Muscle Force Replication Research Articles

Biomechanics of Thoracolumbar Burst and Chance-Type Fractures during Fall from Height.

Study Design In vitro biomechanical study. Objective To investigate the biomechanics of thoracolumbar burst and Chance-type fractures during fall from height. Methods Our model consisted of a three-vertebra human thoracolumbar specimen (n = 4) stabilized with muscle force replication and mounted within an impact dummy. Each specimen was subjected to a single fall from an average height of 2.1 m with average velocity at impact of 6.4 m/s. Biomechanical responses were determined using impact load data combined with high-speed movie analyses. Injuries to the middle vertebra of each spinal segment were evaluated using imaging and dissection. Results Average peak compressive forces occurred within 10 milliseconds of impact and reached 40.3 kN at the ground, 7.1 kN at the lower vertebra, and 3.6 kN at the upper vertebra. Subsequently, average peak flexion (55.0 degrees) and tensile forces (0.7 kN upper vertebra, 0.3 kN lower vertebra) occurred between 43.0 and 60.0 milliseconds. The middle vertebra of all specimens sustained pedicle and endplate fractures with comminution, bursting, and reduced height of its vertebral body. Chance-type fractures were observed consisting of a horizontal split fracture through the laminae and pedicles extending anteriorly through the vertebral body. Conclusions We hypothesize that the compression fractures of the pedicles and vertebral body together with burst fracture occurred at the time of peak spinal compression, 10 milliseconds. Subsequently, the onset of Chance-type fracture occurred at 20 milliseconds through the already fractured and weakened pedicles and vertebral body due to flexion-distraction and a forward shifting spinal axis of rotation.

Hybrid cadaveric/surrogate model of thoracolumbar spine injury due to simulated fall from height

A fall from high height can cause thoracolumbar spine fracture with retropulsion of endplate fragments into the canal leading to neurological deficit. Our objectives were to develop a hybrid cadaveric/surrogate model for producing thoracolumbar spine injury during simulated fall from height, evaluate the feasibility and performance of the model, and compare injuries with those observed clinically. Our model consisted of a 3-vertebra human lumbar specimen (L3–L4–L5) stabilized with muscle force replication and mounted within an impact dummy. The model was subjected to a fall from height of 2.2m with impact velocity of 6.6m/s. Kinetic and kinematic time-history responses were determined using spinal and pelvis load cell data and analyses of high-speed video. Injuries to the L4 vertebra were evaluated by fluoroscopy, radiography, and detailed anatomical dissection. Peak compression forces during the fall from height occurred at 7ms and reached 44.7kN at the ground, 9.1kN at the pelvis, and 4.5kN at the spine. Pelvis acceleration peaks reached 209.9g at 8ms for vertical and 62.8g at 12ms for rearward. Tensile load peaks were then observed (spine: 657.0N at 47ms; pelvis: 569.4N at 61ms). T1/pelvis peak flexion of 68.3° occurred at 38ms as the upper torso translated forward while the pelvis translated rearward. Complete axial burst fracture of the L4 vertebra was observed including endplate comminution, retropulsion of bony fragments into the canal, loss of vertebral body height, and increased interpedicular distance due to fractures anterior to the pedicles and a vertical split fracture of the left lamina. Our dynamic injury model closely replicated the biomechanics of real-life fall from height and produced realistic, clinically relevant burst fracture of the lumbar spine. Our model may be used for further study of thoracolumbar spine injury mechanisms and injury prevention strategies.

