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Vertebrobasilar Stroke

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Vertebrobasilar Stroke Overview of Vertebrobasilar Stroke
Author: Vladimir Kaye, MD; Chief Editor: Denise I Campagnolo, MD, MS more... Updated: Mar 29, 2011

Overview of Vertebrobasilar Stroke
The vertebrobasilar arterial system perfuses the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex. Occlusion of large vessels in this system usually leads to major disability or death. Vertebrobasilar stroke carries a mortality rate of more than 85%. Because of involvement of the brainstem and cerebellum, most survivors have multisystem dysfunction (eg, quadriplegia or hemiplegia, ataxia, dysphagia, dysarthria, gaze abnormalities, cranial neuropathies). However, many vertebrobasilar lesions arise from small vessel disease and are correspondingly small and discrete. The clinical correlates of these smaller lesions consist of a variety of focal neurologic deficits, depending on their location within the brainstem. Patients with small lesions usually have a benign prognosis with reasonable functional recovery. See the images below regarding vertebrobasilar stroke.

Lesion of the medial longitudinal fasciculus (MLF) resulting in internuclear ophthalmoplegia (INO). (Courtesy of BC Decker Inc.)


involving the opposite arm and leg Cerebellar signs (eg. (Courtesy of BC Decker Inc.) Visceral motor component of CN III and pathw ays involved in pupillary constriction. including the following[1] : When cranial nerves or their nuclei are involved. ataxia) are frequent .Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex. dysmetria. the corresponding clinical signs are ipsilateral to the lesion and the corticospinal signs are crossed. (Courtesy of BC Decker Inc.) Vestibular nuclei and their connections. (Courtesy of BC Decker Inc.) Distinction of vertebrobasilar and hemispheric stroke Lesions in the vertebrobasilar system have some characteristic clinical features that distinguish them from lesions in the hemispheres. (Courtesy of BC Decker Inc.) Note the horizontal eye movement. Also note a topographic relationship of the center for vertical gaze.

The damaged arteries may occlude with thrombus or undergo dissection.Involvement of the ascending sensory pathways may affect the spinothalamic pathway or the medial lemniscus (dorsal columns). the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain. At the top of the pons. such as aphasia and cognitive impairments. smaller branches from the vertebral arteries. At the base of the brain. as well as the superior surface of the cerebellum. penetrating branches from the basilar artery and its major branches. The medulla is perfused by the PICA and by direct. chiropractic manipulation or neck rotation may traumatize the vertebral arteries in the neck. and the origin of the vertebral arteries. Etiology of Vertebrobasilar Stroke Vertebrobasilar insufficiency or stroke may be caused by a number of mechanisms. strokes occur because of ischemic events (80-85% of patients) or hemorrhage (15-20% of patients). communicating arteries known as the circle of Willis. embolism. Lipohyalinosis weakens the vessel wall. in which plaques cause narrowing and occlusion of the large vessels. the basilar artery divides into 2 posterior cerebral arteries (PCAs). are absent Anatomy of the Vertebral and Basilar Arteries The vertebral arteries arise from the subclavian arteries. the carotid and basilar systems join to form a circle of large. and the anterior inferior and superior cerebellar arteries from the basilar artery. which frequently occurs in association with hypertension. because the small vessels become occluded by a process called lipohyalinosis. including thrombus. Each vertebral artery usually gives off the posterior inferior cerebellar artery (PICA). Embolic occlusion of the vertebrobasilar system is not common and usually is artery-to-artery with occlusion of the basilar artery. the subclavian artery. resulting in a focal hemorrhage. the PICA. Because of the close anatomical relationship between the vertebral arteries and the cervical spine. Because of this arrangement of collateral vessels. and vomiting. They enter the skull through the foramen magnum and merge at the pontomedullary junction to form the basilar artery. The pathology of small vessel disease (affecting arteries 50-200 µm in diameter) is different from that of atherosclerosis. nausea. represent involvement of the vestibular system Unilateral Horner syndrome occurs with brainstem lesions Occipital lobe lesions result in visual field loss or visuospatial deficits Cortical deficits. resulting in dissociated sensory loss (ie. even when one of the main arteries is occluded. rupture of the artery may occur. and in hypertensive individuals. penetrating vessels. and as they course cephalad in the neck. along with nystagmus. In general. such as the following: Increasing age Family history 3/19 . which may appear as single lesions or may be distributed as multiple lesions scattered widely throughout the subcortex and brainstem. Proximal to its bifurcation into the terminal branches (PCAs). and hemorrhage (secondary to aneurysm or trauma). adequate perfusion of the brain still may be possible. The pons is perfused by small. Occlusions of these small vessels lead to small. Donor sites for the emboli typically are the aortic arch. Almost all intracerebral hemorrhages originate from the rupture of these small. round infarctions called lacunes. they pass through the costotransverse foramina of C6 to C2. and the occipital cortex is perfused by the PCAs. The cerebellum is supplied by long circumferential arteries. loss of 1 sensory modality on one side and preservation of other sensory modalities in the opposite limbs) Dysarthria and dysphagia typically are present Vertigo. A number of risk factors are associated with stroke. Penetrating arteries from the PCAs perfuse the midbrain and thalamus.[2] Pathophysiology of Vertebrobasilar Stroke The most common vascular condition affecting the vertebrobasilar system is atherosclerosis.

