For those of you who have yet to hear about the Smooth Pursuit Neck Torsion test, it's had an impeccable research pedigree. It's one of the few tests that has great separation of the data between normal controls and injured patients, meaning that injured patients produce a value on the test that isn't found in normal subjects. The test is also objective, very difficult to fake, and part of an ENG battery that's been performed since the 1950's. That's why we were surprised to come across the paper by Kongsted which seemed to show that the test result produced by SPNT (Gain), was not statistically different in a whiplash group and a normal control group. As usual, once you peer "under the hood" it becomes pretty clear why they got this result. For more on those details, see below. However, this brings up a much bigger issue about research and academics. Clearly, the Kongsted group is not made up of clinicians, but of academic researchers. Why is this clear? For clinicians performing research, the easiest subjects to recruit are patients (we have lots of those) and the hardest are "normal controls" (we don't see those). As discussed below, this group had no problem finding almost twice as many normal controls as patient subjects.
The bigger issue is why are academics (who don't normally see these patients) getting involved in research about a test that has only clinical value? The motive becomes clear when one investigates that the source of funding for the study was in fact that auto insurance industry in Denmark.
Here's the editorial just submitted by Micheal Freeman any myself...
Editorial Submission on Kongsted, A., et al., Are smooth pursuit eye movements altered in chronic whiplash-associated disorders? A cross-sectional study. Clin Rehabil, 2007. 21(11): p. 1038-49
Christopher J. Centeno, M.D., Michael Freeman, Ph.D., M.P.H.
We read with much interest the research on the Smooth Pursuit Neck Torsion test and WAD published by Kongsted.[1] Since this study had very different conclusions from other research on this diagnostic test, we decided to investigate further.
The authors state, “The sample size needed to reach a power of 90% with a significance level of 5%... Under these conditions we required 40 cases and 60 controls.” With this statement we were surprised to find only 34 subjects. It also seemed odd to us that controls outnumbered subjects almost 2 to 1. Usually normal controls are very difficult to recruit. Table 1 shows that only 15 of their subjects had daily neck pain, 12 had daily headache, and only 4 had daily dizziness. Even if we add back the subjects without daily, but severe pain that occurred on an infrequent basis that leaves at most (15 + 11) 26 WAD subjects who had any type of symptom complaint that would likely cause them to seek specialty care. This is now significantly less than their power calculation revealed would be needed.
Yet another issue with the WAD group is the number of patients with moderate or severe daily neck pain (15/34) vs. the number of patients with moderate or severe daily dizziness (4/34). If one looks at this data from the other direction, there are 2/34 WAD subjects with mild occasional, regular, or daily neck pain, but 11/34 WAD subjects with mild occasional, regular, or daily dizziness. This difference is significant, as Treleaven found that this test to be positive in 90% of patients who reported dizziness vs. 54% of patients who did not.[2] Clearly the group most likely to have a positive test (WAD patients with dizziness) is skewed toward mild symptoms.
In order to compare this tested WAD group to the severity of prior studies, we contacted Treleaven. While her SPNT paper did not include severity data, this study was part of a more comprehensive investigation which did measure this data. Mean (SEM) NDI of their WAD non- dizzy group was 34.4(2.0) and WAD dizzy group was 46.4(2.1). If one looks at the interpretation of this data by the original authors of the neck disability index (NDI), Treleaven’s non-dizzy group would be categorized as “severely disabled” and her dizzy group would be categorized as “completely disabled”.[3] While Kongsted did not use NDI, the review of their pain frequency data above would clearly define these groups as significantly less severe than either of the Trealeven subgroups.
The authors also state, “A box plot revealed that patients with severe neck pain or headache during the previous two weeks tended to obtain lower gains than patients with mild or moderate pain…” This is not surprising, as above, we discuss that the recruited subjects had very mild symptom frequency. Here the authors confirm our suspicion that their own analysis showed that patients with more frequent symptoms tended to have more positive tests. The authors also state, “Lower gains were slightly more frequent in patients with dizziness, but the results were almost similar to those for patients without dizziness (Figure 3).” Again, this trend is not surprising given the fact that the dizziness in the subject group is heavily skewed toward mild symptoms. It should be noted that the total number of subjects with dizziness is only 27, more than 30% lower than the n required by their power calculation to reach significance with an expected gain difference of 5%.
