Basilar Artery Thrombosis

Updated: Jan 11, 2019
Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA; Chief Editor: Helmi L Lutsep, MD 



Acute basilar artery thrombosis is associated with a poor prognosis.[1] However, the advent of high-quality, reliable, and noninvasive technology (eg, magnetic resonance imaging [MRI]) has made its diagnosis possible even in subjects with mild symptoms (see the image below). This has illustrated that some patients have an acute partial occlusion or a slow progressive occlusion with limited ischemic injury and, therefore, a better prognosis. (See Etiology and Workup.)

Diffusion-weighted MRI images showing a right cere Diffusion-weighted MRI images showing a right cerebellar infarct.

Although outcomes continue to be poor in patients with basilar artery thrombosis, advances in pharmacologic and mechanical thrombolysis and in endovascular therapy may reduce the mortality and disability rates associated with this disease. (See Prognosis, Treatment, and Medication.)

Vertigo is one of several common presenting symptoms associated with basilar artery occlusion. See Vertigo: 5 Case-Based Diagnostic Puzzles, a Critical Images slideshow, to help recognize diagnostic clues in vertigo cases.


Complications of basilar artery thrombosis can include the following (see Prognosis, Presentation, and Workup):

  • Aspiration pneumonia

  • Myocardial infarction

  • Deep vein thrombosis and pulmonary embolism

Patient education

For patient education information, see the Cholesterol Center, as well as High Cholesterol and Cholesterol FAQs.


The basilar artery is the most important artery in the posterior circulation. It is formed at the pontomedullary junction by the confluence of both vertebral arteries. It lies on the ventral surface of the pons and, throughout its course, gives off the median, paramedian, short, and long circumferential branches.

Anterior inferior cerebellar artery

The branch of the basilar artery with the larger circumference is the anterior inferior cerebellar artery. It normally arises at the junction of the proximal and middle third of the basilar artery and supplies the lateral pontine tegmentum, brachium pontis or middle cerebellar peduncle, flocculus, and a small part of the anterior cerebellum. The internal auditory artery usually arises from the anterior inferior cerebellar artery; however, it may also arise as a direct branch of the basilar artery.

Posterior cerebral artery

The terminal branch of the basilar artery is the posterior cerebral artery (PCA); it supplies the midbrain, the thalamus, and the medial aspect of the temporal and occipital lobes. Proximal to its bifurcation into the terminal branches (ie, PCA), the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain and the superior surface of the cerebellum.


Given the anatomy of the posterior circulation and the circle of Willis, the clinical manifestations of basilar artery thrombosis depend on the location of the occlusion, the extent of the thrombus, and the collateral flow. Normally, the blood flows in an anterograde fashion from the vertebral arteries to the basilar artery up to its terminal branches. This pattern of flow may vary.

If the proximal segment of the basilar artery is occluded and the occlusion has resulted from a slowly progressive stenosis, collateralization occurs within the cerebellum into the circumferential branches of the basilar artery. Additionally, flow can be reversed from the PCAs into the distal basilar artery.


The risk factors for basilar artery thrombosis are the same as those seen generally in stroke. The most common risk factor is hypertension, which is found in as many as 70% of cases. It is followed by diabetes mellitus, coronary artery disease, peripheral vascular disease, cigarette smoking, and hyperlipidemia.

The mechanism of stroke in basilar artery occlusion differs depending on the segment of the vessel involved. Atherosclerotic occlusive disease predominantly affects the midsegment of the basilar artery, followed by the vertebrobasilar junction.

Embolism, either from a cardiac or arterial source, is much more frequent in the distal third of the basilar artery and the vertebrobasilar junction.

Arterial dissection is much more common in the extracranial vertebral artery. It has been associated with a previous neck injury or chiropractic manipulation. Intracranial dissections are very uncommon.


Occurrence in the United States

The frequency, incidence, and prevalence of basilar artery occlusion are not known. Although basilar artery occlusion has been reported in 2 per 1000 autopsy cases, basilar artery thrombosis may, in stroke registries, explain as many as 27% of ischemic strokes occurring in the posterior circulation.

