Vertebral Artery Dissection

Back

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. See the image below.



View Image

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

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 three 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 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[13] :

See Treatment and Medication for more detail.

Background

Vertebral artery dissection (VAD) is an increasingly recognized cause of stroke in patients younger than 45 years.[4, 14, 15, 16, 17] Although its pathophysiology and treatment closely resemble that of its sister condition, carotid artery dissection (CAD), the clinical presentation, etiology, and epidemiologic profile of VADs are unique. In particular, advances in imaging have contributed to growing awareness of this entity.[8]

Pathophysiology

An expanding hematoma in the vessel wall is the root lesion in vertebral artery dissection (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.[18]

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 four 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.

Etiology

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.

Several risk factors have been associated with the development of VAD. These include the following:

When patients with serious cervical trauma, such as cord injuries or cervical spine fractures, are screened for vertebral artery injury, 20-40% may demonstrate traumatic occlusion. This traumatic vertebral artery occlusion (as opposed to dissection) is asymptomatic, and its management is controversial.

Epidemiology

United States statistics

Dissections of the extracranial cervical arteries are relatively rare. The combined incidence of both verterbral artery dissection (VAD) and carotid artery dissection (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.[1]

Sex- and age-related demographics

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

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.[9]

Prognosis

Extracranial dissection

Most patients with extracranial dissection do remarkably well if they survive the initial crisis. As many as 88% of these patients demonstrate a complete clinical recovery at follow-up. However, this suggests an overall risk of death, recurrent transient ischemic attacks, or stroke of approximately 10%.

One series suggests that the severity of neurologic deficits at the time of presentation is related directly to the functional outcome.

Follow-up angiography demonstrates spontaneous healing in as many as two thirds of these patients.

Intracranial dissection

Patients with intracranial vertebrobasilar dissection constitute a more severely affected subgroup of all patients with verterbral artery dissection (VAD).[13]

The presentation of a dissection involving the intracranial portion of the vertebral artery (segment IV) is characterized by rapidly progressive neurologic deficits, including depressed consciousness.

VAD is associated with subarachnoid hemorrhage, brainstem infarctions, and high mortality rate.[13]

Morbidity/mortality

VAD has been associated with a 10% mortality rate in the acute phase. Death is the result of extensive intracranial dissection, brainstem infarction, or subarachnoid hemorrhage.[6]

Those who survive the initial crisis do remarkably well, with long-term sequelae rare.

Complications

Complications include the following:

Major complications of vertebral artery dissection include stroke and death. Previous observational studies have yielded stroke rates between 0.3% and 8.5% after vertebral or carotid artery dissection. However, one randomized clinical trial observed a much lower stroke rate of 1.2% at 3 month follow-up and no deaths were reported in this time.[27, 28] As recurrences are rare, any definitive study examining complications following dissection will require large sample sizes.

History

The typical presentation of vertebral artery dissection (VAD) is a young person with severe occipital headache and posterior nuchal pain[29, 30] following a recent, relatively minor, head or neck injury.[3, 31] 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 central nervous system (CNS) sequelae is not uncommon. Delays of weeks and years also have been reported. Many patients present only at the onset of neurologic symptoms. Thus, when VAD is suspected, clinicians should evaluate patients for the presence of a unilateral headache and/or neck pain and vertigo, with or without objective neurologic signs.[29]

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:

Physical Examination

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.

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

Cerebellar findings may include the following:

Laboratory Studies

Vertebral artery dissection (VAD) is a disease of young, generally healthy individuals. Laboratory evaluation is directed toward establishing baseline parameters in anticipation of anticoagulant therapy.

Prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR) are the usual monitoring parameters for patients on anticoagulant medication.

Erythrocyte sedimentation rate (ESR), if elevated, may suggest vasculitis involving the cerebrovascular circulation.

Procedures

Patients with suspected subarachnoid hemorrhage and a normal computed tomography (CT) scan may undergo lumbar puncture (LP) if VAD is not pursued by other imaging modalities.

