eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Vertebrobasilar Stroke

Author: Vladimir Kaye, MD, Consulting Staff, Departments of Neurology and Psychiatry, Hoag Hospital
Coauthor(s): Murray E Brandstater, MBBS, PhD, Chairman and Program Director, Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine
Contributor Information and Disclosures

Updated: Jul 15, 2009

Introduction

Background

The vertebrobasilar arterial system perfuses the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex. Occlusion of large vessels in this system usually leads to major disability or death; indeed, most patients who suffer a vertebrobasilar stroke have a significant degree of disability, due to involvement of the brainstem and cerebellum, with resultant multisystem dysfunction (eg, quadriplegia or hemiplegia, ataxia, dysphagia, dysarthria, gaze abnormalities, cranial neuropathies).

However, many vertebrobasilar lesions arise from small vessel disease and are correspondingly small and discrete. The clinical correlates of these smaller lesions consist of a variety of focal neurologic deficits, depending on their location within the brainstem. Patients with small lesions usually have a benign prognosis with reasonable functional recovery.

Lesions in the vertebrobasilar system have some characteristic clinical features that distinguish them from lesions in the hemispheres, including the following1 :

  • When cranial nerves or their nuclei are involved, the corresponding clinical signs are ipsilateral to the lesion and the corticospinal signs are crossed, involving the opposite arm and leg.
  • Cerebellar signs (eg, dysmetria, ataxia) are frequent.
  • Involvement of the ascending sensory pathways may affect the spinothalamic pathway or the medial lemniscus (dorsal columns), resulting in a condition referred to as dissociated sensory loss. This condition occurs when there is loss of 1 sensory modality on one side and preservation of other sensory modalities in the opposite limbs.
  • Dysarthria and dysphagia typically are present.
  • Vertigo, nausea, and vomiting, along with nystagmus, represent involvement of the vestibular system.
  • Additionally, unilateral Horner syndrome occurs with brainstem lesions.
  • Occipital lobe lesions result in visual field loss or visuospatial deficits.
  • In contrast to hemispheric lesions, cortical deficits, such as aphasia and cognitive impairments, are absent.

Related eMedicine topics:
 Acute Stroke Management
Basilar Artery Thrombosis
Vertebral Artery Atherothrombosis
Vertebrobasilar Atherothrombotic Disease

Related Medscape topics:
 CME Research Highlights of 2007: Stroke Management Update
Resource Center Stroke/Cerebrovascular Disease

Pathophysiology

The vertebral arteries arise from the subclavian arteries, and as they course cephalad in the neck, they pass through the costotransverse foramina of C6 to C2. They enter the skull through the foramen magnum and merge at the pontomedullary junction to form the basilar artery. Each vertebral artery usually gives off the posterior inferior cerebellar artery (PICA). At the top of the pons, the basilar artery divides into 2 posterior cerebral arteries (PCAs).

Proximal to its bifurcation into the terminal branches (PCAs), the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain, as well as the superior surface of the cerebellum. The cerebellum is supplied by long circumferential arteries, the PICA, and the anterior inferior and superior cerebellar arteries from the basilar artery.

The medulla is perfused by the PICA and by direct, smaller branches from the vertebral arteries. The pons is perfused by small, penetrating branches from the basilar artery and its major branches. Penetrating arteries from the PCAs perfuse the midbrain and thalamus, and the occipital cortex is perfused by the PCAs.

At the base of the brain, the carotid and basilar systems join to form a circle of large, communicating arteries known as the circle of Willis. Because of this arrangement of collateral vessels, even when one of the main arteries is occluded, adequate perfusion of the brain still may be possible.2

The most common vascular condition affecting the vertebrobasilar system is atherosclerosis, in which plaques cause narrowing and occlusion of the large vessels. The pathology of small vessel disease (affecting arteries 50-200 µm in diameter) is different from that of atherosclerosis, because the small vessels become occluded by a process called lipohyalinosis, which frequently occurs in association with hypertension. Occlusions of these small vessels lead to small, round infarctions called lacunes, which may appear as single lesions or may be distributed as multiple lesions scattered widely throughout the subcortex and brainstem. Lipohyalinosis weakens the vessel wall, and in hypertensive individuals, rupture of the artery may occur, resulting in a focal hemorrhage. Almost all intracerebral hemorrhages originate from the rupture of these small, penetrating vessels.

Because of the close anatomical relationship between the vertebral arteries and the cervical spine, chiropractic manipulation or neck rotation may traumatize the vertebral arteries in the neck. The damaged arteries may occlude with thrombus or undergo dissection.

Embolic occlusion of the vertebrobasilar system is not common and usually is artery-to-artery with occlusion of the basilar artery. Donor sites for the emboli typically are the aortic arch, the subclavian artery, and the origin of the vertebral arteries.

Frequency

United States

The frequency, incidence, and prevalence of the vertebrobasilar syndromes vary, depending on the specific area and syndrome involved. Approximately 80-85% of all strokes are ischemic, and 20% of the lesions producing ischemic strokes occur in the vertebrobasilar system. Overall, hemorrhage is the cause of stroke in 15-20% of patients. Although most intracerebral hemorrhages occur in the region of the putamen and thalamus, about 7% of all hemorrhagic lesions involve the cerebellum in the area of the dentate nucleus, and approximately 6% of hemorrhagic lesions involve the pons.

Related eMedicine topic:
Stroke, Ischemic

Mortality/Morbidity

The mortality of patients with basilar artery occlusion is high. In most of the reported series, mortality has been consistently greater than 75-80%.3 Most survivors of basilar artery occlusion have severe, persisting disability.