Facet Joint and Disc Kinematics During Simulated Rear Crashes With Active Injury Prevention Systems

Experimental and computational biomechanical analyses of simulated rear crashes. The objectives were to determine cervical facet joint and disc kinematics and ligament strains during simulated rear crashes with the Whiplash Protection System (WHIPS) and active head restraint (AHR) and to compare these data with those obtained with no head restraint (NHR). Previous biomechanical studies document abnormal cervical facet kinematics and potentially injurious ligament strains during simulated rear crashes with no injury prevention system. A human model of the neck, consisting of a neck specimen mounted to the torso of BioRID II and carrying a surrogate head and stabilized with muscle force replication, was subjected to simulated rear crashes in a WHIPS seat (n = 6, 12.0 g, ΔV 11.4 km/h) or AHR seat and subsequently with NHR (n = 6: 11.0 g, ΔV 10.2 km/h with AHR; 11.5 g, ΔV 10.7 km/h with NHR). Lower cervical spine facet and disc motions and ligament strains during the crashes were computed and average peak values statistically compared (P < 0.05) between WHIPS, AHR, and NHR. Average peak facet and disc translations and ligament strains could not be statistically differentiated between WHIPS and AHR or between AHR and NHR. WHIPS significantly reduced peak capsular ligament strain and peak disc separation at C6/C7 as compared with NHR. Facet compression at C6/C7 reached 2.9 mm with WHIPS, 1.9 mm with AHR, and 3.2 mm with NHR. WHIPS and AHR generally reduced peak disc separation and anterior longitudinal ligament strain as compared with NHR. WHIPS and AHR limited capsular strain below the subfailure threshold but did not protect against potential facet joint compression injuries, which may occur during or after contact of the head with the head restraint.

Understanding whiplash injury and prevention mechanisms using a human model of the neck

Objectives Various models for rear crash simulation exist and each has unique advantages and limitations. Our goals were to: determine the neck load and motion responses of a human model of the neck (HUMON) during simulated rear crashes; evaluate HUMON's biofidelity via comparisons with in vivo data; and investigate mechanisms of whiplash injury and prevention. Methods HUMON, consisting of a neck specimen ( n = 6) mounted to the torso of BioRID II and carrying a surrogate head and stabilized with muscle force replication, was subjected to simulated rear crashes in an energy-absorbing seat with fixed head restraint (HR) at peak sled accelerations of 9.9 g (Δ V 9.2 kph), 12.0 g (Δ V 11.4 kph), and 13.3 g (Δ V 13.4 kph). Physiologic spinal rotation ranges were determined from intact flexibility tests. Average time–history response corridors (±1 standard deviation) were computed for spinal motions, loads, and injury criteria. Results Neck loads generally increased caudally and consisted of shear, compression, and flexion moment caused by straightening of the kyphotic thoracic and lordotic lumbar curvatures, upward torso ramping, and head inertial and head/HR contact loads. Nonphysiologic rotation occurred in flexion at C7/T1 prior to head/HR contact and in extension at C6/7 and C7/T1 during head/HR contact. Conclusions HUMON's neck load and motion responses compared favorably with in vivo data. Lower cervical spine flexion–compression injuries prior to head/HR contact and extension–compression injuries during head/HR contact may be reduced by refinement of existing seatback, lapbelt, and HR designs and/or development of new injury prevention systems.

Cervical spine curvature during simulated rear crashes with energy-absorbing seat

Background context Epidemiological studies indicate potential benefits of the Whiplash Protection System (WHIPS) for reducing neck injury risk. Purpose Our goal was to evaluate cervical spine curvature during simulated rear crashes of a Human Model of the Neck (HUMON) within a WHIPS seat with fixed head restraint (HR). Study design In vitro biomechanical study. Methods The HUMON consisted of a human neck specimen mounted to the torso of BioRID II (Denton ATD, Inc., Milan, OH, USA) and carrying a surrogate head stabilized with muscle force replication. The HUMON was subjected to simulated rear crashes in a WHIPS seat (n=6) at 9.9, 12.0, and 13.3 g and in a seat with no WHIPS or HR (n=6) at 11.5 g. Statistical tests (p<.05) determined significant increases in spinal motion peaks during the crashes with WHIPS relative to physiologic and significant differences in spinal curvature peaks between WHIPS (12.0 g) and no WHIPS or HR (11.5 g). Results The WHIPS absorbed crash energy during the initial 75 milliseconds, while peak lower cervical spine (LCS) extension occurred as late as 179 milliseconds. The average C7/T1 rotation peaks during the 13.3- g rear crashes with WHIPS significantly exceeded physiologic by 95% in flexion (4.3° vs. 2.2°) and more than 225% in extension (9.8° vs. 3.0°). The WHIPS caused a significant reduction in average peak normalized LCS extension as compared with no WHIPS or HR (1.2 vs. 3.7). Conclusions Although the peak LCS extension was significantly reduced due to WHIPS as compared with no WHIPS or HR, it exceeded physiologic as the cervical spine maintained a prolonged S-shaped curvature. Nonphysiologic LCS motion may occur even if head/HR contact occurs early, and injury is possible before head/HR contact even with a modern energy-absorbing seat. Future whiplash-reduction systems will most likely integrate active injury prevention systems with advanced features such as accident avoidance technology.

