Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Basilar Artery Thrombosis Treatment & Management

  • Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Oct 30, 2015
 

Approach Considerations

All patients should be admitted to a stroke unit. Patients with unstable or fluctuating neurologic symptoms, decreased level of consciousness, active cardiac or respiratory comorbid conditions, hemodynamic instability, or a need for interventional therapies (eg, thrombolysis) must be admitted to a neurologic intensive care unit (ICU).

Recanalization of the basilar artery is key to the successful treatment of basilar artery thrombosis and to improving its prognosis. Some unresolved issues need further clarification, such as the best method of recanalization (intra-arterial thrombolysis, mechanical thrombolysis, or a combination), the time window for the treatment, and patient selection.

In a study of103 patients with basilar artery occlusion recanalized after IV tissue-type plasminogen activator thrombolysis, thrombus length was independently associated with recanalization. Patients who underwent recanalization had shorter thrombi (median, 5.5 mm; mean, 9.7 mm) when compared with those not recanalized (median, 15.0 mm; mean, 16.6 mm; P < 0.001). Thrombi shorter than 10 mm had 70-80% probability of recanalization; 10-20 mm, 50-70% probability; 20-30 mm, 30-50% probability; and greater than 30 mm, 20-30% probability.[14]

In a meta-analysis, recanalization of acute basilar artery occlusion led to reduction in mortality by 2-fold and reduction in the risk of DoD by 1.5-fold. With recanalization, risk ratios (RR) for death or dependency (DoD) in those treated within 12 hours was 0.63; and for those treated after 12 hours, 0.67. RR for DoD in the intravenous thrombolysis subgroup was 0.68, and it was 0.67 in the intra-arterial/endovascular therapy subgroup. Recanalization resulted in mortality RR of 0.46 in those treated within 12 hours and 0.50 for those treated after 12 hours.[15]

In the absence of clear evidence, treating patients with basilar artery thrombosis in the context of a clinical trial seems most reasonable. If this option is not available (and given the limited time window), IV thrombolysis within 3 hours seems to be a reasonable alternative. In institutions in which the service is available, intra-arterial pharmacologic or mechanical thrombolysis can be considered.

General care

Care is required for all indwelling catheters, including monitoring for infection. Control body temperature because evidence suggests that fever worsens the outcome in patients with stroke. Glucose levels should be monitored to avoid hypoglycemia and hyperglycemia. Aggressive pulmonary toilet is instituted to avoid pneumonia.

Stroke-related therapy

Treatment of patients with basilar artery thrombosis includes the following:

  • Hemodynamic management
  • Respiratory management
  • Thrombolysis
  • Intra-arterial thrombolysis
  • Combination therapy - The combination of IV thrombolysis with consecutive, on-demand, mechanical endovascular thrombectomy may allow for early treatment initiation with high recanalization; in one small study, recanalization was achieved in 15 of 16 patients who received the combination therapy [16]

Sedation and paralysis

Sedation and paralysis should be avoided because they interfere with neurologic assessment of the patient. However, sedation alone can and should be used to maintain comfort. Under certain circumstances, such as the occurrence of neurogenic hyperventilation, the use of sedation and paralysis may be required to avoid hypocarbia, which can worsen the ischemic process.

Consultations

Physical and occupational therapy should be started soon after admission, depending on the condition of the patient. Once the symptoms have stabilized, the patient should be mobilized out of bed and allowed full physical and occupational therapy activities.

Speech therapy should address the concerns of aspiration in patients with profound dysarthria and depressed cough reflex.

Diet

The patient should be restricted to taking nothing by mouth until his or her swallowing mechanism has been assessed and cleared and the airway has been protected. If the patient has a high risk of aspiration, a nasogastric or nasoduodenal tube should be placed.

If the swallowing abnormalities are so severe that recovery is expected to take weeks or months, a gastrostomy tube should be placed either surgically or percutaneously.

Activity

Some patients have fluctuating symptoms and signs, and these are often position related. Because of this, bed rest is advised until the symptoms have stabilized. In some patients, the severity of the deficits is such that free ambulation is not possible; however, patients should be mobilized out of bed and be actively involved with physical and occupational therapy.

