eMedicine Specialties > Emergency Medicine > Neurology
Vertebrobasilar Atherothrombotic Disease
Updated: Jun 3, 2008
Introduction
Background
Vertebrobasilar atherothrombotic disease (VBATD) describes a wide spectrum of clinical entities with a common pathophysiology. Transient ischemic attacks (TIAs) in this vascular territory are also referred to as vertebrobasilar insufficiency (VBI). This more commonly used term was developed in the 1950s after Fisher introduced the term carotid insufficiency to describe TIAs of the anterior circulation, which frequently serve as the prodrome to carotid branch infarcts. Although carotid insufficiency has been dropped from common medical jargon, VBI persists as the term that encompasses all TIA syndromes of the posterior circulation. In this article, VBATD describes both transient and permanent ischemic deficits as they affect posterior cerebral circulation.
VBATD deserves special attention among emergency physicians because it is difficult to diagnose and important not to misdiagnose. Signs and symptoms of VBATD overlap those of other more common benign entities (eg, labyrinthitis, vestibular neuronitis, benign paroxysmal positional vertigo).
Pathophysiology
Vertebrobasilar (posterior) circulation constitutes the arterial supply to the brain stem, cerebellum, and occipital cortex. Any interruption in blood flow to these areas may manifest in a myriad of symptoms. These symptoms are determined by which particular branch or branches of the vertebrobasilar circulation have been compromised, extent of any collateral circulation, and degree of occlusion.
The brain stem is a focal point of neurologic activity, housing cranial nerves, the reticular activating system, and a series of ascending and descending neurosensory tracts. When this compact area of neurologic activity malfunctions as a result of impaired blood flow, several different but overlapping clinical syndromes can result.
Studies show that embolic phenomena cause infarction in vertebrobasilar territory in 9-40% of reported cases. The vertebrobasilar bed appears less susceptible than carotid circulation to embolic occlusion.
The vertebral artery is often classified into intracranial and extracranial segments; the atherosclerotic process tends to affect vertebrobasilar circulation at specific intracranial and extracranial sites. The extracranial site is defined as the initial segment of the vertebral artery just proximal to its take-off from the subclavian. The intracranial site is defined as the proximal portion of the basilar artery, just after the joining of the 2 vertebral arteries or just distal to the pontomedullary junction.
Frequency
United States
Approximately one fourth of strokes and TIAs occur in the vertebrobasilar distribution.
- Brainstem infarctions have been reported in autopsy series at a rate of 2 per 1000 cases. One clinical study has suggested that the disease occurs 25% as frequently as occlusions of the carotid artery and its branches.
- Recent developments in neuroimaging provide new perspectives about the disease's prevalence. Some studies using MRI suggest that 40% of patients with vertebrobasilar TIAs have evidence of brainstem infarction.
Mortality/Morbidity
Vertebrobasilar ischemic disease encompasses a vast spectrum of clinical syndromes, extending from subclinical to lethal brainstem infarctions.
- Of patients who suffer infarctions in the vertebrobasilar territory, 50% report TIAs in the days or weeks (rarely months) prior to onset of the permanent deficit. A systematic review suggests that although overall mortality is no different than anterior territory ischemia, the early risk (within 7 d) of recurrent stroke or TIA progression to stroke is higher with VBATD.1
- Basilar artery syndrome, which presents as a locked-in state, is caused by complete occlusion of the intracranial portion of vertebrobasilar circulation. It is a devastating disease with a mortality rate of 75-85%.
Sex
As with atherosclerosis, this disease affects men twice as often as it does women.
Age
Vertebrobasilar ischemic disease occurs in the late decades of life (eg, 70s and 80s).
Clinical
History
Vertebrobasilar TIAs typically have shorter duration than attacks involving the carotid territory, lasting 8 minutes on average compared with 14 minutes for carotid TIAs.
Vertigo is the hallmark symptom of patients experiencing ischemia in the vertebrobasilar distribution. Many patients describe their vertigo as nonviolent or more of a swimming or swaying sensation. Exact incidence of vertigo is unknown, yet as many as one third of patients with VBI may experience vertigo as the sole manifestation of their illness. Visual disturbances (diplopia) as well as auditory phenomena have been described (sudden sensorineural hearing loss).
