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Vertebrobasilar Stroke Overview of VertebrobasilarStroke

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 occipitalcortex. Occlusion of large vessels in this system usually leads to major disability or death. Vertebrobasilar strokecarries a mortality rate of more than 85%. Because of involvement of the brainstem and cerebellum, most survivorshave 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 anddiscrete. The clinical correlates of these smaller lesions consist of a variety of focal neurologic deficits, dependingon their location within the brainstem. Patients with small lesions usually have a benign prognosis with reasonablefunctional 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.)

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Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex. (Courtesy of BC Decker Inc.)

Visceral motor component of CN III and pathw ays involved in pupillary constriction. (Courtesy of BC Decker Inc.)

Note the horizontal eye movement. Also note a topographic relationship of the center for vertical gaze. (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, including the following[1] :

When cranial nerves or their nuclei are involved, the corresponding clinical signs are ipsilateral to the lesionand the corticospinal signs are crossed, involving the opposite arm and legCerebellar signs (eg, dysmetria, ataxia) are frequent

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Involvement of the ascending sensory pathways may affect the spinothalamic pathway or the mediallemniscus (dorsal columns), resulting in dissociated sensory loss (ie, loss of 1 sensory modality on oneside and preservation of other sensory modalities in the opposite limbs)Dysarthria and dysphagia typically are presentVertigo, nausea, and vomiting, along with nystagmus, represent involvement of the vestibular systemUnilateral Horner syndrome occurs with brainstem lesionsOccipital lobe lesions result in visual field loss or visuospatial deficitsCortical deficits, such as aphasia and cognitive impairments, are absent

Anatomy of the Vertebral and Basilar Arteries

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

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

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

At the base of the brain, the carotid and basilar systems join to form a circle of large, communicating arteriesknown as the circle of Willis. Because of this arrangement of collateral vessels, even when one of the main

arteries is occluded, adequate perfusion of the brain still may be possible.[2]

Pathophysiology of Vertebrobasilar Stroke

The most common vascular condition affecting the vertebrobasilar system is atherosclerosis, in which plaquescause narrowing and occlusion of the large vessels.

The pathology of small vessel disease (affecting arteries 50-200 µm in diameter) is different from that ofatherosclerosis, because the small vessels become occluded by a process called lipohyalinosis, which frequentlyoccurs in association with hypertension. Occlusions of these small vessels lead to small, round infarctions calledlacunes, which may appear as single lesions or may be distributed as multiple lesions scattered widely throughoutthe subcortex and brainstem.

Lipohyalinosis weakens the vessel wall, and in hypertensive individuals, rupture of the artery may occur, resultingin a focal hemorrhage. Almost all intracerebral hemorrhages originate from the rupture of these small, penetratingvessels.

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

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

Etiology of Vertebrobasilar Stroke

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

Increasing ageFamily history

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RacePrior history of strokeHypertensionCoronary artery diseaseDiabetes mellitusCigarette smokingHeart diseaseObesityPhysical inactivityDrug or alcohol abuse

Epidemiology of Vertebrobasilar Stroke

The frequency, incidence, and prevalence of the vertebrobasilar syndromes vary, depending on the specific areaand syndrome involved. Approximately 80-85% of all strokes are ischemic, and 20% of the lesions producingischemic strokes occur in the vertebrobasilar system.

Overall, hemorrhage causes 15-20% of strokes. Although most intracerebral hemorrhages occur in the region ofthe putamen and thalamus, about 7% of all hemorrhagic lesions involve the cerebellum in the area of the dentatenucleus, and approximately 6% of hemorrhagic lesions involve the pons.

In most of the reported series, mortality patients with basilar artery occlusion has been consistently greater than

75-80%.[3] Most survivors of basilar artery occlusion have severe, persisting disability.

Clinical Presentation in Vertebrobasilar Stroke

Patient History

The onset and duration of symptoms in vertebrobasilar stroke depends, in large part, upon the etiology. Patientswith basilar artery thrombosis typically have a waxing and waning course of symptoms, with as many as 50% ofpatients experiencing transient ischemic attacks for several days to weeks prior to the occlusion.

In contrast, embolic events are sudden, without prodrome or warning, with acute and dramatic presentation.

