Vertebral Artery Dissection

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Practice Essentials

Vertebral artery dissection (VAD) is a relatively rare but increasingly recognized cause of stroke in patients younger than 45 years. Although the term spontaneous VAD is used to describe cases that do not involve significant blunt or penetrating trauma as a precipitating factor, many patients with so-called spontaneous VAD have a history of trivial or minor injury involving some degree of cervical distortion.

Essential update: Long-term benefit from endovascular therapy for vertebral artery dissection

In a study of 73 patients treated for VAD with endovascular internal trapping, stable and durable results were demonstrated over a mean follow-up of 55.6 months. Recanalization was rare and observed only in 2 patients with ruptured VAD, both within 3 months after initial treatment without rupture. Cranial nerve paresis was observed in 8.21% of patients, perforating ischemia was seen in 9.59%, and spinal cord infarction was seen in 2.74%. Patient ratings of quality of life were good.[6]

Signs and symptoms

The typical patient with VAD is a young person who experiences severe occipital headache and posterior nuchal pain following a head or neck injury and subsequently develops focal neurologic signs attributable to ischemia of the brainstem or cerebellum. The focal signs may not appear until after a latent period lasting as long as 3 days, however, and delays of weeks and years also have been reported. Many patients present only at the onset of neurologic symptoms.

When neurologic dysfunction does occur, patients most commonly report symptoms attributable to lateral medullary dysfunction (ie, Wallenberg syndrome). Patient history may include the following:

Rarely, patients may manifest the following symptoms of a medial medullary syndrome:

Depending upon which areas of the brainstem or cerebellum are experiencing ischemia, the following signs may be present:

Cerebellar findings may include the following:

See Clinical Presentation for more detail.

Diagnosis

Imaging studies in patients with suspected VAD may include the following:

Because VAD occurs in young, generally healthy individuals, laboratory evaluation is directed toward establishing baseline parameters in anticipation of anticoagulant therapy, as follows:

In addition, elevation of the erythrocyte sedimentation rate (ESR) may suggest vasculitis involving the cerebrovascular circulation.

See Workup for more detail.

Management

Acute management of proven or suspected spontaneous VAD is as follows[16] :

See Treatment and Medication for more detail.

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A, Dissection of the left vertebral artery secondary to guidewire injury. B, Complete resolution occurred in 6 months with only aspirin and clopidogre....

Background

Vertebral artery dissection (VAD) is an increasingly recognized cause of stroke in patients younger than 45 years.[1, 2, 3, 4] Although its pathophysiology and treatment closely resemble that of its sister condition, carotid artery dissection (CAD), the clinical presentation, etiology, and epidemiological profile of VADs are unique. In particular, advances in imaging have contributed to growing awareness of this entity.[5]

Pathophysiology

An expanding hematoma in the vessel wall is the root lesion in VAD. This intramural hematoma can arise spontaneously or as a secondary result of minor trauma, through hemorrhage of the vasa vasorum within the media of the vessel. It also can be introduced through an intimal flap that develops at the level of the inner lumen of the vessel. Major trauma is also an increasingly recognized cause of VAD.[17]

This intramural hemorrhage can evolve in a variety of ways, resulting in any of the following consequences:

An understanding of the anatomy of the vertebral artery is helpful. The course of the vertebral artery usually is divided into 4 sections as follows:

Spontaneous dissection of the vertebral artery usually occurs in the tortuous distal extracranial segment (segment III) but may extend into the intracranial portion or segment IV.

Epidemiology

Frequency

United States

Dissections of the extracranial cervical arteries are relatively rare. The combined incidence of both VAD and CAD is estimated to be 2.6 per 100,000. However, cervical dissections are the underlying etiology in as many as 20% of the ischemic strokes presenting in younger patients aged 30-45 years. Among all extracranial cervical artery dissections, CAD is 3-5 times more common than VAD.[7]

Mortality/Morbidity

Sex

The female-to-male ratio is 3:1.

Age

In contrast to atherothrombotic disease of the vertebrobasilar circulation, VAD occurs in a much younger population. The average age is 40 years; the average age of a patient with CAD is closer to 47 years.[12]

History

The typical presentation of vertebral artery dissection (VAD) is a young person with severe occipital headache and posterior nuchal pain following a recent, relatively minor, head or neck injury.[9] The trauma is generally from a trivial mechanism but is associated with some degree of cervical distortion.

