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:

Ipsilateral facial dysesthesia (pain and numbness)^[6]: 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^[1]
Nausea and vomiting
Diplopia or oscillopsia (image movement experienced with head motion)
Dysphagia (CN IX and X)
Disequilibrium
Unilateral hearing loss^[2]

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

Contralateral weakness or paralysis (pyramidal tract)
Contralateral numbness (medial lemniscus)

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:

Limb or truncal ataxia
Nystagmus^[3]
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 syndrome^[6]

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)

Differential Diagnoses

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Media Gallery

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).

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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

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association 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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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

Inderjeet (Indy) S Sahota, MD, MSc, CCFP is a member of the following medical societies: Canadian Association of Emergency Physicians, Canadian Cardiovascular Society, Canadian Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Amin Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Program Director, Emergency Medicine, Einstein Medical Center Montgomery

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, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.