CT Scanning, MRI, and MRA

Diagnosis of vertebral artery dissection (VAD) is usually made by neuroimaging, which has largely replaced conventional angiography in most centers.[32] The 2011 combined ASA/ACCF/AHA guidelines gave a class I recommendation to noninvasive computed tomography angiography (CTA) or magnetic resonance angiography (MRA) as the initial diagnostic study for suspected VAD.[33] These studies were favored over ultrasonography, but there was no specific guidance on CTA over MRA provided. If these imaging modalities are inconclusive for VAD but the clinical suspicion remains high, the guidelines gave a class IIa recommendation to either serial noninvasive imaging or invasive contrast angiography (if the patients would be candidates for revascularization).[33]

Computed tomography scanning

Data examining CTA versus magnetic resonance imaging-angiography (MRI-A)/MRA for VAD are limited, but there may be a slight preference for CTA for identifying VAD given the smaller arterial diameters compared to internal carotid dissections.[34] However, CTA is less accurate if heavy calcifications are present. CTA studies have a reported 90%-99% specificity and 40%-100% sensitivity for VAD.

CT scanning is useful in identifying patients with the complication of subarachnoid hemorrhage.[3]

Absence of hemorrhage, as demonstrated by CT scan, is a prerequisite for instituting anticoagulant therapy. Ease of access to CT scanners may provide the impetus for using CTA over MRA as the inital diagnostic study.

Magnetic resonance imaging

MRI detects both the intramural thrombus and intimal flap that are characteristic of VAD.[7]

Hyperintensity of the vessel wall seen on T1-weighted axial images is considered by some to be pathognomonic of VAD.[7, 8, 9, 10, 11]

Park et al conducted a retrospective study of 41 vertebral arteries to evaluate radiologic findings according to the stages in spontaneous and unruptured, intracranial VAD (IVAD) on 3T high-resolution MRI (HR-MRI).[35] The 3T HR-MRI revealed the vessel wall characteristics as well as provided distinguishing findings between earlier stages and the chronic stage in spontaneous and unruptured IVAD. The investigators concluded that the characterization of these radiologic findings according to stages may help with the age estimation of the dissection.[35]

In a review of VAD cases registered between April 2008 and October 2014 that compared radiologic findings between patients with extracranial VAD (EVAD) and intracranial VAD (IVAD), Kobayashi et al found that intramural hematomas were more commonly revealed by MRI in patients with EVAD.[36] By contrast, in patients with IVAD, MRI and CT scanning more frequently revealed aneurysm formation.

Magnetic resonance angiography

MRA can identify abnormalities that are characteristic of the disturbed arterial flow seen in VAD. These include the presence of a pseudolumen and aneurysmal dilation of the artery.[7]

New generation MRI and MRA appear to be as sensitive as cerebral angiography for the detection of VAD, although they probably have equivalent specificity.[8, 9, 10, 11, 12, 37]

Cerebral angiography may still have a role when clinical suspicion is high but MRI/MRA has failed to isolate the lesion. In these situations, the choice can be made between serial noninvasive imaging (if symptoms are suggestive of VAD) or invasive angiography (if the patient is a candidate for revascularization and might benefit from simultaneous diagnosis and therapy).

Four-Vessel Cerebral Angiography

Prior to the development of noninvasive techniques such as magnetic resonance imaging (MRI) and Doppler ultrasonography, cerebral angiography was the criterion standard in diagnosing vertebral artery dissection (VAD). These noninvasive techniques are supplanting angiography as the imaging techniques of choice for patients in whom VAD is suspected.[7]

A French retrospective study that evaluated clinical and imaging features with outcomes in 20 pediatric patients with extracranial VAD over 14 years indicated that the initial imaging studies should include the posterior fossa vessels and the craniocervical region with V2-V3 segments.[38] In the presence of inconclusive findings on nonivasive imaging studies, the investigators suggested use of conventional angiography for definitive diagnosis.[38]

The characteristic angiographic finding in a dissected vertebral artery is the string or "string and pearl" appearance of the stenotic vessel lumen.[10] Angiograms are shown in the images below.