Although most intracerebral hemorrhages occur in the region of the putamen and thalamus. in large part. Patients with basilar artery thrombosis typically have a waxing and waning course of symptoms. hemiparesis. and 20% of the lesions producing ischemic strokes occur in the vertebrobasilar system. Overall. about 7% of all hemorrhagic lesions involve the cerebellum in the area of the dentate erv iew#aw2aab6c20 structures result in ipsilateral lateral gaze or conjugate gaze palsy. nystagmus. diplopia. and dysphagia.[3] Most survivors of basilar artery occlusion have severe. and bulbar manifestations. and/or the medial longitudinal fasciculus (MLF). the horizontal gaze center located in the pontine paramedian reticular formation (PPRF). In contrast. with acute and dramatic presentation. embolic events are sudden. contiguous to the abducens nucleus. upon the etiology. and approximately 6% of hemorrhagic lesions involve the pons.11. lateral gaze abnormalities. pupillary changes) Ipsilateral cranial nerve weakness (eg. hemorrhage causes 15-20% of strokes. dysphagia. and prevalence of the vertebrobasilar syndromes vary. mortality patients with basilar artery occlusion has been consistently greater than 75-80%. Commonly reported symptoms associated with vertebrobasilar strokes include the following[1] : Vertigo Nausea and vomiting Headache Abnormalities in the level of consciousness Abnormal oculomotor signs (eg. Approximately 80-85% of all strokes are ischemic. quadriparesis) Pain and temperature loss Incontinence Visual-field defects Presence of central pain Abnormal swelling Sweating in the face or extremities Physical Examination Common clinical findings observed in more than 70% of patients with vertebrobasilar stroke include an abnormal level of consciousness. with as many as 50% of patients experiencing transient ischemic attacks for several days to weeks prior to the occlusion. dysarthria. dysphonia. dysphonia.medscape. weakness of facial muscles and tongue) Sensory loss (in the face and scalp) Ataxia Contralateral motor weakness (eg.2012 Vertebrobasilar Stroke Race Prior history of stroke Hypertension Coronary artery disease Diabetes mellitus Cigarette smoking Heart disease Obesity Physical inactivity Drug or alcohol abuse Epidemiology of Vertebrobasilar Stroke The frequency. In most of the reported series. occur in more than 40% of patients. Pupillary abnormalities and oculomotor signs are common. Lesions to these emedicine. incidence. persisting disability. without prodrome or warning. as well as hemiparesis or quadriparesis. Oculomotor signs usually reflect the involvement of the abducens nucleus. which usually is asymmetric. dysarthria. depending on the specific area and syndrome involved. Clinical Presentation in Vertebrobasilar Stroke Patient History The onset and duration of symptoms in vertebrobasilar stroke depends. such as facial weakness.10. 4/19 .

) Center for vertical gaze and pathw ays involved in vertical eye movement (Courtesy of Cranial Nerves--Anatomy and Clinical erv iew#aw2aab6c20 5/19 . (Courtesy of BC Decker Inc.2012 Vertebrobasilar Stroke longitudinal fasciculus (MLF). (Courtesy of BC Decker Inc. Lesion of the medial longitudinal fasciculus (MLF) resulting in internuclear ophthalmoplegia (INO). Toronto. Lesions to these structures result in ipsilateral lateral gaze or conjugate gaze palsy.11.) Vestibular reflex illustrating horizontal eye movements only. (Courtesy of BC Decker Inc.) emedicine.10. See the images below. BC Decker Inc. 1988) Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex.medscape.

Horner syndrome. Some examples are as follows: Lateral medullary (Wallenberg) syndrome Medial medullary (Dejerine) syndrome Cerebellar infarction Locked-in syndrome Top-of-the-basilar syndrome Internuclear ophthalmoplegia One-and-a-half syndrome Ventral pontine (Millard-Gubler) syndrome Upper dorsal pontine (Raymond-Cestan) syndrome Upper dorsal pontine (Raymond-Cestan) syndrome Lower dorsal pontine (Foville) syndrome Ventral midbrain (Weber) syndrome Dorsal midbrain (Benedikt) syndrome Posterior Cerebral Artery occlusion Lateral medullary (Wallenberg) syndrome This syndrome is most often due to vertebral artery occlusion erv iew#aw2aab6c20 6/19 . Certain constellations of findings may serve as clues to the location of the lesion. downward movement of the eyeball with a subsequent return to the primary position. to posterior inferior cerebellar emedicine. (Courtesy of BC Decker Inc. less commonly. vocal cord. Other reported signs of pontine ischemia include ataxia and tremor associated with mild hemiparesis. and ipsilateral paralysis of the tongue.cranial nerve (CN) III lesion and vertical gaze palsy Pontine syndromes .medscape.2012 Vertebrobasilar Stroke Visceral motor component of CN III and pathw ays involved in pupillary constriction.10.CN VI lesion. or sternocleidomastoid [SCM] muscle Posterior cerebral artery . horizontal gaze palsy. ipsilateral ataxia. contralateral loss of pain and temperature sensation. including the following examples: Midbrain syndromes . soft palate. presenting a diagnostic challenge in lesion localization.) Ocular bobbing is described as a brisk. This deficit localizes the lesion to the pons. The signs described can occur in different combinations. and VII nerve palsy Medullary syndromes .11. based on constellations of findings.contralateral hemianopia with macular sparing Complications Potential complications of vertebrobasilar stroke include the following: Aspiration pneumonia Deep venous thrombosis Pulmonary embolism Myocardial infarction Vertebrobasilar Artery Stroke Syndromes A variety of specific neurologic syndromes [4] have been described in vertebrobasilar artery stroke.ipsilateral facial pain and temperature loss.