Commonly reported symptoms associated with vertebrobasilar strokes include the following[1] :

VertigoNausea and vomitingHeadacheAbnormalities in the level of consciousnessAbnormal oculomotor signs (eg, nystagmus, lateral gaze abnormalities, diplopia, pupillary changes)Ipsilateral cranial nerve weakness (eg, dysarthria, dysphagia, dysphonia, weakness of facial muscles andtongue)Sensory loss (in the face and scalp)AtaxiaContralateral motor weakness (eg, hemiparesis, quadriparesis)Pain and temperature lossIncontinenceVisual-field defectsPresence of central painAbnormal swellingSweating in the face or extremities

Physical Examination

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

Oculomotor signs usually reflect the involvement of the abducens nucleus; the horizontal gaze center located inthe pontine paramedian reticular formation (PPRF), contiguous to the abducens nucleus; and/or the medial

longitudinal fasciculus (MLF). Lesions to these structures result in ipsilateral lateral gaze or conjugate gaze palsy.

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longitudinal fasciculus (MLF). Lesions to these structures result in ipsilateral lateral gaze or conjugate gaze palsy.

See the images below.

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

Center for vertical gaze and pathw ays involved in vertical eye movement (Courtesy of Cranial Nerves--Anatomy and Clinical Comments.

BC Decker Inc; Toronto. 1988)

Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex. (Courtesy of BC Decker Inc.)

Vestibular reflex illustrating horizontal eye movements only. (Courtesy of BC Decker Inc.)

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Visceral motor component of CN III and pathw ays involved in pupillary constriction. (Courtesy of BC Decker Inc.)

Ocular bobbing is described as a brisk, downward movement of the eyeball with a subsequent return to theprimary position. This deficit localizes the lesion to the pons. Other reported signs of pontine ischemia includeataxia and tremor associated with mild hemiparesis. The signs described can occur in different combinations,presenting a diagnostic challenge in lesion localization.

Certain constellations of findings may serve as clues to the location of the lesion, including the followingexamples:

Midbrain syndromes - cranial nerve (CN) III lesion and vertical gaze palsyPontine syndromes - CN VI lesion, horizontal gaze palsy, and VII nerve palsyMedullary syndromes - ipsilateral facial pain and temperature loss, Horner syndrome, ipsilateral ataxia,contralateral loss of pain and temperature sensation, and ipsilateral paralysis of the tongue, soft palate,vocal cord, or sternocleidomastoid [SCM] musclePosterior cerebral artery - contralateral hemianopia with macular sparing

Complications

Potential complications of vertebrobasilar stroke include the following:

Aspiration pneumoniaDeep venous thrombosisPulmonary embolismMyocardial infarction

Vertebrobasilar Artery Stroke Syndromes

A variety of specific neurologic syndromes[4] have been described in vertebrobasilar artery stroke, based onconstellations of findings. Some examples are as follows:

Lateral medullary (Wallenberg) syndromeMedial medullary (Dejerine) syndromeCerebellar infarctionLocked-in syndromeTop-of-the-basilar syndromeInternuclear ophthalmoplegiaOne-and-a-half syndromeVentral pontine (Millard-Gubler) syndromeUpper dorsal pontine (Raymond-Cestan) syndromeUpper dorsal pontine (Raymond-Cestan) syndromeLower dorsal pontine (Foville) syndromeVentral midbrain (Weber) syndromeDorsal midbrain (Benedikt) syndromePosterior Cerebral Artery occlusion

Lateral medullary (Wallenberg) syndrome

This syndrome is most often due to vertebral artery occlusion or, less commonly, to posterior inferior cerebellar

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artery (PICA) occlusion. Patients present with nausea, vomiting, and vertigo from involvement of the vestibularsystem.

Ipsilateral clinical features include the following:

Ataxia and dysmetria, due to damage to the inferior cerebellar peduncle and cerebellumHorner syndrome (eg, ptosis, miosis, hypohidrosis or anhidrosis, enophthalmos), due to damage todescending sympathetic fibersFacial pain and temperature lossReduced corneal reflex, from damage to the descending spinal tract and nucleus of CN VNystagmusHypoacusis (cochlear nucleus)DysarthriaDysphagiaParalysis of the pharynx, palate, and vocal cordLoss 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, indicatinginvolvement of the anterior spinothalamic tract. Other findings include tachycardia and dyspnea (dorsal nucleus ofCN X) and palatal myoclonus, a rhythmic involuntary jerking movement of the soft palate, pharyngeal muscles, anddiaphragm. Palatal myoclonus sometimes follows infarction of the dentate nucleus of the cerebellum and inferioroliva.