View Image

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



View Image

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 ....

Because of the high incidence (up to 40% in some series) of multiple extracranial cervical artery dissections occurring simultaneously in the same patient, 4-vessel angiography is the angiographic technique of choice in all patients with potential carotid artery dissection (CAD) or VAD.[10]

Ultrasonography

Vascular duplex scanning

Duplex ultrasonography of the vertebral arteries demonstrates abnormal flow in 95% of patients with vertebral artery dissection (VAD).[8]

Ultrasonographic signs specific to VAD (eg, segmental dilation of the vessel, eccentric channel) are detectable in only 20% of patients. Thus, ultrasonography may be useful as an initial test only if computed tomography angiography (CTA) or magnetic resonance angiography (MRA) are not readily available.

Transcranial Doppler

Transcranial Doppler is approximately 75% sensitive to the flow abnormalities seen in VAD. It is useful also in detecting high-intensity signals (HITS), which are characteristic of microemboli propagating distally as a result of the dissection. HITS are associated with symptomatic ischemic symptoms both in VAD and in other types of cerebrovascular disease.

Emergency Department 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 vertebral artery dissection (VAD).

Immediate management for dissections leading to acute ischemia includes the initiation of thrombolytic agents provided there are no contraindications to their administration. This therapy is best reserved for patients presenting within 4.5 hours of symptom onset. Beyond this phase, treatment with either anticoagulation or antiplatelet agents are the treatments of choice.

The accepted management of proven or suspected spontaneous VAD consists of antithrombotic therapy (with either antiplatelet or anticoagulant agents) in those patients who are not also affected by the complication of subarachnoid hemorrhage.[13, 39] This approach is intended to prevent thrombogenic or embolic occlusion of the vertebrobasilar network and subsequent infarction of posterior CNS structures, brain stem, and cerebellum.

Data guiding this management strategy comes from the 2015 Cervical Artery Dissection in Stroke Study (CADISS) trial discussed in the Medical Care section.[40] The pathophysiologic mechanism underlying VAD includes hemorrhage into the arterial wall and subarachnoid hemorrhage as a devastating complication of the condition.

Consultations

Consult with a neurosurgeon.

Hospitalization

Patients with vertebral artery dissection (VAD) warrant admission and close neurologic monitoring until anticoagulation with warfarin is complete and patient's clinical condition is stable.

Medical Care

Findings from the Cervical Artery Dissection in Stroke Study (CADISS) trial, the only randomized trial to examine antiplatelets versus anticoagulants in the treatment of extracranial carotid and vertebral artery dissections (VADs) were published in 2015, in which no differences in outcomes between groups receiving antiplatelets versus anticoagulants were found.[40] Two hundred and fifty patients (118 with carotid artery dissection [CAD]; 132 with VAD) were randomized to either antiplatelet therapy or anticoagulant therapy and followed out to a 3 month period. Recurrent stroke was rare within this time frame (2%).[40] There was a very low incidence of postdissection adverse effects in both groups, meaning randomized studies examining treatment effects on secondary outcomes will be lacking.

Similar findings to those discussed above have been reported in previous meta-analyses examining antithrombotic treatments for CAD and VADs.[41, 42]

At this time, therefore, it would be reasonable to treat patients who are not candidates for surgical therapy, to receive either antiplatelet therapy (aspirin, with or without clopidogrel) or anticoagulant therapy (warfarin, with or without heparin).