WHIPS Seat and Occupant Motions During Simulated Rear Crashes

Objective: Objectives of this study were to investigate the motions of Volvo's Whiplash Protection System (WHIPS) seat and occupant during simulated rear crashes of a human model of the neck (HUMON). Methods: HUMON consisted of a human neck specimen (n = 6) mounted to the torso of BioRID II and carrying an anthropometric head stabilized with muscle force replication. HUMON was seated and secured in a 2005 Volvo XC90 minivan seat that included WHIPS and a fixed head restraint. Rear crashes of 9.9 g (ΔV 9.2 kph), 12.0 g (ΔV 11.4 kph), and 13.3 g (ΔV 13.4 kph) were simulated and WHIPS and occupant motions were monitored. Linear regression analyses (P < .05) were used to determine relationships between WHIPS and occupant motion peaks using data from all crashes combined. Results: WHIPS motions consisted of simultaneous rearward and downward translations and extension of the seatback and plastic deformation of the bilateral WHIPS energy-absorbing components. Peak WHIPS motions were linearly correlated only with peak rearward occupant translations. Less rearward pelvis translation was required to cause WHIPS activation as compared to T1 translation. Conclusions: WHIPS reduced peak T1 horizontal acceleration by 39 percent compared to sled acceleration. This was within the range previously reported for WHIPS, between 30 and 60 percent, but higher than the 16 percent reduction previously reported due to active head restraint. Absorption of crash energy occurred during the initial 75 ms and the onset of head support occurred at 114 ms. Differential head–torso motions occurred prior to and during head support, indicating the potential for neck injury even with WHIPS.

Whiplash injury prevention with active head restraint

Background Previous epidemiological studies have observed that an initial head restraint backset greater than 10 cm is associated with a higher risk of neck injury and persistent symptoms. The objective of this study was to investigate the relation between the active head restraint position and peak neck motion using a new human model of the neck. Methods The model consisted of an osteoligamentous neck specimen mounted to the torso of a rear impact dummy and carrying an anthropometric head stabilized with muscle force replication. Rear impacts (7.1 and 11.1 g) were simulated with and without the active head restraint. Physiologic rotation was determined from intact flexibility tests. Significant reductions ( P < 0.05) in the spinal motion peaks with the active head restraint, as compared to without, were identified. Linear regression analyses identified correlation between head restraint backset and peak spinal rotations ( R 2 > 0.3 and P < 0.001). Findings The active head restraint significantly reduced the average peak spinal rotations, however, these peaks exceeded the physiologic range in flexion at head/C1 and in extension at C4/5 through C7/T1. Correlation was observed between the head restraint backset and the extension peaks at C4/5 and C5/6. Interpretation Correlation between head restraint backset and spinal rotation peaks indicated that a head restraint backset in excess of 8.0 cm may cause hyperextension injuries at the middle and lower cervical spine. The active head restraint may not be fully activated at the time of peak spinal motions, thus reducing its potential protective effects.

