Manohar M. Panjabi

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.

Study Design. 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. Objectives. 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. Summary of Background Data. 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. Methods. 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. Results. 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. Conclusions. 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.

Objective. Intervertebral Neck Injury Criterion (IV-NIC) is based on the hypothesis that dynamic three-dimensional intervertebral motion beyond physiological limits may cause multiplanar injury of cervical spine soft tissues. Goals of this study, using a biofidelic whole human cervical spine model with muscle force replication and surrogate head in simulated side impacts, were to correlate IV-NIC with multiplanar injury and determine IV-NIC injury threshold for each intervertebral level. Methods. Using a bench-top apparatus, side impacts were simulated at 3.5, 5, 6.5, and 8 g horizontal accelerations of the T1 vertebra. Pre- and post-impact flexibility testing in three-motion planes measured the soft tissue injury, i.e., significant increase (p < 0.05) in neutral zone (NZ) or range of motion (RoM) at any intervertebral level, above corresponding physiological limit. Results. IV-NIC in left lateral bending correlated well with total lateral bending RoM (R = 0.61, P < 0.001) and NZ (R = 0.55, P < 0.001). Additionally, the same IV-NIC correlated well with left axial rotation RoM (R = 0.50, P < 0.001). IV-NIC injury thresholds (95% confidence limits) varied among intervertebral levels and ranged between 1.5 (0.6–2.4) at C3-C4 and 4.0 (2.4–5.7) at C7-T1. IV-NIC injury threshold times were attained beginning at 84.5 ms following impact. Conclusions. Present results suggest that IV-NIC is an effective tool for determining multiplanar soft tissue neck injuries by identifying the intervertebral level, mode, time, and severity of injury.

Between 23 and 70% of occupants involved in frontal impacts sustain cervical spine injuries, many with neurological involvement. It has been hypothesized that cervical spinal cord compression and injury may explain the variable neurological profile described by frontal impact victims. The goals of the present study, using a biofidelic whole cervical spine model with muscle force replication, were to quantify canal pinch diameter (CPD) narrowing during frontal impact and to evaluate the potential for cord compression. The biofidelic model and a sled apparatus were used to simulate frontal impacts at 4, 6, 8, and 10 g horizontal accelerations of the T1 vertebra. The CPD was measured in the intact specimen in the neutral posture (neutral posture CPD), under static sagittal pure moments of 1.5 Nm (pre-impact CPD), during dynamic frontal impact (dynamic impact CPD), and again under static pure moments following each impact (post-impact CPD). Frontal impact caused significant (P<0.05) dynamic CPD narrowing at C0-dens, C2-C3, and C6-C7. The narrowest dynamic CPD was observed at C0-dens during the 10 g impact and was 25.9% narrower than the corresponding neutral posture CPD. Interpretation of the present results indicate that the neurological symptomatology reported by frontal impact victims is most likely not due to cervical spinal cord compression. Cord compression due to residual spinal instability is also not likely.

Clinical reports and research studies have documented the behavior of chronic low back and neck pain patients. A few hypotheses have attempted to explain these varied clinical and research findings. A new hypothesis, based upon the concept that subfailure injuries of ligaments (spinal ligaments, disc annulus and facet capsules) may cause chronic back pain due to muscle control dysfunction, is presented. The hypothesis has the following sequential steps. Single trauma or cumulative microtrauma causes subfailure injuries of the ligaments and embedded mechanoreceptors. The injured mechanoreceptors generate corrupted transducer signals, which lead to corrupted muscle response pattern produced by the neuromuscular control unit. Muscle coordination and individual muscle force characteristics, i.e. onset, magnitude, and shut-off, are disrupted. This results in abnormal stresses and strains in the ligaments, mechanoreceptors and muscles, and excessive loading of the facet joints. Due to inherently poor healing of spinal ligaments, accelerated degeneration of disc and facet joints may occur. The abnormal conditions may persist, and, over time, may lead to chronic back pain via inflammation of neural tissues. The hypothesis explains many of the clinical observations and research findings about the back pain patients. The hypothesis may help in a better understanding of chronic low back and neck pain patients, and in improved clinical management.

