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(Stroke. 2002;33:1945.)
© 2002 American Heart Association, Inc.

Letters to the Editor

"Spontaneous" Cervical Arterial Dissection

J.W. Norris, MD

University of Toronto, Ontario, Canada

V. Beletsky, MD

University of Western Ontario, Ontario, Canada

Z. Nadareishvili, MD

National Institutes of Health, Bethesda, Md

To the Editor:

The editorial on "spontaneous" cervical arterial dissection (CAD) by Brandt and Grond-Ginsbach¹ was an interesting and informed review of a subject that in the past has received inappropriately little attention, considering that CAD represents possibly the most common cause of ischemic stroke in persons below 45 years of age. However, the heavy emphasis on constitutional and genetic factors could prove misleading, and there is no conclusive evidence that such factors play a major role in CAD.

The diagnosis of "spontaneous" dissection is entirely dependent on history, and retrospectively reviewing patient’s medical charts is unlikely to accurately reflect the events occurring at the time of dissection. In a current study of this topic by the Canadian Stroke Consortium, dissections were initially diagnosed as spontaneous in patients doing push-ups or lifting heavy weights and engaged in other activities where violent or trivial neck movements were involved. The moment of arterial dissection is easily determined because neck pain occurs in most cases (82% in our series) at the moment of dissection, but unless patients are carefully questioned this factor is easily overlooked.

True, as the authors state, chiropractic maneuvers produce CAD only in a minority of cases,² but they were responsible for 42 of 178 (24%) in our series, so this cause cannot be dismissed as a rare occurrence.

The jury is still out regarding the role of homocysteine in stroke, the usual relationship being an acceleration of atherosclerosis, so its role in CAD must still remain tentative and uncertain.³ Only a minority of the patients in our series had demonstrated abnormalities such as fibromuscular dysplasia on angiogram (15%), although histopathology may prove more sensitive.⁴ However, only a tiny minority of patients have a family history of dissection. There is clearly a spectrum of trauma versus a genetic factor as the causal agent for dissection, but in most cases trauma, severe in a minority of cases and trivial in many, seems to play a major role.

References

1. Brandt T, Grond-Ginsbach C. Spontaneous cervical artery dissection: from risk factors toward pathogenesis. Stroke. 2002; 33: 657–658.[Free Full Text]
2. Rothwell DM, Bondy SJ, Williams JI. Chiropractic manipulation and stroke: a population-based case-control study. Stroke. 2001; 32: 1054–1060.[Abstract/Free Full Text]
3. Pezzini A, Del Zotto E, Archetti S, Negrini R, Bani P, Albertini A, Grassi M, Assanelli D, Gasparotti R, Vignolo LA, Magoni M, Padovani A. Plasma homocysteine concentration, C677T MTHFR genotype, and 844ins68bp CBS genotype in young adults with spontaneous cervical artery dissection and atherothrombotic stroke. Stroke. 2002; 33: 664–669.[Abstract/Free Full Text]
4. Brandt T, Hausser I, Orberk E, Grau A, Hartschuh W, Anton-Lamprecht I, Hacke W. Ultrastructural connective tissue abnormalities in patients with spontaneous cervicocerebral artery dissections. Ann Neurol. 1998; 44: 281–285.[CrossRef][Medline] [Order article via Infotrieve]

Response

Tobias Brandt, MD Caspar Grond-Ginsbach, PhD

Department of Neurology, University of Heidelberg, Germany

We thank Dr Norris and colleagues for their comments on our editorial on spontaneous cervical artery dissections (sCAD). Our finding of electron microscopic connective tissue aberrations in the majority of skin biopsies from patients with sCAD, but not in skin biopsies from healthy control subjects,¹ suggests that the majority of patients have a predisposition for dissection. Moreover, we recently demonstrated in some families from patients with sCAD that the connective tissue aberrations are inherited and follow an autosomal dominant pattern.² These findings show that genetic factors do play a role in the development of sCAD at least in a subgroup of patients.

We agree with Dr Norris and colleagues that constitutional and genetic factors alone do not sufficiently explain why sCAD occurs at a certain moment and in typical locations.³ Furthermore, only very few patients have a family history of dissection. It is an important finding of the Canadian Stroke Consortium that many dissections that were initially diagnosed as "spontaneous" were in fact triggered by minor or severe injury that was overlooked in earlier records. This underlines that mechanical stress can indeed be an important (co-) factor in the etiology of sCAD. In our first prospective series, however, with inclusion of sCAD patients only within 4 weeks after the event and the history very carefully taken, in 12 of 25 (48%) of the patients no possible trigger movement at all could be found.⁴

We do not believe in an opposition between genetic factors on one side and trauma or injury on the other. Dissection is probably in most cases the outcome of a complex interplay of genetic and environmental factors.³ Severe trauma alone can lead to cervical artery occlusions⁵ and mechanical trauma might even be a triggering factor for the development of most dissections. However, the finding of preceding trivial trauma in the majority of patients does not rule out the possible importance of constitutional and genetic factors. In fact, trivial trauma is a common event, but dissections are rare; and similarly most of a patient’s relatives with a connective tissue phenotype do not develop dissections.³

References

1. Brandt T, Orberk E, Weber R, Werner I, Busse O, Muller BT, Wigger F, Grau A, Grond-Ginsbach C, Hausser I. Pathogenesis of cervical artery dissections: association with connective tissue abnormalities. Neurology. 2001; 57: 24–30.[Abstract/Free Full Text]
2. Grond-Ginsbach C, Klima B, Weber R, Striegel J, Fischer C, Hacke W, Brandt T, Hauser I. Exclusion mapping of the genetic predisposition for cerebral artery dissections by linkage analysis. Ann Neurol. In press.
3. Brandt T, Grond-Ginsbach C. Spontaneous cervical artery dissection: from risk factors toward pathogenesis. Stroke. 2002; 33: 657–658.[Free Full Text]
4. Brandt T, Hausser I, Orberk E, Grau A, Hartschuh W, Anton-Lamprecht I, Hacke W. Ultrastructural connective tissue abnormalities in patients with spontaneous cervico-cerebral artery dissections. Ann Neurol. 1998; 44: 281–285.[CrossRef][Medline] [Order article via Infotrieve]
5. Sim E, Vaccaro AR, Berzlanovich A, Pienaar S. The effects of staged static cervical flexion-distraction deformities on the patency of the vertebral arterial vasculature. Spine. 2000; 25: 2180–2186.[Medline] [Order article via Infotrieve]

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