Comparison of the whiplash injury criteria

Whiplash injury criteria are based upon the hypothesis that neck injuries are caused by excessive loads, displacements, or head/T1 relative acceleration and velocity. The objectives of this study were to evaluate and compare the whiplash injury criteria (IV-NIC, NIC, Nkm, Nij, and NDC) during simulated rear impacts of a new Human Model of the Neck (HUMON) with and without an active head restraint (AHR). HUMON consisted of a neck specimen mounted to the torso of BioRID II and carrying an anthropometric head stabilized with muscle force replication. HUMON was seated and secured in a Kia Sedona seat with AHR on a sled. Rear impacts (7.1 and 11.1 g) were simulated with the AHR in five different positions followed by an impact with no HR. Statistical differences ( P < 0.05) were determined in the peak NIC and NDC due to the AHR, as compared to no HR, and in the peak IV-NIC relative to physiologic limits. Linear regression analyses identified correlation between IV-NIC and NIC, Nkm, Nij, and NDC ( R 2 ≥ 0.35 and P < 0.001). The AHR caused significant decreases in peak NIC and NDC as compared to no HR. The IV-NIC identified significantly increased motion above the physiologic limit at the middle and lower cervical spine with and without the AHR. Correlation was observed between IV-NIC and NIC, Nkm, Nij, and NDC. Extrapolation using the present correlations and the IV-NIC injury thresholds suggests neck injuries may occur at peak NIC of 14.4 m 2/s 2, Nkm of 0.33, or Nij of 0.09. Nonphysiologic spinal rotation at one or more spinal levels may occur even if head/T1 motions are small.

Biomechanics of Cervical Facet Dislocation

Objectives: The goal of this study was to compute the dynamic neck loads during simulated high-speed bilateral facet dislocation and investigate the injury mechanism. Methods: Ten osteoligamentous functional spinal units (C3/4, n = 4; C5/6, n = 3; C7/T1, n = 3) were prepared with muscle force replication, motion tracking flags, and a 3.3-kg mass rigidly attached to the upper vertebra. Frontal impacts of increasing severity were applied to the lower vertebra until dislocation was achieved. Inverse dynamics was used to calculate the dynamic neck loads during dislocation. Average peak impact acceleration required to cause dislocation ranged between 7.6 and 11.6 g. This resulted in dynamic neck loads applied at average peak rates of 906 Nm/s for flexion moment, 8017 N/ for anterior shear, and 8100 N/s for axial compression. To determine the temporal event patterns, the average occurrence Results: Among average peak loads, axial compression of 233.6 N was first to occur followed by anterior shear force of 73.1 N and flexion moment of 30.7 Nm. Among average peak motions, axial separation of 5.3 mm was first to occur followed by flexion rotation of 63.1 degrees and anterior shear of 21.5 mm. Subsequently, average peak posterior shear force of 110.3 N was observed as the upper facet became locked in the intervertebral foramina. Average peak axial compression of 6.6 mm occurred significantly later than all preceding events. Conclusions: During bilateral facet dislocation, the main loads included flexion moment and forces of axial compression and anterior shear. These loads caused flexion rotation, facet separation, and anterior translation of the upper facet relative to the lower. The present data help elucidate the injury mechanism of cervical facet dislocation.

The compensation mechanism of cervical muscle dysfunction on spinal stability – an in vitro study using porcine model

Muscle injury/impairment results in decreased muscle forces. Decreased muscle forces can be compensated by synergic muscle forces. However, the effects of muscle dysfunction and compensation on spinal stability are not clear yet. Eight porcine cervical spine specimens (C2‐T1) were tested by the spine flexibility testing apparatus. The apparatus was equipped with muscle force replication of three paired cervical muscles. The simulations of muscle recruitment included; no muscle recruitment, normal muscle recruitment, muscle dysfunction without compensation, and muscle dysfunction with two compensation strategies: the minimized muscle forces and the minimized axial forces. The spinal stability was examined by the neutral zone (NZ) and range of motion (ROM), which was the sagittal motion of specimen applied with external moment at 0.5 and 2 Nm respectively. Initial positions of specimens were also recorded. NZ and ROM were largest in the no muscle test, and smallest in the muscle dysfunction without compensation test. NZ and ROM of muscle dysfunction with minimal axial force compensation were larger than those with minimal muscle force compensation. This study concluded that: (1) the muscle dysfunction without compensation constrains spinal motion; (2) impaired muscle with compensations cannot stabilize cervical spine efficiently as normal muscles does; and (3) compensation strategy of minimal muscle forces provides better spinal stability than that of minimal axial forces.