Race-, sex-, and age-related demographics

Atherosclerotic basilar artery stenosis, like stenosis of any other intracranial artery, is more frequent in the African American and Asian populations than in white populations. The male-to-female ratio for basilar artery thrombosis is 2:1.

Basilar artery occlusion secondary to atherosclerosis is most prevalent in the sixth and seventh decades of life. Occlusion of the distal basilar artery is usually secondary to embolism and is most frequent in the fourth decade. Women with basilar artery occlusion are typically older than men.


Patients with acute basilar artery occlusion have a mortality rate of greater than 85%, although the mortality rate may be as low as 40% in patients with recanalization. Good functional outcomes can be expected in as many as 24-35% of patients treated with intravenous (IV) or intra-arterial thrombolysis, respectively. For symptomatic patients who survive, the risk of recurrent stroke is 10-15%.

Morbidity and mortality

The prognosis for basilar artery occlusion is generally poor, with the mortality rate for this condition consistently reported at greater than 70%. However, the prognosis depends on several factors, including the following[2] :

  • Decreased level of consciousness

  • Dysarthria

  • Pupillary abnormalities

  • Bulbar symptoms

  • Diplopia

  • Bilateral cerebellar lesions

  • Tetraplegia

  • Cardiac cause of embolism

Up to 90% of patients with no such factors have a good functional outcome, while in one study, all patients with such factors either died or had severe disability.[2]

Recanalization is an important requisite for a good functional outcome.[3] A Barthel index of 85 can reportedly be achieved in as many as 58% of patients with vessel recanalization. Recanalization may decrease the mortality rate from basilar artery thrombosis by 50%, although the outcome in a series of patients with the condition who were treated with antithrombotics was similar to that reported in the available series of patients treated with thrombolytic therapy.

A study by Schonewille et al involving 82 patients with symptomatic basilar artery occlusion found that conventional therapy with antiplatelets, anticoagulation, or both was associated with a poor outcome in almost 80% of patients. The case fatality are in the study was 40%, with 65% of survivors remaining dependent (Rankin score 4-5).[4]




A stuttering and progressive course of symptoms or transient ischemic attacks in the vertebrobasilar territory is seen in patients with atherosclerotic occlusion. As many as 50% of patients experience transient ischemic attacks or a waxing and waning course for several days to weeks prior to the occlusion.

The most common heralding symptoms include the following:

  • Motor deficits such as hemiparesis or tetraparesis and facial paresis - 40-67% of cases

  • Dysarthria and speech impairment - 30-63% of cases

  • Vertigo, nausea, and vomiting - 54-73% of cases

  • Headache - 40-42% of cases

  • Visual disturbances - 21-33% of cases

  • Altered consciousness - 17-33% of cases

In a few cases, convulsive-like movements along with hemiparesis (herald hemiparesis) may be the only diagnostic clues.

In very rare cases, patients may present with isolated vertigo or dizziness, with no other neurologic symptoms. The presence of vascular risk factors, headache, and the inability to walk may suggest the diagnosis of vertebrobasilar insufficiency. Any associated neurologic signs of brainstem dysfunction also support the diagnosis of vertebrobasilar insufficiency.

Based on the temporal profile of the symptoms, basilar artery thrombosis may manifest in at least these 3 different ways, as follows:

  • Sudden onset of severe motor and bulbar symptoms with impaired consciousness

  • Gradual or stuttering course of a combination of the symptoms described above that ends with disabling motor and bulbar symptoms, impaired consciousness, or both

  • Prodromal symptoms that may include loss of vision, diplopia, dysarthria, vertigo, hemiparesis, paresthesias, imbalance, and convulsive-like movements (these symptoms may precede monophasic basilar artery thrombosis by several days or even by months)

Physical Examination

An abnormal level of consciousness and motor signs, such as hemiparesis or quadriparesis (usually asymmetrical), are seen in more than 70% of patients.

Bulbar and pseudobulbar signs are the most common findings in one series, reportedly affecting 74% of patients.