From our review of this paper, the conclusion should read, "When we compared a statically underpowered group of mild WAD and even more mild dizzy WAD patients to a larger control group, we did not detect significant differences in gain between our small mild WAD group and the normal control group."
1. Kongsted, A., et al., Are smooth pursuit eye movements altered in chronic whiplash-associated disorders? A cross-sectional study. Clin Rehabil, 2007. 21(11): p. 1038-49.
2. Treleaven, J., G. Jull, and N. LowChoy, The relationship of cervical joint position error to balance and eye movement disturbances in persistent whiplash. Man Ther, 2006. 11(2): p. 99-106.
3. Vernon, H. and S. Mior, The Neck Disability Index: a study of reliability and validity. J Manipulative Physiol Ther, 1991. 14(7): p. 409-15.
Monday, November 19, 2007
Wednesday, November 7, 2007
A Greek with Whiplash...
Partheni M, Miliaras G, Constantoyannis C, Papadakis N.
Related Articles,
Links
Whiplash injury.J Rheumatol. 1999 May;26(5):1206-7; author reply 1208-10. No abstract available. PMID: 10332996 [PubMed - indexed for MEDLINE]
In 1999, a paper was published by Partheni presuming to show that chronic whiplash injury didn't exist in Greece. This paper was widely criticized in the research community because it had poor methodology. The problem was that it failed to send questionnaires to enough Greeks to find cases of chronic whiplash. It was followed up with numerous papers that again seemed to be following on this same concept.
When George showed up in my clinic in 2003, I had a big chuckle. He was a Greek with chronic whiplash who had traveled thousands of miles for care here in the US. His work-up eventually showed upper cervical instability and objective MRI changes in the alar ligaments. He had a VNG in Greece showing severe abnormal nystagmus and his Smooth Pursuit Neck Torsion Test (SPNT) performed here by our clinic was grossly abnormal. So not only was there chronic whiplash in Greece, it can be objectified just as it can be here in the US, in Australia, or any other country. The Greek literature barrage was busted.
When you speak with George, it becomes clear why whiplash is not identified in Greece. George's family clearly has means. The medical system in Greece completely misidentified his injury. It wasn't until he bought his way to see some of the best specialists in the country that he met an ENT physician who was able to give him a diagnosis. So the problem isn't that whiplash doesn't exist in Greece or Lithuania, it's that poor nationalized health care systems strained with taking care of life threatening illnesses can't spend the resources to worry about traumatic neck pain. If you have money in those poor countries, you can get your whiplash diagnosed and handled. If you don't, you're at the mercy of an underfunded and overworked system.
Related Articles,
Links
Whiplash injury.J Rheumatol. 1999 May;26(5):1206-7; author reply 1208-10. No abstract available. PMID: 10332996 [PubMed - indexed for MEDLINE]
In 1999, a paper was published by Partheni presuming to show that chronic whiplash injury didn't exist in Greece. This paper was widely criticized in the research community because it had poor methodology. The problem was that it failed to send questionnaires to enough Greeks to find cases of chronic whiplash. It was followed up with numerous papers that again seemed to be following on this same concept.
When George showed up in my clinic in 2003, I had a big chuckle. He was a Greek with chronic whiplash who had traveled thousands of miles for care here in the US. His work-up eventually showed upper cervical instability and objective MRI changes in the alar ligaments. He had a VNG in Greece showing severe abnormal nystagmus and his Smooth Pursuit Neck Torsion Test (SPNT) performed here by our clinic was grossly abnormal. So not only was there chronic whiplash in Greece, it can be objectified just as it can be here in the US, in Australia, or any other country. The Greek literature barrage was busted.
When you speak with George, it becomes clear why whiplash is not identified in Greece. George's family clearly has means. The medical system in Greece completely misidentified his injury. It wasn't until he bought his way to see some of the best specialists in the country that he met an ENT physician who was able to give him a diagnosis. So the problem isn't that whiplash doesn't exist in Greece or Lithuania, it's that poor nationalized health care systems strained with taking care of life threatening illnesses can't spend the resources to worry about traumatic neck pain. If you have money in those poor countries, you can get your whiplash diagnosed and handled. If you don't, you're at the mercy of an underfunded and overworked system.
Tuesday, November 6, 2007
Shannon AL, Ferrari R, Russell AS.
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Alberta rodeo athletes do not develop the chronic whiplash syndrome.J Rheumatol. 2006 May;33(5):975-7. PMID: 16652428 [PubMed - indexed for MEDLINE]
We have gotten several e-mails about this article and have spoken to several of our Canadian brethren at the IWTC about this publication. As a result, we have chosen to reprint here our formal rebuttal.