Next

Hemodynamic Management

The goal of hemodynamic management is to minimize ischemic injury. Cerebral ischemia results in impaired autoregulation. Therefore, under ischemic conditions, cerebral blood flow becomes dependent on blood pressure. In patients with severe cerebral vascular occlusive disease, mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) become critical in maintaining cerebral blood flow (CPP = MAP - intracranial pressure).

Hypertension

If the patient has a fluctuating neurologic condition and his or her blood pressure requires close monitoring, an arterial catheter should be placed.

No evidence from randomized trials indicates that treating hypertension is better than not treating it. However, currently available guidelines for the management of acute stroke recommend the use of antihypertensives to lower blood pressure to a systolic value of less than 185 mm Hg or a diastolic value of less than 110 mm Hg if thrombolysis is being considered. (Some evidence, however, suggests that in selected cases, induced hypertension may be beneficial for limiting ischemic injury.)

Hypertension should also be treated if the patient has evidence of acute end organ damage, such as hypertensive encephalopathy, unstable angina or acute myocardial infarction, heart failure, or acute renal failure. Otherwise, treatment is indicated only when the diastolic blood pressure is greater than 120 mm Hg or the systolic blood pressure is greater than 220 mm Hg.

The preferred antihypertensive agents are nicardipine and labetalol. When diastolic blood pressure is greater than 140 mm Hg and not responsive to nicardipine and labetalol, then nitroprusside should be used.

Overzealous treatment of hypertension should be avoided because it can exacerbate the ongoing ischemia.

Hypotension

Patients with hypotension should be treated to normalize the MAP and therefore to improve blood pressure–dependent cerebral blood flow. Every effort should be made to maintain a normal intravascular volume by administering isotonic solutions.

If the MAP continues to be low despite fluid management, vasopressors such as dopamine, dobutamine, or phenylephrine should be used.

Dopamine can cause significant tachycardia; therefore, phenylephrine (Neo-Synephrine) and norepinephrine (Levophed) are the vasopressors of choice after dopamine. Dobutamine should be used with caution and with close monitoring of the cardiac index, because it can often cause vasodilatation and hypotension. Dobutamine is the pressor of choice in patients with congestive heart failure.

Unknown intravascular volume status

In patients whose intravascular volume status is unknown or who have comorbid conditions such as congestive heart failure or pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary wedge pressure. This allows better management and optimization of the intravascular volume to avoid volume overload.

Previous
Next

Respiratory Management

Early assessment and management of the airway is vital, given the frequent involvement of lower cranial nerves and impairment of consciousness in patients with brainstem ischemia. Other important aspects include assessment of the respiratory drive, the gag reflex, and the ability to handle secretions by a forceful cough.

Ventilation

Generally, endotracheal intubation should be considered in patients with a decreased level of consciousness and Glasgow Coma Scale score of less than 8.

Endotracheal intubation is recommended in most patients to keep their airway clear while maintaining normal ventilation. Of the mechanical ventilation modes, pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation are used most often.

For patients with good respiratory drive, the most comfortable mode is PSV. In this mode, the ventilator does not deliver a set of breaths but provides enough pressure support to maintain the desired tidal volume. The usual goal is to maintain a tidal volume of 5 mL/kg. Most patients with no comorbid pulmonary condition reach this goal with a PSV of 5-10.

Synchronized, intermittent, mandatory ventilation may be a better mode for patients with poor respiratory drive. This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with the patient's inspiratory effort but allows the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort during the extra breaths.

Previous
Next

Thrombolysis

Tissue plasminogen activator (tPA) is the only pharmaceutical agent approved by the US Food and Drug Administration (FDA) for the treatment of acute ischemic stroke within the first 3 hours of onset. Its approval was based on data from the trial by the National Institute for Neurological Disorders and Stroke. However, the trial did not include patients in stupor or coma and, thus, probably excluded patients who experienced basilar artery occlusion. Moreover, the trial did not systematically study vascular anatomy in all patients.

Previous
Next

Intra-Arterial Thrombolysis

This has emerged as a therapeutic strategy despite the absence of randomized, controlled clinical trials examining its use in vertebrobasilar occlusion.

Several case series have been published on intra-arterial thrombolysis, with the average time to treatment ranging from 8-48 hours. Overall mortality rates have decreased from 46-75% to 26-60%.