patients may die in the acute phase from aspiration pneumonia. due to damage to descending sympathetic fibers Facial pain and temperature loss Reduced corneal reflex. intention tremor. contralateral hemiplegia with sparing of the face (corticospinal tract). because swelling may cause brainstem compression or hydrocephalus. indicating involvement of the anterior spinothalamic tract. (Courtesy of BC Decker Inc. Ipsilateral clinical features include the following: Ataxia and dysmetria. Other findings include tachycardia and dyspnea (dorsal nucleus of CN X) and palatal myoclonus.) LMN Lesion of the hypoglossal nerve producing tongue deviation to the side of the lesion. erv iew#aw2aab6c20 7/19 . and diaphragm. The prognosis of patients with the lateral medullary syndrome usually is quite good for functional outcome. Locked-in syndrome This dramatic clinical syndrome occurs when there is an infarction of the upper ventral pons. central pontine myelinolysis. sometimes. The clinical features include ipsilateral paresis of the tongue with deviation toward the lesion (lower motor neuron lesion of CN XII). Locked-in syndrome can result from occlusion of the proximal and middle segments of the basilar artery or from hemorrhage involving that region. Patients present with nausea. pharyngeal muscles. encephalitis. from damage to the descending spinal tract and nucleus of CN V Nystagmus Hypoacusis (cochlear nucleus) Dysarthria Dysphagia Paralysis of the pharynx. (See the image below. and loss of ipsilateral vibration and proprioception (medial lemniscus). Early diagnosis of cerebellar infarctions is important. Medial medullary (Dejerine) syndrome This syndrome is an uncommon lesion resulting from occlusion of a vertebral artery or its branch to the anterior spinal artery. hypohidrosis or anhidrosis. the hypoglossal nerve.medscape. Palatal myoclonus sometimes follows infarction of the dentate nucleus of the cerebellum and inferior oliva. miosis. enophthalmos). clumsiness. and. and death has been reported from sleep apnea in a number of cases. It can also be caused by trauma. emedicine. scanning speech. and vocal cord Loss of taste from the posterior third of the tongue (nuclei or fibers of CN IX and X) Contralateral findings include the loss of pain and temperature sense in the body and extremities.10.11.2012 Vertebrobasilar Stroke artery (PICA) occlusion. due to damage to the inferior cerebellar peduncle and cerebellum Horner syndrome (eg. ataxia. however. or a tumor. dysarthria. ptosis. a rhythmic involuntary jerking movement of the soft palate.) Cerebellar infarction A stroke involving the cerebellum may result in a lack of coordination. it involves the pyramid. the medial lemniscus. palate. and vertigo from involvement of the vestibular system. and even difficulties with memory and motor planning.

it results from a brainstem lesion affecting the MLF between the nuclei of CN VI and III.10. Coma generally is associated with oculomotor abnormalities. convergence spasm resulting in pseudoabducens palsy. Convergence is preserved. Internuclear ophthalmoplegia Clinically. the occlusion usually results from an embolism. and visual symptoms (eg. The only movements preserved are vertical eye movements and blinking. away from the involved side). Some recovery of facial muscle movement and horizontal gaze may occur with time or in an incomplete form of this syndrome. Coma may occur with bilateral involvement of the pontine tegmentum or with lesions of the midbrain reticular formation. including small pupils with decreased light reactivity (diencephalic). skew deviation. Top-of-the-basilar syndrome This syndrome is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery. disruption of the communication pathway (ie. Patients present with sudden changes in the level of consciousness. it may occur due to multiple sclerosis (MS). there is no adduction to either side with nystagmus of the abducting eye in both directions. because the nuclei of CN III and peripheral innervation of the medial recti muscles are intact. the patient's consciousness is preserved. thalamus. or posturing. commonly with bilateral involvement. Sleep-wake cycles are absent in patients with coma. In elderly patients. and ectopic or oval pupils. By the same logic. These patients can also demonstrate oculomotor abnormalities.[5] Varying degrees of involvement of the midbrain. emedicine. erv iew#aw2aab6c20 8/19 . or to look to either side (horizontal eye movement is impaired due to a lesion of bilateral CN VI nuclei). sensate. confusion. cortical blindness. large/mid-position and fixed pupils (midbrain). Because horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI (relative to the lesion). most commonly of the vertical gaze. (See the image below. also are frequent. (Courtesy of BC Decker Inc. In younger adults. or convergence-retraction nystagmus.medscape. to produce facial movement (damage to the corticobulbar tracts). Other abnormalities include varying degrees of weakness.) Lesion of the medial longitudinal fasciculus (MLF) resulting in internuclear ophthalmoplegia (INO). and aware. and motor abnormalities may be present. he/she shows no adduction of the right eye and full abduction of the left eye with the end-point abduction nystagmus. Because the tegmentum of the pons is spared. CN III palsy and pupillary abnormalities. A comatose patient is unresponsive. with the patient fully awake. sensory deficits. such as gaze palsy.) When a patient with a lesion in the right MLF attempts to look to his/her left (ie.2012 Vertebrobasilar Stroke Bilateral ventral pontine lesions involving corticospinal and corticobulbar tracts lead to quadriplegia. abnormal color vision/color dysnomia).11. The patient is unable to speak. internuclear ophthalmoplegia (INO) is a horizontal gaze palsy. INO is caused most often by occlusion of the basilar artery or its paramedian branches. The patient is paralyzed completely and communicates only by blinking. and the coma may be prolonged when it is due to basilar artery occlusion. hemianopia. the MLF) between the nuclei of CN III (in the midbrain) and CN VI (in the pons) results in the inability of the eye ipsilateral to the lesion to adduct and the contralateral eye to exhibit abduction nystagmus when looking away from the involved side. in the case of bilateral INO. and portions of the temporal and occipital lobes may occur and can produce severe disability. most commonly in the pons.

