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(Stroke. 2002;33:657.)
© 2002 American Heart Association, Inc.

Editorials

Spontaneous Cervical Artery Dissection

From Risk Factors Toward Pathogenesis

Tobias Brandt, MD Caspar Grond-Ginsbach, PhD

From the Department of Neurology (T.B., C.G-G.), University of Heidelberg, and the Department of Neurological Rehabilitation (T.B.), Schmieder-Kliniken Heidelberg, Germany.

Correspondence to Dr T. Brandt, Department of Neurology, University of Heidelberg. Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany. E-mail Tobias_Brandt@med.uni-heidelberg.de

Key Words: cervical artery dissection • connective tissue disorders • homocysteine • methylenetetrahydrofolate reductase

The pathogenesis of a cervical artery dissection (CAD) remains unknown in most cases.^1,2 Dissections are usually classified as either traumatic or spontaneous.³ However, mechanical trauma did not appear to be an important and frequent cause for the development of CAD, neither in clinical nor in histopathological studies. Chiropractic maneuver, for instance, was repeatedly discussed as a risk factor for CAD, but its pathogenetic effect could be proven only in a minority of cases.⁴ Signs of mechanical damage could not be observed in the majority of preparations in a histopathological study of 50 dissected carotid arteries.⁵ As a result, factors other than mechanical were increasingly taken into consideration in the pathogenesis of cervical artery dissections.

Several constitutional risk factors have been associated with nontraumatic, spontaneous cervical artery dissection (sCAD).

• Hereditary connective tissue disorders, in particular the vascular Ehlers-Danlos syndrome (EDS), are known to be a risk factor for spontaneous dissections. Vascular EDS is an autosomal dominant disorder. Most patients carry mutations in the gene that encodes the pro-1(III) collagen.⁶ Also, other subtypes of EDS (hypermobility and classic forms) are known to predispose for sCAD. Collagen defects, mostly mutations in the pro-1(V) and pro-2(V) encoding genes, have been identified as the pathogenetic cause in the majority of patients with classic EDS.⁷ The molecular defect in the hypermobility subtype of EDS is not yet known⁸.
  
• The morphology of connective tissue elements was found to be aberrant in the majority of skin biopsies from patients with sCAD lacking clinical stigmata . . . [Full Text of this Article]

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