Whole cervical spine model with muscle force replication was subjected to simulated frontal impacts of increasing severity, and resulting injuries were evaluated via flexibility testing.
To identify and quantify cervical spine soft tissue injury and the injury threshold acceleration due to frontal impact.
Cervical spine instability may result from automotive collisions. No previous studies have quantified soft tissue injuries due to frontal impact.
Six human cervical specimens (occiput-T1) with muscle force replication were subjected to frontal impacts of 4, 6, 8, and 10 g. Before frontal impact, baseline flexibility data were collected following a 2 g simulation. Flexibility parameters of total (flexion plus extension) neutral zone (NZ), flexion NZ, total range of motion (ROM), and flexion ROM were obtained following each impact and compared with baseline flexibility. Injury was a significant increase (P < 0.05) in intervertebral flexibility due to frontal impact over baseline. Injury threshold was the lowest T1 peak acceleration that caused injury.
The injury threshold acceleration was 8 g, as determined by significant increases of 12.6 to 51.4% over the baseline flexibility, in the C4–C5 total NZ, and the C6–C7 total NZ, flexion NZ, total ROM, and flexion ROM. Following 10 g, significant increases in flexibility parameters were observed at C2–C3, C3–C4, C4–C5, C6–C7, and C7–T1.
Middle (C2–C3 to C4–C5) and lower (C6–C7 and C7–T1) cervical spine were at risk for injury during frontal impacts, for the experimental conditions studied.
The whole cervical spine model with muscle force replication underwent incremental frontal impacts, and resulting increases in flexibility parameters were monitored. The injury threshold acceleration was 8 g. The middle (C2–C3–C4–C5) and lower (C6–C7 and C7–T1) cervical spine regions were injured because of intervertebral hyperflexion.
From the *Department of Orthopaedic Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire; the †Biomechanics Research Laboratory, Department of Orthopedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticut; the ‡Department of Orthopaedic Surgery, St. Marianna University School of Medicine, Kanagawa, Japan; and the §Orthopaedic Biomechanics Laboratory, Union Memorial Hospital, Baltimore, Maryland.
Acknowledgment date: May 7, 2004. First revision date: July 12, 2004. Acceptance date: July 14, 2004.
This research was supported by NIH Grant 1 R01 AR45452 1A2 and the Doris Duke Charitable Foundation.
The manuscript submitted does not contain information about medical device(s)/drug(s).
Federal and Institutional funds were received to support this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.
Address correspondence and requests for reprints to Manohar M. Panjabi, PhD, Biomechanics Research Laboratory, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, 333 Cedar St. P.O. Box 208071, New Haven, CT 06520-8071; E-mail: firstname.lastname@example.org