Surgical Care

New technological advancements in endovascular procedures indicate the growing popularity of endovascular recanalization of dissections. These procedures are viable, effective, and tolerable treatment alternatives with impressive radiographic results.[43] However, endovascular treatments are controversial, as most of the related mortality and morbidity is secondary to emboli formation in the vessel, which is amenable to antiplatelet or anticoagulation therapy. Furthermore, most dissections heal spontaneously. Surgical or endovascular repair of dissections is best reserved for patients who experience recurrent ischemic episodes despite antithrombotic therapy. It may also have a role for patients with intracranial dissections who present with subarachnoid hemorrhage.[44]

A 2014 meta-analysis of vertebral artery dissections (VADs) treated endovascularly found that 86.3% of procedures were associated with good or excellent outcomes.[45] Postoperative complications occurred in 10.5% (complications included vasospasm, postoperative rebleeding, and ischemia) with an overall mortality of 8.7%. The authors suggested that reduced operating time, minimal invasiveness, and comparative safety make endovascular procedures suitable options for intervention-amenable dissections.[45]

Surgical treatment is reserved for those patients in whom symptoms are persistent and refractory to maximal medical therapy and who are not candidates for endovascular procedures. Surgical options for vertebral artery dissections include in situ interposition grafting or extracranial-intracranial bypasses.[46]

Long-Term Monitoring

Medications

No clear guidelines exist on the duration of anticoagulation in patients with VAD. Consider treatment regimens of 3-6 months or until radiographic resolution is established by either MRI or follow-up angiography.

Rarely, patients experience reocclusion when removed from anticoagulant therapy, which subjects them to longer regimens.

Other considerations

Most authors support follow-up imaging at 3 months after diagnosis, preferably with a noninvasive technique such as MRI.

As with all patients on warfarin therapy, monitor INR at regular intervals.

Therapy recommendations for patients with stroke and arterial dissection are available from the American Heart Association/American Stroke Association.[47, 48]

For patient education resources, see the Brain and Nervous System Center, as well as Stroke.

Medication Summary

Anticoagulant and antiplatelet agents are the drugs of choice (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.

In a randomized controlled trial of 250 patients with vertebral artery (n = 132) or extracranial carotid (n = 118) dissections who were randomly assigned to antiplatelet therapy versus anticoagulation therapy within 7 days of symptom onset, the investigators found no difference between either agent in preventing stroke and death after 3 months.[27] Indeed, there were only 4 strokes in the entire cohort and no deaths, far lower than reported in other observational studies.[27] These results were similar to a previous meta-analysis.[28]

Studies in recent years suggest that novel oral anticoagulants (NOACs) such as dabigatran, rivaroxaban, and apixaban may be viable alternatives with similar efficacy and safety outcomes to vitamin K antagonists.[49] NOACs may be associated with similar rates of stroke at follow-up, but they have fewer hemorrhagic complications.[50] Nonetheless, further research is required.

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]).