Race

The prevalence of all types of stroke tends to be higher in African Americans than in whites.

Sex

Stroke occurs slightly more commonly in men than in women.

Age

The incidence of stroke increases with age.

Clinical

History

The onset and duration of symptoms depends, in large part, upon the etiology. Patients with basilar artery thrombosis typically have a waxing and waning course of symptoms, with as many as 50% of patients experiencing transient ischemic attacks for several days to weeks prior to the occlusion. In contrast, embolic events are sudden, without prodrome or warning, with acute and dramatic presentation. Commonly reported symptoms associated with the vertebrobasilar strokes include the following1 :

  • Vertigo
  • Nausea and vomiting
  • Headache
  • Abnormalities in the level of consciousness
  • Abnormal oculomotor signs (eg, nystagmus, lateral gaze abnormalities, diplopia, pupillary changes)
  • Ipsilateral cranial nerve weakness (eg, dysarthria, dysphagia, dysphonia, weakness of facial muscles and tongue)
  • Sensory loss (in the face and scalp)
  • Ataxia
  • Contralateral motor weakness (eg, hemiparesis, quadriparesis)
  • Pain and temperature loss
  • Incontinence
  • Visual-field defects
  • Presence of central pain
  • Abnormal swelling
  • Sweating in the face or extremities

Related eMedicine topic:
Transient Ischemic Attack

Physical

Common clinical findings observed in more than 70% of patients with vertebrobasilar stroke include an abnormal level of consciousness, as well as hemiparesis or quadriparesis, which usually is asymmetric. Pupillary abnormalities and oculomotor signs are common, and bulbar manifestations, such as facial weakness, dysphonia, dysarthria, and dysphagia, occur in more than 40% of patients.

Oculomotor signs usually reflect the involvement of the abducens nucleus; the horizontal gaze center located in the pontine paramedian reticular formation (PPRF), contiguous to the abducens nucleus; and/or the medial longitudinal fasciculus (MLF). Lesions to these structures result in ipsilateral lateral gaze or conjugate gaze palsy. Ocular bobbing is described as a brisk, downward movement of the eyeball with a subsequent return to the primary position. This deficit localizes the lesion to the pons. Other reported signs of pontine ischemia include ataxia and tremor associated with mild hemiparesis. The signs described can occur in different combinations, presenting a diagnostic challenge in lesion localization.

Certain constellations of findings may serve as clues that help to narrow the search, including the following examples:

  • Midbrain syndromes - Clues are a cranial nerve [CN] III lesion and vertical gaze palsy.
  • Pontine syndromes - Clues are a CN VI lesion, horizontal gaze palsy, and VII nerve palsy.
  • Medullary syndromes - Clues are ipsilateral facial pain and temperature loss, Horner syndrome, ipsilateral ataxia, contralateral loss of pain and temperature sensation, and ipsilateral paralysis of the tongue, soft palate, vocal cord, or sternocleidomastoid [SCM] muscle
  • Posterior cerebral artery - Clues are contralateral hemianopia with macular sparing.

A variety of specific neurologic syndromes4 have been described based on constellations of findings. Some examples are as follows:

  • Lateral medullary (Wallenberg) syndrome
    • This syndrome is most often due to vertebral artery occlusion or, less commonly, to PICA occlusion.
    • Patients present with nausea, vomiting, and vertigo from involvement of the vestibular system.
    • Ipsilateral clinical features include the following:
      • Ataxia and dysmetria, due to damage to the inferior cerebellar peduncle and cerebellum
      • Horner syndrome (eg, ptosis, miosis, hypohidrosis or anhidrosis, enophthalmos), due to damage to descending sympathetic fibers
      • Facial pain and temperature loss
      • Reduced corneal reflex, from damage to the descending spinal tract and nucleus of CN V
      • Nystagmus
      • Hypoacusis (cochlear nucleus)
      • Dysarthria
      • Dysphagia
      • Paralysis of the pharynx, palate, and vocal cord
      • Loss of taste from the posterior third of the tongue (nuclei or fibers of CN IX and X)
    • Contralateral findings include the loss of pain and temperature sense in the body and extremities, indicating involvement of the anterior spinothalamic tract. Other findings include tachycardia and dyspnea (dorsal nucleus of CN X), and palatal myoclonus, a rhythmic involuntary jerking movement of the soft palate, pharyngeal muscles, and diaphragm. Palatal myoclonus sometimes follows infarction of the dentate nucleus of the cerebellum and inferior oliva.
    • The prognosis of patients with the lateral medullary syndrome usually is quite good for functional outcome; however, patients may die in the acute phase from aspiration pneumonia, and death has been reported from sleep apnea in a number of cases.
  • Medial medullary (Dejerine) syndrome
    • This syndrome is an uncommon lesion resulting from occlusion of a vertebral artery or its branch to the anterior spinal artery; it involves the pyramid, the medial lemniscus, and, sometimes, the hypoglossal nerve.
    • The clinical features include ipsilateral paresis of the tongue with deviation toward the lesion (lower motor neuron lesion of CN XII), contralateral hemiplegia with sparing of the face (corticospinal tract), and loss of ipsilateral vibration and proprioception (medial lemniscus).
  • Cerebellar infarction
    • A stroke involving the cerebellum may result in a lack of coordination, clumsiness, intention tremor, ataxia, dysarthria, scanning speech, and even difficulties with memory and motor planning.
    • Early diagnosis of cerebellar infarctions is important, because swelling may cause brainstem compression or hydrocephalus.
  • Locked-in syndrome
    • This dramatic clinical syndrome occurs when there is an infarction of the upper ventral pons. Locked-in syndrome can result from occlusion of the proximal and middle segments of the basilar artery or from hemorrhage involving that region. It can also be caused by trauma, central pontine myelinolysis, encephalitis, or a tumor.
    • Bilateral ventral pontine lesions involving corticospinal and corticobulbar tracts lead to quadriplegia. The patient is unable to speak, to produce facial movement (damage to the corticobulbar tracts), or to look to either side (horizontal eye movement is impaired due to a lesion of bilateral CN VI nuclei). Because the tegmentum of the pons is spared, the patient's consciousness is preserved, with the patient fully awake, sensate, and aware. The only movements preserved are vertical eye movements and blinking. The patient is paralyzed completely and communicates only by blinking. Some recovery of facial muscle movement and horizontal gaze may occur with time or in an incomplete form of this syndrome.
    • Coma may occur with bilateral involvement of the pontine tegmentum or with lesions of the midbrain reticular formation. Coma generally is associated with oculomotor abnormalities, and motor abnormalities may be present. A comatose patient is unresponsive, and the coma may be prolonged when it is due to basilar artery occlusion. Sleep-wake cycles are absent in patients with coma.
  • Top-of-the-basilar syndrome5
    • This syndrome is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery; the occlusion usually results from an embolism. Varying degrees of involvement of the midbrain, thalamus, and portions of the temporal and occipital lobes may occur and can produce severe disability.
    • Patients present with sudden changes in the level of consciousness, confusion, amnesia, and visual symptoms (eg, hemianopia, cortical blindness, abnormal color vision/color dysnomia). These patients can also demonstrate oculomotor abnormalities, most commonly of the vertical gaze, such as gaze palsy, skew deviation, convergence spasm resulting in pseudoabducens palsy, or convergence-retraction nystagmus.
    • CN III palsy and pupillary abnormalities, including small pupils with decreased light reactivity (diencephalic), large/mid-position and fixed pupils (midbrain), and ectopic or oval pupils, also are frequent.
    • Other abnormalities include varying degrees of weakness, sensory deficits, or posturing.
  • Internuclear ophthalmoplegia (INO)
    • Clinically, INO is a horizontal gaze palsy; it results from a brainstem lesion affecting the MLF between the nuclei of CN VI and III, most commonly in the pons.
    • When a patient with a lesion in the right MLF attempts to look to his/her left (ie, away from the involved side), he/she shows no adduction of the right eye and full abduction of the left eye with the end-point abduction nystagmus.
    • By the same logic, in the case of bilateral INO, there is no adduction to either side with nystagmus of the abducting eye in both directions. Convergence is preserved, because the nuclei of CN III and peripheral innervation of the medial recti muscles are intact.
    • Because horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI (relative to the lesion), disruption of the communication pathway (ie, the MLF) between the nuclei of CN III (in the midbrain) and CN VI (in the pons) results in the inability of the eye ipsilateral to the lesion to adduct and the contralateral eye to exhibit abduction nystagmus when looking away from the involved side.
    • In elderly patients, INO is caused most often by occlusion of the basilar artery or its paramedian branches. In younger adults, it may occur due to multiple sclerosis (MS), commonly with bilateral involvement.
  • One-and-a-half syndrome6
    • This syndrome is caused by a lesion affecting the PPRF and MLF simultaneously, resulting in ipsilateral conjugate gaze palsy and INO.
    • The patient with a lesion in the ipsilateral PPRF or abducens nucleus and MLF connecting to the contralateral CN VI exhibits horizontal gaze palsy when looking toward the side of the lesion (1) and exhibits INO when looking away from the side of the lesion (half). Associated features may include vertical nystagmus, exotropia of the contralateral eye, and skew deviation. Vertical gaze and convergence generally are preserved. A patient with this syndrome is completely unable to move the ipsilateral eye, and he/she is able only to abduct the contralateral eye, with resulting nystagmus.
  • Ventral pontine (Millard-Gubler) syndrome
    • This syndrome occurs after paramedian infarction in the pons and results in ipsilateral lateral rectus palsy (CN VI) with diplopia, complete facial paresis (unilateral CN VII palsy), and contralateral hemiparesis/hemiplegia (corticospinal tract involvement) with sparing of the face.
  • Upper dorsal pontine (Raymond-Cestan) syndrome
    • This syndrome is due to obstruction of flow in the long circumferential branches of the basilar artery. This occlusion results in ipsilateral ataxia and coarse intention tremor (indicating involvement of the superior and middle cerebellar peduncles), weakness of mastication and sensory loss in the face (suggesting sensory and motor trigeminal nuclei and tracts), and contralateral loss of all sensory modalities (due to damage to medial lemniscus and spinothalamic tract) with or without facial weakness and hemiparesis (corticospinal tract).
    • Horizontal gaze palsy also may occur.
  • Lower dorsal pontine (Foville) syndrome
    • This syndrome may result from lesions to the dorsal tegmentum of the lower pons.
    • The patient exhibits ipsilateral paresis of the whole face (nucleus and fibers of CN VII), horizontal gaze palsy on the ipsilateral side (PPRF+/- CN VI nucleus), and contralateral hemiplegia (corticospinal tract) with sparing of the face.
  • Ventral midbrain (Weber) syndrome
    • Weber syndrome occurs with an occlusion of the median and/or paramedian perforating branches of the basilar artery.
    • Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (ie, damage to parasympathetic fibers of CN III) with contralateral hemiplegia. Weakness of the lower face (corticospinal and corticobulbar tracts) may be noted.
  • Dorsal midbrain (Benedikt) syndrome
    • This syndrome is due to a lesion in the midbrain tegmentum resulting from occlusion of paramedian branches of either the basilar artery, the PCA, or both.
    • The patient demonstrates ipsilateral oculomotor palsy, ptosis, and mydriasis (as in Weber syndrome), along with the contralateral involuntary movements, such as those of intention tremor, ataxia, or chorea (due to the involvement of the red nucleus).
  • PCA occlusion
    • The most common finding is occipital lobe infarction leading to contralateral hemianopia with macular sparing.
    • Clinical symptoms associated with occlusion of the PCA vary depending on the location of the occlusion and may include the thalamic syndrome, thalamic perforate syndrome, Weber syndrome, cortical blindness, color blindness, failure to see to-and-fro movements, verbal dyslexia, and hallucinations.

