It has been true that the cause of symptoms remains obscure in many whiplash patients; Castro et al’s contention that it is true in "virtually all 'whiplash' patients" is definitely not true. One must question the motivation of such a statement right from the start of this paper. Perhaps that is why it was published in a defense-oriented legal journal and not a medical or engineering journal. In any case, the cause of many injuries after whiplash is often very clear, for example, when one or more herniated discs visible on MRI after whiplash were not present on MRI in days or weeks before the crash.
In any case, it remains true that "it is impossible to identify acute pathology in many cases", as Castro et al stated. Certainly MRI is not sensitive to detect many of the other connective tissue tears and lesions after whiplash. A recent study by Yoganandan et al clearly showed that x-ray, CT and MRI are most often insensitive to serious connective tissue injuries after whiplash (see Yoganandan N, Cusick JF, Pintar FA, Rao RD. Whiplash injury determination with conventional spine imaging and cryomicrotomy. Spine 2001; 26: 2443-2448). Many other studies show this to be true as well (see review by Uhrenholt L, Grunnett-Nilson N, Hartvigsen J. Cervical spine lesions after road traffic accidents. Spine 2002; 27(17): 1934-1941).
One of the reasons why MRI is not sensitive enough to view even serious lesions, such as ligament avulsions, ligament tears, hematomas, intervertebral disc rim lesions, disc avulsions and cartilage contusions, is because MRI image slices are spaced no closer than about 1/8 inch. The injured cervical spine structures are very small, often less than 1/8 inch. Therefore, serious and painful injuries to ligamentous structures are simply not visible. MRI is certainly not a “gold standard” for identifying these serious lesions. Yoganandan’s brilliant study illustrates this point very well for cadavers that were crashed at delta V’s of 9.8 mph and 15.2 mph delta V’s. The authors state: "The change in velocity was 4.4 m/sec or 6.8 m/sec with a pulse duration of 137 msec or 154 msec. This level of acceleration pulse was chosen on the basis of published reports indicating that 75–90% of whiplash injuries occur at speeds less than 6.9 m/sec".
Another problem with MRI is that injured persons must lie down for an MRI exam. Lying down takes much of the pressure off the intervertebral discs. What appears to be a “normal” disc lying down may not be when standing up. The potential for false negatives on MRI is very large. Further, MRI pictures are taken with the injured patient stationary. If the patient moves, then a blurry, useless picture may result.
Fortunately, motion study MRI, where the patient may be placed in any position is rapidly becoming available. "Stand-up MRI" is here (see Fonar Corporation), although not yet widely used. Many persons whose cervical intervertebral discs appeared "normal" on supine (laying flat) MRI were shown to have, in fact, seriously herniated discs when they underwent MRI in the upright position with neck extended. This is one of the reasons why spinal surgeons cannot rely solely on MRI to make a decision to operate. Discs appear in better shape than they truly are, due to the lack of pressure placed on them when they are lying down. Most of us don’t spend our days in the supine position.
A third defect with the Castro et al study is that, contrary to the statements by the authors, there may have been biomechanical stress imparted to the subjects in this study. In the study, before any subject testing was done, the authors crashed an Audi 200 into the rear end of an Opel Ascona at a Vc of 13 mph, with the vehicles aligned at an offset of 30% to the left rear of the Opel. There was visible damage to the Opel, and the authors placed crash debris and broken glass behind the Opel prior to the placebo crash. The Opel’s rear tires were elevated on a ramp that was 2 inches high and fastened with a steel cable. To simulate restitution after the placebo impact, the cable was released to allow the Opel to travel about 4 feet down the ramp. The authors also suspended a 242-lb. metal plate in the trunk of the Opel which fell 6 inches onto a glass bottle to simulate the sound of a crash.
While the authors did evaluate horizontal acceleration of the Opel (minimal at 0.03 g horizontal), the authors did not comment on the vertical acceleration forces imparted to the Opel’s occupants, resulting from dropping the 242-lb. plate in to the trunk of the Opel.
A fourth flaw of this study is that directly following the collisions, 9 of 51 subjects (17.6%) had symptoms including tachycardia, palpitations, and "trembling knees", according to these authors. All of the subjects reported that these symptoms were the result of the placebo collision. Three days after the placebo collision, 10 subjects reported symptoms. At four weeks, 5 subjects reported symptoms, but 4 of these 5 stated that they did not think their symptoms were related to the placebo collision.
Based on these results, Castro et al concluded that "Approximately 20% of subjects exposed to placebo, low-velocity rear-end collisions will thus indicate WAD [whiplash-associated disorders], even though no biochemical potential for injury exists. Certain psychological profiles place an individual at higher risk for phenomenon".
But Castro et al. simply scared the hell out of their research subjects. The authors simply produced a startle response in their subjects, a frightening event that the subjects did not expect because they were told it would not occur (subjects were told that they would be subjected to a rear-end collision that would "definitely not exceed the effects of rear-end collisions in a bumper car at the fun fair"). They therefore lied to the research subjects, because they subjected them to the sound of breaking glass, screeching brakes or skidding tires that are certainly not present with bumper cars. A startle response in humans is known to cause involuntary muscle contractions greater than voluntary contractions, and this has even been seen in human subject auto crash tests (see Szabo TJ, Welcher JB. Human subject kinematics and electromyographic activity during low speed rear impacts. SAE Tech Paper Series 1996; 962432: 295-315). Therefore, Castro et al likely had a biomechanical str
ess in that regard as well.
The fifth and perhaps most serious flaw in the Castro et al study is that the symptoms reported by the subjects in this study would be expected after being frightened. To then try to extrapolate this experience to a true rear-end collision is ludicrous. The forces involved in a true rear-end impact collision are very different than this "placebo" collision. Yet the authors claim that the psychological response of their subjects must also be the cause of symptoms in a real-world crash. It just doesn’t make sense. This conclusion is not scientific. The alleged "whiplash-associated disorders" found in these research subjects were not related to whiplash in any way. They were related to being unexpectedly startled and jolted in a way thoroughly unrelated to the whiplash-injury mechanism.
Many other have criticized this study, including Michael D. Freeman, Ph.D., D.C., M.P.H. (see Injury Forum, courtesy of Richard Serrousi, M.D.) and Gunther Siegmund at MacInnes Engineering (see Siegmund GP, Brault JR, Wheeler JB. Placebo whiplash data need cautious interpretation. Int J Legal Med. 2002 Aug;116(4):251). One must question what motivates the authors of this "placebo" study. It appears that Castro et al group began with the premise that symptoms after low speed rear impacts are not the result of real physical injury, and then embark on a project to prove this hypothesis, rather than test its validity (see Freeman MD).
It is impossible to state that physical inj