What is the role of vertebral artery dissection (VAD) in stroke?What are common characteristics of vertebral artery dissection (VAD)?What are common symptoms of vertebral artery dissection (VAD)?What are atypical symptoms of vertebral artery dissection (VAD)?What are the signs of ischemia in patients with vertebral artery dissection (VAD)?What are the cerebellar findings in patients with vertebral artery dissection (VAD)?Which imaging studies are used in the diagnosis of vertebral artery dissection (VAD)?What is the role of lab studies in the diagnosis of vertebral artery dissection (VAD)?How is vertebral artery dissection (VAD) treated?What is vertebral artery dissection (VAD)?What is the pathogenesis of vertebral artery dissection (VAD)?What is the pathophysiology of vertebral artery dissection (VAD)?What is the relevant anatomy in vertebral artery dissection (VAD)?What causes vertebral artery dissection (VAD)?What are the risk factors associated with vertebral artery dissection (VAD)?How common is vertebral artery dissection (VAD) in the US?What are the demographics of vertebral artery dissection (VAD)?What is the prognosis of extracranial vertebral artery dissection (VAD)?What is the prognosis of intracranial vertebral artery dissection (VAD)?What is the morbidity and mortality of vertebral artery dissection (VAD)?What are the complications of vertebral artery dissection (VAD)?What is the typical presentation of vertebral artery dissection (VAD)?What is the clinical history of vertebral artery dissection (VAD)?What are the symptoms of medial medullary syndrome in vertebral artery dissection (VAD)?What are the physical exam findings in patients with vertebral artery dissection (VAD) who do not have neurologic symptoms?What are the signs of ischemia in vertebral artery dissection (VAD)?What are the cerebellar findings in vertebral artery dissection (VAD)?What are the diagnostic considerations in vertebral artery dissection (VAD)?What are the differential diagnoses for Vertebral Artery Dissection?Which lab studies are indicated in the workup of vertebral artery dissection (VAD)?Which procedures are used in the workup of vertebral artery dissection (VAD)?What is the role of neuroimaging in the workup of vertebral artery dissection (VAD)?What is the role of CT scanning in the workup of vertebral artery dissection (VAD)?What is the role of MRI in the workup of vertebral artery dissection (VAD)?What is the role of MRA in the workup of vertebral artery dissection (VAD)?What is the role of 4-vessel cerebral angiography in the workup of vertebral artery dissection (VAD)?What is the role of duplex ultrasonography in the workup of vertebral artery dissection (VAD)?What is the role of transcranial Doppler sonography in the workup of vertebral artery dissection (VAD)?What is the emergent care of vertebral artery dissection (VAD)?Which specialist consultations are indicated in the treatment of vertebral artery dissection (VAD)?What is the role of inpatient care in the treatment of vertebral artery dissection (VAD)?What is the medical care for vertebral artery dissection (VAD)?What is the role of endovascular procedures in the treatment of vertebral artery dissection (VAD)?How long is anticoagulation therapy needed for vertebral artery dissection (VAD)?What is the long-term monitoring of patients with vertebral artery dissection (VAD)?What is the medication of choice for treatment of vertebral artery dissection (VAD)?Which medications in the drug class Thrombolytics are used in the treatment of Vertebral Artery Dissection?Which medications in the drug class Antiplatelet Agents, Cardiovascular are used in the treatment of Vertebral Artery Dissection?Which medications in the drug class Anticoagulants, Cardiovascular are used in the treatment of Vertebral Artery Dissection?

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)

Inderjeet (Indy) S Sahota, MD, MSc, CCFP, Resident Physician, CCFP-EM Emergency Medicine R3, University of British Columbia Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

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

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.

Amin Antoine Kazzi, MD, Professor of Clinical Emergency Medicine, Department of Emergency Medicine, American University of Beirut, Lebanon

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, Sanz Laniado Medical Center, Netanya, Israel

Disclosure: Nothing to disclose.

Additional Contributors

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

Disclosure: Nothing to disclose.