The Mechanics of Cervical Muscle Recruitment on Cervical Spine Stability —A Biomechanical in Vitro Study using Porcine Model

ABSTRACTCervical muscles are crucial in providing the stability of the cervical spine. Many in vitro studies have investigated the relationship between muscle force and stability directly. However, the effects of different muscle dysfunctions or muscle recruitments on cervical spine stability are not yet clear and therefore, worthy of study. A spine testing apparatus with muscle force replication activated by pneumatic cylinders was developed to find the effect of muscles on spinal stability. Seven porcine cervical spines (C2-T1) were used. Three pairs of cervical muscles, including neck flexors (sternocleidomastoid, SCM) and neck extensors (splenius capitis, SPL; semispinalis capitis, SSC), were simulated. The experimental tests included: 1. no muscle recruitment, 2. full muscle recruitments, 3. SCM dysfunction, 4. SPL dysfunction, and 5. SSC dysfunction. The external pure moment in sagittal plane was applied from 0 Nm to 2 Nm to examine the stability/flexibility of specimens. The spinal stability was evaluated by the neutral zone (NZ), the range of motion (ROM), the reduced NZ (R_NZ), and the reduced ROM (R_ROM). Loading responses of C7-T1 disc were also measured. The results of this study showed: The activation of cervical muscles decreased the NZ and ROM. The degree of decrease among different muscle dysfunctions, however, was not significantly different. The SPL dysfunction induced larger anterior shear force, while the SCM dysfunction exclusively induced extension moment. In conclusion, the muscle forces could stabilize the cervical spine, but significant decrease in spinal stability was not found among dysfunctions of different muscles. The SCM and SPL dysfunction may result in abnormal stress at the C7-T1 disc.

Mechanism of Cervical Spinal Cord Injury During Bilateral Facet Dislocation

An in vitro biomechanical study. The objectives were to: quantify dynamic canal pinch diameter (CPD) narrowing during simulated bilateral facet dislocation of a cervical functional spinal unit model with muscle force replication, determine if peak dynamic CPD narrowing exceeded that observed post-trauma, and evaluate dynamic cord compression. Previous biomechanical models are limited to quasi-static loading or manual ligament transection. No studies have comprehensively analyzed dynamic CPD narrowing during simulated dislocation. Bilateral facet dislocation was simulated using 10 cervical functional spinal units (C3-C4: n = 4; C5-C6: n = 3; C7-T1: n = 3) with muscle force replication by frontal impact of the lower vertebra. Rigid body transformation of kinematic data recorded optically was used to compute the CPD in neutral posture (before dislocation), during dynamic impact (peak during dislocation), and post-impact (flexion rotation = 0(0) degrees ). Peak dynamic impact and post-impact CPD narrowing were statistically compared. Average peak dynamic impact CPD narrowing significantly exceeded (P < 0.05) post-impact narrowing and occurred as early as 71.0 ms following impact. The greatest dynamic impact narrowing of 7.2 mm was observed at C3-C4, followed by 6.4 mm at C5-C6, and 5.1 mm at C7-T1, with average occurrence times ranging between 71.0 ms at C7-T1 and 97.0 ms at C5-C6. Extrapolation of the present results indicated dynamic spinal cord compression of up to 88% in those with stenotic canals and 35% in those with normal canal diameters. These results are consistent with the wide range of neurologic injury severity observed clinically due to bilateral facet dislocation.