2012 Vertebrobasilar Stroke One-and-a-half syndrome This syndrome is caused by a lesion affecting the PPRF and MLF simultaneously. and skew deviation. ptosis. and mydriasis (as in Weber syndrome). color blindness. and is able only to abduct the contralateral eye. Weakness of the lower face (corticospinal and corticobulbar tracts) may be noted. exotropia of the contralateral eye. and hallucinations. This occlusion results in ipsilateral ataxia and coarse intention tremor (indicating involvement of the superior and middle cerebellar peduncles).11. verbal dyslexia. ataxia. Ventral pontine (Millard-Gubler) syndrome This syndrome occurs after paramedian infarction in the pons and results in ipsilateral lateral rectus palsy (CN VI) with diplopia. Weber syndrome. Horizontal gaze palsy also may occur. Vertical gaze and convergence generally are preserved. Typical clinical findings include ipsilateral CN III palsy. Lower dorsal pontine (Foville) syndrome This syndrome may result from lesions to the dorsal tegmentum of the lower pons. Dorsal midbrain (Benedikt) syndrome This syndrome is due to a lesion in the midbrain tegmentum resulting from occlusion of paramedian branches of the basilar artery. Ventral midbrain (Weber) syndrome Weber syndrome occurs with an occlusion of the median and/or paramedian perforating branches of the basilar artery. complete facial paresis (unilateral CN VII palsy).medscape. Diagnostic Considerations The differential diagnosis of vertebrobasilar stroke includes the following: emedicine. horizontal gaze palsy on the ipsilateral side (ie. Posterior cerebral artery occlusion The most common finding is occipital lobe infarction leading to contralateral hemianopia with macular sparing. The patient with a lesion in the ipsilateral PPRF or abducens nucleus and MLF connecting to the contralateral CN VI exhibits horizontal gaze palsy when looking toward the side of the lesion and exhibits INO when looking away from the side of the lesion. The patient exhibits ipsilateral paresis of the whole face (nucleus and fibers of CN VII). resulting in ipsilateral conjugate gaze palsy and INO[6] A patient with this syndrome is completely unable to move the ipsilateral eye. and mydriasis (ie. or chorea (due to the involvement of the red nucleus). such as those of intention tremor. failure to see to-and-fro movements. and contralateral hemiparesis/hemiplegia (corticospinal tract involvement) with sparing of the face. damage to parasympathetic fibers of CN III) with contralateral hemiplegia. along with the contralateral involuntary movements. Associated features may include vertical nystagmus. PPRF with or without CN VI nucleus). Clinical symptoms associated with occlusion of the PCA vary depending on the location of the occlusion and may include the thalamic syndrome. Upper dorsal pontine (Raymond-Cestan) syndrome This syndrome is due to obstruction of flow in the long circumferential branches of the basilar artery. or both. the ‘one’ in the syndrome name refers to the former. ptosis. cortical blindness. with resulting nystagmus. and the ‘half’ to the erv iew#aw2aab6c20 9/19 . the PCA. thalamic perforate syndrome. and contralateral hemiplegia (corticospinal tract) with sparing of the face.10. and contralateral loss of all sensory modalities (due to damage to medial lemniscus and spinothalamic tract) with or without facial weakness and hemiparesis (corticospinal tract). The patient demonstrates ipsilateral oculomotor palsy. weakness of mastication and sensory loss in the face (suggesting sensory and motor trigeminal nuclei and tracts).

14. herniation.[8.[10] Spiral CT angiography is used further to identify occluded and dolichoectatic vessels.[8. and troponin level should be tested in the following persons: All patients with suggestive symptoms (eg.[11. A limitation of MRA is its tendency to overestimate the degree of stenosis. tumors. hence. 15] MRI and magnetic resonance angiography (MRA) are very helpful in finding occult lesions. because of the high incidence of concomitant coronary artery disease)[7] Computed Tomography CT scanning usually is the first imaging study performed. protein erv iew#aw2aab6c20 10/19 . and antithrombin III deficiencies Factor V Leiden mutation Creatine kinase. This overestimation occurs because the production of a vessel's image in MRA is a based on a flow-related phenomenon. and brainstem compression Laboratory Studies for Vertebrobasilar Artery Stroke The laboratory workup should include the following: Complete blood count (CBC) Electrolytes Blood urea nitrogen (BUN) and creatinine Prothrombin time and activated partial thromboplastin time (aPTT) Cholesterol level Lipid profile Patients who are younger than 45 years or who have no evidence of atherosclerosis should be investigated for the presence of hypercoagulable states. Magnetic Resonance Imaging MRI is more sensitive than CT in the identification of ischemia (since bone does not degrade the image). 9. such as demyelinating plaques. 12] The disadvantages of CT scanning include a low sensitivity for early ischemia and the presence of significant artifacts caused by the bony structures surrounding the brainstem and cerebellum. 17.11. such as the following: Lupus anticoagulant and anticardiolipin antibodies Protein C. chest pain) Patients with evidence of ischemic changes in the electrocardiogram (ECG.2012 Vertebrobasilar Stroke Central pontine myelinolysis Metastatic disease of the brain Subarachnoid hemorrhage Basilar meningitis Basilar migraine Cerebellopontine angle tumors Supratentorial hemispheric mass lesions with mass effect. Newer techniques. 18] MRA has a sensitivity of up to 97% and a specificity of up to 98% when used to identify vertebrobasilar occlusion.medscape. vertebrobasilar dolichoectasia.[16. because it has a sensitivity of more than 95% when used in the identification intra-axial or extra-axial hemorrhage within the first 24 hours of onset. 9] Other helpful findings include evidence of infarcts in the thalamus or occipital lobes (implicating involvement of the rostral basilar artery) and evidence that a hyperdense basilar artery is present (suggesting a probable occlusion).10. cardiac isoenzymes. or dissection. make MRI a very powerful tool for the exclusion of intraparenchymal hemorrhage or edema and for the identification of early and potentially reversible ischemia. including flow suppression and the production of diffusion-weighted and perfusion-weighted images. the presence of severe stenosis with significant flow compromise may result in poor visualization of a vessel and cause the MRA image to resemble vascular occlusion. 13. emedicine.