References

  1. Kim YK, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. 2009 Apr. 123(6):810-21. [View Abstract]
  2. Raupp SF, Jellema K, Sluzewski M, de Kort PL, Visser LH. Sudden unilateral deafness due to a right vertebral artery dissection. Neurology. 2004 Apr 27. 62(8):1442. [View Abstract]
  3. Garry D, Forrest-Hay A. A headache not to be sneezed at. Emerg Med J. 2009 May. 26(5):384-5. [View Abstract]
  4. Stahmer SA, Raps EC, Mines DI. Carotid and vertebral artery dissections. Emerg Med Clin North Am. 1997 Aug. 15(3):677-98. [View Abstract]
  5. Lyrer PA, Brandt T, Metso TM, et al. Clinical import of Horner syndrome in internal carotid and vertebral artery dissection. Neurology. 2014 May 6. 82(18):1653-9. [View Abstract]
  6. 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. 2000 Nov. 27(4):292-6. [View Abstract]
  7. 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. 1994 Jan. 190(1):97-103. [View Abstract]
  8. 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. 2009 Oct. 193(4):1167-74. [View Abstract]
  9. Silbert PL, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology. 1995 Aug. 45(8):1517-22. [View Abstract]
  10. Yoshimoto Y, Wakai S. Unruptured intracranial vertebral artery dissection. Clinical course and serial radiographic imagings. Stroke. 1997 Feb. 28(2):370-4. [View Abstract]
  11. [Guideline] Daffner RH, Hackney DB, Dalinka MK, et al. Suspected spine trauma. [online publication]. Reston (VA): American College of Radiology (ACR). 2007.
  12. Grau AJ, Brandt T, Buggle F, et al. Association of cervical artery dissection with recent infection. Arch Neurol. 1999 Jul. 56(7):851-6. [View Abstract]
  13. de Bray JM, Penisson-Besnier I, Dubas F, Emile J. Extracranial and intracranial vertebrobasilar dissections: diagnosis and prognosis. J Neurol Neurosurg Psychiatry. 1997 Jul. 63(1):46-51. [View Abstract]
  14. Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A, Norris JW. Cervical arterial dissection: time for a therapeutic trial?. Stroke. 2003 Dec. 34(12):2856-60. [View Abstract]
  15. Norris JW, Beletsky V, Nadareishvili ZG. Sudden neck movement and cervical artery dissection. The Canadian Stroke Consortium. CMAJ. 2000 Jul 11. 163(1):38-40. [View Abstract]
  16. Rubinstein SM, Peerdeman SM, van Tulder MW, Riphagen I, Haldeman S. A systematic review of the risk factors for cervical artery dissection. Stroke. 2005 Jul. 36(7):1575-80. [View Abstract]
  17. Jaffre A, Ruidavets JB, Calviere L, Viguier A, Ferrieres J, Larrue V. Risk factor profile by etiological subtype of ischemic stroke in the young. Clin Neurol Neurosurg. 2014 May. 120:78-83. [View Abstract]
  18. Lleva P, Ahluwalia BS, Marks S, et al. Traumatic and spontaneous carotid and vertebral artery dissection in a level 1 trauma center. J Clin Neurosci. 2012 Aug. 19(8):1112-4. [View Abstract]
  19. Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection--clinical features, risk factors, therapy and outcome in 126 patients. J Neurol. 2003 Oct. 250(10):1179-84. [View Abstract]
  20. Haldeman S, Kohlbeck FJ, McGregor M. Stroke, cerebral artery dissection, and cervical spine manipulation therapy. J Neurol. 2002 Aug. 249(8):1098-104. [View Abstract]
  21. Smith WS, Johnston SC, Skalabrin EJ, et al. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology. 2003 May 13. 60(9):1424-8. [View Abstract]
  22. Stevinson C, Honan W, Cooke B, Ernst E. Neurological complications of cervical spine manipulation. J R Soc Med. 2001 Mar. 94(3):107-10. [View Abstract]
  23. [Guideline] Anderson-Peacock E, Blouin JS, Bryans R, et al. Chiropractic clinical practice guideline: evidence-based treatment of adult neck pain not due to whiplash. J Can Chiropr Assoc. 2005 Sep. 49(3):158-209. [View Abstract]
  24. Zhou M, Zheng H, Gong S, et al. Vertebral artery hypoplasia and vertebral artery dissection: a hospital-based cohort study. Neurology. 2015 Feb 24. 84(8):818-24. [View Abstract]
  25. 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. 2006 Jan. 77(1):95-7. [View Abstract]