Related eMedicine topics:
Posterior Cerebral Artery Stroke [Neurology]
Posterior Cerebral Artery Stroke [Physical Medicine and Rehabilitation]

Causes

Vertebrobasilar insufficiency or stroke may be caused by a number of mechanisms, including thrombus, embolism, and hemorrhage (secondary to aneurysm or trauma). In general, strokes occur because of ischemic events (80-85% of patients) or hemorrhage (15-20% of patients). Several risk factors are associated with stroke, such as the following:

Related Medscape topic:
CME A Case of Cocaine-induced Basilar Artery Thrombosis

More on Vertebrobasilar Stroke

Overview: Vertebrobasilar Stroke
Differential Diagnoses & Workup: Vertebrobasilar Stroke
Treatment & Medication: Vertebrobasilar Stroke
Follow-up: Vertebrobasilar Stroke
Multimedia: Vertebrobasilar Stroke
References
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References

  1. Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke. Aug 1990;21(8):1135-42. [Medline].

  2. Archer CR, Horenstein S. Basilar artery occlusion: clinical and radiological correlation. Stroke. May-Jun 1977;8(3):383-90. [Medline].

  3. Kamper L, Rybacki K, Mansour M, et al. Time management in acute vertebrobasilar occlusion. Cardiovasc Intervent Radiol. Aug 13 2008;[Medline].

  4. Chaves CJ, Caplan LR, Chung CS, et al. Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. Neurology. Aug 1994;44(8):1385-90. [Medline].

  5. Caplan LR. "Top of the basilar" syndrome. Neurology. Jan 1980;30(1):72-9. [Medline].

  6. Wall M, Wray SH. The one-and-a-half syndrome--a unilateral disorder of the pontine tegmentum: a study of 20 cases and review of the literature. Neurology. Aug 1983;33(8):971-80. [Medline].

  7. Adams RJ, Chimowitz MI, Alpert JS, et al. Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the AHA/ASA. Circulation. Sep 9 2003;108(10):1278-90. [Medline]. [Full Text].

  8. Bahouth MN, LaMonte MP. Acute ischemic stroke: evaluation and management strategies. Top Adv Pract Nurs. 2005;5(4):[Full Text].

  9. Kim D, Liebeskind DS. Neuroimaging advances and the transformation of acute stroke care. Semin Neurol. Dec 2005;25(4):345-61. [Medline].

  10. Ehsan T, Hayat G, Malkoff MD, et al. Hyperdense basilar artery. An early computed tomography sign of thrombosis. J Neuroimaging. Oct 1994;4(4):200-5. [Medline].

  11. Puetz V, Sylaja PN, Coutts SB, et al. Extent of hypoattenuation on CT angiography source images predicts functional outcome in patients with basilar artery occlusion. Stroke. Sep 2008;39(9):2485-90. [Medline].

  12. Sylaja PN, Puetz V, Dzialowski I, et al. Prognostic value of CT angiography in patients with suspected vertebrobasilar ischemia. J Neuroimaging. Jan 2008;18(1):46-9. [Medline].

  13. Bogousslavsky J, Regli F, Maeder P, et al. The etiology of posterior circulation infarcts: a prospective study using magnetic resonance imaging and magnetic resonance angiography. Neurology. Aug 1993;43(8):1528-33. [Medline].

  14. Biller J, Yuh WT, Mitchell GW, et al. Early diagnosis of basilar artery occlusion using magnetic resonance imaging. Stroke. Mar 1988;19(3):297-306. [Medline].

  15. Kidwell CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA. Oct 20 2004;292(15):1823-30. [Medline]. [Full Text].

  16. Aichner FT, Felber SR, Birbamer GG. Magnetic resonance imaging and magnetic resonance angiography of vertebrobasilar dolichoectasia. Cerebrovasc Dis. 1993;3:280-4.

  17. Kitanaka C, Tanaka J, Kuwahara M, et al. Magnetic resonance imaging study of intracranial vertebrobasilar artery dissections. Stroke. Mar 1994;25(3):571-5. [Medline].

  18. Knepper L, Biller J, Adams HP Jr, et al. MR imaging of basilar artery occlusion. J Comput Assist Tomogr. Jan-Feb 1990;14(1):32-5. [Medline].

  19. Kinsella LJ, Feldmann E, Brooks JM. The clinical utility of transcranial Doppler ultrasound in suspected vertebrobasilar ischemia. J Neuroimaging. Apr 1993;3(2):115-22. [Medline].