Focal neurologic signs attributable to ischemia of the brainstem or cerebellum ultimately develop in 85% of patients; however, a latent period as long as 3 days between the onset of pain and the development of CNS sequelae is not uncommon. Delays of weeks and years also have been reported. Many patients present only at the onset of neurologic symptoms.

When neurologic dysfunction does occur, patients most commonly report symptoms attributable to lateral medullary dysfunction (ie, Wallenberg syndrome).

Physical

The physical examination of patients who have not yet manifested neurologic dysfunction may be misleading. The occipital and nuchal pain associated with vertebral artery dissection (VAD) mimics musculoskeletal pain and often is attributed to the mechanical strain that precipitated the dissection.

Causes

Spontaneous vertebral artery dissection (VAD) is the term used to describe all cases that do not involve blunt or penetrating trauma as a precipitating factor. However, a history of trivial or minor injury is elicited frequently from patients with so-called spontaneous VAD. The diagnosis of traumatic VAD is reserved for those patients with a history of significant trauma, including motor vehicle accidents (MVAs), falls, or penetrating injuries. Despite the severity of the injury mechanism, dissections of the vertebral artery are exceedingly rare in these contexts.

Laboratory Studies

Imaging Studies

Procedures

Prehospital Care

Patients who demonstrate significant neurologic deficits merit transport to stroke centers or other health care institutions able to offer appropriate care of either spontaneous or traumatic VAD.

Emergency Department Care

Consultations

Medication Summary

Anticoagulant and antiplatelet agents are the DOCs to prevent thromboembolic disorders associated with vertebral artery dissection (VAD). More potent agents (eg, intra-arterial thrombolytics) have also been described in treating selective cases.

Heparin

Clinical Context:  Potentiates antithrombin III activity. Does not actively lyse, but blocks further thrombogenesis. Prevents reaccumulation of a clot after spontaneous fibrinolysis. aPTT value 1.5-2 times control (50-80 s) is considered therapeutic.

Warfarin (Coumadin)

Clinical Context:  For prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Interferes with hepatic vitamin K-dependent carboxylation. Usually prolongs PT in 48 h.

Class Summary

These agents are indicated in patients with VAD to prevent recurrent or ongoing thromboembolic occlusion of vertebrobasilar circulation.

Aspirin (Zorprin, Bayer Buffered Aspirin)

Clinical Context:  Inhibits cyclooxygenase, which produces thromboxane A2, a potent platelet activator.

Ticlopidine (Ticlid)

Clinical Context:  Second-line antiplatelet therapy for patients who are intolerant to aspirin or in whom aspirin therapy fails.

Class Summary

Antiplatelet agents have been used effectively in treating VAD but are reserved for those patients who cannot tolerate or have contraindications to anticoagulants.

Alteplase (Activase, TPA)

Clinical Context:  Tissue plasminogen activator exerts effect on fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII Serum half-life is 4-6 min but half-life lengthened when bound to fibrin in clot.

Intra-arterial dose: 0.3 mg/kg; not to exceed 10-20 mg

Class Summary

Lysis of the occluding embolus may be considered by localized intra-arterial injection of alteplase (ie, tissue plasminogen activator [TPA]).

Further Inpatient Care

Further Outpatient Care

Complications

Prognosis

Author

Eddy S Lang, MDCM, CCFP(EM), CSPQ, Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Marc Afilalo, MD, FACEP, FRCPC, MCFP (EM), CSPQ, Director, Emergency Department, Associate Professor, Faculty of Medicine, Section of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center

Disclosure: Nothing to disclose.

Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

A Antoine Kazzi, MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

Disclosure: Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Disclosure: Nothing to disclose.