The rate of hemorrhagic transformation is approximately 8%, which is a little higher than that for IV thrombolysis in anterior circulation, confirmed by a study in animal models. Indeed, a systematic analysis demonstrated that the morbidity and mortality of patients treated with intra-arterial thrombolysis are not all that different from those associated with IV thrombolysis, although recanalization was achieved more frequently with intra-arterial thrombolysis.[17]

The patient's condition at presentation appears to be the major prognostic factor for intra-arterial thrombolysis; patients with quadriplegia and/or coma have worse outcomes than do other patients.

Ideally, patients with basilar artery occlusion should be treated within the context of a randomized trial. In the absence of this option, many stroke experts would advocate the use of intra-arterial thrombolysis. This decision, however, should be made with knowledge of the background information described below and with recognition of the absence of evidence from randomized trials.

Thrombolytic agents

Thrombolytic agents include urokinase, pro-urokinase, streptokinase, and tPA. Urokinase is not on the market in the United States because of concerns regarding its production. Streptokinase has been discontinued by the manufacturer.

Pro-urokinase was tested in a prospective, randomized fashion. The trial involved only patients with occlusion of the middle cerebral artery stem. Results showed a better outcome in treated patients. However, pro-urokinase was not approved for use in acute stroke; therefore, the only option in the United States is tPA. This drug has been studied prospectively in trials involving combined IV and intra-arterial thrombolysis; the dosage used is 0.3 mg/kg, up to a maximum of 10-20 mg intra-arterially.

Because the rate of reocclusion is approximately 30%, some investigators have reported limited experience with the use of glycoprotein IIb/IIIa inhibitors, such as abciximab, to block platelet function and rethrombosis.

Guidelines

Some general guidelines should be followed when treating a patient with IV or intra-arterial thrombolysis.

Patients with a stuttering course of longer than 3 hours and up to 12 hours should be considered for intra-arterial thrombolysis, provided that ischemic changes are not present on the CT scan. However, the care team should recognize that under these circumstances, the therapy is being offered in a compassionate fashion, given the poor prognosis of basilar artery occlusion.

Despite reports of the successful use of anticoagulation immediately following thrombolysis, avoiding systemic anticoagulation is recommended for the first 24 hours after thrombolysis, given the risk of hemorrhagic complications.

Although treatment as late as 24-48 hours after symptom onset has been reported, the authors recommend caution because of the high risk of hemorrhagic complications. Systemic anticoagulation may be an alternative for patients with contraindications for thrombolysis, although no evidence clearly indicates any beneficial effect.

With rare exceptions, patients should not be treated with thrombolysis if more than 12 hours have elapsed since the onset of more major symptoms or if they have marked ischemic changes on the CT scan, regardless of the time course.

The benefits of intra-arterial thrombolysis in selected groups of patients with basilar artery thrombosis, such as patients with minor deficit or old patients with extensive brainstem infarcts, is even less clear than for other individuals with this type of occlusion

Previous
Next

Additional Pharmacologic and Mechanical Therapies

Anticoagulant and antiplatelet agents

Anticoagulation with heparin or low–molecular-weight heparinoids has been used, but no evidence shows that this has an impact on outcome. The role of antiplatelets, such as clopidogrel and the combination of aspirin and dipyridamole, in the treatment of acute basilar artery occlusion is not known.

Angioplasty

Angioplasty with or without stent placement has been performed to treat patients with atherosclerotic stenosis or to mechanically dislodge thrombi. The advantage of angioplasty is excellent and quick anatomic recanalization, but the success rate is still low.

Angioplasty has been performed in patients with acute vertebrobasilar occlusion and in patients selected electively. The morbidity rates cited in the published case series range from 0-50%; the mortality rate is as high as 33%. The role of angioplasty in the therapy for this disorder is not known.

Embolectomy

Only one case report has described successful endovascular embolectomy in basilar artery thrombosis.[18] In the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) and Multi MERCI trials, mechanical embolectomy in 27 patients resulted in a 78% recanalization rate, a mortality rate of 44%, and a good clinical outcome in 41% of patients. Patients who underwent recanalization had better outcomes than did those without recanalization.[19]

Thrombus retrieval

Thrombus retrieval has been added to the armamentarium by way of the Merci Retriever device. The FDA approved its use for blood vessel recanalization, although its impact in improving neurologic outcome is not known.