The supraspinous and interspinous ligaments, ligamentum flavum, and capsular and posterior longitudinal ligament strains were monitored during simulated frontal impact of whole cervical spine specimens with muscle force replication and compared with corresponding physiologic strain limits. To quantify the strains in the cervical spine ligaments during simulated frontal impact and investigate injury mechanisms. Clinical and biomechanical studies have documented injuries to cervical spine ligaments during frontal impact. There are no biomechanical studies investigating subfailure injury mechanisms to these ligaments during simulated frontal impacts of increasing severity. The whole cervical spine with muscle force replication model and a bench-top sled were used to simulate frontal impacts at 4, 6, 8, and 10g horizontal accelerations of the T1 vertebra. The peak ligament strains during frontal impacts were compared with physiologic strain limits determined during intact flexibility testing. Significant increases (P < 0.05) in the supraspinous and interspinous ligaments and the ligamentum flavum strains beyond physiologic limits were observed throughout the cervical spine, with the highest strains occurring at C3–C4. Significant increases were observed in the capsular ligament strains only during the 10g impact, whereas the posterior longitudinal ligament strains did not exceed physiologic limits. The supraspinous and interspinous ligaments and the ligamentum flavum may be at risk for injury due to excessive strains during frontal impacts.

Whiplash has been simulated using volunteers, whole cadavers, mathematical models, anthropometric test dummies, and whole cervical spines. Many previous in vitro whiplash models lack dynamic biofidelity. The goals of this study were to (1) develop a new dynamic whole cervical spine whiplash model that will incorporate anterior, lateral and posterior muscle force replication, (2) evaluate its performance experimentally and (3) compare the results with in vivo data. To evaluate the new model, rear-impact whiplash simulations were performed using the incremental trauma approach at maximum measured T1 horizontal accelerations of 3.6 g, 4.7 g, 6.6 g, and 7.9 g. The kinematic response of the new model, e.g., peak head–T1 extension and peak intervertebral rotations, were compared with the corresponding in vivo data. The average peak head–T1 extension was within the in vivo corridor during the 3.6 g whiplash simulation (9.1 kph delta V). The peak in vivo intervertebral rotations obtained during a 4.6 g whiplash simulation of a young volunteer were within, or only marginally in excess of, the 95% confidence limits of the average peak intervertebral rotations measured during the 4.7 g whiplash simulation of the present study. Thus, the new whole cervical spine model with muscle force replication produced biofidelic dynamic responses to simulated whiplash. The new model is capable of generating important biomechanical data that may help improve our understanding of whiplash injuries and injury mechanisms.

Cervical disc injury due to frontal impact has been observed in both clinical and biomechanical investigations; however, there is a lack of data that elucidate the mechanisms of disc injury during these collisions. The goals of the current study were to determine the peak dynamic disc annular tissue strain and disc shear strain during simulated frontal impact of the whole human cervical spine model with muscle force replication at 4 g, 6 g, 8 g and 10 g horizontal accelerations of the T1 vertebra. These data were compared with those obtained during physiological loading, and with previously reported rear impact data. Peak disc shear strain and peak annular tissue strain during frontal impact exceeded (p<0.05) corresponding physiological limits at the C2–C3 intervertebral level, beginning at 4 g and 6 g, respectively. These subsequently spread throughout the entire cervical spine at 10 g, with the exception of C4–C5. The C5–C6 intervertebral level was at high risk for injury during both frontal and rear impacts, while during frontal impact, in addition to C5–C6, subfailure injuries were likely at superior intervertebral levels, including C2–C3. The disc injuries occurred at lower impact accelerations during rear impact as compared with frontal impact. The subfailure injuries of the cervical intervertebral disc that occur during frontal impact may lead to the chronic symptoms reported by patients, such as head and neck pain.