  20. Rem JA, Hachinski VC, Boughner DR, et al. Value of cardiac monitoring and echocardiography in TIA and stroke patients. Stroke. Nov-Dec 1985;16(6):950-6. [Medline].

  21. Reeves MJ, Arora S, Broderick JP, et al. Acute stroke care in the US: results from 4 pilot prototypes of the Paul Coverdell National Acute Stroke Registry. Stroke. Jun 2005;36(6):1232-40. [Medline]. [Full Text].

  22. Dirnagl U, Pulsinelli W. Autoregulation of cerebral blood flow in experimental focal brain ischemia. J Cereb Blood Flow Metab. May 1990;10(3):327-36. [Medline].

  23. Huemer M, Niederwieser V, Ladurner G. Thrombolytic treatment for acute occlusion of the basilar artery. J Neurol Neurosurg Psychiatry. Feb 1995;58(2):227-8. [Medline]. [Full Text].

  24. Lutsep HL, Rymer MM, Nesbit GM. Vertebrobasilar revascularization rates and outcomes in the MERCI and multi-MERCI trials. J Stroke Cerebrovasc Dis. Mar-Apr 2008;17(2):55-7. [Medline].

  25. Del Zoppo GJ, Saver JL, Jauch EC, et al. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator. A science advisory from the American Heart Association/American Stroke Association. Stroke. May 28 2009;[Medline]. [Full Text].

  26. Rothwell PM. Is intravenous recombinant plasminogen activator effective up to 4.5 h after onset of ischemic stroke?. Nat Clin Pract Cardiovasc Med. Mar 2009;6(3):164-5. [Medline].

  27. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. Sep 25 2008;359(13):1317-29. [Medline]. [Full Text].

  28. Wahlgren N, Ahmed N, Davalos A, et al. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. Oct 11 2008;372(9646):1303-9. [Medline].

  29. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. May 2007;38(5):1655-711. [Medline]. [Full Text].

  30. Nenci GG, Gresele P, Taramelli M, et al. Thrombolytic therapy for thromboembolism of vertebrobasilar artery. Angiology. Sep 1983;34(9):561-71. [Medline].

  31. Albers GW, Diener HC, Frison L, et al. Ximelagatran vs warfarin for stroke prevention in patients with nonvalvular atrial fibrillation: a randomized trial. JAMA. Feb 9 2005;293(6):690-8. [Medline]. [Full Text].

  32. Ois A, Gomis M, Rodríguez-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].

  33. Bader MK, Littlejohns LR, eds. AANN Core Curriculum for Neuroscience Nursing. 4th ed. Philadelphia, Pa: WB Saunders; 2004.

  34. Amarenco P, Duyckaerts C, Tzourio C, et al. The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med. Jan 23 1992;326(4):221-5. [Medline].

  35. Appel LJ, Brands MW, Daniels SR, et al. Dietary approaches to prevent and treat hypertension: a scientific statement from the American Heart Association. Hypertension. Feb 2006;47(2):296-308.

  36. Astrup J, Siesjo BK, Symon L. Thresholds in cerebral ischemia - the ischemic penumbra. Stroke. Nov-Dec 1981;12(6):723-5. [Medline].

  37. Bockenheimer S, Reinhuber F, Mohs C. [Intra-arterial thrombolysis of vessels supplying the brain]. Radiologe. Apr 1991;31(4):210-5. [Medline].

  38. Boysen G, Engell HC, Pistolese GR, et al. Editorial: On the critical lower level of cerebral blood flow in man with particular reference to carotid surgery. Circulation. Jun 1974;49(6):1023-5. [Medline].

  39. Brandstater ME. Stroke rehabilitation. In: Delisa JA, Gans BM, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia, Pa: Lippincott-Raven; 1998:1165-89.

  40. Bruckmann H, Ferbert A, del Zoppo GJ, et al. Acute vertebral-basilar thrombosis. Angiologic-clinical comparison and therapeutic implications. Acta Radiol Suppl. 1986;369:38-42. [Medline].

  41. Castaigne P, Lhermitte F, Gautier JC, et al. Arterial occlusions in the vertebro-basilar system. A study of 44 patients with post-mortem data. Brain. 1973;96(1):133-54. [Medline].

  42. Center-Smith M. Surface electromyography (SEMG) biofeedback treatment for dysphagia. In: Focus on Physiatry. vol 5. Kessler Medical Rehabilitation Research and Education Corp.

  43. Chimowitz MI, Lynn MJ, Howlett-Smith H, et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. Mar 31 2005;352(13):1305-16. [Medline]. [Full Text].

  44. Coert BA, Chang SD, Marks MP, et al. Revascularization of the posterior circulation. Skull Base. Feb 2005;15(1):43-62.

  45. Coull BM, Goodnight SH. Antiphospholipid antibodies, prethrombotic states, and stroke. Stroke. Sep 1990;21(9):1370-4. [Medline].

  46. Cravioto H, Rey-Bellet PH, Prose I. Occlusion of the basilar artery; a clinical and pathologic study of 14 autopsied cases. Neurology. Feb 1958;8(2):145-52. [Medline].

  47. Daffertshofer M, Mielke O, Pullwitt A, et al. Transient ischemic attacks are more than "ministrokes". Stroke. Nov 2004;35(11):2453-8.

  48. Denny-Brown D. Basilar artery-syndromes. Bull New Engl Med Cent. Jun 1953;15(2):53-60. [Medline].

  49. Denny-Brown D. The treatment of recurrent cerebrovascular symptoms and the question of "vasospasm". Med Clin North Am. Sep 1951;35(5):1457-74. [Medline].

