eMedicine Specialties > Emergency Medicine > Cardiovascular

Dissection, Vertebral Artery

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
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

Updated: Aug 5, 2009

Introduction

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.

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.

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

• The hematoma may seal off and, if sufficiently small, remain largely asymptomatic.
• If the dissection is subintimal, the expanding hematoma may partially or completely occlude the vertebral artery or one of its branches. Extensive dissections (those that extend intracranially and involve the basilar artery) result in infarctions of the brain stem, cerebellum or, rarely, the spinal cord. Subintimal dissections also may rupture back into the vertebral artery, thus creating a false lumen (pseudolumen).
• Subadventitial dissections tend to cause pseudoaneurysmal dilation of the vertebral artery, which may compress adjacent neurologic structures. These subadventitial dissections are prone to rupture through the adventitia, resulting in subarachnoid hemorrhage. In an autopsy series of more than 100 patients with subarachnoid hemorrhage, 5% of the hemorrhages were deemed the result of VAD.
• The intimal disruption and low flow states that arise in VAD create a thrombogenic milieu in which emboli may form and propagate distally. This results in transient ischemia or infarction.

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:

• Segment I runs from its takeoff at the first branch of the subclavian artery to the transverse foramina of cervical vertebra C5 or C6.
• Segment II runs entirely within the transverse foramina of C5/C6 to C2.
• Segment III, a tortuous segment, begins at the transverse foramen of C2, runs posterolaterally to loop around the posterior arch of C1, and passes subsequently between the atlas and the occiput. This segment is encased in muscles, nerves, and the atlanto-occipital membrane.
• Segment IV, the intracranial segment, begins as it pierces the dura at the foramen magnum and continues until the junction of the pons and medulla, where the vertebral arteries merge to join the larger proximal basilar trunk.

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.

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.

Mortality/Morbidity

• 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.⁵
• Those who survive the initial crisis do remarkably well, with long-term sequelae rare.

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.⁶

Clinical

History

The typical presentation of VAD is a young person with severe occipital headache and posterior nuchal pain following a recent, relatively minor, head or neck injury.⁷ 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 brain stem 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).

• Patient history may include the following:
  • Ipsilateral facial dysesthesia (pain and numbness)⁵ - Most common symptom
  • Dysarthria or hoarseness (cranial nerves [CN] IX and X)
  • Contralateral loss of pain and temperature sensation in the trunk and limbs
  • Ipsilateral loss of taste (nucleus and tractus solitarius)
  • Hiccups
  • Vertigo⁵
  • Nausea and vomiting
  • Diplopia or oscillopsia (image movement experienced with head motion)
  • Dysphagia (CN IX and X)
  • Disequilibrium
  • Unilateral hearing loss⁸
• Rarely, patients may manifest the following symptoms of a medial medullary syndrome:
  • Contralateral weakness or paralysis (pyramidal tract)
  • Contralateral numbness (medial lemniscus)

Physical

The physical examination of patients who have not yet manifested neurologic dysfunction may be misleading. The occipital and nuchal pain associated with 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:
  • Limb or truncal ataxia
  • Nystagmus⁷
  • Ipsilateral Horner syndrome in as many as one third of patients with VAD (ie, impairment of descending sympathetic tract)⁴
  • Ipsilateral hypogeusia or ageusia (ie, diminished or absent sense of taste)
  • Ipsilateral impairment of fine touch and proprioception
  • Contralateral impairment of pain and thermal sensation in the extremities (ie, spinothalamic tract)
  • Lateral medullary syndrome⁵
• Cerebellar findings may include the following:
  • Nystagmus
  • Medial medullary syndrome
  • Tongue deviation to the side of the lesion (impairment of CN XII)
  • Contralateral hemiparesis
  • Ipsilateral impairment of fine touch and proprioception (nucleus gracilis)
  • Internuclear ophthalmoplegia (lesion of the medial longitudinal fasciculus)

Causes

Spontaneous 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:
  • Spinal manipulation^{9,10,2,3,5,11,12} - Has one of the best studied and strongest demonstrated associations with VAD
  • Yoga
  • Ceiling painting
  • Nose blowing
  • Minor neck trauma
  • Judo
  • Medical risk factors
  • Hypertension¹³ (48% in one series)
  • Oral contraceptive use
  • Chronic headache syndromes/migraines^3,5,6
  • Intrinsic vascular pathology
  • Fibromuscular dysplasia
  • Cystic medial necrosis
  • Female sex
  • Recent infection¹⁴
• 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.

Differential Diagnoses

Other Problems to Be Considered

Vasculitis affecting the vertebrobasilar circulation

Workup

Laboratory Studies

• 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.

