Vertebral artery disease can be caused by a number of factors that narrow the vertebral arteries supplying the brain stem. It causes symptoms mainly because the brain stem does not get sufficient blood. The two vertebral arteries join to form a single artery at the base of the brain. Usually, if one vertebral artery is not narrowed it will be sufficient to supply blood to the brainstem.
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 (DO NOT EDIT)[1]
Vascular Imaging in Patients with Vertebral Artery Disease (DO NOT EDIT)[1]
"1. Noninvasive imaging by CTA or MRA for detection of vertebral artery disease should be part of the initial evaluation of patients with neurological symptoms referable to the posterior circulation and those with subclavian steal syndrome. (Level of Evidence: C)"
"2. Patients with asymptomatic bilateral carotid occlusions or unilateral carotid artery occlusion and incomplete circle of Willis should undergo noninvasive imaging for detection of vertebral artery obstructive disease. (Level of Evidence: C)"
"3. In patients whose symptoms suggest posterior cerebral or cerebellar ischemia, MRA or CTA is recommended rather than ultrasound imaging for evaluation of the vertebral arteries. (Level of Evidence: C)"
"1. In patients with symptoms of posterior cerebral or cerebellar ischemia, serial noninvasive imaging of the extracranial vertebral arteries is reasonable to assess the progression of atherosclerotic disease and exclude the development of new lesions. (Level of Evidence: C)"
"2. In patients with posterior cerebral or cerebellar ischemic symptoms who may be candidates for revascularization, catheter-based contrast angiography can be useful to define vertebral artery pathoanatomy when noninvasive imaging fails to define the location or severity of stenosis. (Level of Evidence: C)"
"3. In patients who have undergone vertebral artery revascularization, serial noninvasive imaging of the extracranial vertebral arteries is reasonable at intervals similar to those for carotid revascularization. (Level of Evidence: C)"
Management of Atherosclerotic Risk Factors in Patients with Vertebral Artery Disease (DO NOT EDIT)[1]
"1. Medical therapy and lifestyle modification to reduce atherosclerotic risk are recommended in patients with vertebral atherosclerosis according to the standards recommended for those with extracranial carotid atherosclerosis[2][3]. (Level of Evidence: B)"
"3. Antiplatelet drug therapy is recommended as part of the initial management for patients who sustain ischemic stroke or TIA associated with extracranial vertebral atherosclerosis. Aspirin (81 to 325 mg daily), the combination of aspirin plus extended-release dipyridamole (25 and 200 mg twice daily, respectively), and clopidogrel (75 mg daily) are acceptable options. Selection of an antiplatelet regimen should be individualized on the basis of patient risk factor profiles, cost, tolerance, and other clinical characteristics, as well as guidance from regulatory agencies[6][4][7][8][9][10]. (Level of Evidence: B)"
"1. For patients with atherosclerosis of the extracranial vertebral arteries in whom aspirin is contraindicated by factors other than active bleeding, including those with allergy to aspirin, either clopidogrel (75 mg daily) or ticlopidine (250 mg twice daily) is a reasonable alternative. (Level of Evidence: C)"
↑"Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report". Circulation. 106 (25): 3143–421. 2002. PMID12485966. Unknown parameter |month= ignored (help)
↑Ginsberg HN, Kris-Etherton P, Dennis B; et al. (1998). "Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1". Arterioscler. Thromb. Vasc. Biol. 18 (3): 441–9. PMID9514413. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Adams RJ, Albers G, Alberts MJ; et al. (2008). "Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack". Stroke. 39 (5): 1647–52. doi:10.1161/STROKEAHA.107.189063. PMID18322260. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑"A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee". Lancet. 348 (9038): 1329–39. 1996. PMID8918275. Unknown parameter |month= ignored (help)
↑Diener HC, Bogousslavsky J, Brass LM; et al. (2004). "Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial". Lancet. 364 (9431): 331–7. doi:10.1016/S0140-6736(04)16721-4. PMID15276392.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Diener HC, Cunha L, Forbes C, Sivenius J, Smets P, Lowenthal A (1996). "European Stroke Prevention Study. 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke". J. Neurol. Sci. 143 (1–2): 1–13. PMID8981292. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)