  50. Ellrodt A. Assessing the risks of cervical manipulation for neck pain. CMAJ. Apr 30 2002;166(9):1134-5. [Medline]. [Full Text].

  51. Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial. The EC/IC Bypass Study Group. N Engl J Med. Nov 7 1985;313(19):1191-200. [Medline].

  52. Feldmann E, Daneault N, Kwan E, et al. Chinese-white differences in the distribution of occlusive cerebrovascular disease. Neurology. Oct 1990;40(10):1541-5. [Medline].

  53. Fieschi C, Agnoli A, Battistini N, et al. Derangement of regional cerebral blood flow and of its regulatory mechanisms in acute cerebrovascular lesions. Neurology. Dec 1968;18(12):1166-79. [Medline].

  54. Fisher CM. Atherosclerosis of the carotid and vertebral arteries – extracranial and intracranial. J Neuropathol Exp Neurol. 1965;24:455-76.

  55. Fisher CM. Ocular bobbing. Arch Neurol. Nov 1964;11:543-6. [Medline].

  56. Fisher CM. Some neuro-ophthalmological observations. J Neurol Neurosurg Psychiatry. Oct 1967;30(5):383-92. [Medline]. [Full Text].

  57. Garcia JH. Stroke Pathophysiology, Diagnosis, and Management. NY:. Churchill Livingstone;1992:125.

  58. Gomez CR, Cruz-Flores S, Malkoff MD, et al. Isolated vertigo as a manifestation of vertebrobasilar ischemia. Neurology. Jul 1996;47(1):94-7. [Medline].

  59. Gorelick PB, Caplan LR, Hier DB, et al. Racial differences in the distribution of posterior circulation occlusive disease. Stroke. Sep-Oct 1985;16(5):785-90. [Medline].

  60. Gustafsson D, Elg M. The pharmacodynamics and pharmacokinetics of the oral direct thrombin inhibitor ximelagatran and its active metabolite melagatran: a mini-review. Thromb Res. Jul 15 2003;109 Suppl 1:S9-15. [Medline].

  61. Hacke W, Albers G, Al-Rawi Y, et al. The Desmoteplase in Acute Ischemic Stroke Trial (DIAS): a phase II MRI-based 9-hour window acute stroke thrombolysis trial with intravenous desmoteplase. Stroke. Jan 2005;36(1):66-73. [Medline]. [Full Text].

  62. Hacke W, Kaste M, Fieschi C, et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS). JAMA. Oct 4 1995;274(13):1017-25. [Medline].

  63. Hacke W, Zeumer H, Ferbert A, et al. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke. Oct 1988;19(10):1216-22. [Medline].

  64. Haley EC Jr, Kassell NF, Torner JC. Failure of heparin to prevent progression in progressing ischemic infarction. Stroke. Jan 1988;19(1):10-4. [Medline].

  65. Hayem MG. Sur la thrombose par arterite tronc basilaire. Comme cause du mort rapide. Arch Physiol Norm Pathol. 1868;1:270-89.

  66. Heiss WD, Rosner G. Functional recovery of cortical neurons as related to degree and duration of ischemia. Ann Neurol. Sep 1983;14(3):294-301. [Medline].

  67. Herdman SJ. Physical therapy management of vestibular disorders in older patients. Phys Ther Pract. 1992;1(1):77-87.

  68. Higashida RT, Tsai FY, Halbach VV, et al. Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries. J Neurosurg. Feb 1993;78(2):192-8. [Medline].

  69. Horn LB. Differentiating between vestibular and nonvestibular balance disorders. Neurol Rep. 1997;21:23-8.

  70. Horner J, Buoyer FG, Alberts MJ, et al. Dysphagia following brain-stem stroke. Clinical correlates and outcome. Arch Neurol. Nov 1991;48(11):1170-3. [Medline].

  71. Hurd K, Chopp M, Vande Linde AM, et al. Effects of moderate hyperglycemia on the temporal profile of brain tissue intracellular pH and [Mg2+] after global cerebral ischemia in rats. J Neurol Sci. Apr 1995;129(2):90-6. [Medline].

  72. Johansson B, Strandgaard S, Lassen NA. On the pathogenesis of hypertensive encephalopathy. Circ Res. 1974;34-5 (Suppl 1):I167-71.

  73. Kahrilas PJ. Pharyngeal structure and function. Dysphagia. Fall 1993;8(4):303-7. [Medline].

  74. Kay R, Wong KS, Yu YL. Low-molecular-weight heparin for the treatment of acute ischemic stroke. N Engl J Med. Dec 14 1995;333(24):1588-93. [Medline]. [Full Text].

  75. Kubik S, Adams RA. Occlusion of the basilar artery. A clinical and pathological study. Brain. 1946;69:6-121.

  76. Labauge R, Pages M, Marty-Double C, et al. [Occlusion of the basilar artery. A review with 17 personal cases (author's transl)]. Rev Neurol (Paris). 1981;137(10):545-71. [Medline].

  77. Lauretti WJ. Clarifying chiropractic manipulation risks. CMAJ. Apr 2 2002;166(7):886. [Medline]. [Full Text].

  78. Leopold J. Vestibular rehabilitation. In: Focus on Physiatry. vol 5. Kessler Medical Rehabilitation Research and Education Corp.

  79. Lhermitte J, Trelles JO. L'arteriosclerose du tronc basilaire et ses consequences anatomo-cliniques. Jahrbucher f Psychiatrie Neurologie. 1934;51:91-107.

