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Classical description of the whiplash injury restricts the definition to movements of the neck in the sagittal plane only, with forced flexion and extension only. It has been found that both the axial compression and the unnatural double curvature of the cervical spine are important in the initial response of the cervical spine to the load. One common misperception about the whiplash injury is that if a vehicle does not sustain damage, or if the damage to the vehicle is minimal, then the occupants could not have sustained a severe whiplash injury. However, scientific studies have shown that low-speed collisions may produce whiplash injuries just as severe as in high-speed collisions. In higher-speed collisions, the metal of the vehicle crushes and deforms, which dissipates much of the energy of the collision. It was inferred from this experiment that substantial compressive forces were exerted on the cervical range of motion. In this experiment, the subjects reported mild discomfort and neck pain that lasted 2a€“4 days, but none had any long-term sequelae. The segments achieved peak initial flexion between 50 and 110 ms after impact and peak extension between 100 and 200 ms after impact.
However, what constitutes a low-speed impact can vary according to the different authorities performing the studies.

In particular, whilst extension occurs about an abnormally high axis of rotation, the vertebra rotates which results in abnormal separation of the anterior elements of the neck and abnormal patterns of compression posteriorly.
Head restraints have also proved to be effective in preventing whiplash injury only when they are properly positioned.
Due to the infolding of the ligamentum flavum on extension, the cross-sectional area of the spinal canal actually decreases on extension and increases on flexion7 (Figure 2). The nerve tissues within the spinal canal are incompressible during a typical whiplash injury with rapid flexion-extension, and so there are changes of the cerebrospinal fluid (CSF) as well as the blood flow in order to compensate any change in space. Hence, in a typical whiplash injury, pressure gradients in the spinal fluid column form, causing mechanical stress on the nerve tissues8 (Figure 3).
These joints act as a barrier between the intervertebral disc and the neural contents of the foramen. Thus, when the head is turned in a whiplash injury, the rotary forces on the adjacent vertebra may cause tearing of the annular fibers at the moment of the impact9 (Figure 4).
This a€?inflammatory soupa€™ in turn, sensitizes the calcium channels of the nerve, with increased sensitization of the dorsal root ganglia and the dorsal horn neurons.
The exact mechanism of spinal cord hyperexcitability is unknown but it is postulated that the inflammation produces cyclooxygenase-2 (COX-2) in the spinal cord, which leads to production of prostaglandin, which secondarily produces hyperexcitability of the spinal neurons. This hyperexcitability is also observed in the entire spinal cord and the supraspinal centers. The term a€?muscle spasma€™ has proved to have poor reliability because of the apparent reason that there is a huge inter-observer discrepancy. Abnormal stretch reflex is likely a major cause of muscular symptoms after a whiplash injury. Cephalalgia may be present and the discomfort is felt around the scalp area, or at the base of the occiput (Figure 10). Treatments involve various modalities such as oral analgesics, heat, massage, local injection of anesthetics and steroids. Cloward, as early as the 1950a€™s, had already demonstrated that interscapular pain may be produced by intranuclear discograms, where there is irritation of the anterior part of the disc23 (Figure 12).

Monitor liver function, hemoglobin, hematocrit, prostate specific antigen (PSA), cholesterol, bone age. However, with further experimentation and scientific studies, this belief will need to be further re-considered for it has been revealed that the movements involved are more complex than was previously ascertained. Thus, the overall result is that the cervical spine assumed an S shaped curve at about 100 ms, while the lower segments started extension while the higher segments were still undergoing flexion. The standard suggestion is that the restraint is placed at least 27.5 inches above the seating reference point.
Typical lesions are those with avulsion of the disc from the vertebral end-plate and tears of the annulus fibrosus of the disc.
Rim lesions are a separation of the outer annular fibers of the disc from the outer avascular cartilage plates, which are connected to the outer, highly vascular bony endplate14 (Figure 5). Activation of the glial cells in the spinal cord is also involved in the widespread hyperexcitability of the spinal cord neurons (Figure 7). A stretch reflex is initiated by the passive, unexpected stretch of a voluntary muscle that causes the spindle system to discharge (Figure 9). After reaching the inferior oblique muscle, it bends and then courses in a medial and superior direction through the semispinalis muscle forming the 2nd bend.
Surgery may be indicated which involves releasing the nerve by dividing the inferior oblique muscle. It is performed while placing the head laterally and turned towards the affected side with axial compression. It then transverses between the trapezius muscle and travels upward and laterally (Figure 11). It is considered to be positive if there is reproduction of the radicular pain (Figure 13).

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