You are in: eMedicine Specialties > Neurosurgery > Vascular Vertebral Artery AtherothrombosisArticle Last Updated: Feb 20, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Mark K Eskandari, MD, Associate Professor, Departments of Radiology and Division of Vascular Surgery, Feinberg School of Medicine, Northwestern University; Attending Surgeon, Division of Vascular Surgery, Northwestern Memorial Hospital; Consulting Staff, Division of Vascular Surgery, Northwestern Medical Faculty Foundation; Consulting Staff, Department of Surgery, Jesse Brown Veterans Affairs Medical Center; Consulting Staff, Department of Surgery, Evanston Northwestern Healthcare Mark K Eskandari is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, International Society of Endovascular Specialists, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Society of Interventional Radiology, Society of University Surgeons, and Western Surgical Association Coauthor(s): Mark D Morasch, MD, Clinical Practice Director, Division of Vascular Surgery, Assistant Professor of Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine Editors: Michael G Nosko, MD, PhD, Chief, Division of Neurosurgery, Director of Neurovascular Surgery, Medical Director of Neuroscience Unit, Associate Professor, Department of Surgery, University of Medicine and Dentistry at New Jersey; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Ryszard M Pluta, MD, PhD, Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences at Warsaw, Poland; Senior Researcher, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH; Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy; Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc Author and Editor Disclosure Synonyms and related keywords: vertebral artery atherothrombosis, atherosclerosis, atherosclerotic lesions, atherosclerotic plaque, vertebral artery stenosis, hemodynamic symptoms, vertebrobasilar ischemia, fibromuscular dysplasia, FMD, carotid artery disease, vasculopathy, Takayasu disease, osteophyte compression, aneurysms, arteritides, anticoagulation, vertebral artery reconstruction, subclavian-vertebral artery endarterectomy, saphenous vein bypass INTRODUCTIONSection 2 of 12
  ProblemIschemic mechanisms are either hemodynamic or embolic in nature. For hemodynamic symptoms to occur, significant disease must be present in both of the vertebrals, and compensatory contribution from the anterior circulation via the circle of Willis must be incomplete. Alternatively, hemodynamic ischemia may occur with proximal subclavian artery stenosis leading to a subclavian-vertebral steal phenomenon. Such pathologic states can result in transient "end-organ" (brainstem, cerebellum, and/or occipital lobes) hypoperfusion. Regardless of the specific pathology, patients usually demonstrate reproducible symptoms following postural or positional changes. Hypoperfusion has also been described in the face of underlying cardiac insufficiency. In general, ischemia attributable to hemodynamic causes rarely results in infarction. Patients typically present with repetitive, short-lived symptoms, which are more of a nuisance than a danger. However, they are prone to succumb to traumatic injuries resulting from loss of balance. Embolic causes of vertebrobasilar ischemia may not be as well recognized. However, current estimates suggest that up to a third of vertebrobasilar ischemic episodes are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, and/or basilar arteries. These patients are at high risk for infarction within the tissues supplied by the posterior circulation. Emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and (rarely) from fibromuscular lesions, aneurysms, or dissections. Compared to hemodynamic mechanisms of ischemia, emboli are more likely to cause dangerous infarcts that leave patients with permanent and debilitating strokes. The manifestations of vertebrobasilar ischemia are varied and vague, often making the diagnosis difficult. A number of medical conditions may mimic vertebrobasilar ischemia, thus confounding the selection of patients in need of posterior circulation treatment. These include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, benign vertiginous states, basilar artery migraine, and postsubarachnoid hemorrhage vasospasm. In contradistinction to carotid disease, vertebrobasilar symptoms are poorly defined. The classic symptoms of vertebrobasilar ischemia are dizziness, vertigo, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, drop attacks, ataxia, and homonymous hemianopsia (see Image 7). Ischemia affecting the temporo-occipital areas of the cerebral hemispheres and segments of the brainstem and cerebellum characteristically produces bilateral symptoms. EtiologyAtherosclerosis is the primary etiology, although fibromuscular dysplasia (FMD) is an occasional cause PathophysiologyVertebrobasilar ischemia is certainly less common than internal carotid artery disease, yet it must be diagnosed appropriately because it is a treatable vasculopathy. The most common disease affecting the vertebral artery is atherosclerosis. Less common pathologic processes include trauma, FMD, Takayasu disease, osteophyte compression, dissections, aneurysms, and other arteritides. INDICATIONSSection 3 of 12
Once the diagnosis of vertebrobasilar ischemia has been confirmed with appropriate imaging, surgical correction may be considered. The mere presence of vertebral artery stenosis in an asymptomatic patient is rarely an indication for surgery. Surgical reconstruction is based on the specific etiology. The indication for surgery in patients with hemodynamic symptoms depends on the ability to demonstrate insufficient blood flow to the basilar artery. In other words, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels. In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. However, as in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings. RELEVANT ANATOMYSection 4 of 12
Atherosclerosis involving the vertebrobasilar system is known to cause posterior circulation ischemia. The posterior circulation, or vertebrobasilar system, supplies blood to the brainstem, cerebellum, and occipital lobes via paired vertebral arteries. The vertebrals converge beyond the base of the skull and form the basilar artery at the base of the pons. The vertebral artery is arbitrarily segmented into the following four parts:
The anterior spinal artery arises from branches off each of the vertebral arteries prior to their convergence to form the basilar artery. Pontine and cerebellar arteries arise from the basilar artery before it bifurcates into the paired posterior cerebral arteries. CONTRAINDICATIONSSection 5 of 12
As discussed previously, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels. In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. However, as in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings. Patients with symptomatic vertebrobasilar ischemia who are not amenable to surgery or investigational endoluminal therapy may be treated medically with long-term anticoagulation to prevent thrombosis. WORKUPSection 6 of 12
Imaging Studies
TREATMENTSection 7 of 12
Medical therapyPatients with symptomatic vertebrobasilar ischemia who are not amenable to surgery or investigational endoluminal therapy may be treated medically with long-term anticoagulation to prevent thrombosis. Surgical therapyPrevious experience has shown that with appropriate diagnosis and surgical correction, complete resolution of hemodynamic and embolic symptoms can occur predictably. Vertebral artery reconstruction can be performed successfully with fewer ischemic complications than carotid artery surgery and with durable long-term results. The location of disease dictates the type of surgical reconstruction required. Intraoperative detailsThe two main options for treating offending ostial lesions (V1 segment) are transposition of the proximal vertebral artery onto the common carotid artery or vertebral artery bypass. The bypass can originate from either the common carotid artery or the adjacent subclavian artery (see Image 4). Choices of conduit include either saphenous vein grafts or prosthetic material (polytetrafluoroethylene [PTFE] or Dacron). Subclavian-vertebral artery endarterectomy is less commonly performed. The V2 segment, which ascends within the foramina of the cervical vertebrae, is the site of a wide variety of disorders. External compression is most likely to occur in this segment because of osteophytes, the edge of the transverse foramina, or the intervertebral joints. Positional changes, such as rotation or extension of the neck, usually trigger compression of the vertebral artery in this segment. The V2 segment is also the site of aneurysmal degeneration (see Image 5), fibromuscular diseases, and embolizing atherosclerotic plaques (see Image 6). Elective surgical reconstruction is very rarely undertaken within this segment; however, ligation (at the C1-C2 level) and bypass to the distal (V3 segment) vertebral artery may be indicated. Extrinsic lesions can be corrected to relieve kinking or compression of the artery. The most common indication for exposure of this segment of the artery is for control of hemorrhage, which is best relieved with proximal and distal ligation of the artery. An alternative for traumatic injuries to the V2 segment includes coil embolization. Neither of these has been associated with worsening neurologic sequelae. Reconstruction of the distal (V3 segment) vertebral artery is usually performed at the C1-C2 level. The techniques most often used to reconstruct the distal vertebral artery at this level include (1) saphenous vein bypass from the common carotid, subclavian, or proximal vertebral artery; (2) transposition of the external carotid or hypertrophied occipital artery to the distal vertebral; and (3) transposition of the distal vertebral artery to the side of the distal internal carotid artery. More distal pathology can be accessed surgically above the level of the transverse process of C1. At this level, the vertebral artery is vulnerable to direct trauma and stretch injuries that can lead to intimal damage, thrombosis, embolization, and dissection. This segment is also prone to arteriovenous fistula formation and aneurysmal degeneration. Surgical exposure at the suboccipital segment requires resection of the C1 transverse process and part of its posterior arch. Reconstruction at this level is limited to saphenous vein bypass from the distal internal carotid artery. Postoperative detailsPostoperatively, patients should be monitored and should receive long-term antiplatelet therapy (eg, aspirin). Follow-upFollow-up care and monitoring is primarily based on clinical assessment of recurrent symptoms. The presence of new symptoms consistent with vertebrobasilar ischemia mandates imaging studies as previously outlined. COMPLICATIONSSection 8 of 12
The perioperative complication rates differ for proximal versus distal vertebral artery repairs. The technically easier proximal operations have been reported to have a combined morbidity/mortality rate of 0.9%. Distal reconstructions have a combined morbidity/mortality rate of 3-4%. Perioperative complications include stroke, hematoma, thrombosis, lymphocele, and nerve injury (eg, Horner syndrome, spinal accessory nerve, vagus nerve). The occurrence of ptosis (drooping of the eyelid) on the operative side is a known complication of proximal vertebral artery reconstructions. This condition is usually temporary and is attributed to a traction injury of the lower cervical sympathetic nerves. OUTCOME AND PROGNOSISSection 9 of 12
Results following both proximal and distal vertebral artery reconstructions are generally equal to or better than those reported for other forms of cerebrovascular revascularizations. In experienced hands, the combined stroke and death rates are 4% or less. Long-term patency of the reconstructions is excellent. More than 80% of patients experience symptom relief following surgical reconstruction. FUTURE AND CONTROVERSIESSection 10 of 12
Modern surgical advances have resulted in a safe and durable mode of therapy for patients with documented symptomatic vertebrobasilar ischemia. On the horizon is the application of minimally invasive endovascular interventions, which have spread throughout the field of vascular and cardiovascular surgery. Balloon angioplasty, along with endoluminal stent placement, has already been tried in proximal vertebral disease with some reported early technical success. The complication rate and long-term success of endoluminal procedures are still unknown; therefore, this form of therapy is currently considered investigational. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Vertebral Artery Atherothrombosis excerpt Article Last Updated: Feb 20, 2007 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