  80. McDowell FH, Potes J, Groch S. The natural history of internal carotid and vertebral-basilar artery occlusion. Neurology. Apr 1961;11(4)Pt2:153-7. [Medline].

  81. Mehler MF. The neuro-ophthalmologic spectrum of the rostral basilar artery syndrome. Arch Neurol. Sep 1988;45(9):966-71. [Medline].

  82. Mehler MF. The rostral basilar artery syndrome: diagnosis, etiology, prognosis. Neurology. Jan 1989;39(1):9-16. [Medline].

  83. Meyer JS. Circulatory changes following occlusion of the middle cerebral artery and their relation to function. J Neurosurg. Nov 1958;15(6):653-73. [Medline].

  84. Millikan CH, Siekert RG. Studies in cerebrovascular disease. I. The syndrome of intermittent insufficiency of the basilar arterial system. Mayo Clin Proc. Feb 23 1955;30(4):61-8. [Medline].

  85. Moufarrij NA, Little JR, Furlan AJ, et al. Basilar and distal vertebral artery stenosis: long-term follow-up. Stroke. Sep-Oct 1986;17(5):938-42. [Medline].

  86. Myers MG, Norris JW, Hachinski VC, et al. Cardiac sequelae of acute stroke. Stroke. Nov-Dec 1982;13(6):838-42. [Medline].

  87. Nachman RL, Silverstein R. Hypercoagulable states. Ann Intern Med. Oct 15 1993;119(8):819-27. [Medline].

  88. Nadeau S, Jordan J, Mishra S. Clinical presentation as a guide to early prognosis in vertebrobasilar stroke. Stroke. Feb 1992;23(2):165-70. [Medline].

  89. Nedergaard M. Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarction. Brain Res. Apr 7 1987;408(1-2):79-85. [Medline].

  90. Nelson JR, Johnston CH. Ocular bobbing. Arch Neurol. Apr 1970;22(4):348-56. [Medline].

  91. Norris JW, Hachinski VC, Myers MG, et al. Serum cardiac enzymes in stroke. Stroke. Sep-Oct 1979;10(5):548-53. [Medline].

  92. Pessin MS, Gorelick PB, Kwan ES, et al. Basilar artery stenosis: middle and distal segments. Neurology. Nov 1987;37(11):1742-6. [Medline].

  93. Pulsinelli WA, Waldman S, Rawlinson D, et al. Moderate hyperglycemia augments ischemic brain damage: a neuropathologic study in the rat. Neurology. Nov 1982;32(11):1239-46. [Medline].

  94. Restrepo L, Quiroga-Chand A, Tomatore C, et al. "Rubral" tremor after cardiac catheterization: report of 2 cases. Tex Heart Inst J. 2005;32(3):427-9. [Medline]. [Full Text].

  95. Ringelstein EB, Zeumer H, Poeck K. Non-invasive diagnosis of intracranial lesions in the vertebrobasilar. Stroke. 1945;16:848-54.

  96. Rolak L. Neurology Secrets. Philadelphia, Pa: Hanley & Belfus; 1993.

  97. Rother J, Wentz KU, Rautenberg W, et al. Magnetic resonance angiography in vertebrobasilar ischemia. Stroke. Sep 1993;24(9):1310-5. [Medline].

  98. Sacco RL, Sivenius J, Diener HC. Efficacy of aspirin plus extended-release dipyridamole in preventing recurrent stroke in high-risk populations. Arch Neurol. Mar 2005;62(3):403-8. [Medline]. [Full Text].

  99. Sandercock PA, van den Belt AG, Lindley RI, et al. Antithrombotic therapy in acute ischaemic stroke: an overview of the completed randomised trials. J Neurol Neurosurg Psychiatry. Jan 1993;56(1):17-25. [Medline]. [Full Text].

  100. Schwamm LH, Pancioli A, Acker JE 3rd, et al. Recommendations for the establishment of stroke systems of care: recommendations from the American Stroke Association's Task Force on the Development of Stroke Systems. Stroke. Mar 2005;36(3):690-703. [Medline]. [Full Text].

  101. Schwartz A, Rautenberg W, Hennerici M. Dolichoectatic intracranial arteries: review of selected aspects. Cerebrovasc Dis. 1993;3:273.

  102. Secondary prevention of vascular disease by prolonged antiplatelet treatment. Antiplatelet Trialists' Collaboration. Br Med J (Clin Res Ed). Jan 30 1988;296(6618):320-31. [Medline]. [Full Text].

  103. Seger JJ. Syncope evaluation and management. Tex Heart Inst J. 2005;32(2):204-6. [Medline]. [Full Text].

  104. Sharpe JA, Rosenberg MA, Hoyt WF, et al. Paralytic pontine exotropia. A sign of acute unilateral pontine gaze palsy and internuclear ophthalmoplegia. Neurology. Nov 1974;24(11):1076-81. [Medline].

  105. Siekert RG, Millikan CH. Studies in cerebrovascular disease. II. Some clinical aspects of thrombosis of the basilar artery. Mayo Clin Proc. Mar 9 1955;30(5):93-100. [Medline].

  106. Smith E, Delargy M. Locked-in syndrome. BMJ. Feb 19 2005;330(7488):406-9. [Medline]. [Full Text].

  107. Strandgaard S, MacKenzie ET, Sengupta D, et al. Upper limit of autoregulation of cerebral blood flow in the baboon. Circ Res. Apr 1974;34(4):435-40. [Medline].

  108. Streptokinase in acute myocardial infarction. European Cooperative Study Group for Streptokinase Treatment in Acute Myocardial Infarction. N Engl J Med. Oct 11 1979;301(15):797-802. [Medline].