Previous
Next

Rehabilitation

Patients with brainstem, cerebellar, diencephalic, or occipital infarcts secondary to basilar artery occlusion have a significant degree of disability because of weakness, ataxia, swallowing difficulties, or other cranial neuropathies or due to a combination of these.

Patients with dysphagia are at significant risk for aspiration and pneumonia. Evaluation of these patients should be thorough and should include videofluoroscopy with modified barium swallow to assess for silent aspiration. Interventions for prevention of aspiration include compensatory strategies such as oromotor exercises, postural changes while swallowing, and facilitative strategies (including modification of bolus consistency, volume, and delivery).

Patients also need training on balance and gait. Using a patch on 1 eye or prisms can help diplopia.

Previous
Next

Stroke Prevention

Prevention strategies for basilar artery thrombosis, in addition to risk factor control, depend pharmacologically on the cause of the occlusion. For example, patients with a definite cardioembolic source, such as atrial fibrillation, should be treated with warfarin to maintain an INR of between 2 and 3.

For patients with atherosclerotic stenosis who survive basilar artery occlusion, the estimated annual risk of recurrent stroke is 20%. Antiplatelet agents such as aspirin, clopidogrel, and the combination aspirin/dipyridamole (Aggrenox) can be used for stroke prophylaxis. No trials have been reported that directly compare clopidogrel with aspirin/dipyridamole. Secondary prevention trials showed that these agents are marginally better than aspirin alone; therefore, they may be the drugs of choice.

Long-term anticoagulation with warfarin was advocated as the treatment of choice, but the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study Group demonstrated that warfarin is no better than aspirin in preventing strokes in patients with intracranial artery stenosis and is associated with bleeding complications.

No definite indication currently exists for long-term anticoagulation in patients with noncardioembolic stroke.

Previous
 
 
Contributor Information and Disclosures
Author

Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA Professor and Founding Chair, Department of Neurology, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center

Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Neurology, American College of Physicians, American Heart Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, Society of Critical Care Medicine

Disclosure: Received honoraria from Lilly for review panel membership; Received honoraria from Novo Nordisk for review panel membership.

Coauthor(s)

Sombat Muengtaweepongsa, MD, MSc Associate Professor, Department of Neurology, Faculty of Medicine, Thammasat University, Thailand

Sombat Muengtaweepongsa, MD, MSc is a member of the following medical societies: American Academy of Neurology, Royal College of Physicians of Thailand

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Boehringer.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Acknowledgements

Draga Jichici, MD, FRCP, FAHA Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care Medicine (USA)

Disclosure: Nothing to disclose.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Lindsberg PJ, Soinne L, Tatlisumak T, et al. Long-term outcome after intravenous thrombolysis of basilar artery occlusion. JAMA. 2004 Oct 20. 292(15):1862-6. [Medline].

  2. Devuyst G, Bogousslavsky J, Meuli R, et al. Stroke or transient ischemic attacks with basilar artery stenosis or occlusion: clinical patterns and outcome. Arch Neurol. 2002 Apr. 59(4):567-73. [Medline].

  3. Davis SM, Donnan GA. Basilar artery thrombosis: recanalization is the key. Stroke. 2006 Sep. 37(9):2440. [Medline].

  4. Schonewille WJ, Algra A, Serena J, Molina CA, Kappelle LJ. Outcome in patients with basilar artery occlusion treated conventionally. J Neurol Neurosurg Psychiatry. 2005 Sep. 76(9):1238-41. [Medline]. [Full Text].

  5. Muengtaweepongsa S, Singh NN, Cruz-Flores S. Pontine warning syndrome: case series and review of literature. J Stroke Cerebrovasc Dis. 2010 Sep-Oct. 19(5):353-6. [Medline].

  6. Mortimer AM, Saunders T, Cook JL. Cross-sectional imaging for diagnosis and clinical outcome prediction of acute basilar artery thrombosis. Clin Radiol. 2011 Jun. 66(6):551-8. [Medline].

  7. Arnold M, Nedeltchev K, Schroth G, et al. Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis. J Neurol Neurosurg Psychiatry. 2004 Jun. 75(6):857-62. [Medline].

  8. Goldmakher GV, Camargo EC, Furie KL, et al. Hyperdense basilar artery sign on unenhanced CT predicts thrombus and outcome in acute posterior circulation stroke. Stroke. 2009 Jan. 40(1):134-9. [Medline].