Cervical facet joint kinematics during bilateral facet dislocation

Previous biomechanical models of cervical bilateral facet dislocation (BFD) are limited to quasi-static loading or manual ligament transection. The goal of the present study was to determine the facet joint kinematics during high-speed BFD. Dislocation was simulated using ten cervical functional spinal units with muscle force replication by frontal impact of the lower vertebra, tilted posteriorly by 42.5 degrees. Average peak rotations and anterior sliding (displacement of upper articulating facet surface along the lower), separation and compression (displacement of upper facet away from and towards the lower), and lateral shear were determined at the anterior and posterior edges of the right and left facets and statistically compared (P < 0.05). First, peak facet separation occurred, and was significantly greater at the left posterior facet edge, as compared to the anterior edges. Next, peak flexion rotation and anterior facet sliding occurred, followed by peak facet compression. The highest average facet translation peaks were 22.0 mm for anterior sliding, 7.9 mm for separation, 9.9 mm for compression and 3.6 mm for lateral shear. The highest average rotation of 63 degrees occurred in flexion, significantly greater than all other directions. These events occurred, on average, within 0.29 s following impact. During BFD, the main sagittal motions included facet separation, flexion rotation, anterior sliding, followed by compression, however, non-sagittal motions also existed. These motions indicated that unilateral dislocation may precede bilateral dislocation.

Cervical Spine Loads and Intervertebral Motions During Whiplash

Objective. To quantify the dynamic loads and intervertebral motions throughout the cervical spine during simulated rear impacts. Methods. Using a biofidelic whole cervical spine model with muscle force replication and surrogate head and bench-top mini-sled, impacts were simulated at 3.5, 5, 6.5, and 8 g horizontal accelerations of the T1 vertebra. Inverse dynamics was used to calculate the dynamic cervical spine loads at the centers of mass of the head and vertebrae (C1-T1). The average peak loads and intervertebral motions were statistically compared (P < 0.05) throughout the cervical spine. Results. Load and motion peaks generally increased with increasing impact acceleration. The average extension moment peaks at the lower cervical spine, reaching 40.7 Nm at C7-T1, significantly exceeded the moment peaks at the upper and middle cervical spine. The highest average axial tension peak of 276.9 N was observed at the head, significantly greater than at C4 through T1. The average axial compression peaks, reaching 223.2 N at C5, were significantly greater at C4 through T1, as compared to head-C1. The highest average posterior shear force peak of 269.5 N was observed at T1. Conclusion. During whiplash, the cervical spine is subjected to not only bending moments, but also axial and shear forces. These combined loads caused both intervertebral rotations and translations.

Dynamic sagittal flexibility coefficients of the human cervical spine

The goal of the present study was to determine the dynamic sagittal flexibility coefficients, including coupling coefficients, throughout the human cervical spine using rear impacts. A biofidelic whole cervical spine model ( n = 6) with muscle force replication and surrogate head was rear impacted at 5 g peak horizontal accelerations of the T1 vertebra within a bench-top mini-sled. The dynamic main and coupling sagittal flexibility coefficients were calculated at each spinal level, head/C1 to C7/T1. The average flexibility coefficients were statistically compared ( p < 0.05) throughout the cervical spine. To validate the coefficients, the average computed displacement peaks, obtained using the average flexibility matrices and the measured load vectors, were statistically compared to the measured displacement peaks. The computed and measured displacement peaks showed good overall agreement, thus validating the computed flexibility coefficients. These peaks could not be statistically differentiated, with the exception of extension rotation at head/C1 and posterior shear translation at C7/T1. Head/C1 was significantly more flexible than all other spinal levels. The cervical spine was generally more flexible in posterior shear, as compared to axial compression. The coupling coefficients indicated that extension moment caused coupled posterior shear translation while posterior shear force caused coupled extension rotation. The present results may be used towards the designs of anthropometric test dummies and mathematical models that better simulate the cervical spine response during dynamic loading.