References

  1. Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A, Norris JW. Cervical arterial dissection: time for a therapeutic trial?. Stroke. Dec 2003;34(12):2856-60. [View Abstract]
  2. Norris JW, Beletsky V, Nadareishvili ZG. Sudden neck movement and cervical artery dissection. The Canadian Stroke Consortium. CMAJ. Jul 11 2000;163(1):38-40. [View Abstract]
  3. Rubinstein SM, Peerdeman SM, van Tulder MW, Riphagen I, Haldeman S. A systematic review of the risk factors for cervical artery dissection. Stroke. Jul 2005;36(7):1575-80. [View Abstract]
  4. Stahmer SA, Raps EC, Mines DI. Carotid and vertebral artery dissections. Emerg Med Clin North Am. Aug 1997;15(3):677-98. [View Abstract]
  5. Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. Oct 2009;193(4):1167-74. [View Abstract]
  6. Kashiwazaki D, Ushikoshi S, Asano T, Kuroda S, Houkin K. Long-term clinical and radiological results of endovascular internal trapping in vertebral artery dissection. Neuroradiology. Feb 2013;55(2):201-6. [View Abstract]
  7. Kim YK, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. Apr 2009;123(6):810-21. [View Abstract]
  8. Raupp SF, Jellema K, Sluzewski M, de Kort PL, Visser LH. Sudden unilateral deafness due to a right vertebral artery dissection. Neurology. Apr 27 2004;62(8):1442. [View Abstract]
  9. Garry D, Forrest-Hay A. A headache not to be sneezed at. Emerg Med J. May 2009;26(5):384-5. [View Abstract]
  10. Saeed AB, Shuaib A, Al-Sulaiti G, Emery D. Vertebral artery dissection: warning symptoms, clinical features and prognosis in 26 patients. Can J Neurol Sci. Nov 2000;27(4):292-6. [View Abstract]
  11. Levy C, Laissy JP, Raveau V, et al. Carotid and vertebral artery dissections: three-dimensional time-of-flight MR angiography and MR imaging versus conventional angiography. Radiology. Jan 1994;190(1):97-103. [View Abstract]
  12. Silbert PL, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology. Aug 1995;45(8):1517-22. [View Abstract]
  13. Yoshimoto Y, Wakai S. Unruptured intracranial vertebral artery dissection. Clinical course and serial radiographic imagings. Stroke. Feb 1997;28(2):370-4. [View Abstract]
  14. [Guideline] Daffner RH, Hackney DB, Dalinka MK, Davis PC, Resnik CS, Rubin DA, et al. Suspected spine trauma. [online publication]. Reston (VA): American College of Radiology (ACR). 2007;
  15. Grau AJ, Brandt T, Buggle F, et al. Association of cervical artery dissection with recent infection. Arch Neurol. Jul 1999;56(7):851-6. [View Abstract]
  16. de Bray JM, Penisson-Besnier I, Dubas F, Emile J. Extracranial and intracranial vertebrobasilar dissections: diagnosis and prognosis. J Neurol Neurosurg Psychiatry. Jul 1997;63(1):46-51. [View Abstract]
  17. Lleva P, Ahluwalia BS, Marks S, Sahni R, Tenner M, Risucci DA, et al. Traumatic and spontaneous carotid and vertebral artery dissection in a level 1 trauma center. J Clin Neurosci. Aug 2012;19(8):1112-4. [View Abstract]
  18. Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection--clinical features, risk factors, therapy and outcome in 126 patients. J Neurol. Oct 2003;250(10):1179-84. [View Abstract]
  19. Haldeman S, Kohlbeck FJ, McGregor M. Stroke, cerebral artery dissection, and cervical spine manipulation therapy. J Neurol. Aug 2002;249(8):1098-104. [View Abstract]
  20. Smith WS, Johnston SC, Skalabrin EJ, et al. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology. May 13 2003;60(9):1424-8. [View Abstract]
  21. Stevinson C, Honan W, Cooke B, Ernst E. Neurological complications of cervical spine manipulation. J R Soc Med. Mar 2001;94(3):107-10. [View Abstract]
  22. [Guideline] Anderson-Peacock E, Blouin JS, Bryans R, Danis N, Furlan A, Marcoux H, et al. Chiropractic clinical practice guideline: evidence-based treatment of adult neck pain not due to whiplash. J Can Chiropr Assoc. Sep 2005;49(3):158-209. [View Abstract]
  23. Pezzini A, Caso V, Zanferrari C, et al. Arterial hypertension as risk factor for spontaneous cervical artery dissection. A case-control study. J Neurol Neurosurg Psychiatry. Jan 2006;77(1):95-7. [View Abstract]
  24. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2003;(3):CD000255.
  25. [Guideline] Adams RJ, Albers G, Alberts MJ, Benavente O, Furie K, Goldstein LB, et al. Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack. Stroke. May 2008;39(5):1647-52. [View Abstract]
  26. [Guideline] Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Stroke. Feb 2006;37(2):577-617. [View Abstract]
  27. Caplan LR. Barnett H, ed. Stroke: Pathophysiology, Diagnosis and Management. Vol 1. London, England: Churchill Livingstone; 1986:549-619.
  28. Condie J, Shaibani A, Wainwright MS. Successful treatment of recurrent basilar artery occlusion with intra-arterial thrombolysis and vertebral artery coiling in a child. Neurocrit Care. Feb 2012;16(1):158-62. [View Abstract]
  29. De Giorgio F, Vetrugno G, De Mercurio D, et al. 1. Dissection of the vertebral artery during a basketball game: a case report. Med Sci Law. Jan 2004;44(1):80-6. [View Abstract]
  30. Hamada J, Kai Y, Morioka M, Yano S, Todaka T, Ushio Y. Multimodal treatment of ruptured dissecting aneurysms of the vertebral artery during the acute stage. J Neurosurg. Dec 2003;99(6):960-6. [View Abstract]
  31. Mokri B. Traumatic and spontaneous extracranial internal carotid artery dissections. J Neurol. Oct 1990;237(6):356-61. [View Abstract]
  32. Prabhu V, Kizer J, Patil A, Hellbusch L, Taylon C, Leibrock L. Vertebrobasilar thrombosis associated with nonpenetrating cervical spine trauma. J Trauma. Jan 1996;40(1):130-7. [View Abstract]
  33. Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. Oct 2009;193(4):1167-74. [View Abstract]
  34. Ramphul N, Geary U. Caveats in the management and diagnosis of cerebellar infarct and vertebral artery dissection. Emerg Med J. Apr 2009;26(4):303-4. [View Abstract]
  35. Rodallec MH, Marteau V, Gerber S, Desmottes L, Zins M. Craniocervical arterial dissection: spectrum of imaging findings and differential diagnosis. Radiographics. Oct 2008;28(6):1711-28. [View Abstract]
  36. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. Mar 22 2001;344(12):898-906. [View Abstract]
  37. Sturzenegger M, Mattle HP, Rivoir A, Rihs F, Schmid C. Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke. Dec 1993;24(12):1910-21. [View Abstract]