The prognosis of patients with the lateral medullary syndrome usually is quite good for functional outcome;however, patients may die in the acute phase from aspiration pneumonia, and death has been reported from sleepapnea in a number of cases.

Medial medullary (Dejerine) syndrome

This syndrome is an uncommon lesion resulting from occlusion of a vertebral artery or its branch to the anteriorspinal artery; it involves the pyramid, the medial lemniscus, and, sometimes, the hypoglossal nerve.

The clinical features include ipsilateral paresis of the tongue with deviation toward the lesion (lower motor neuronlesion of CN XII), contralateral hemiplegia with sparing of the face (corticospinal tract), and loss of ipsilateralvibration and proprioception (medial lemniscus). (See the image below.)

LMN Lesion of the hypoglossal nerve producing tongue deviation to the side of the lesion. (Courtesy of BC Decker Inc.)

Cerebellar infarction

A stroke involving the cerebellum may result in a lack of coordination, clumsiness, intention tremor, ataxia,dysarthria, scanning speech, and even difficulties with memory and motor planning. Early diagnosis of cerebellarinfarctions is important, because swelling may cause brainstem compression or hydrocephalus.

Locked-in syndrome

This dramatic clinical syndrome occurs when there is an infarction of the upper ventral pons. Locked-in syndromecan result from occlusion of the proximal and middle segments of the basilar artery or from hemorrhage involvingthat region. It can also be caused by trauma, central pontine myelinolysis, encephalitis, or a tumor.

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Bilateral ventral pontine lesions involving corticospinal and corticobulbar tracts lead to quadriplegia. The patient isunable to speak, to produce facial movement (damage to the corticobulbar tracts), or to look to either side(horizontal eye movement is impaired due to a lesion of bilateral CN VI nuclei). Because the tegmentum of thepons is spared, the patient's consciousness is preserved, with the patient fully awake, sensate, and aware. Theonly movements preserved are vertical eye movements and blinking. The patient is paralyzed completely andcommunicates only by blinking. Some recovery of facial muscle movement and horizontal gaze may occur withtime or in an incomplete form of this syndrome.

Coma may occur with bilateral involvement of the pontine tegmentum or with lesions of the midbrain reticularformation. Coma generally is associated with oculomotor abnormalities, and motor abnormalities may be present.A comatose patient is unresponsive, and the coma may be prolonged when it is due to basilar artery occlusion.Sleep-wake cycles are absent in patients with coma.

Top-of-the-basilar syndrome

This syndrome is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the

rostral basilar artery; the occlusion usually results from an embolism.[5] Varying degrees of involvement of themidbrain, thalamus, and portions of the temporal and occipital lobes may occur and can produce severe disability.

Patients present with sudden changes in the level of consciousness, confusion, amnesia, and visual symptoms(eg, hemianopia, cortical blindness, abnormal color vision/color dysnomia). These patients can also demonstrateoculomotor abnormalities, most commonly of the vertical gaze, such as gaze palsy, skew deviation, convergencespasm resulting in pseudoabducens palsy, or convergence-retraction nystagmus.

CN III palsy and pupillary abnormalities, including small pupils with decreased light reactivity (diencephalic),large/mid-position and fixed pupils (midbrain), and ectopic or oval pupils, also are frequent.

Other abnormalities include varying degrees of weakness, sensory deficits, or posturing.

Internuclear ophthalmoplegia

Clinically, internuclear ophthalmoplegia (INO) is a horizontal gaze palsy; it results from a brainstem lesion affectingthe MLF between the nuclei of CN VI and III, most commonly in the pons. (See the image below.)

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

When a patient with a lesion in the right MLF attempts to look to his/her left (ie, away from the involved side),he/she shows no adduction of the right eye and full abduction of the left eye with the end-point abductionnystagmus.

By the same logic, in the case of bilateral INO, there is no adduction to either side with nystagmus of theabducting eye in both directions. Convergence is preserved, because the nuclei of CN III and peripheral innervationof the medial recti muscles are intact.