Shannon et al claimed that Rodeo riders have little if any sequelae of whiplash, and the people in the audience had more complaints from whiplash, hence whiplash must be a biopsychosocial phenomenon.
For a link to Pubmed for these citations, click here...
Centeno C, Freeman MD.
Related Articles,
Links
Alberta rodeo riders do not develop late whiplash.J Rheumatol. 2007 Feb;34(2):451-2; author reply 452. No abstract available. PMID: 17304671 [PubMed - indexed for MEDLINE]
We were quite surprised to see that Shannon et al’s paper regarding the comparative rates of chronic whiplash in Alberta rodeo athletes versus members of the rodeo audience merited publication in the Archives of Rheumatology[1]. Despite these authors’ claim that “we have no reason to believe that the distribution of such injuries should be strikingly different in these 2 groups” we would have surmised that the peer-reviewers of this paper would have found the reason that escaped Shannon et al. and yet would be readily apparent to most lay readers of the study. We find the authors’ conclusions just as publication-worthy as those of a study of the average height of NBA basketball players versus the members of the audience, with the conclusion that the difference of more than a foot in height is best explained by the theory that the audience must be lacking in nutrition. In a similar vein, Shannon et al explained the difference in symptom duration between rodeo athletes and audience members as the result of a specious biopsychosocial theory that sidesteps the enormous amount of literature indicating an organic etiology of most chronic whiplash symptoms, instead blaming the chronic symptoms on an irrational fear of whiplash injury in the patient..[2-10]
In arriving at their biopsychosocial model explanation for their findings, Shannon et al managed to overlook the fact that rodeo athletes are self-selected ultra-hardy members of the population, located at the furthest right extreme of the injury susceptibility bell curve. While few lay people are aware of the definitions of the epidemiologic terms “bias” and “confounding,” most are aware of the intuitive concept that professional athletes should not be compared to non-professional athletes for the characteristics that make them most likely to become professional athletes; physical prowess. It is rather surprising that the reviewers who green-lighted this paper for the Archives were not more attentive. In our opinion, this paper should not have been published in its current form.
1. Shannon, A.L., R. Ferrari, and A.S. Russell, Alberta rodeo athletes do not develop the chronic whiplash syndrome. J Rheumatol, 2006. 33(5): p. 975-7.
2. Barnsley, L., et al., The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine, 1995. 20(1): p. 20-5; discussion 26.
3. Krakenes, J., et al., MRI assessment of the alar ligaments in the late stage of whiplash injury--a study of structural abnormalities and observer agreement. Neuroradiology, 2002. 44(7): p. 617-24.
4. Kristjansson, E., et al., Increased sagittal plane segmental motion in the lower cervical spine in women with chronic whiplash-associated disorders, grades I-II: a case-control study using a new measurement protocol. Spine, 2003. 28(19): p. 2215-21.
5. Lord, S.M., et al., Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine, 1996. 21(15): p. 1737-44; discussion 1744-5.
6. Panjabi, M.M., et al., Injury mechanisms of the cervical intervertebral disc during simulated whiplash. Spine, 2004. 29(11): p. 1217-25.
7. Siegmund, G.P., et al., Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading. Spine, 2001. 26(19): p. 2095-101.
8. Sterling, M., et al., Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain, 2003. 104(3): p. 509-17.
9. Treleaven, J., G. Jull, and M. Sterling, Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. J Rehabil Med, 2003. 35(1): p. 36-43.
10. Wallis, B.J., S.M. Lord, and N. Bogduk, Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial. Pain, 1997. 73(1): p. 15-22.
Related Articles,
Links
Alberta rodeo athletes do not develop the chronic whiplash syndrome.J Rheumatol. 2006 May;33(5):975-7. PMID: 16652428 [PubMed - indexed for MEDLINE]
We have gotten several e-mails about this article and have spoken to several of our Canadian brethren at the IWTC about this publication. As a result, we have chosen to reprint here our formal rebuttal.
Shannon et al claimed that Rodeo riders have little if any sequelae of whiplash, and the people in the audience had more complaints from whiplash, hence whiplash must be a biopsychosocial phenomenon.
For a link to Pubmed for these citations, click here...
Centeno C, Freeman MD.