  9. Ng KW, Venketasubramanian N, Yeo LL, et al. Usefulness of CT Angiography for Therapeutic Decision Making in Thrombolyzing Intubated Patients with Suspected Basilar Artery Thrombosis. J Neuroimaging. 2012 Feb 3. [Medline].

  10. 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. 2008 Sep. 39(9):2485-90. [Medline]. [Full Text].

  11. Mortimer AM, Saunders T, Cook JL. Cross-sectional imaging for diagnosis and clinical outcome prediction of acute basilar artery thrombosis. Clin Radiol. 2011 Jun. 66(6):551-8. [Medline].

  12. Cho TH, Nighoghossian N, Tahon F, et al. Brain stem diffusion-weighted imaging lesion score: a potential marker of outcome in acute basilar artery occlusion. AJNR Am J Neuroradiol. 2009 Jan. 30(1):194-8. [Medline].

  13. Kermer P, Wellmer A, Crome O, et al. Transcranial color-coded duplex sonography in suspected acute basilar artery occlusion. Ultrasound Med Biol. 2006 Mar. 32(3):315-20. [Medline].

  14. Strbian D, Sairanen T, Silvennoinen H, Salonen O, Lindsberg PJ. Intravenous thrombolysis of basilar artery occlusion: thrombus length versus recanalization success. Stroke. 2014 Jun. 45(6):1733-8. [Medline].

  15. Kumar G, Shahripour RB, Alexandrov AV. Recanalization of acute basilar artery occlusion improves outcomes: a meta-analysis. J Neurointerv Surg. 2014 Sep 30. [Medline].

  16. Pfefferkorn T, Mayer TE, Opherk C, et al. Staged escalation therapy in acute basilar artery occlusion: intravenous thrombolysis and on-demand consecutive endovascular mechanical thrombectomy: preliminary experience in 16 patients. Stroke. 2008 May. 39(5):1496-500. [Medline]. [Full Text].

  17. Lindsberg PJ, Mattle HP. Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke. 2006 Mar. 37(3):922-8. [Medline].

  18. Yu W, Binder D, Foster-Barber A, et al. Endovascular embolectomy of acute basilar artery occlusion. Neurology. 2003 Nov 25. 61(10):1421-3. [Medline].

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

  20. Aichner FT, Felber SR, Birbamer GG. Magnetic resonance imaging and magnetic resonance angiography of vertebrobasilar dolichoectasia. Cerebrovasc Dis. 1993. 3:280-284.

  21. 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. 1992 Jan 23. 326(4):221-5. [Medline].

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

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

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

  25. Bergui M, Stura G, Daniele D, et al. Mechanical thrombolysis in ischemic stroke attributable to basilar artery occlusion as first-line treatment. Stroke. 2006 Jan. 37(1):145-50. [Medline].

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

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

  28. 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. 1993 Aug. 43(8):1528-33. [Medline].

  29. 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. 1974 Jun. 49(6):1023-5. [Medline].

  30. 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].

  31. Calvin SA, Beall DP, Ly JQ, et al. Basilar artery thrombosis. J Okla State Med Assoc. 2004 Aug. 97(8):334-6. [Medline].

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

  33. Caplan LR, Wityk RJ, Glass TA, et al. New England Medical Center Posterior Circulation registry. Ann Neurol. 2004 Sep. 56(3):389-98. [Medline].

  34. 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].

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

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

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

  38. Cruz-Flores S, Gomez CR, Malkoff MD. Isolated vertigo as the presentation of severe basilar artery occlusive disease. Neurology. 1994. 4(Suppl):A225.

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

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

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

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

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

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

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

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

  47. Fisher CM. Ocular Bobbing. Arch Neurol. 1964 Nov. 11:543-6. [Medline].

  48. Fisher CM. Atherosclerosis of the carotid and vertebral arteries: extracranial and intracranial. J Neuropathol Exp Neurol. 1965. 24:455-476.

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

  50. Ford GA. Intra-arterial thrombolysis is the treatment of choice for basilar thrombosis: con. Stroke. 2006 Sep. 37(9):2438-9. [Medline].

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

  52. 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. 2003 Jul 15. 109 Suppl 1:S9-15. [Medline].

  53. 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. 1995 Oct 4. 274(13):1017-25. [Medline].