Because horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI (relative tothe lesion), disruption of the communication pathway (ie, the MLF) between the nuclei of CN III (in the midbrain)and CN VI (in the pons) results in the inability of the eye ipsilateral to the lesion to adduct and the contralateraleye to exhibit abduction nystagmus when looking away from the involved side.

In elderly patients, INO is caused most often by occlusion of the basilar artery or its paramedian branches. Inyounger adults, it may occur due to multiple sclerosis (MS), commonly with bilateral involvement.

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One-and-a-half syndrome

This syndrome is caused by a lesion affecting the PPRF and MLF simultaneously, resulting in ipsilateral

conjugate gaze palsy and INO[6] A patient with this syndrome is completely unable to move the ipsilateral eye,and is able only to abduct the contralateral eye, with resulting nystagmus; the ‘one’ in the syndrome name refersto the former, and the ‘half’ to the latter.

The patient with a lesion in the ipsilateral PPRF or abducens nucleus and MLF connecting to the contralateral CNVI exhibits horizontal gaze palsy when looking toward the side of the lesion and exhibits INO when looking awayfrom the side of the lesion. Associated features may include vertical nystagmus, exotropia of the contralateral eye,and skew deviation. Vertical gaze and convergence generally are preserved.

Ventral pontine (Millard-Gubler) syndrome

This syndrome occurs after paramedian infarction in the pons and results in ipsilateral lateral rectus palsy (CN VI)with diplopia, complete facial paresis (unilateral CN VII palsy), and contralateral hemiparesis/hemiplegia(corticospinal tract involvement) with sparing of the face.

Upper dorsal pontine (Raymond-Cestan) syndrome

This syndrome is due to obstruction of flow in the long circumferential branches of the basilar artery. Thisocclusion results in ipsilateral ataxia and coarse intention tremor (indicating involvement of the superior and middlecerebellar peduncles), weakness of mastication and sensory loss in the face (suggesting sensory and motortrigeminal nuclei and tracts), and contralateral loss of all sensory modalities (due to damage to medial lemniscusand spinothalamic tract) with or without facial weakness and hemiparesis (corticospinal tract).

Horizontal gaze palsy also may occur.

Lower dorsal pontine (Foville) syndrome

This syndrome may result from lesions to the dorsal tegmentum of the lower pons. The patient exhibits ipsilateralparesis of the whole face (nucleus and fibers of CN VII), horizontal gaze palsy on the ipsilateral side (ie, PPRFwith or without CN VI nucleus), and contralateral hemiplegia (corticospinal tract) with sparing of the face.

Ventral midbrain (Weber) syndrome

Weber syndrome occurs with an occlusion of the median and/or paramedian perforating branches of the basilarartery. Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (ie, damage toparasympathetic fibers of CN III) with contralateral hemiplegia. Weakness of the lower face (corticospinal andcorticobulbar tracts) may be noted.

Dorsal midbrain (Benedikt) syndrome

This syndrome is due to a lesion in the midbrain tegmentum resulting from occlusion of paramedian branches ofthe basilar artery, the PCA, or both.

The patient demonstrates ipsilateral oculomotor palsy, ptosis, and mydriasis (as in Weber syndrome), along withthe contralateral involuntary movements, such as those of intention tremor, ataxia, or chorea (due to theinvolvement of the red nucleus).

Posterior cerebral artery occlusion

The most common finding is occipital lobe infarction leading to contralateral hemianopia with macular sparing.Clinical symptoms associated with occlusion of the PCA vary depending on the location of the occlusion and mayinclude the thalamic syndrome, thalamic perforate syndrome, Weber syndrome, cortical blindness, colorblindness, failure to see to-and-fro movements, verbal dyslexia, and hallucinations.

Diagnostic Considerations

The differential diagnosis of vertebrobasilar stroke includes the following:

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Central pontine myelinolysisMetastatic disease of the brainSubarachnoid hemorrhageBasilar meningitisBasilar migraineCerebellopontine angle tumorsSupratentorial hemispheric mass lesions with mass effect, herniation, and brainstem compression

Laboratory Studies for Vertebrobasilar Artery Stroke

The laboratory workup should include the following:

Complete blood count (CBC)ElectrolytesBlood urea nitrogen (BUN) and creatinineProthrombin time and activated partial thromboplastin time (aPTT)Cholesterol levelLipid profile

Patients who are younger than 45 years or who have no evidence of atherosclerosis should be investigated for thepresence of hypercoagulable states, such as the following:

Lupus anticoagulant and anticardiolipin antibodiesProtein C, protein S, and antithrombin III deficienciesFactor V Leiden mutation

Creatine kinase, cardiac isoenzymes, and troponin level should be tested in the following persons:

All patients with suggestive symptoms (eg, chest pain)Patients with evidence of ischemic changes in the electrocardiogram (ECG; because of the high incidence

of concomitant coronary artery disease)[7]

Computed Tomography

CT scanning usually is the first imaging study performed, 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.[8, 9] Other helpfulfindings 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]

Spiral CT angiography is used further to identify occluded and dolichoectatic vessels.[11, 12]

The disadvantages of CT scanning include a low sensitivity for early ischemia and the presence of significantartifacts caused by the bony structures surrounding the brainstem and cerebellum.

Magnetic Resonance Imaging

MRI is more sensitive than CT in the identification of ischemia (since bone does not degrade the image). Newertechniques, including flow suppression and the production of diffusion-weighted and perfusion-weighted images,make MRI a very powerful tool for the exclusion of intraparenchymal hemorrhage or edema and for the identification

of early and potentially reversible ischemia.[8, 9, 13, 14, 15]

MRI and magnetic resonance angiography (MRA) are very helpful in finding occult lesions, such as demyelinating

plaques, tumors, vertebrobasilar dolichoectasia, or dissection.[16, 17, 18] MRA has a sensitivity of up to 97% and aspecificity of up to 98% when used to identify vertebrobasilar occlusion.

A limitation of MRA is its tendency to overestimate the degree of stenosis. This overestimation occurs becausethe production of a vessel's image in MRA is a based on a flow-related phenomenon; hence, the presence ofsevere stenosis with significant flow compromise may result in poor visualization of a vessel and cause the MRAimage to resemble vascular occlusion.

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Angiography

While the role of cerebral (catheter) angiography has changed due to the availability of noninvasive imagingmodalities (eg, MRI, MRA, TCD), it still is considered the criterion standard for imaging. Catheter cerebralangiography is performed in the following circumstances:

The patient has an absolute contraindication to MRA (eg, a pacemaker, metallic implant)The quality of noninvasive studies is not satisfactoryThe results of noninvasive studies do not explain the clinical findings

Angiography should be considered a first-line diagnostic test after a CT scan, once it has been decided thatrecanalization with thrombolysis should be completed. The most important goal of the workup is to establish thetype of vascular lesion and the mechanism of the stroke.

Ultrasonography

Transcranial Doppler (TCD) is used in the evaluation of cerebrovascular disease, but it often is inaccurate.Absence of signal in an initial examination does not necessarily mean occlusion.

TCD is helpful for purposes of follow-up once an initial evaluation has demonstrated the lesion. TCD has a

sensitivity of 72% and a specificity of 94% in patients with basilar artery disease.[19]

Electrocardiography

Electrocardiography should be performed in all patients on initial evaluation. All patients should be monitoredcontinuously for the first few days. Ischemic changes in the ECG should be investigated further with assays ofserum creatine kinase, cardiac isoenzymes, and troponin, for reasons that include the following:

Up to 20% of patients with acute stroke have an arrhythmiaMyocardial infarction occurs in 2-3% of patientsThe presence of arrhythmias (eg, atrial fibrillation) has an impact on long-term patient management relatedto stroke prevention

Echocardiography

Echocardiography[20] should be considered in the following patients:

Those younger than 45 yearsThose with explained basilar artery occlusion

Findings that may affect management include valvular disorders, vegetations, intramural or extramural thrombi,ventricular aneurisms, cardiac tumors (myxoma), right-to-left shunts, and poor ejection fraction.

Treatment of Acute Vertebrobasilar Artery Stroke

Ideally, all patients who have suffered a vertebrobasilar stroke should be admitted to a unit specializing in the careof stroke patients. Admission to a neurologic intensive care unit (ICU) is indicated for patients who are candidates

for interventional therapies (eg, thrombolysis) or who have any of the following[21] :

Unstable or fluctuating neurologic symptomsDecreased level of consciousnessHemodynamic instabilityActive cardiac or respiratory problems

Hemodynamic management

Hemodynamic management should be aimed at minimizing the ischemic injury. Cerebral ischemia impairs thebrain’s ability to autoregulate its circulation through vasoconstriction and vasodilatation. Therefore, under ischemic

conditions, the cerebral blood flow becomes blood pressure–dependent.[22] An increase in the mean arterialpressure (MAP) results in vasoconstriction. This response limits the perfusion pressure and the blood volume. A

decrease in the MAP results in vasodilatation.