Predicting Multiplanar Cervical Spine Injury Due to Head-Turned Rear Impacts Using IV-NIC

Objective. Intervertebral Neck Injury Criterion (IV-NIC) hypothesizes that dynamic three-dimensional intervertebral motion beyond physiological limit may cause multiplanar soft-tissue injury. Present goals, using biofidelic whole human cervical spine model with muscle force replication and surrogate head in head-turned rear impacts, were to: (1) correlate IV-NIC with multiplanar injury, (2) determine IV-NIC injury threshold at each intervertebral level, and (3) determine time and mode of dynamic intervertebral motion that caused injury. Methods. Impacts were simulated at 3.5, 5, 6.5, and 8 g horizontal accelerations of T1 vertebra (n = 6; average age: 80.2 years; four male, two female donors). IV-NIC was defined at each intervertebral level and in each motion plane as dynamic intervertebral rotation divided by physiological limit. Three-plane pre- and post-impact flexibility testing measured soft-tissue injury; that is significant increase in neutral zone (NZ) or range of motion (RoM) at any intervertebral level, above baseline. IV-NIC injury threshold was average IV-NIC peak at injury onset. Results. IV-NIC extension peaks correlated best with multiplanar injuries (P < 0.001): extension RoM (R = 0.55) and NZ (R = 0.42), total axial rotation RoM (R = 0.42) and NZ (R = 0.41), and total lateral bending NZ (R = 0.39). IV-NIC injury thresholds ranged between 1.1 at C0–C1 and C3–C4 to 2.9 at C7–T1. IV-NIC injury threshold times were attained between 83.4 and 150.1 ms following impact. Conclusions. Correlation between IV-NIC and multiplanar injuries demonstrated that three-plane intervertebral instability was primarily caused by dynamic extension beyond the physiological limit during head-turned rear impacts.

Head-turned rear impact causing dynamic cervical intervertebral foramen narrowing: implications for ganglion and nerve root injury

A rotated head posture at the time of vehicular rear impact has been correlated with a higher incidence and greater severity of chronic radicular symptoms than accidents occurring with the occupant facing forward. No studies have been conducted to quantify the dynamic changes in foramen dimensions during head-turned rear-impact collisions. The objectives of this study were to quantify the changes in foraminal width, height, and area during head-turned rear-impact collisions and to determine if dynamic narrowing causes potential cervical nerve root or ganglion impingement. The authors subjected a whole cervical spine model with muscle force replication and a surrogate head to simulated head-turned rear impacts of 3.5, 5, 6.5, and 8 G following a noninjurious 2-G baseline acceleration. Continuous dynamic foraminal width, height, and area narrowing were recorded, and peaks were determined during each impact; these data were then statistically compared with those obtained at baseline. The authors observed significant increases (p < 0.05) in mean peak foraminal width narrowing values greater than baseline values, of up to 1.8 mm in the left C5-6 foramen at 8 G. At the right C2-3 foramen, the mean peak dynamic foraminal height was significantly narrower than baseline when subjected to rear-impacts of 5 and 6.5 G, but no significant increases in foraminal area were observed. Analysis of the results indicated that the greatest potential for cervical ganglion compression injury existed at C5-6 and C6-7. Greater potential for ganglion compression injury existed at C3-4 and C4-5 during head-turned rear impact than during head-forward rear impact. Extrapolation of present results indicated potential ganglion compression in patients with a non-stenotic foramen at C5-6 and C6-7; in patients with a stenotic foramen the injury risk greatly increases and spreads to include the C3-4 through C6-7 as well as C4-5 through C6-7 nerve roots.

