Facet joint components may be at risk for injury due to facet joint compression during rear-impact accelerations of 3.5 g and above. Capsular ligaments are at risk for injury at higher accelerations.

STUDY DESIGN Non-systematic review of cervical spine lesions in whiplash-associated disorders (WAD). OBJECTIVE To describe whiplash injury models in terms of basic and clinical science, to summarize what can and cannot be explained by injury models, and to highlight future research areas to better understand the role of tissue damage in WAD. SUMMARY OF BACKGROUND DATA The frequent lack of detectable tissue damage has raised questions about whether tissue damage is necessary for WAD and what role it plays in the clinical context of WAD. METHODS Non-systematic review. RESULTS Lesions of various tissues have been documented by numerous investigations conducted in animals, cadavers, healthy volunteers and patients. Most lesions are undetected by imaging techniques. For zygapophysial (facet) joints, lesions have been predicted by bioengineering studies and validated through animal studies; for zygapophysial joint pain, a valid diagnostic test and a proven treatment are available. Lesions of dorsal root ganglia, discs, ligaments, muscles and vertebral artery have been documented in biomechanical and autopsy studies, but no valid diagnostic test is available to assess their clinical relevance. The proportion of WAD patients in whom a persistent lesion is the major determinant of ongoing symptoms is unknown. Psychosocial factors, stress reactions and generalized hyperalgesia have also been shown to predict WAD outcomes. CONCLUSION There is evidence supporting a lesion-based model in WAD. Lack of macroscopically identifiable tissue damage does not rule out the presence of painful lesions. The best available evidence concerns zygapophysial joint pain. The clinical relevance of other lesions needs to be addressed by future research.

BACKGROUND CONTEXT-Most previous studies have investigated ligaments mechanical properties at slow elongation rates of less than 25 mm/s.

Whiplash injury is the most common motor vehicle injury, yet it is also one of the most poorly understood. Here we examine the evidence supporting an organic basis for acute and chronic whiplash injuries and review the anatomical sites within the neck that are potentially injured during these collisions. For each proposed anatomical site--facet joints, spinal ligaments, intervertebral discs, vertebral arteries, dorsal root ganglia, and neck muscles--we present the clinical evidence supporting that injury site, its relevant anatomy, the mechanism of and tolerance to injury, and the future research needed to determine whether that site is responsible for some whiplash injuries. This article serves as a snapshot of the current state of whiplash biomechanics research and provides a roadmap for future research to better understand and ultimately prevent whiplash injuries.

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A rear-end collision is most likely to injure the lower cervical spine by intervertebral hyperextension at a peak T1 horizontal acceleration of 5 g and above. These results may aid in the design of injury prevention systems and more precise diagnoses of whiplash injuries.

The purpose of the present study was to investigate whether increased intra-abdominal pressure (IAP) can be achieved without elevating the overall trunk muscle co-contraction that causes increased spine compression force. Ten subjects performed isometric trunk flexion, extension, and lateral bending exertions while generating 0%, 40% and 80% of their maximal IAP or while co-contracting trunk muscles without consciously raising IAP. An additional three subjects performed a variety of ramp IAP, co-contraction and isometric exertion tasks while holding their breaths and while exhaling. An 18 degree-of-freedom, electromyogram (EMG)-assisted biomechanical model was used to quantify trunk muscle co-contraction with calculations of spine compression force and stability. Spine stability and compression force increased proportionally with increased IAP regardless of whether the subjects intentionally generated IAP or consciously avoided it. This increase was accomplished with significantly greater co-contraction of 12 major trunk muscles. The EMG activation of all muscles was highly correlated with IAP and intra-thoracic pressure (ITP) ( r from 0.59 to 0.95). Activity of the thoracic erector spinae correlated the best with ITP ( r=0.81), which in turn was correlated with IAP ( r=0.91). It was not possible to co-contract trunk muscles without generating IAP and ITP, or conversely to generate IAP without trunk muscle co-contraction and increased ITP.

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