A, Dissection of the left vertebral artery secondary to guidewire injury. B, Complete resolution occurred in 6 months with only aspirin and clopidogrel (Plavix; Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Bridgewater, NJ) therapy.

A, Dissection of the left vertebral artery secondary to guidewire injury. B, Complete resolution occurred in 6 months with only aspirin and clopidogrel (Plavix; Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Bridgewater, NJ) therapy.

Gunshot wound to the right side of the neck. A, The angiogram shows transections of the right vertebral artery (RVA) and the right internal maxillary artery (RIMAX), with partial transection and pseudoaneurysm formation of the midcervical right internal carotid artery (RICA). The transected segments of the RVA and RIMAX were embolized with coils. B and C, The RICA pseudoaneurysm was successfully treated with a 7 x 40-mm covered stent (Wallgraft; Boston Scientific Corp, Natick, Mass).

A, Dissection of the left vertebral artery secondary to guidewire injury. B, Complete resolution occurred in 6 months with only aspirin and clopidogrel (Plavix; Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Bridgewater, NJ) therapy.

Gunshot wound to the right side of the neck. A, The angiogram shows transections of the right vertebral artery (RVA) and the right internal maxillary artery (RIMAX), with partial transection and pseudoaneurysm formation of the midcervical right internal carotid artery (RICA). The transected segments of the RVA and RIMAX were embolized with coils. B and C, The RICA pseudoaneurysm was successfully treated with a 7 x 40-mm covered stent (Wallgraft; Boston Scientific Corp, Natick, Mass).