Dynamic Intervertebral Foramen Narrowing During Simulated Rear Impact

A biomechanical study of intervertebral foraminal narrowing during simulated automotive rear impacts. To quantify foraminal width, height, and area narrowing during simulated rear impact, and evaluate the potential for nerve root and ganglion impingement in individuals with and without foraminal spondylosis. Muscle weakness and paresthesias, documented in whiplash patients, have been associated with neural compression within the cervical intervertebral foramen. To our knowledge, no studies have comprehensively examined dynamic changes in foramen dimensions. There were 6 whole cervical spine specimens (average age 70.8 years) with muscle force replication and surrogate head that underwent simulated rear impact at 3.5, 5, 6.5, and 8 g, following noninjurious baseline 2 g acceleration. Peak dynamic narrowing of foraminal width, height, and area were determined during each impact and statistically compared to baseline narrowing. Significant increases (P < 0.05) in average peak foraminal width narrowing above baseline were observed at C5-C6 beginning with 3.5 g impact. No significant increases in average peak foraminal height narrowing were observed, while average peak foraminal areas were significantly narrower than baseline at C4-C5 at 3.5, 5, and 6.5 g. Extrapolation of the present results indicated that the highest potential for ganglia compression injury was at the lower cervical spine, C5-C6 and C6-C7. Acute ganglia compression may produce a sensitized neural response to repeat compression, leading to chronic radiculopathy following rear impact.

Alar, Transverse, and Apical Ligament Strain due to Head-Turned Rear Impact

Determination of alar, transverse, and apical ligament strains during simulated head-turned rear impact. To quantify the alar, transverse, and apical ligament strains during head-turned rear impacts of increasing severity, to compare peak strains with baseline values, and to investigate injury mechanisms. Clinical and epidemiologic studies have documented upper cervical spine ligament injury due to severe whiplash trauma. There are no previous biomechanical studies investigating injury mechanisms during head-turned rear impacts. Whole cervical spine specimens (C0-T1) with surrogate head and muscle force replication were used to simulate head-turned rear impacts of 3.5, 5, 6.5, and 8 g horizontal accelerations of the T1 vertebra. The peak ligament strains during impact were compared (P < 0.05) to baseline values, obtained during a noninjurious 2 g acceleration. The highest right and left alar ligament average peak strains were 41.1% and 40.8%, respectively. The highest transverse and apical ligament average strain peaks were 17% and 21.3%, respectively. There were no significant increases in the average peak ligament strains at any impact acceleration compared with baseline. The alar, transverse, and apical ligaments are not at risk for injury due to head-turned rear impacts up to 8 g. The upper cervical spine symptomatology reported by whiplash patients may, therefore, be explained by other factors, including severe whiplash trauma in excess of 8 g peak acceleration and/or other impact types, e.g., offset, rollover, and multiple collisions.

Multiplanar Cervical Spine Injury Due to Head-Turned Rear Impact

Head-turned whole cervical spine model was stabilized with muscle force replication and subjected to simulated rear impacts of increasing severity. Multiplanar flexibility testing evaluated any resulting injury. To identify and quantify cervical spine soft tissue injury and injury threshold acceleration for head-turned rear impact, and to compare these data with previously published head-forward rear and frontal impact results. Epidemiologically and clinically, head-turned rear impact is associated with increased injury severity and symptom duration, as compared to forward facing. To our knowledge, no biomechanical data exist to explain this finding. Six human cervical spine specimens (C0-T1) with head-turned and muscle force replication were rear impacted at 3.5, 5, 6.5, and 8 g, and flexibility tests were performed before and after each impact. Soft tissue injury was defined as a significant increase (P < 0.05) in intervertebral flexibility above baseline. Injury threshold was the lowest T1 horizontal peak acceleration that caused the injury. The injury threshold acceleration was 5 g with injury occurring in extension or axial rotation at C3-C4 through C7-T1, excluding C6-C7. Following 8 g, 3-plane injury occurred in extension and axial rotation at C5-C6, while 2-plane injury occurred at C7-T1. Head-turned rear impact caused significantly greater injury at C0-C1 and C5-C6, as compared to head-forward rear and frontal impacts, and resulted in multiplanar injuries at C5-C6 and C7-T1.