  26. Kelly JC, Safain MG, Roguski M, Edlow AG, Malek AM. Postpartum internal carotid and vertebral arterial dissections. Obstet Gynecol. 2014 Apr. 123(4):848-56. [View Abstract]
  27. CADISS trial investigators, Markus HS, Hayter E, Levi C, et al. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr. 14(4):361-7. [View Abstract]
  28. Kennedy F, Lanfranconi S, Hicks C, et al. Antiplatelets vs anticoagulation for dissection: CADISS nonrandomized arm and meta-analysis. Neurology. 2012 Aug 14. 79(7):686-9. [View Abstract]
  29. Fukuhara K, Ogata T, Ouma S, et al. Impact of initial symptom for accurate diagnosis of vertebral artery dissection. Int J Stroke. 2015 Oct. 10 Suppl A100:30-3. [View Abstract]
  30. Kim JG, Choi JY, Kim SU, et al. Headache characteristics of uncomplicated intracranial vertebral artery dissection and validation of ICHD-3 beta diagnostic criteria for headache attributed to intracranial artery dissection. Cephalalgia. 2015 May. 35(6):516-26. [View Abstract]
  31. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015 Jul. 45(7):503-11. [View Abstract]
  32. Robertson JJ, Koyfman A. Cervical artery dissections: a review. J Emerg Med. 2016 Nov. 51(5):508-18. [View Abstract]
  33. [Guideline] Brott TG, Halperin JL, Abbara S, et al, for the ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology... Vasc Med. 2011 Feb. 16(1):35-77. [View Abstract]
  34. Long A, Lepoutre A, Corbillon E, Branchereau A. Critical review of non- or minimally invasive methods (duplex ultrasonography, MR- and CT-angiography) for evaluating stenosis of the proximal internal carotid artery. Eur J Vasc Endovasc Surg. 2002 Jul. 24(1):43-52. [View Abstract]
  35. Park KJ, Jung SC, Kim HS, et al. Multi-contrast high-resolution magnetic resonance findings of spontaneous and unruptured intracranial vertebral artery dissection: qualitative and quantitative analysis according to stages. Cerebrovasc Dis. 2016. 42(1-2):23-31. [View Abstract]
  36. Kobayashi H, Morishita T, Ogata T, et al. Extracranial and intracranial vertebral artery dissections: a comparison of clinical findings. J Neurol Sci. 2016 Mar 15. 362:244-50. [View Abstract]
  37. Ben Hassen W, Machet A, Edjlali-Goujon M, et al. Imaging of cervical artery dissection. Diagn Interv Imaging. 2014 Dec. 95(12):1151-61. [View Abstract]
  38. Simonnet H, Deiva K, Bellesme C, et al. Extracranial vertebral artery dissection in children: natural history and management. Neuroradiology. 2015 Jul. 57(7):729-38. [View Abstract]
  39. Lansberg MG, O'Donnell MJ, Khatri P, et al, for the American College of Chest Physicians. Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb. 141 (2 suppl):e601S-36S. [View Abstract]
  40. Markus HS, Hayter E, Levi C, et al, for the CADISS trial investigators. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr. 14(4):361-7. [View Abstract]
  41. Kennedy F, Lanfranconi S, Hicks C, et al, for the CADISS Investigators. Antiplatelets vs anticoagulation for dissection: CADISS nonrandomized arm and meta-analysis. Neurology. 2012 Aug 14. 79(7):686-9. [View Abstract]
  42. Chowdhury MM, Sabbagh CN, Jackson D, Coughlin PA, Ghosh J. Antithrombotic treatment for acute extracranial carotid artery dissections: a meta-analysis. Eur J Vasc Endovasc Surg. 2015 Aug. 50(2):148-56. [View Abstract]
  43. Nam KH, Ko JK, Cha SH, Choi CH, Lee TH, Lee JI. Endovascular treatment of acute intracranial vertebral artery dissection: long-term follow-up results of internal trapping and reconstructive treatment using coils and stents. J Neurointerv Surg. 2015 Nov. 7(11):829-34. [View Abstract]
  44. Kernan WN, Ovbiagele B, Black HR, et al, for the American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Jul. 45(7):2160-236. [View Abstract]
  45. Hernandez-Duran S, Ogilvy CS. Clinical outcomes of patients with vertebral artery dissection treated endovascularly: a meta-analysis. Neurosurg Rev. 2014 Oct. 37(4):569-77. [View Abstract]