Cerebral ischemia impairs the brain’s ability to autoregulate its circulation through vasoconstriction and vasodilatation. and troponin. but it often is inaccurate. Absence of signal in an initial examination does not necessarily mean occlusion. ervin iew#aw2aab6c20 11/19 .2012 Vertebrobasilar Stroke Angiography While the role of cerebral (catheter) angiography has changed due to the availability of noninvasive imaging modalities (eg. ventricular aneurisms. for reasons that include the following: Up to 20% of patients with acute stroke have an arrhythmia Myocardial infarction occurs in 2-3% of patients The presence of arrhythmias (eg.medscape. TCD is helpful for purposes of follow-up once an initial evaluation has demonstrated the lesion. The most important goal of the workup is to establish the type of vascular lesion and the mechanism of the stroke. Ischemic changes in the ECG should be investigated further with assays of serum creatine kinase. This response limits the perfusion pressure and the blood volume. emedicine. Therefore. Ultrasonography Transcranial Doppler (TCD) is used in the evaluation of cerebrovascular disease.10. TCD). the cerebral blood flow becomes blood pressure–dependent. All patients should be monitored continuously for the first few days. metallic implant) The quality of noninvasive studies is not satisfactory The results of noninvasive studies do not explain the clinical findings Angiography should be considered a first-line diagnostic test after a CT scan. all patients who have suffered a vertebrobasilar stroke should be admitted to a unit specializing in the care of stroke patients. once it has been decided that recanalization with thrombolysis should be completed. cardiac tumors (myxoma). under ischemic conditions. a pacemaker. cardiac isoenzymes. vegetations. right-to-left shunts. thrombolysis) or who have any of the following[21] : Unstable or fluctuating neurologic symptoms Decreased level of consciousness Hemodynamic instability Active cardiac or respiratory problems Hemodynamic management Hemodynamic management should be aimed at minimizing the ischemic injury. it still is considered the criterion standard for imaging. A decrease in the MAP results vasodilatation. atrial fibrillation) has an impact on long-term patient management related to stroke prevention Echocardiography Echocardiography [20] should be considered in the following patients: Those younger than 45 years Those with explained basilar artery occlusion Findings that may affect management include valvular disorders. TCD has a sensitivity of 72% and a specificity of 94% in patients with basilar artery disease. Catheter cerebral angiography is performed in the following circumstances: The patient has an absolute contraindication to MRA (eg. Admission to a neurologic intensive care unit (ICU) is indicated for patients who are candidates for interventional therapies (eg.11. MRA.[19] Electrocardiography Electrocardiography should be performed in all patients on initial evaluation. intramural or extramural thrombi. Treatment of Acute Vertebrobasilar Artery Stroke Ideally.[22] An increase in the mean arterial pressure (MAP) results in vasoconstriction. and poor ejection fraction.

the limits of autoregulation are within the range of 50-150 mm Hg of the MAP. consequently. usually in the range of 5-8 mL/kg. Respiratory management Early assessment and management of the airway are critical due to the frequent involvement of lower cranial nerves and the impairment of consciousness in patients with brainstem ischemia. CPP = MAP-ICP). should be used.[8] Approval was based on data from the National Institute of Neurological Disorders and Stroke trial. In this mode. vasopressors. This form of ventilation delivers a set number of breaths with a set tidal erv iew#aw2aab6c20 12/19 . Thrombolysis In 1996. synchronized intermittent mandatory ventilation may be a better mode. such as hypertensive encephalopathy. Moreover. Endotracheal intubation may be considered in patients with a decreased level of consciousness and a Glasgow coma score of less than 8.medscape. In patients with unknown intravascular volume status or those with complications. a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary wedge pressure. overzealous treatment of hypertension should be avoided.2012 Vertebrobasilar Stroke decrease in the MAP results in vasodilatation. nitroprusside is the preferred drug. and phenylephrine. In chronic hypertensive patients. such as dopamine. because they may obscure the neurologic assessment. or acute renal failure. Maximal effort should be made to maintain a normal intravascular volume using isotonic solutions. No existing information from randomized trials indicates whether treating hypertension is better than not treating it. For patients with good respiratory drive. The US Food and Drug Administration (FDA) approved tissue plasminogen activator (tPA) for the treatment of acute ischemic stroke within the first 3 hours of onset. the most comfortable mode is PSV. For patients with poor respiratory drive. and ability to handle secretions with a forceful cough also is of great importance. when thrombolysis is a strong consideration. In the patients with severe cerebral vascular occlusive disease. Commonly used antihypertensives are labetalol and nitroprusside. Of the mechanical ventilation modes. CPP is equal to MAP less intracranial pressure (ICP) (ie. hypertension should not be treated unless there is evidence of end-organ damage. Adding PSV during the extra breaths can minimize the patient's respiratory effort when taking them. which is synchronized with the patient's inspiratory effort while allowing the patient to take extra breaths. which showed that a higher number of treated versus untreated patients had minimal deficit and minimal or no disability. Based on evidence from experimental models and on data from clinical experience. Assessment of the respiratory drive. pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation are used most often. unstable angina. Sedation and paralysis should be avoided. Hypertension should be treated when the diastolic blood pressure is greater than 120 mm Hg or when the systolic blood pressure is over 200 mm Hg. and that criterion probably excluded patients who suffered a basilar artery occlusion. neurogenic hyperventilation) to avoid hypocarbia and worsening of the ischemic process. Patients with hypotension need to be treated to optimize the MAP and. Most patients with no pulmonary comorbidities reach this goal with a PSV of 5-10. gag reflex. Therefore. the blood pressure– dependent cerebral blood flow. heart failure.11.10. If the MAP continues to be low despite fluid management. dobutamine. the trial did not study the vascular anatomy systematically in all emedicine. such as congestive heart failure and pulmonary edema. the curve of autoregulation is shifted upward. In normotensive patients. this trial did not include patients in stupor or coma. the MAP and the cerebral perfusion pressure (CPP) become critical in maintaining the cerebral blood flow. Otherwise. because it can decrease the cerebral perfusion pressure and exacerbate the ongoing ischemia. However. provided that no contraindications exist. acute myocardial infarction. the treatment parameters become 110 mm Hg or more for diastolic blood pressure or greater than 180 mm Hg for systolic blood pressure. Circumstances may exist that require the use of sedation and paralysis (eg. When diastolic blood pressure is greater than 140 mm Hg. This approach would improve monitoring of the intravascular volume to avoid overload. the ventilator does not deliver a set of breaths but provides enough pressure support to maintain the desired tidal volume.

