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. See the image below.



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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....

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[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 epidemiological 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 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 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.

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 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.[1]

Sex- and age-related statistics

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 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]

Mortality/Morbidity

Vertebral artery dissection (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 include the following:

Complications

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 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

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

A French retrospective study that evaluated clinical and imaging features with outcomes in 20 pediatric patients with extracranial vertebral artery dissection (VAD) over 14 years indicated that the initial imaging studies should include the posterior fossa vessels and the craniocervical region with V2-V3 segments.[32] In the presence of inconclusive findings on nonivasive imaging studies, the investigators suggested use of conventional angiography for definitive diagnosis.[32]

Computed tomography scanning

Computed tomography (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.

Magnetic resonance imaging

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]

Magnetic resonance angiography

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, 33]

Cerebral angiography may still have a role when clinical suspicion is high but MRI/MRA has failed to isolate the lesion.

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]

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.

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).

Once contraindications to anticoagulation have been ruled out, the accepted management of proven or suspected spontaneous VAD consists of anticoagulant therapy in those patients who are not also affected by the complication of subarachnoid hemorrhage.[13]  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.

This management strategy is adhered to despite the fact that no randomized controlled studies support this approach.[34]  Furthermore, the pathophysiologic mechanism underlying VAD includes hemorrhage into the arterial wall and subarachnoid hemorrhage as a devastating complication of the condition.

Evidence in favor of anticoagulation is suggested by a number of published series that demonstrate an encouraging prognosis for those patients who survive their initial presentation and subsequently undergo anticoagulation.[1]  Most of these patients underwent head CT to exclude frank subarachnoid hemorrhage before beginning anticoagulant therapy. Anticoagulation therapy is further supported by the fact that no published cases have documented brainstem hemorrhage or clinical deterioration as a result of this therapy. Recent studies suggest that treatment with novel anticoagulants may yield outcomes and safety profiles similar to therapy with conventional vitamin K antagonists.[35]

Antiplatelet therapy is a reasonable option to consider in patients who are suspected of suffering from a VAD while awaiting definitive investigations.

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.

Transcranial Doppler may be used to monitor the intracranial vertebral artery both for patency and for the abnormal flow associated with embolic phenomena.

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.[36] 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.

A 2014 meta-analysis of vertebral artery dissections (VADs) treated endovascularly found that 86.3% of procedures were associated with good or excellent outcomes.[37] 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.[37]

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.[38]

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.[35]  NOACs may be associated with similar rates of stroke at follow-up, but they have fewer hemorrhagic complications.[39] 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]).

Further Outpatient Care

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.[40, 41]

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

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 Singh Sahota, MSc, Research Assistant, Emergency Medicine and Cardiology and Medical Student, Cumming School of Medicine, University of Calgary

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.

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.

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.

Additional Contributors

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

Disclosure: Nothing to disclose.

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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 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).