Pupillary abnormalities, oculomotor signs, and pseudobulbar manifestations (ie, facial weakness, dysphonia, dysarthria, dysphagia) are seen in more than 40% of patients.

The signs described can be present in different combinations. The recognized syndromes more commonly associated with basilar artery occlusion are locked-in syndrome and top-of-the-basilar syndrome.

Locked-in syndrome

This is caused by infarction of the basis pontis secondary to occlusive disease of the proximal and middle segments of the basilar artery, resulting in quadriplegia. Because the tegmentum of the pons is spared, the patient has a spared level of consciousness, preserved vertical eye movements, and blinking.

Coma associated with oculomotor abnormalities and quadriplegia also indicates proximal basilar and midbasilar occlusive disease with pontine ischemia.

Top-of-the-basilar syndrome

This is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery, usually by an embolus. Patients present with changes in the level of consciousness. They may experience visual symptoms such as hallucinations and/or blindness. Third nerve palsy and pupillary abnormalities are also frequent. Motor abnormalities include abnormal movements or posturing.

Pontine warning syndrome

This is the manifestation of motor fluctuation that resembles the so-called capsular warning syndrome. Clinical features cannot definitely distinguish between these 2 syndromes. The most common features are waxing and waning of hemiparesis. The postulate mechanism is the plaque in the basilar artery at the orifice of the branch to the pons, resulting in paramedian pontine infarction.[5]

Oculomotor symptoms

Oculomotor signs are common and can be associated with the syndromes described above. They usually reflect involvement of the vertical gaze center in the midbrain and/or the abducens nucleus, the horizontal gaze center located in the paramedian reticular formation contiguous to the abducens nucleus, and/or the medial longitudinal fasciculus. Lesions to these structures result in the following:

  • Ipsilateral abducens palsy

  • Ipsilateral conjugate gaze palsy

  • Internuclear ophthalmoplegia

  • One-and-a-half syndrome caused by a lesion simultaneously affecting the paramedian reticular formation and the medial longitudinal fasciculus, resulting in ipsilateral conjugate gaze palsy and internuclear ophthalmoplegia

  • Ocular bobbing, which localizes the lesion to the pons - This is characterized by a brisk, downward movement of the eyeball with a subsequent return to the primary position.

  • Skew deviation

Additional symptoms

In addition to those discussed above, reported signs of pontine ischemia include the following:

  • Limb shaking

  • Ataxia - Usually associated with mild hemiparesis

  • Facial weakness

  • Dysarthria

  • Dysphagia

  • Hearing loss



Diagnostic Considerations

Conditions to consider in the differential diagnosis of basilar artery thrombosis include the following:

  • Basilar meningitis

  • Basilar migraine

  • Cerebellar hemorrhage with brainstem compression

  • Cerebellar infarct with edema and brainstem compression

  • Pontine hemorrhage

  • Space-occupying lesions in the posterior fossa

  • Supratentorial hemispheric mass lesions with mass effect, herniation, and brainstem compression

Differential Diagnoses



Approach Considerations

The primary goals of the workup are to (1) establish the type of vascular lesion and the mechanism of the stroke and, if early enough, (2) establish whether acute intervention is needed to achieve recanalization.

The laboratory workup should include the following:

  • Complete blood count (CBC)

  • Electrolyte values

  • Blood urea nitrogen (BUN) and creatinine determination

  • International normalized ratio (INR)

  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT)

  • Lipid profile

Young patients (< 45 y) or patients with no evidence of atherosclerosis should be investigated for the presence of procoagulant conditions. However, these tests may need to be repeated several weeks after the acute event to establish whether the abnormality was a response to the acute event or an actual abnormality. These patients are typically screened for the following procoagulant conditions:

  • Protein C, protein S, and antithrombin III deficiencies, especially if the patients has evidence of paradoxical embolism, because these disorders have a stronger association with venous rather than arterial thrombosis

  • Lupus anticoagulant and anticardiolipin antibodies

  • Homocysteine level

Creatine kinase levels, cardiac isoenzyme values, and troponin levels should be tested in the following:

  • All symptomatic patients - Eg, those with chest pain

  • Patients with electrocardiographic evidence of ischemic changes - These patients should be tested because of the high incidence of concomitant coronary artery disease in patients with cerebrovascular disease

CT Scanning of the Head

Computed tomography (CT) scanning is usually the first imaging study performed.[6] It has a sensitivity of greater than 95% for identifying hemorrhage within the first 24 hours of onset and helps to exclude intra- or extra-axial hemorrhage.

