

ce

t jo

int m

otio

n (

mm

)

Time (msec)

C6-C7, Anterior

effects of reflexive cervical muscle ......muscle contraction likely has a significant affect on...

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