Letter: Traumatic and Spontaneous Vertebral Artery Dissections: An Analysis of Tertiary-Center 310 Patient Cohort

To the Editor: The authors have presented an important series of patients with vertebral artery dissection (VAD), comparing populations with spontaneous VAD (sVAD) and traumatic VAD (tVAD) etiologies.1 The analysis presented is limited in several ways. Addressing these limitations would make the analysis more impactful, moving toward a better understanding of genesis of different types of dissections. Arterial tortuosity (AT) or redundancy is not assessed in the patient groups. The literature supports the correlation between AT, underlying ultrastructural abnormalities of the vessel wall, and connective tissue disorders all potentially leading to increased risk of sVAD.2-4 It is postulated that AT does not necessarily predispose to tVAD. It would be a straightforward task to provide this analysis because all patients had vascular imaging of the cervicocerebral vessels. The data set is also an opportunity to look at the imaging appearance of VADs themselves. Comparing the characteristics of traumatic and spontaneous events could provide some perspective on those VADs that fall in the gray area between those obviously traumatic or spontaneous. This gray zone comprises VADs from innocuous or minor traumas. Understanding the true origin of these dissections is critical for patient care, development of preventative measures, family counseling, and avoidance of unnecessary litigation. The authors do not discuss the recent literature supporting the idea that VADs in general should not be causally attributed chiropractic adjustment. A recent review of cervical arterial dissection from the American Heart Association Stroke Council and American Stroke Association came to this conclusion.5 A subsequent study from the Penn State Neurosurgery provided a meta-analysis of the published literature on this topic with the same conclusion.6 This analysis went further and applied the Hill criteria for causation to the question, finding that causation was not supported across most of the criteria. The authors should determine whether their patients with chiropractic-related VAD had symptoms or imaging findings to suggest that the VAD antedated the chiropractic care. Commonly, the onset of stroke symptoms is conflated with the onset of the symptoms of VAD, but these events are most commonly distinct. Acknowledging the symptoms that occurred in association with the chiropractic care is helpful in determining which of these events occurred in temporal proximity to the chiropractic care. Furthermore, there is no report of the time interval between chiropractic care and diagnosis of dissection, nor any relevant intercurrent events. It would be helpful to know what type of chiropractic care was provided. Some chiropractic techniques do not carry any significant risk of stroke or vascular injury. We should not simply attribute a patient's VAD to chiropractic care without a more granular understanding of these factors. This raises the question of whether those tVADs reported in this study as being associated with chiropractic care are actually sVADs. Because the energy transfer of the “trauma” associated with chiropractic care is of a different order of magnitude from true high-energy traumas,7 such as motor vehicle accidents, it would be worth looking at this data set considering the likelihood that non–high-energy tVADs are likely sVADs. Unfortunately, our lack of clarity on the role of chiropractic care in the genesis of VAD vs “stroke from” VAD leads to unnecessary legal action and incomplete evaluation of patients with stroke due to VAD. This data set provides an opportunity to further understand the different characteristics of traumatic vs spontaneous VAD.