Imaging Studies

• CT scanning
  • CT scan is useful in identifying patients with the complication of subarachnoid hemorrhage.⁷
  • Absence of hemorrhage, as demonstrated by CT scan, is a prerequisite for instituting anticoagulant therapy.
• Four-vessel cerebral angiography¹⁵
  • Prior to development of noninvasive techniques such as MRI and Doppler ultrasound, cerebral angiography was the criterion standard in diagnosing VAD. These noninvasive techniques are supplanting angiography as the imaging techniques of choice for patients in whom VAD is suspected.
  • The characteristic angiographic finding in a dissected vertebral artery is the string or "string and pearl" appearance of the stenotic vessel lumen.¹⁶
  • 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 CAD or VAD.¹⁷
• Magnetic resonance imaging^7,15
  • MRI detects both the intramural thrombus and intimal flap that are characteristic of VAD.¹⁶
  • Hyperintensity of the vessel wall seen on T1-weighted axial images is considered by some to be pathognomonic of VAD.
• Magnetic resonance angiography^7,15
  • 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.¹⁶
  • MRI and MRA are less sensitive than cerebral angiography for the detection of VAD, although they probably have equivalent specificity.
  • Cerebral angiography is indicated when clinical suspicion is high but MRI/MRA has failed to isolate the lesion.
• Vascular duplex scanning
  • Duplex sonography of the vertebral arteries demonstrates abnormal flow in 95% of patients with VAD.
  • 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.

Procedures

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

Treatment

Emergency Department Care

• 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.¹⁸
• 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 controlled studies support this approach.
• 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.
• All 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.

Consultations

• Neurosurgery

Medication

Anticoagulant and antiplatelet agents are the DOCs to prevent thromboembolic disorders associated with VAD.

Anticoagulant agents

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

Heparin

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.

Dosing

Adult

Loading dose: 80 U/kg IV; followed by continuous infusion mixed as follows: 25,000 U in 250 mL D5W (100 U/mL); initiate infusion at 18 U/kg/h; adjust prn according to aPTT results
This regimen increases anticoagulation up to 85% on initial aPTT; some EDs, especially those with many older patients, use a regimen of 70 U/kg loading dose and 15 U/kg/h continuous infusion
Alternatively, infuse 50 U/kg/h IV to start, followed by 15-25 U/kg/h as a continuous infusion; increase by 5 U/kg/h q4h prn depending on aPTT results

Pediatric

Loading dose: 50 U/kg/h IV; followed by 15-25 U/kg/h continuous infusion; increase dose by 2-4 U/kg/h q6-8h prn depending on aPTT results

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity; active bleeding; subacute bacterial endocarditis; history of heparin-induced thrombocytopenia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Exclude radiographically evident CNS hemorrhage prior to use in VAD; in neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock

Warfarin sodium (Coumadin)

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.

Dosing

Adult

5-15 mg/d PO qd for 2-5 d; tailor dose to maintain INR in range of 2-3

Pediatric

0.05-0.34 mg/kg/d PO; infants may require doses at or near the high end of this range

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; open wounds or GI ulcers; severe liver or kidney disease

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brands after achieving therapeutic response; caution in active TB or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Antiplatelet agents

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

Aspirin (Anacin, Bufferin, Ecotrin, Bayer aspirin)

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

Dosing

Adult

650 mg PO divided bid/qid; not to exceed 1.3 g/d; 300 mg/d as effective as larger dose and may be associated with fewer side effects

Pediatric

Not established

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; caution if liver damage, hypoprothrombinemia, or vitamin K deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, history of blood coagulation defects, or taking anticoagulants

Ticlopidine (Ticlid)

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

Dosing

Adult

250 mg PO bid

Pediatric

Not established

Interactions

Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDS may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution if liver damage, neutropenia, thrombocytopenia, or active bleeding disorders; discontinue if ANC decreases to <1200/mm³ or if platelet count falls to <80,000/mm³

Follow-up

Further Inpatient Care

• Patients with 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.

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.
• 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.

Complications

• Brainstem infarction
• Cerebellar infarction
• Subarachnoid hemorrhage
• Vertebral artery pseudoaneurysm causing compressive cranial neuropathy

Prognosis

• Extracranial dissection
  • Most patients 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.¹⁹
  • 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.¹⁹

Patient Education

• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider diagnosis of VAD. The routine ED evaluation of headache (CT scan and LP) fails to identify patients with VAD. Most patients are evaluated by one other physician before the diagnosis of VAD is established.
• Failure to differentiate between the pain associated with VAD and musculoskeletal pain in the absence of a significant mechanism of injury
• Failure to consider occipital headache as a sign of VAD. Occipital headache lacks features that traditionally indicate a serious etiology. Headaches associated with VAD lack a thunderclap onset, are not associated with meningismus or fever, and are not associated with a history of significant head trauma.
• Failure to consider etiologies of the stroke syndrome, other than atherosclerosis, if the patient presents with brainstem or cerebellar dysfunction. This is especially true in the context of a negative CT scan and/or LP.

References

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Keywords

VAD, vertebral artery dissection, stroke, aneurysm, arteria vertebralis, hematoma, carotid artery dissection, CAD, stroke rehabilitation

Contributor Information and Disclosures

Author

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
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
Marc Afilalo, MD, FACEP, FRCPC, MCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Royal College of Physicians and Surgeons of Canada, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center
Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

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
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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