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

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

  56. Hayem MG. Surla thrombose par arterite tronc basilaire. Comme cause du mort rapide. Arch Physiol Norm Pathol. 1868. 1:270-289.

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

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

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

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

  61. 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. 1995 Apr. 129(2):90-6. [Medline].

  62. Johansson B, Strandgaard S, Lassen NA. On the pathogenesis of hypertensive encephalopathy. Circ Res. 1974. 34-35 Suppl 1:I167-I171.

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

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

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

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

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

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

  69. 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].

  70. Lhermitte J, Trelles JO. [L arteriosclerose du tronc basilaire et ses consequences anatomo-cliniques]. Jahrbucher Psychiatrie Neurologie. 1934. 51:91-107.

  71. Lindsberg PJ, Soinne L, Roine RO, Tatlisumak T. Options for recanalization therapy in basilar artery occlusion. Stroke. 2005 Feb. 36(2):203-4. [Medline].

  72. Lisboa RC, Jovanovic BD, Alberts MJ. Analysis of the safety and efficacy of intra-arterial thrombolytic therapy in ischemic stroke. Stroke. 2002 Dec. 33(12):2866-71. [Medline].

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

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

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

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

  77. Millikan CH, Siekert RG. Studies in cerebrovascular disease. IV. The syndrome of intermittent insufficiency of the carotid arterial system. Mayo Clin Proc. 1955 May 4. 30(9):186-91. [Medline].

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

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

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

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

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

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

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

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

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

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

  88. Qureshi AI, Boulos AS, Hanel RA, et al. Randomized comparison of intra-arterial and intravenous thrombolysis in a canine model of acute basilar artery thrombosis. Neuroradiology. 2004 Dec. 46(12):988-95. [Medline].

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

  90. Ringelstein EB, Zeumer H, Poeck K. Non-invasive diagnosis of intracranial lesions in the vertebrobasilar artery. Stroke. 1945. 16:848-854.

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

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

  93. Schellinger PD, Hacke W. Intra-arterial thrombolysis is the treatment of choice for basilar thrombosis: pro. Stroke. 2006 Sep. 37(9):2436-7. [Medline].

  94. Schwartz A, Rautenberg W, Hennerici M. Dolichoectatic intracranial arteries: review of selected aspects. Cerebrovascular Disease. 1993. 3:273-279.

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

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

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

  98. 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. 1974 May-Jun. 5(3):355-64. [Medline].

  99. Tettenborn B, Estol C, DeWitt LD. Accuracy of transcranial Doppler in the vertebrobasilar circulation. J Neurol. 1990. 237:159.

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

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

  102. The Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study Group. Prognosis of patients with symptomatic vertebral or basilar artery stenosis. Stroke. 1998 Jul. 29(7):1389-92. [Medline].

  103. Thompson JR, Simmons CR, Hasso AN, Hinshaw DB Jr. Occlusion of the intradural vertebrobasilar artery. Neuroradiology. 1978 Feb 17. 14(5):219-29. [Medline].

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

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

  106. Voetsch B, DeWitt LD, Pessin MS, Caplan LR. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 2004 Apr. 61(4):496-504. [Medline].

  107. Von Kummer R, Brandt T, Muller-Kuypers M. Thrombolytic therapy of basilar artery occlusion: preconditions for recanalization and good clinical outcome. Yamaguchi T, Mori E, Minematsu K, del Zoppo G, eds. Thrombolytic Therapy. 1995. 343-348.

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

  109. 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. 1983 Aug. 33(8):971-80. [Medline].

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

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

  112. Weinberger J. Noninvasive imaging of the cervical vertebral artery in the diagnosis of vertebrobasilar insufficiency. J Stroke Cerebrovasc Dis. 1991. 1:21-25.

  113. 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. 1978 Feb. 3(2):107-15. [Medline].

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

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

 
Previous
Next
 
Diffusion-weighted MRI images showing a right cerebellar infarct.
Magnetic resonance angiography demonstrating the absence of flow in the vertebrobasilar system.
Right vertebral artery angiography showing an occlusion with no flow in the basilar artery.
Angiography performed after intra-arterial thrombolysis and angioplasty showing recanalization and perfusion of the basilar artery and its branches.
Hyperdense basilar artery (arrow).
Spiral CT angiography showing occluded basilar artery.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.