However, CT scanning has a low sensitivity for early ischemia and usually has the disadvantage of significant artifacts caused by the bony structures surrounding the brainstem and cerebellum.

Helpful findings include infarcts in the thalamus and/or occipital lobe or lobes, which indicate involvement of the rostral basilar artery; a hyperdense basilar artery, which indicates probable occlusion[7] ; and a dilated vertebral and/or basilar artery, which indicates a dolichoectatic vessel. (See the image below.)[8]

Spiral CT angiography is helpful in identifying occluded and dolichoectatic vessels. CT angiogram should be helpful in assisting treatment decision making. (See the image below.)[9]

Hyperdense basilar artery (arrow). Hyperdense basilar artery (arrow).
Spiral CT angiography showing occluded basilar art Spiral CT angiography showing occluded basilar artery.

Functional outcome score

The posterior circulation Acute Stroke Prognosis Early CT Score (pc-ASPECTS) with CT Angiography Source Images (CTASI) is a predictive scale of functional outcome in patients with basilar artery thrombosis.

Pc-ASPECTS allocates 10 points to the posterior circulation. One point each is subtracted for hypoattenuation on CTASI in the left or right thalamus, cerebellum, or posterior cerebral artery territory, respectively, and 2 points each are subtracted for hypoattenuation on CTASI in any part of the midbrain or pons. A pc-ASPECTS score of 10 indicates absence of visible posterior circulation ischemia; a score of 0 indicates hypoattenuation in all pc-ASPECTS territories.

The CTASI pc-ASPECTS score can identify patients with basilar artery thrombosis who will have a poor clinical outcome despite recanalization.[10]


Magnetic resonance imaging (MRI) and MR angiography (MRA) are more sensitive than CT scanning for identifying ischemia and vascular occlusion.[6]

Gradient echo technique, with its higher sensitivity for identifying blood, and diffusion/perfusion-weighted images, with their higher sensitivity for identifying ischemia and hypoperfusion, make MRI a more powerful tool for the treatment of patients with basilar artery occlusion. (See the image below.)[11]

Diffusion-weighted MRI images showing a right cere Diffusion-weighted MRI images showing a right cerebellar infarct.

Helpful findings include lesions that suggest microbleeds, tumors, vertebral/basilar dolichoectasia, and vertebral/basilar dissections.

MRA can identify vertebral/basilar occlusion with sensitivity of as high as 97% and a specificity of 98%. (See the image below.)

Magnetic resonance angiography demonstrating the a Magnetic resonance angiography demonstrating the absence of flow in the vertebrobasilar system.

MRA has limitations, however, because it frequently overestimates the degree of stenosis. Severe stenosis may resemble vascular occlusion. This occurs because the image of the vessel with MRA is a flow-related phenomenon; therefore, severe stenosis with significant flow compromise may result in poor visualization of the vessel.

DWI lesion score

A baseline brainstem diffusion-weighted imaging (DWI) lesion score can be used as an independent predictor for clinical outcome in patients with basilar artery thrombosis.[12]

The total number of brainstem arterial territories with abnormal DWI defines the brainstem DWI lesion score, which ranges between 0 and 22. A score of 0 indicates absence of visible posterior circulation ischemia; a score of 22 indicates DWI restriction in the entire brainstem.[12]


Transcranial Doppler (TCD) ultrasonography is a useful tool for evaluating cerebrovascular disease; however, it is often inaccurate. In patients with basilar artery disease, the reported sensitivity is 72% and the specificity is 94%. TCD ultrasonography is helpful in follow-up once an initial evaluation has demonstrated the lesion.

