Like the ghost of Christmas Past, the specters of arterial dissection and stroke continue to haunt the chiropractic profession.
John Kinsinger, MD, and Stephen Barrett, MD, for example, have pilloried your practice with scenarios of stroke victims attributing their condition to the last time they experienced a cervical manipulation at the hands of a chiropractor.
Articles in both the peer-reviewed and lay press—and even radio—have fanned the flames of this controversy and have demanded lengthy responses from the chiropractic profession.1-6
But these attacks have missed the point. Studies appearing in the New England Journal of Medicine offer the first clue that these attacks upon cervical manipulation have been largely misdirected, as the annual rates of spontaneous vertebral artery dissection (VAD) have been estimated to occur between 2.5 and 3 times per 100,000 patients, as much as 30 times greater than dissection rates attributed to chiropractic manipulation.7,8
This suggests strongly that a far more significant mechanism must underlie arterial dissections, a belief reinforced by a comprehensive interdisciplinary task force report released almost a decade ago that found that the risks of VAD for neck pain patients is the same whether they consult a chiropractor or a primary care physician.9
In addition to these statistics, once you manage to “look under the hood” to ask yourself what are the actual mechanisms and most plausible causes of VAD, you can place the risk of adjustments at a considerable distance from cervical manipulations as being the culprit in the vast majority of cases. The mystery starts to unravel with early studies that found elastic fiber degradations in bundles of collagen—a major component of arterial walls—in a majority of cases in a study of patients with acute nontraumatic dissections of cervicocerebral arteries.10
A second study found that patients with cervical artery dissections registered blood levels of the amino acid homocysteine that were on the average three times higher than age-matched patients without stroke.11
The link to homocysteine strengthens when looking at another study that showed patients with stroke caused by arterial dissections compared to stroke patients without such dissections were more than twice as likely to have blood homocysteine concentrations exceeding 12 micromoles per liter.12
Yet a fourth study of patients who survived a cerebral infarct caused by spontaneous artery dissection when matched against healthy controls showed that the chances of experiencing a spontaneous cervical artery dissection were nearly 8 times greater with blood homocysteine levels at or greater than the 95th percentile of controls.
In addition, this same elevation of risk was found in patients whose serum folate concentrations were below the 5th percentile of controls.13
Etiology of VAD
Now it’s time to unsheathe your knowledge of biochemistry to tie all these observations together and reach a more informed understanding of what events lead to cervical arterial dissections.
First, it’s been found that homocysteine activates metalloproteinases and serine elastases enzymes that actively degrade the elastin and collagen of the arterial wall.14,15 Then it turns out that homocysteine has been shown to block chemical components in elastin (aldehydes) that are critical in cross-linking and strengthening elastin.16 This has the effect of robbing the arterial wall of a critical stabilizing element.
The cross-linking and stabilization of collagen may also be impaired by homocysteine.17 Folate vitamin B12 and vitamin B6 have all been shown to reduce blood homocysteine levels, the biochemical pathways having been well established.18,19 [See Figure 1.]
Your first reaction might be to wonder how you can determine homocysteine levels in your patients to reduce what appears to be a significant risk factor in causing VAD. That is absolutely the correct approach to take.
Although the reference method often used in earlier research involve high-pressure liquid chromatography, gas chromatography, and mass spectrometry, new inexpensive and automated enzyme conversion immunoassay techniques are available that require just microliters of blood.20-22
With homocysteine determinations becoming more incorporated into standard commercial clinical laboratory measurements, you now have at your disposal a means—in addition to patient histories and symptoms—to determine who is at elevated risk for cervical artery dissection (and who is not).
Reports have appeared in the literature that describe chiropractors experiencing their patients encountering arterial dissections without any manual interventions on the part of the practitioner.23 This finding strongly suggests that you should thoroughly review a patient’s history, including assessing common risk factors associated with
- Atherosclerosis (hypertension, diabetes mellitus, smoking),
- Environmental exposure (infection, oral contraceptive use), and
- Genetic predispositions that point directly toward vessel abnormalities and elevated homocysteine levels.24
The take-home message here is straightforward: Elevated homocysteine levels appear to provide a pathway to VAD, a fact supported by both clinical evidence and established biochemical mechanisms.
As such, homocysteine measurement appears to be a useful screening procedure—not only for manipulation but also for all individuals who may be at risk for spontaneous events involving the vertebral arteries.
But it should not be construed as grounds for performing cervical manipulation without full consideration of the patient’s history and common warning signs. With this approach and in consideration of the evidence presented above, you should feel well defended against the charge that chiropractic manipulation is a frequent direct cause of VAD and stroke.
Anthony Rosner, PhD, is a champion of interdisciplinary research methodology in the health sciences, having previously served as director of research and education at the Foundation for Chiropractic Education and Research. He was designated Humanitarian of the Year in 2000 by the American Chiropractic Association and holds an honorary degree from the National University of Health Sciences. He obtained his PhD from Harvard in medical sciences and biochemistry. He can be contacted at email@example.com.
1 Barrett S. Chiropractors Angry About Bus Ad. https://www.chirobase.org/08Legal/bus_ad.html. Published April 2010. Accessed Sept. 2017.
2 Hufnagel A, Hammers A, Schonle P-W, Bohm K-D Leonhardt G. Stroke following chiropractic manipulation of the cervical spine. Journal of Neurology. 1999;246:683-8.
3 Norris JW, Beletsky V, Nadareishvillei ZG. Canadan Stroke Consortium. Canadian Medical Association Journal. 2000;163:38-40.
4 Rothwell DM, Bondy SJ, Williams JI. Chiropractic manipulation and stroke: a population-based case-control study. Stroke. 2001;32(5):1054-60.
5 Body J. When simple actions ravage arteries. New York Times. April 30, 2001:D6.
6 Bill Caroll Show [transcript]. CFRB 1010 radio. February 6, 2002.
7 Shieving WT, Mokri B, Whisnant JP. Internal carotid artery dissection in a community: Rochester, Minnesota, 1987-1992. Stroke. 1993;24(11):1678-80.
8 Carey RF. A report on the occurrence of cerebral vascular accidents in chiropractic practice. Journal of the Canadian Chiropractic Association. 1993;57(2):104-106.
9 Haldeman S, Caroll L, et al. The Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders: Executive summary. Eur Spine J. 2008; 17(Suppl 1):5-7.
10 Brandt T, Hausser I, Orberk E, Hacke W. Ultrastructural connective tissue components in patients with spontaneous cervicocerebral artery dissections. Annals of Neurology. 1998;44(2):281-285.
11 Gallai V, Caso V, Paciaroni M, et al. Mild hyperhomocyst(e)inemia: a possible risk factor for cervical artery dissection. Stroke. 2001;32(3):714-8.