Reports describe angioplasty performed in patients with acute vertebrobasilar occlusion. but there is no evidence that it has an impact on outcome.5 hours are similar to those employed for treatment prior to 3 hours. did show a better outcome at 7 days for patients with large vessel disease. From experimental evidence and thrombolytic trials. At this time. This drug has been studied prospectively in trials involving combined intravenous and intra-arterial therapy. prourokinase. streptokinase. Anticoagulation Anticoagulation therapy with heparin has been used. 30] To date.medscape. the American Heart Association/American Stroke Association (AHA/ASA) published a science advisory recommending that the time window for tPA administration be increased to 4. Streptokinase has not been used for stroke since the multicenter European and Australian trials documented a greater mortality in the treated patients.5-hour window.[26.[25] Research indicates that tPA is effective in patients even when administered within the 3. as well as electively. controlled trials. in doses of 0. Overall mortality has decreased from 46-75% to 26-60%. urokinase is not currently available in the United States. 28] but the AHA/ASA stated that. 23.11.[29] but with the exclusion criteria expanded to include any of the following patient characteristics: Age greater than 80 years Use of oral anticoagulants Baseline National Institutes of Health (NIH) Stroke Scale score >25 A history of both stroke and diabetes In the early 1980s. Of the different agents currently used for thrombolysis (urokinase. but prourokinase has not been approved for use in acute stroke.[3. Limited experience with the use of GPIIb/IIIa inhibitors. several case series have been published. with a maximum of 10-20 mg. the only viable option for thrombolysis in the United States continues to be tPA. to block the platelet function and rethrombosis has shown an overall reocclusion rate of approximately 30%. 27. Results showed a better outcome in treated patients. however. patients with quadriplegia and/or coma have demonstrated the least favorable outcomes.[8. intraarterial thrombolysis for vertebrobasilar occlusion has not been studied systematically in randomized. prourokinase and tPA seem to have more selectivity for thrombi. Results from a trial using low–molecular weight heparin intravenously in patients with acute stroke. it is apparent that recanalization improves outcome. randomized fashion. The patient's condition at presentation appears to be the major prognostic factor. although negative overall.10. Angioplasty Angioplasty has been performed to treat patients with atherosclerotic basilar artery stenosis. is not yet known.3 mg/kg. such as abciximab. despite its 4.5 hours after a stroke. The use of angioplasty is based on the tendency of thrombosis to occur in stenosed arterial segments. Nenci and colleagues reported the first 4 cases of local thrombolysis for vertebrobasilar occlusion. 24] In 2009. Prourokinase was tested in a prospective. Because of concerns with its production. within that time period. establishing a trend to treat patients with intra-arterial erv iew#aw2aab6c20 13/19 . The published case series report a morbidity rate of 0-16% and a mortality rate of up to 33%. The average time to treatment has ranged from 8-48 hours. The eligibility criteria for treatment between 3 and 4. tPA). Other Treatment Other aspects of treatment for vertebrobasilar stroke should include the following: Aggressive pulmonary toilet to prevent mucous congestion and pneumonia Prevention of aspiration pneumonitis Early establishment of bowel and bladder programs emedicine. although this change has not been approved by the FDA. Despite the above efforts. as established in the AHA/ASA's 2007 guidelines. the role of angioplasty in the treatment of vertebrobasilar occlusion is not well defined.2012 Vertebrobasilar Stroke patients. including only patients with middle cerebral artery stem occlusion. the effectiveness of tPA administration in comparison with other treatments for thrombosis.