The flow direction detected by TCD ultrasonography, in combination with CT angiography, may be useful before performing invasive angiography, to help predict the area of stenosis or occlusion.[13]

Electrocardiography and Echocardiography


Electrocardiography (ECG) should be performed in all patients during the initial evaluation because it can reveal paroxysmal arrhythmias such as atrial fibrillation. Additionally, the prevalence of coronary disease is high in patients with cerebrovascular disease.

Ischemic changes seen on ECG should be investigated further with serum creatine kinase measurements, cardiac isoenzyme profiles, and/or troponin levels for the following reasons:

  • Of patients with acute stroke, 5-20% have an arrhythmia.

  • Additionally, 2-3% have a myocardial infarction.

  • The presence of arrhythmias (eg, atrial fibrillation) has an impact on the long-term management plan for stroke prevention


Echocardiography should be considered in all patients because cardioembolism is frequent enough in this population to warrant such consideration. Moreover, even patients with documented atherothrombosis may have a concomitant cardiac source of embolism.

Catheter Angiography

With the availability of noninvasive imaging modalities such as MRI, MRA, and TCD ultrasonography, the role of angiography has changed; however, it still is considered the criterion standard. Angiography is performed (1) when MRA cannot be performed because the patient has an absolute contraindication, such as a pacemaker, or (2) when the quality of noninvasive studies is not satisfactory or the results of other tests do not explain clinical findings. (See the images below.)

Right vertebral artery angiography showing an occl Right vertebral artery angiography showing an occlusion with no flow in the basilar artery.
Angiography performed after intra-arterial thrombo Angiography performed after intra-arterial thrombolysis and angioplasty showing recanalization and perfusion of the basilar artery and its branches.

Angiography should be pursued as a first-line diagnostic test after CT scanning and once the decision is made that recanalization should be performed.



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]

While the largest randomized embolectomy trials to date did not include basilar occlusions and treating patients with basilar artery thrombosis in the context of a clinical trial may be reasonable, intra-arterial pharmacologic or mechanical thrombolysis should be considered given the poor prognosis of these patients when clinical trials aren't available.  Consideraton of IV thrombolysis with tPA is also reasonable.

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.


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.


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.


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.

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).


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.


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.

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.


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.


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.

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 embolectomy or 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.


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

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 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.


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

Two stent retriever devices, the Trevo Retriever and Solitaire Device, were susequently shown to have better angiographic and clinical outcomes than the Merci Retriever.[20, 21]   While these trials included patients with primarily anterior circulation strokes, vertebrobasilar occlusions were also included.


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.

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, or with a novel anticoagulant such as dabigatran, rivaroxaban or apixaban.

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.  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.



Medication Summary

The medications used in the treatment of patients with basilar artery thrombosis include thrombolytic agents, anticoagulants, antihypertensive agents, and antiplatelet agents. Some patients, particularly those with severe and active comorbid conditions, such as an acute myocardial infarction, require inotropic agents and vasopressors.

Several new oral anticoagulant medications are in the final stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke. Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Antihypertensive agents

Class Summary

These agents control severe hypertension. They are recommended for patients considered candidates for thrombolytic therapy who have a systolic blood pressure of greater than 185mm Hg and/or a diastolic blood pressure of greater than 110mm Hg.

Nicardipine (Cardene)

Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.


Labetalol blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Nitroprusside sodium (Nitropress)

Nitroprusside sodium produces vasodilation and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate.

Enalapril (Vasotec, Epaned)

Enalapril is a competitive inhibitor of angiotensin-converting enzyme (ACE). It reduces angiotensin II levels, decreasing aldosterone secretion.


Class Summary

The potential benefits of thrombolytic therapy for the treatment of thrombosis include fast dissolution of physiologically compromising pulmonary emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.

Alteplase (Activase)

Alteplase is a tPA. Its safety and efficacy with concomitant heparin or aspirin during the first 24 hours after symptom onset have not been investigated. It is the only drug approved for use in patients within 3 hours of onset of acute ischemic stroke.

Anticoagulant Agents

Class Summary

The rationale for the use of these agents is to prevent recurrent embolism or extension of the thrombosis.


Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of a clot after spontaneous fibrinolysis.

Enoxaparin (Lovenox)

Enoxaparin is a low–molecular-weight heparin (LMWH) produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). It binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from UFH by having a higher ratio of anti–factor Xa to anti–factor IIa.

Enoxaparin does not actively lyse thrombi but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Its advantages include intermittent dosing and a decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. There is no point in checking the aPTT; the drug has a wide therapeutic window, and aPTT does not correlate with anticoagulant effect.

Desirudin (Iprivask)

Desirudin is a highly selective thrombin inhibitor. It inhibits fibrin formation, activation of coagulation factors, and thrombin-induced platelet aggregation. This results in prolongation of activated partial thromboplastin time.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with the hepatic synthesis of vitamin K–dependent coagulation factors. It is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain the INR in the range of 2-3. Warfarin is used for long-term stroke prophylaxis.

Dabigatran (Pradaxa)

Dabigatran etexilate is a selective thrombin inhibitor that inhibits thrombin formation by binding to the active thrombin site of free and fibrin-bound thrombin. It inhibits thrombin-induced platelet aggregation.

Rivaroxaban (Xarelto)

Rivaroxaban is a selective and reversible inhibition factor of Xa (FXa) in the intrinsic and extrinsic coagulation pathways. This interrupts the blood coagulation cascade, which in turn inhibits thrombin formation and thrombus development.

Apixaban (Eliquis)

Inhibits platelet activation and fibrin clot formation via direct, selective, and reversible inhibition of free and clot-bound factor Xa. Factor Xa, as part of the prothrombinase complex, catalyzes the conversion of prothrombin to thrombin. Thrombin activates platelets and catalyzes the conversion of fibrinogen to fibrin.

Antiplatelet Agents, Cardiovascular

Class Summary

Antiplatelet agents inhibit the cyclo-oxygenase system, decreasing the level of thromboxane A2, a potent platelet activator.

Aspirin (Bayer Aspirin, Ascriptin, Bufferin, Ecotrin)

Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It may be used in low doses to inhibit platelet aggregation and improve complications of venous stasis and thrombosis. Aspirin is used for long-term stroke prophylaxis.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to the platelet receptor and subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Aspirin 25 mg/dipyridamole 200 mg (Aggrenox)

This drug combination has antithrombotic action. Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It may be used in low doses to inhibit platelet aggregation and to improve the complications of venous stasis and thrombosis.

Dipyridamole is a platelet adhesion inhibitor that possibly inhibits red blood cell uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, dipyridamole may inhibit phosphodiesterase activity, leading to increased cyclic adenosine monophosphate (cAMP) within platelets and the formation of thromboxane A2.


Ticlopidine is second-line antiplatelet therapy for patients in whom aspirin is not tolerated or is ineffective.


Class Summary

These agents augment coronary and cerebral blood flow during the low-flow state associated with hypotension. If the MAP continues to be low despite fluid management, vasopressors such as dopamine, dobutamine, norepinephrine or phenylephrine should be used.


Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.


Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It produces systemic vasodilation and increases the inotropic state. Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia. Dobutamine is the pressor of choice in patients with congestive heart failure.

Norepinephrine (Levophed)

Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.

Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic blood pressure <70mm Hg) or hypotension unresponsive to other medication.

Phenylephrine (Vazculep)

Produces systemic arterial vasoconstriction, which in turn results in dose dependent increases in systolic and diastolic blood pressure and reductions in heart rate and cardiac output, especially in patients with heart failure. As a second-line treatment, phenylephrine (Neo-Synephrine) may be added to or substituted for dopamine.


Questions & Answers


What is basilar artery thrombosis?

What are the possible complications of basilar artery thrombosis?

What is the anatomy of the basilar artery relevant to thrombosis?

What is the anatomy of the anterior inferior cerebellar artery relevant to basilar artery thrombosis?

What is the anatomy of the posterior cerebral artery relevant to basilar artery thrombosis?

What is the pathophysiology of basilar artery thrombosis?

What causes basilar artery thrombosis?