Related Articles,
Links
Alberta rodeo riders do not develop late whiplash.J Rheumatol. 2007 Feb;34(2):451-2; author reply 452. No abstract available. PMID: 17304671 [PubMed - indexed for MEDLINE]
We were quite surprised to see that Shannon et al’s paper regarding the comparative rates of chronic whiplash in Alberta rodeo athletes versus members of the rodeo audience merited publication in the Archives of Rheumatology[1]. Despite these authors’ claim that “we have no reason to believe that the distribution of such injuries should be strikingly different in these 2 groups” we would have surmised that the peer-reviewers of this paper would have found the reason that escaped Shannon et al. and yet would be readily apparent to most lay readers of the study. We find the authors’ conclusions just as publication-worthy as those of a study of the average height of NBA basketball players versus the members of the audience, with the conclusion that the difference of more than a foot in height is best explained by the theory that the audience must be lacking in nutrition. In a similar vein, Shannon et al explained the difference in symptom duration between rodeo athletes and audience members as the result of a specious biopsychosocial theory that sidesteps the enormous amount of literature indicating an organic etiology of most chronic whiplash symptoms, instead blaming the chronic symptoms on an irrational fear of whiplash injury in the patient..[2-10]
In arriving at their biopsychosocial model explanation for their findings, Shannon et al managed to overlook the fact that rodeo athletes are self-selected ultra-hardy members of the population, located at the furthest right extreme of the injury susceptibility bell curve. While few lay people are aware of the definitions of the epidemiologic terms “bias” and “confounding,” most are aware of the intuitive concept that professional athletes should not be compared to non-professional athletes for the characteristics that make them most likely to become professional athletes; physical prowess. It is rather surprising that the reviewers who green-lighted this paper for the Archives were not more attentive. In our opinion, this paper should not have been published in its current form.
1. Shannon, A.L., R. Ferrari, and A.S. Russell, Alberta rodeo athletes do not develop the chronic whiplash syndrome. J Rheumatol, 2006. 33(5): p. 975-7.
2. Barnsley, L., et al., The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine, 1995. 20(1): p. 20-5; discussion 26.
3. Krakenes, J., et al., MRI assessment of the alar ligaments in the late stage of whiplash injury--a study of structural abnormalities and observer agreement. Neuroradiology, 2002. 44(7): p. 617-24.
4. Kristjansson, E., et al., Increased sagittal plane segmental motion in the lower cervical spine in women with chronic whiplash-associated disorders, grades I-II: a case-control study using a new measurement protocol. Spine, 2003. 28(19): p. 2215-21.
5. Lord, S.M., et al., Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine, 1996. 21(15): p. 1737-44; discussion 1744-5.
6. Panjabi, M.M., et al., Injury mechanisms of the cervical intervertebral disc during simulated whiplash. Spine, 2004. 29(11): p. 1217-25.
7. Siegmund, G.P., et al., Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading. Spine, 2001. 26(19): p. 2095-101.
8. Sterling, M., et al., Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain, 2003. 104(3): p. 509-17.
9. Treleaven, J., G. Jull, and M. Sterling, Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. J Rehabil Med, 2003. 35(1): p. 36-43.
10. Wallis, B.J., S.M. Lord, and N. Bogduk, Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial. Pain, 1997. 73(1): p. 15-22.
The Insurance Indusrty is at it again...
Cote P, Hogg-Johnson S, Cassidy JD, Carroll L, Frank JW, Bombardier C.
Related Articles,
Links
Initial patterns of clinical care and recovery from whiplash injuries: a population-based cohort study.Arch Intern Med. 2005 Oct 24;165(19):2257-63. PMID: 16246992 [PubMed - indexed for MEDLINE]
Yet another study funded by the auto insurers. This one purports to show that more care (primarily chiropractic and PT) leads to delayed recovery. The problem is that this premise would only work if there was some way to independently severity adjust these patients. Meaning, how do we know that some patients were not more severely injuried and needed more care? In fact, the study just shows that more severely injured people use more care, what a surprise! How these guys were able to get to their final conclusion is a mystery, as their study design ignores all the published research of the past decade showing that spinal trauma with prolonged symptoms is an organic injury.
Freeman and I published a rebuttal...
Art Croft published a rebuttal...