due to a high prevalence of vestibular and cerebellar involvement in vertebrobasilar strokes. Prior to a discussion of the specific therapy disciplines. the severity of the deficits makes ambulation impossible. of appropriate precautions. with resultant multisystem dysfunction ( iew#aw2aab6c20 A premorbid vestibular status determination is of great 14/19 . swallowing function. acute rehabilitation. emedicine. dysphagia. dysarthria. ataxia. Nursing staff always should involve family members in the care of a person who has sustained a stroke. subcutaneous heparin. Nursing issues A wide variation in symptoms may be seen with stroke. depending on the severity of the brain damage. and wheelchair mobility. which will allow them to participate in full PT and OT activities. patients should be mobilized out of bed and should be actively involved in physical and occupational therapy. The patient and family members may be unfamiliar with stroke and its effects. If the upper extremity is flaccid or paretic.2012 Vertebrobasilar Stroke Monitoring of skin and all indwelling catheters for signs of infection Control of body temperature (fever may worsen the outcome in stroke patients) Tight blood glucose control Heel protectors or L'Nard Multi Podus boots with regular skin inspection for breakdown/decubitus Deep vein thrombosis prophylaxis with sequential compression devices or arteriovenous pumps and/or anticoagulants (eg. Patients often need extensive balance and gait training. balance. They often require ongoing. establishing a bowel and bladder program. adjusted-dose. low–molecular weight heparin. precautions are necessary with activities that can be undertaken until the symptoms have stabilized. nurses often are the first to suggest initiation of therapy services. because they have the most extensive involvement with the patient. The rehabilitation and planning are performed best in a multidisciplinary and interdisciplinary setting. Positioning in bed and in a chair assures the patient's comfort and prevents complications from skin breakdown. Other important nursing issues include communication with the treating clinician in order to initiate therapy services for the assessment of ambulation. with attention paid to specific patient issues and the formulation of short-term and long-term care plans. Vestibular evaluation and training are very important. positioning is critical to the prevention of shoulder subluxation and pain from shoulder-hand syndrome. Some patients have fluctuating symptoms and signs. and of continuing therapy upon discharge to home. Evaluation always should begin with a detailederv and focused history. provided that there are no contraindications Further inpatient care Most patients with vertebrobasilar stroke have a significant degree of disability. and ensuring the person's safety from injury. Physicians and nurses play crucial roles on the rehabilitation team. warfarin).11. and the performance of activities of daily living (ADL). Once the symptoms have stabilized. transfers. patients should be mobilized out of bed. transfers.10. depending on the condition of the patient. maintaining nutrition. address nursing issues in the care of patients with vertebrobasilar stroke. Education must be provided to make the patient and his/her family members aware of the importance of continuing with activities. due to involvement of the brainstem and cerebellum. Physical therapy (PT) and occupational therapy (OT) should be initiated soon after admission. Physical therapy The physical therapist is responsible for retraining of gross motor skills. Because of this possibility. Training of the patient and family members in the use of lower extremity orthotics may be necessary to provide for functional mobility. however. cranial neuropathies).medscape. The physical therapist also develops a PT program and instructs the patient in general strengthening and range of motion. which often are related to position. bed mobility. Initial nursing intervention involves maintaining skin integrity. gaze abnormalities. In some patients. Rehabilitation After Vertebrobasilar Artery Stroke Rehabilitation services have been shown to play a critical role in recovery from acute stroke. quadriplegia or hemiplegia. The physical or occupational therapist may be involved with assessing the patient for the proper wheelchair and seating system. such as gait.

Patients move into the provoking position 2-3 times during each session. grooming). Surface electromyography is used in training a patient to perform maneuvers that compensate for the weak swallow. These include adaptation. modification of bolus consistency. Further clinical testing may include the following: Oculomotor examination . due to several possible mechanisms. The patient's vocalization and possible reading. sharpened Romberg. Substitution for the loss of function by the remaining intact visual and somatosensory systems is used in treating patients with bilateral vestibular lesions (complete or partial loss of both labyrinths).Visual tracking.2012 Vertebrobasilar Stroke should begin with a detailed and focused history.Thorough gait assessment. speech and language skills. bathing. The Mendelsohn maneuver. and vestibulo-ocular reflex (VOR) Positional testing . Increased pooling of a bolus in the vallecula and/or pyriform sinuses. Interventions for the prevention of aspiration include compensatory strategies. the brain modulates the gain of the vestibular response. swallowing assessment. for example. dressing. Habituation for postural vertigo results in decreased response to repeated provoking stimuli. Alternating eye patches or prisms can help diplopia. including head turning. and single leg stance (each test is performed on even and uneven surfaces. Occupational therapy OT is used for retraining fine motor skills that are needed to perform ADL (eg. General conditioning also is incorporated into the overall rehabilitation plan. because dizziness is the third most frequent complaint during physician visits from patients aged 65 years and the most frequent complaint from patients aged 75 years and older. The speech and language therapist often performs the initial swallowing evaluation and determines the risk for aspiration and the consistency of the patient's diet. tandem gait.10. Epley maneuver) are used for positional vertigo. upper extremity orthotics. habituation. the cricopharyngeus muscle may fail to open erv iew#aw2aab6c20 . convergence/divergence. negotiating obstacles. Repositioning maneuvers (eg. delivery). resulting in an impaired passage of the bolus from the pharynx to the esophagus. and turning An exercise-based approach has been successful in the treatment of vestibular disorders. OT also is involved in general strengthening. substitution. and processing deficits also are addressed. and repeat these sessions 3-5 times per day. with eyes open and closed) Dynamic balance . safety skills. attempting to correct for a retinal slip (error signal) caused by the decreased gain of the VOR. Surface electromyography biofeedback for dysphagia has shown promising results. volume. resulting in further widening of the opening of the cricopharyngeus muscle and easier emedicine. and the evaluation of needs for adaptive equipment.medscape.11. encouraging an increase in the performance of ADL as tolerated. static/dynamic visual acuity. writing. Evaluation of these patients should be thorough and should include a videofluoroscopy with a modified barium swallow to assess for silent aspiration. wheelchair mobility. spontaneous and gaze-evoked nystagmus. With adaptation by the central vestibular system. The VOR training strategy includes focusing on a stationary or moving target while rotating the head. retro walking. In patients with dysphagia from brainstem lesions. and repositioning. as well as in family training and cognitive retraining for safety and ADL.Romberg. A premorbid vestibular status determination is of great importance. as well as for improving hand and arm function. which spills into the airway. poses a significant risk for aspiration and pneumonia. such as oromotor exercises and postural changes while swallowing. as well as facilitative strategies (eg. saccades and smooth pursuit movement. and family training.Hallpike-Dix maneuver Static balance . requires voluntary maintenance of the thyroid cartilage in an elevated position for a few seconds. Speech therapy Speech therapy (ST) is used for cognitive retraining. resulting in a retinal slip that facilitates adaptation. based on the mechanical displacement of the debris from the affected canal(s) by a series of head movements.