What is the prevalence of basilar artery thrombosis?

Which patient groups have the highest prevalence of basilar artery thrombosis?

What is the prognosis of basilar artery thrombosis?

What are the prognostic factors of basilar artery thrombosis?

How does recanalization affect the prognosis of basilar artery thrombosis?

How does conventional therapy with antiplatelets and/or anticoagulation affect the prognosis of basilar artery thrombosis?


Which clinical history findings are characteristic of basilar artery thrombosis?

What are the signs and symptoms of basilar artery thrombosis?

What are the clinical manifestations of basilar artery thrombosis?

Which physical findings are characteristic of basilar artery thrombosis?

Which physical findings are characteristic of locked-in syndrome in basilar artery thrombosis?

Which physical findings are characteristic of top-of-the-basilar syndrome in basilar artery thrombosis?

Which physical findings are characteristic of pontine warning syndrome in basilar artery thrombosis?

What are the oculomotor findings of basilar artery thrombosis?

What are the signs and symptoms of pontine ischemia in basilar artery thrombosis?


Which conditions should be included in the differential diagnoses of basilar artery thrombosis?

What are the differential diagnoses for Basilar Artery Thrombosis?


What is the role of lab tests in the workup of basilar artery thrombosis?

When is screening for procoagulant conditions included in the workup of basilar artery thrombosis?

When are creatine kinase levels, cardiac isoenzyme values, and troponin levels obtained in the workup of basilar artery thrombosis?

What is the role of CT scanning of the head in the workup of basilar artery thrombosis?

What is the functional outcome score for basilar artery thrombosis?

What is the role of MRI and MRA in the workup of basilar artery thrombosis?

What is the DWI lesion score for basilar artery thrombosis?

What is the role of ultrasonography in the workup of basilar artery thrombosis?

What is the role of ECG in the workup of basilar artery thrombosis?

What is the role of echocardiography in the workup of basilar artery thrombosis?

What is the role of catheter angiography in the workup of basilar artery thrombosis?


How is basilar artery thrombosis treated?

What is the role of sedation and paralysis in the treatment of basilar artery thrombosis?

Which specialist consultations are beneficial to patients with basilar artery thrombosis?

Which dietary modifications are used in the treatment of basilar artery thrombosis?

Which activity modifications are used in the treatment of basilar artery thrombosis?

What is the role of hemodynamic management in the treatment of basilar artery thrombosis?

How is hypertension treated in basilar artery thrombosis?

How is hypotension treated in basilar artery thrombosis?

What is the role of a pulmonary artery catheter in the treatment of basilar artery thrombosis?

What is the role of respiratory management in the treatment of basilar artery thrombosis?

What is the role of mechanical ventilation in the treatment of basilar artery thrombosis?

What is the role of tPA in the treatment of basilar artery thrombosis?

What is the role of intra-arterial thrombolysis in the treatment of basilar artery thrombosis?

Which thrombolytic agents are used in the treatment of basilar artery thrombosis?

What are the guidelines on intra-arterial thrombolysis for basilar artery thrombosis?

What is the role of anticoagulant and antiplatelet therapies in the treatment of basilar artery thrombosis?

What is the role of angioplasty in the treatment of basilar artery thrombosis?

What is the role of embolectomy in the treatment of basilar artery thrombosis?

What is the role of thrombus retrieval in the treatment of basilar artery thrombosis?

What is the role of rehabilitation therapies in the treatment of basilar artery thrombosis?

How is stroke prevented in patients with basilar artery thrombosis?


Which medications are used to treat basilar artery thrombosis?

Which medications in the drug class Vasopressors are used in the treatment of Basilar Artery Thrombosis?

Which medications in the drug class Antiplatelet Agents, Cardiovascular are used in the treatment of Basilar Artery Thrombosis?

Which medications in the drug class Anticoagulant Agents are used in the treatment of Basilar Artery Thrombosis?

Which medications in the drug class Thrombolytics are used in the treatment of Basilar Artery Thrombosis?

Which medications in the drug class Antihypertensive agents are used in the treatment of Basilar Artery Thrombosis?