eMedicine Specialties > Emergency Medicine > Cardiovascular

Dissection, Vertebral Artery

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
Coauthor(s): Marc Afilalo, MD, MCFP (EM), FACEP, CSPQ, FRCP(C), Director, Emergency Department, Associate Professor, Faculty of Medicine, Section of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Contributor Information and Disclosures

Updated: Nov 1, 2007

Introduction

Background

Vertebral artery dissection (VAD) is an increasingly recognized cause of stroke in patients younger than 45 years. 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.
• 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.

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. 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) - 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
  • Vertigo
  • Nausea and vomiting
  • Diplopia or oscillopsia (image movement experienced with head motion)
  • Dysphagia (CN IX and X)
  • Disequilibrium
  • Unilateral hearing loss
• 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
  • Nystagmus
  • Ipsilateral Horner syndrome in as many as one third of patients with VAD (ie, impairment of descending sympathetic tract)
  • 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 syndrome
• 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 - Has one of the best studied and strongest demonstrated associations with VAD
  • Yoga
  • Ceiling painting
  • Nose blowing
  • Minor neck trauma
  • Judo
  • Medical risk factors
  • Hypertension (48% in one series)
  • Oral contraceptive use
  • Chronic headache syndromes/migraines
  • Intrinsic vascular pathology
  • Fibromuscular dysplasia
  • Cystic medial necrosis
  • Female sex
  • Recent infection
• 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.

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