Related Articles,
Links
Initial patterns of clinical care and recovery from whiplash injuries: a population-based cohort study.Arch Intern Med. 2005 Oct 24;165(19):2257-63. PMID: 16246992 [PubMed - indexed for MEDLINE]
Yet another study funded by the auto insurers. This one purports to show that more care (primarily chiropractic and PT) leads to delayed recovery. The problem is that this premise would only work if there was some way to independently severity adjust these patients. Meaning, how do we know that some patients were not more severely injuried and needed more care? In fact, the study just shows that more severely injured people use more care, what a surprise! How these guys were able to get to their final conclusion is a mystery, as their study design ignores all the published research of the past decade showing that spinal trauma with prolonged symptoms is an organic injury.
Freeman and I published a rebuttal...
Art Croft published a rebuttal...
Impact Direction linked to Specific Patterns of Instability
Centeno CJ, Elkins W, Freeman M, Elliott J, Sterling M, Katz E.
Related Articles,
Links
Total cervical translation as a function of impact vector as measured by flexion-extension radiography.Pain Physician. 2007 Sep;10(5):667-71. PMID: 17876363 [PubMed - in process]
I like these authors :). Again, more evidence that ligament injury likely plays a key role in traumatic axial neck injuries. In this case, impact direction is tied to instability as seen on motion based imaging. In other words, the direction you were hit can determine which neck ligaments get damaged. Makes sense.
Related Articles,
Links
Total cervical translation as a function of impact vector as measured by flexion-extension radiography.Pain Physician. 2007 Sep;10(5):667-71. PMID: 17876363 [PubMed - in process]
I like these authors :). Again, more evidence that ligament injury likely plays a key role in traumatic axial neck injuries. In this case, impact direction is tied to instability as seen on motion based imaging. In other words, the direction you were hit can determine which neck ligaments get damaged. Makes sense.
More upper cervical ligaments...
Kaale BR, Krakenes J, Albrektsen G, Wester K.
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Links
Clinical assessment techniques for detecting ligament and membrane injuries in the upper cervical spine region-A comparison with MRI results.Man Ther. 2007 Oct 10; [Epub ahead of print] PMID: 17936054 [PubMed - as supplied by publisher]
More evidence of upper cervical ligament injury as seen on MRI. This was a hot topic at the 2007 IWTC in Miami. When these injuries are grouped into low signal and high signal changes, the agreement between clinician and radiologist is high.
Krakenes has published a number of articles on alar, transverse, tectorial membrane, and posterior AO membrane injuries as detected on MRI. We've had great success getting the radiology community to identify these injuries using the new 3.0T MRI scanners (higher resolution).
Related Articles,
Links
Clinical assessment techniques for detecting ligament and membrane injuries in the upper cervical spine region-A comparison with MRI results.Man Ther. 2007 Oct 10; [Epub ahead of print] PMID: 17936054 [PubMed - as supplied by publisher]
More evidence of upper cervical ligament injury as seen on MRI. This was a hot topic at the 2007 IWTC in Miami. When these injuries are grouped into low signal and high signal changes, the agreement between clinician and radiologist is high.
Krakenes has published a number of articles on alar, transverse, tectorial membrane, and posterior AO membrane injuries as detected on MRI. We've had great success getting the radiology community to identify these injuries using the new 3.0T MRI scanners (higher resolution).
Facet Capsule Damage?
Ivancic PC, Ito S, Tominaga Y, Rubin W, Coe MP, Ndu AB, Carlson EJ, Panjabi MM.
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Links
Whiplash causes increased laxity of cervical capsular ligament.Clin Biomech (Bristol, Avon). 2007 Oct 22; [Epub ahead of print] PMID: 17959284 [PubMed - as supplied by publisher]
More evidence that instability plays a role in many patients with traumatic neck pain. This time facet capsule ligament injury is documented. This fits with clinical observations seen on DMX.
We often see incompetent facet capsules when performing facet injections, so this study fits with my clinical observations. We've had success in healing these tears using prolotherapy and will be trying autologous mesenchymal stem cells in the near future.
Related Articles,
Links
Whiplash causes increased laxity of cervical capsular ligament.Clin Biomech (Bristol, Avon). 2007 Oct 22; [Epub ahead of print] PMID: 17959284 [PubMed - as supplied by publisher]
More evidence that instability plays a role in many patients with traumatic neck pain. This time facet capsule ligament injury is documented. This fits with clinical observations seen on DMX.
We often see incompetent facet capsules when performing facet injections, so this study fits with my clinical observations. We've had success in healing these tears using prolotherapy and will be trying autologous mesenchymal stem cells in the near future.
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