Other symptoms include the following:
- Facial numbness or paresthesias
- Dysphagia, dysarthria, hoarseness
- Syncope (drop attacks)
- Hemisensory extremity symptoms (eg, contralateral to facial component)
- Lateral medullary infarct (Wallenberg syndrome): When VBI progresses to a complete brainstem infarction, a common syndrome is impaired neurologic functioning in the lateral aspect of the medulla, first described by Wallenberg. This is characterized by the following:
- Ipsilateral facial pain and numbness
- Ipsilateral ataxia (falling to side of lesion)
- Vertigo, nausea, vomiting
- Contralateral pain and thermal impairment over body and occasionally face
- Medial medullary infarct: Occlusion of a vertebral artery or branch of the lower basilar artery may produce the following symptoms:
- Contralateral arm and leg weakness (facial sparing)
- Diplopia
- Basilar artery syndrome: Caused by complete basilar artery occlusion, this is characterized by the following:
- Locked-in state (awake quadriplegia)
- Paralysis or weakness of all extremities
- Horizontal gaze paresis, stupor, coma
- Subclavian steal syndrome: This syndrome results from retrograde blood flow down the vertebral artery in response to increased demands from the left upper limb.
- One of the earliest descriptions of VBI was reported in patients who suffered from stenotic lesions of their left subclavian arteries, just proximal to the take-off of the vertebral artery. Half of these patients reported vertigo symptoms consistent with posterior circulation ischemia when exercising their left arms.
- Some series suggest that arm claudication and headache are the most prominent features in patients with symptomatic subclavian steal syndrome.
Physical
Most patients with early stage VBI have only transient episodes of neurologic dysfunction. As a result, most commonly cited physical symptoms may be minimal or nonexistent. Patients with ongoing symptoms, or those who already have incurred an ischemic deficit, demonstrate physical findings that reflect brainstem and cerebellar dysfunction. Crossed signs (eg, contralateral motor and sensory findings) are hallmarks of many types of brainstem strokes.
- Vertebrobasilar insufficiency
- Nystagmus
- Limb ataxia
- Truncal ataxia (falling to side of lesion)
- Contralateral deficit in pain and temperature perception
- Ipsilateral limb and trunk numbness
- Ipsilateral loss of taste
- Visual field defects
- Lateral medullary infarct (Wallenberg syndrome)
- Contralateral impairment of pain and thermal sensation to the extremities
- Nystagmus
- Ipsilateral Horner syndrome (eg, ptosis, miosis, anhydrosis)
- Medial medullary syndrome
- Ipsilateral paralysis and atrophy of the tongue
- Contralateral deficit in proprioception and fine touch (facial sparing)
- Internuclear ophthalmoplegia
- Basilar artery syndrome
- Bifacial and oropharyngeal palsy
- Horizontal gaze paresis
- Decreased level of consciousness
Causes
Atherosclerosis is by far the most common cause of VBI, making VBI most common among patients with cardiovascular risk factors such as age, hypertension, diabetes mellitus, smoking, and dyslipidemias. VBI may result from any disease process that has an impact on the arterial supply to the posterior fossa, including the following:
- Fibromuscular dysplasia
- Rotational occlusion (Bow hunter's stroke) - Mechanical occlusion or stenosis of the vertebral artery at the C1-C2 level caused by lateral flexion
- Vertebral artery dissection
- Vertebrobasilar aneurysms
- Dolichoectasia of basilar artery
More on Vertebrobasilar Atherothrombotic Disease |
 Overview: Vertebrobasilar Atherothrombotic Disease |
| Differential Diagnoses & Workup: Vertebrobasilar Atherothrombotic Disease |
| Treatment & Medication: Vertebrobasilar Atherothrombotic Disease |
| Follow-up: Vertebrobasilar Atherothrombotic Disease |
| References |
| Next Page » |
References
Flossmann E, Rothwell PM. Prognosis of vertebrobasilar transient ischaemic attack and minor stroke. Brain. Sep 2003;126(Pt 9):1940-54. [Medline].
Feinberg WM, Albers GW, Barnett HJ. Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. Circulation. Jun 1994;89(6):2950-65. [Medline].