  109. Symon L, Pasztor E, Branston NM. The distribution and density of reduced cerebral blood flow following acute middle cerebral artery occlusion: an experimental study by the technique of hydrogen clearance in baboons. Stroke. May-Jun 1974;5(3):355-64. [Medline].

  110. Tettenborn B, Estol C, De Witt LD. Accuracy of transcranial Doppler in the vertebrobasilar circulation. J Neurol. 1990;237:159.

  111. Thompson JR, Simmons CR, Hasso AN, et al. Occlusion of the intradural vertebrobasilar artery. Neuroradiology. Feb 17 1978;14(5):219-29. [Medline].

  112. Thömke F, Hopf HC. Abduction paresis with rostral pontine and/or mesencephalic lesions: pseudoabducens palsy and its relation to the so-called posterior internuclear ophthalmoplegia of Lutz. BMC Neurol. Dec 18 2001;1:4.

  113. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med. Dec 14 1995;333(24):1581-7. [Medline]. [Full Text].

  114. Tran H, Anand SS. Oral antiplatelet therapy in cerebrovascular disease, coronary artery disease, and peripheral arterial disease. JAMA. Oct 20 2004;292(15):1867-74. [Medline]. [Full Text].

  115. Verstraete M. The search for the ideal thrombolytic agent. J Am Coll Cardiol. Nov 1987;10(5 Suppl B):4B-10B. [Medline].

  116. Vingerhoets F, Bogousslavsky J. Respiratory dysfunction in stroke. Clin Chest Med. Dec 1994;15(4):729-37. [Medline].

  117. Von Kummer R, Brandt T, Muller-Kuypers M. Thrombolytic therapy of basilar artery occlusion: preconditions for recanalization and good clinical outcome. In: Yamaguchi T, Mori E, Minematsu K, et al, eds. Thrombolytic Therapy in Acute Ischemic Stroke III. Tokyo, Japan: Springer-Verlag; 1995:343-8.

  118. Vonofakos D, Marcu H, Hacker H. CT diagnosis of basilar artery occlusion. AJNR Am J Neuroradiol. May-Jun 1983;4(3):525-8. [Medline].

  119. Waltz AG. Effect of blood pressure on blood flow in ischemic and in nonischemic cerebral cortex. The phenomena of autoregulation and luxury perfusion. Neurology. Jul 1968;18(7):613-21. [Medline].

  120. Warach S, Davis L, ROSIE Study Group. Open-label, dose escalation, safety and proof of principle study of the combination of IV abciximab and reteplase in the treatment of acute ischemic stroke with proven perfusion defects. American Stroke Association 28th International Stroke Conference.

  121. Wardlaw JM, Warlow CP. Thrombolysis in acute ischemic stroke: does it work?. Stroke. Dec 1992;23(12):1826-39. [Medline].

  122. Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study Group. Prognosis of patients with symptomatic vertebral or basilar artery stenosis. Stroke. 1998;29:1389-92. [Full Text].

  123. Weinberger J. Noninvasive imaging of the cervical vertebral artery in the diagnosis of vertebrobasilar insufficiency. J Stroke Cerebrovasc Dis. 1991;1:21-5.

  124. 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].

  125. Wildemann B, Hutschenreuter M, Krieger D, et al. Infusion of recombinant tissue plasminogen activator for treatment of basilar artery occlusion. Stroke. Oct 1990;21(10):1513-4. [Medline].

  126. Williams AN. Cerebrovascular disease in Dumas' The Count of Monte Cristo. J R Soc Med. Aug 2003;96(8):412-4. [Medline]. [Full Text].

  127. Winn HR. Carotid endarterectomy. In: Winn HR, ed. Youman's Neurological Surgery. vol 2. 5th ed. Philadelphia, Pa: WB Saunders; 2004:1623-6.

  128. Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96(4):380-5. [Medline].

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Further Reading

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Keywords

vertebrobasilar stroke, vertebrobasilar, stroke, vertebrobasilar cerebrovascular accident, vertebrobasilar CVA, ischemic stroke, ischemic attack transient, transient ischemic attack, ischaemic stroke, intracerebral hemorrhages, neurologic deficits, vertebral artery, vertebral arteries, basilar artery, basilar arteries, cerebral artery, cerebral arteries, dysmetria, ataxia, dysarthria, dysphagia, vertigo, nausea, vomiting, nystagmus, unilateral Horner syndrome, brainstem lesions, brain stem lesions, occipital lobe lesions, visual field loss, visuospatialdeficits, hemisphericlesions, cortical deficits, aphasia, cognitive impairments

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Contributor Information and Disclosures

Author

Vladimir Kaye, MD, Consulting Staff, Departments of Neurology and Psychiatry, Hoag Hospital
Vladimir Kaye, MD is a member of the following medical societies: American Academy of Anti-Aging Medicine, American Academy of Physical Medicine and Rehabilitation, and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Murray E Brandstater, MBBS, PhD, Chairman and Program Director, Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine
Murray E Brandstater, MBBS, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Congress of Rehabilitation Medicine, American Medical Association, Association for Academic Psychiatry, California Society of Physical Medicine and Rehabilitation, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, Canadian Society of Clinical Neurophysiologists, Catholic Medical Association, National Stroke Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, and Royal College of Physicians and Surgeons of the United States
Disclosure: Nothing to disclose.

Medical Editor

Milton J Klein, DO, MBA, Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital, Allegheny General Hospital, and Ohio Valley General Hospital.
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

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