  46. Schievink WI. The treatment of spontaneous carotid and vertebral artery dissections. Curr Opin Cardiol. 2000 Sep. 15(5):316-21. [View Abstract]
  47. [Guideline] Adams RJ, Albers G, Alberts MJ, et al. Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack. Stroke. 2008 May. 39(5):1647-52. [View Abstract]
  48. [Guideline] Sacco RL, Adams R, Albers G, 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. 2006 Feb. 37(2):577-617. [View Abstract]
  49. Mustanoja S, Metso TM, Putaala J, et al. Helsinki experience on nonvitamin K oral anticoagulants for treating cervical artery dissection. Brain Behav. 2015 Aug. 5(8):e00349. [View Abstract]
  50. Caprio FZ, Bernstein RA, Alberts MJ, et al. Efficacy and safety of novel oral anticoagulants in patients with cervical artery dissections. Cerebrovasc Dis. 2014. 38(4):247-53. [View Abstract]
  51. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2003. (3):CD000255.
  52. Caplan LR. Barnett H, ed. Stroke: Pathophysiology, Diagnosis and Management. London, England: Churchill Livingstone; 1986. Vol 1: 549-619.
  53. 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. 2012 Feb. 16(1):158-62. [View Abstract]
  54. De Giorgio F, Vetrugno G, De Mercurio D, et al. Dissection of the vertebral artery during a basketball game: a case report. Med Sci Law. 2004 Jan. 44(1):80-6. [View Abstract]
  55. 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. 2003 Dec. 99(6):960-6. [View Abstract]
  56. 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. 2013 Feb. 55(2):201-6. [View Abstract]
  57. Mokri B. Traumatic and spontaneous extracranial internal carotid artery dissections. J Neurol. 1990 Oct. 237(6):356-61. [View Abstract]
  58. Prabhu V, Kizer J, Patil A, Hellbusch L, Taylon C, Leibrock L. Vertebrobasilar thrombosis associated with nonpenetrating cervical spine trauma. J Trauma. 1996 Jan. 40(1):130-7. [View Abstract]
  59. 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. 2009 Oct. 193(4):1167-74. [View Abstract]
  60. Ramphul N, Geary U. Caveats in the management and diagnosis of cerebellar infarct and vertebral artery dissection. Emerg Med J. 2009 Apr. 26(4):303-4. [View Abstract]
  61. Rodallec MH, Marteau V, Gerber S, Desmottes L, Zins M. Craniocervical arterial dissection: spectrum of imaging findings and differential diagnosis. Radiographics. 2008 Oct. 28(6):1711-28. [View Abstract]
  62. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001 Mar 22. 344(12):898-906. [View Abstract]
  63. Sturzenegger M, Mattle HP, Rivoir A, Rihs F, Schmid C. Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke. 1993 Dec. 24(12):1910-21. [View Abstract]
  64. Park MS, Albuquerque FC, Nanaszko M, et al. Critical assessment of complications associated with use of the Pipeline Embolization Device. J Neurointerv Surg. 2015 Sep. 7(9):652-9. [View Abstract]
  65. Cohen JE, Gomori JM, Rajz G, Itshayek E, Eichel R, Leker RR. Urgent off-label use of the pipeline flow diverter stent in selected ischemic cerebrovascular conditions: thrombotic segments and tortuous arteries. J Neurointerv Surg. 2015 Sep. 7(9):671-5. [View Abstract]
  66. Robertson JJ, Koyfman A. Extracranial cervical artery dissections. Emerg Med Clin North Am. 2017 Nov. 35(4):727-41. [View Abstract]
  67. Takahara M, Ogata T, Abe H, et al. The comparison of clinical findings and treatment between unilateral and bilateral vertebral artery dissection. J Stroke Cerebrovasc Dis. 2019 Jan 30. [View Abstract]
  68. Hajnovic L, Sefranek V, Schutz L. Trauma of the extracranial cerebral arteries due to injuries of the cervical spine. Rozhl Chir. 2018 Winter. 97(11):504-8. [View Abstract]
  69. MacArthur AM, Mehdi S. Early detection of vertebral artery dissection. BMJ Case Rep. 2018 Nov 28. 11(1):[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) 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) 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).

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