Patients with a definite cardioembolic source. should be treated with warfarin to maintain an international normalized ratio of 2-3. The patient observes the plateau (as opposed to the peak) of the generated waveform on the screen. pain. and social issues). the social services representative may be a licensed social worker or may instead be someone with a more limited background. such as atrial fibrillation. the risk of recurrent stroke is 10-15%. including the physiatrist. functional gains. although neither completely eliminates the aspiration risk.11. Other consultations In addition to consultations with physical. If the swallowing abnormalities are so severe that recovery is expected to take weeks or months. memory. The patient requires continued reassessment of various factors (eg. for that matter. spasticity management. mood. Depending on the setting. Prevention of recurrent stroke Strict risk factor control is important to decrease the risk of stroke recurrence.medscape. and continue with the outpatient rehabilitation program. vocational needs. psychological status. and speech therapists. neurologist. or processing deficits. the social worker usually is not licensed or certified. consultation with a neuropsychologist and a social services worker may also be required in the management of patients with vertebrobasilar stroke. All of these may affect future participation in and compliance with rehabilitation. Recreational therapy The recreational therapist should concentrate on finding alternative recreational activities for patients who are unable to perform at their premorbid level. and other specialists.[32] If approved for use. a nasogastric or nasoduodenal tube should be placed. Evaluation by a neuropsychologist is recommended to screen for depression. For symptomatic patients who survive. occupational. bowel and bladder function.10. family dysfunction.2012 Vertebrobasilar Stroke position for a few seconds. The social services department is responsible for coordinating intake and planning discharge. Home health agencies typically employ licensed social erv iew#aw2aab6c20 16/19 . Treatment of patients with basilar artery stenosis and. skin care. The ongoing warfarin-aspirin trial for symptomatic intracranial disease will provide valuable information in that regard. Engaging in these activities provides a creative outlet and a positive emotional gain that potentially enhance the patient's psychological recovery. reinforcing the concept of muscle activation in the desired position (thyroid cartilage elevation). home and other modifications. the potential of such drugs in the arena of stroke treatment is significant. coping skills. emedicine. Survivors usually are left with significant neurologic deficit. vertebral artery stenosis is less clear. Follow-up After Vertebrobasilar Stroke Patients should follow up with the primary care provider. Prognosis Patients with acute basilar artery occlusion have a mortality rate of more than 85%. then a gastrostomy tube should be placed either surgically or percutaneously. the need for further equipment. Retrospective evidence suggests that warfarin is better than aspirin for the prevention of stroke recurrence in patients with greater than 50% basilar artery stenosis. and subtle cognitive. The patient should be on a nothing-by-mouth restriction until the swallowing mechanism has been assessed and cleared and the airway has been protected. Several oral anticoagulant medications are in various stages of clinical trials for the prophylaxis of ischemic thromboembolic stroke. If there is a high risk of aspiration.[31] Prevention strategies depend on the primary cause of the stroke. resulting in further widening of the opening of the cricopharyngeus muscle and easier passage of the food bolus through to the esophagus. but in nursing homes.

Catholic Medical Association. Professor. Erdman Professor of Rehabilitation. American Osteopathic College of Physical Medicine and Rehabilitation. MD. DO. Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital Milton J Klein. Canadian Medical Association. MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist. Loma Linda University School of Medicine Murray E Brandstater. see the Stroke Center. Department of Physical Medicine and Rehabilitation. Specialty Editor Board Milton J Klein. and Consortium of Multiple Sclerosis Centers emedicine. as well as Stroke. Chief Editor Denise I Campagnolo. American Congress of Rehabilitation Medicine. Departments of Neurology and Psychiatry. Coauthor(s) Murray E Brandstater. University of Pennsylvania School of Medicine Richard erv iew#aw2aab6c20 17/19 . MD is a member of the following medical societies: American Academy of Anti-Aging Medicine. MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians. and Pennsylvania Medical Society Disclosure: Nothing to disclose. Investigator for Barrow Neurology Clinics. St Joseph's Hospital and Medical Center. American Osteopathic Association.medscape. MS is a member of the following medical societies: Alpha Omega Alpha. American College of Physician Executives. American Academy of Physical Medicine and Rehabilitation. MBBS. American Association of Neuromuscular and Electrodiagnostic Medicine. California Society of Physical Medicine and Rehabilitation. Director. MBA Consulting Physiatrist. American Medical Association. University of Nebraska Medical Center College of Pharmacy. MD is a member of the following medical societies: American Academy of Pain Medicine. Barrow Neurology Clinics. PharmD. Francisco Talavera. PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation. and American Paraplegia Society Disclosure: Nothing to disclose. American Paraplegia Society.10.11. Department of Physical Medicine and Rehabilitation. NARCOMS Project for Consortium of MS Centers Denise I Campagnolo. American Pain Society. American Association of Neuromuscular and Electrodiagnostic Medicine. MD Chairman. Hoag Hospital Vladimir Kaye. MD. and Royal College of Physicians and Surgeons of the United States Disclosure: Nothing to disclose. PhD Chairman and Program Director. and North American Spine Society Disclosure: Nothing to disclose. Association for Academic Psychiatry. DO.2012 Vertebrobasilar Stroke Patient Education For patient education information. eMedicine Disclosure: eMedicine Salary Employment Richard Salcido. Canadian Society of Clinical Neurophysiologists. American Medical Association. American Academy of Physical Medicine and Rehabilitation. MD Consulting Staff. Canadian Association of Physical Medicine and Rehabilitation. Senior Pharmacy Editor. Royal College of Physicians and Surgeons of Canada. National Stroke Association. American Medical Association. American Academy of Osteopathy. Association of Academic Physiatrists. PhD Adjunct Assistant Professor. American Academy of Medical Acupuncture. MBBS. American Academy of Physical Medicine and Rehabilitation. Contributor Information and Disclosures Author Vladimir Kaye. Ontario Medical Association.

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