Coull BM, Williams LB, Goldstein LS. Anticoagulants and antiplatelet agents in acute ischemic stroke. Report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a Division of the American Heart Association). Neurology. 2002;59 (1):13-22. [Medline].
Brandt T, von Kummer R, Muller-Kuppers M. Thrombolytic therapy of acute basilar artery occlusion. Variables affecting recanalization and outcome. Stroke. May 1996;27(5):875-81. [Medline].
Sivenius J, Riekkinen PJ, Smets P. The European Stroke Prevention Study (ESPS): results by arterial distribution. Ann Neurol. Jun 1991;29(6):596-600. [Medline].
International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet. May 31 1997;349(9065):1569-81. [Medline].
Whisnant JP, Cartlidge NE, Elveback LR. Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. Ann Neurol. Feb 1978;3(2):107-15. [Medline].
Becker KJ, Purcell LL, Hacke W. Vertebrobasilar thrombosis: diagnosis, management, and the use of intra- arterial thrombolytics. Crit Care Med. Oct 1996;24(10):1729-42. [Medline].
Caplan LR. Vertebrobasilar occlusive disease. In: Stroke: Pathophysiology, Diagnosis and Management. Vol 1. 1992:549-619.
Culebras A, Kase CS, Masdeu JC. Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke. A report of the Stroke Council, American Heart Association. Stroke. Jul 1997;28(7):1480-97. [Medline].
Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med. Dec 2003;10(12):1388-95. [Medline].
Froehling DA, Silverstein MD, Mohr DN. The rational clinical examination. Does this dizzy patient have a serious form of vertigo?. JAMA. Feb 2 1994;271(5):385-8. [Medline].
Libman RB, Kwiatkowski TG, Hansen MD. Differences between anterior and posterior circulation stroke in TOAST. Cerebrovasc Dis. 2001;11(4):311-6. [Medline].
Lipinski CA, Swanson ER. Vertebrobasilar distribution stroke mimicking transtentorial herniation. Ann Emerg Med. May 1998;31(5):640-2. [Medline].
Macleod MR, Davis SM, Mitchell PJ. Results of a multicentre, randomised controlled trial of intra-arterial urokinase in the treatment of acute posterior circulation ischaemic stroke. Cerebrovasc Dis. 2005;20(1):12-7. [Medline].
Ois A, Gomis M, Rodriguez-Campello A, et al. Factors associated with a high risk of recurrence in patients with transient ischemic attack or minor stroke. Stroke. Jun 2008;39(6):1717-21. [Medline]. [Full Text].
Phan TG, Wijdicks EF. Intra-arterial thrombolysis for vertebrobasilar circulation ischemia. Crit Care Clin. Oct 1999;15(4):719-42, vi. [Medline].
Piechowski-Jozwiak B, Bogousslavsky J. Basilar occlusive disease: the descent of the feared foe?. Arch Neurol. Apr 2004;61(4):471-2. [Medline].
Sauvaget E, Kici S, Petelle B. Vertebrobasilar occlusive disorders presenting as sudden sensorineural hearing loss. Laryngoscope. Feb 2004;114(2):327-32. [Medline].
Terada T, Higashida RT, Halbach VV. Transluminal angioplasty for arteriosclerotic disease of the distal vertebral and basilar arteries. J Neurol Neurosurg Psychiatry. Apr 1996;60(4):377-81. [Medline].
Voetsch B, DeWitt LD, Pessin MS. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. Apr 2004;61(4):496-504. [Medline].
Further Reading
Keywords
vertebrobasilar atherothrombotic disease, VBATD, vertebrobasilar insufficiency, basilar artery occlusion, lateral medullary infarction, Wallenberg syndrome, stroke, transient ischemic attacks, TIA, vertebrobasilar atherothrombotic disease, vertebrobasilar insufficiency, VBI, labyrinthitis, vestibular neuronitis, benign paroxysmal positional vertigo, brainstem infarction, atherosclerosis, syncope, medial medullary infarct, basilar artery syndrome, subclavian steal syndrome, Horner syndrome, hypertension, diabetes mellitus, smoking, fibromuscular dysplasia, rotational occlusion, Bow hunter's stroke, vertebral artery dissection, vertebrobasilar aneurysm