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decrease in the MAP results in vasodilatation.

In normotensive patients, the limits of autoregulation are within the range of 50-150 mm Hg of the MAP. In chronichypertensive patients, the curve of autoregulation is shifted upward. In the patients with severe cerebral vascularocclusive disease, the MAP and the cerebral perfusion pressure (CPP) become critical in maintaining the cerebralblood flow. CPP is equal to MAP less intracranial pressure (ICP) (ie, CPP = MAP-ICP). Therefore, overzealoustreatment of hypertension should be avoided, because it can decrease the cerebral perfusion pressure andexacerbate the ongoing ischemia.

No existing information from randomized trials indicates whether treating hypertension is better than not treating it.Based on evidence from experimental models and on data from clinical experience, hypertension should not betreated unless there is evidence of end-organ damage, such as hypertensive encephalopathy, unstable angina,acute myocardial infarction, heart failure, or acute renal failure.

Hypertension should be treated when the diastolic blood pressure is greater than 120 mm Hg or when the systolicblood pressure is over 200 mm Hg. Otherwise, when thrombolysis is a strong consideration, the treatmentparameters become 110 mm Hg or more for diastolic blood pressure or greater than 180 mm Hg for systolic bloodpressure.

Commonly used antihypertensives are labetalol and nitroprusside. When diastolic blood pressure is greater than140 mm Hg, nitroprusside is the preferred drug, provided that no contraindications exist.

Patients with hypotension need to be treated to optimize the MAP and, consequently, the blood pressure–dependent cerebral blood flow. Maximal effort should be made to maintain a normal intravascular volume usingisotonic solutions. If the MAP continues to be low despite fluid management, vasopressors, such as dopamine,dobutamine, and phenylephrine, should be used.

In patients with unknown intravascular volume status or those with complications, such as congestive heart failureand pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure andthe pulmonary capillary wedge pressure. This approach would improve monitoring of the intravascular volume toavoid overload.

Respiratory management

Early assessment and management of the airway are critical due to the frequent involvement of lower cranialnerves and the impairment of consciousness in patients with brainstem ischemia. Assessment of the respiratorydrive, gag reflex, and ability to handle secretions with a forceful cough also is of great importance.

Endotracheal intubation may be considered in patients with a decreased level of consciousness and a Glasgowcoma score of less than 8. Of the mechanical ventilation modes, pressure support ventilation (PSV) andsynchronized intermittent mandatory ventilation are used most often. For patients with good respiratory drive, themost comfortable mode is PSV. In this mode, the ventilator does not deliver a set of breaths but provides enoughpressure support to maintain the desired tidal volume, usually in the range of 5-8 mL/kg. Most patients with nopulmonary comorbidities reach this goal with a PSV of 5-10.

For patients with poor respiratory drive, synchronized intermittent mandatory ventilation may be a better mode.This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with thepatient's inspiratory effort while allowing the patient to take extra breaths. Adding PSV during the extra breathscan minimize the patient's respiratory effort when taking them.

Sedation and paralysis should be avoided, because they may obscure the neurologic assessment. Circumstancesmay exist that require the use of sedation and paralysis (eg, neurogenic hyperventilation) to avoid hypocarbia andworsening of the ischemic process.

Thrombolysis

In 1996, 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.[8] Approval was based on data from theNational Institute of Neurological Disorders and Stroke trial, which showed that a higher number of treated versusuntreated patients had minimal deficit and minimal or no disability.

However, this trial did not include patients in stupor or coma, and that criterion probably excluded patients whosuffered a basilar artery occlusion. Moreover, the trial did not study the vascular anatomy systematically in all

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patients. From experimental evidence and thrombolytic trials, it is apparent that recanalization improves

outcome.[3, 23, 24]

In 2009, the American Heart Association/American Stroke Association (AHA/ASA) published a science advisoryrecommending that the time window for tPA administration be increased to 4.5 hours after a stroke, although this

change has not been approved by the FDA.[25] Research indicates that tPA is effective in patients even when

administered within the 3- to 4.5-hour window,[26, 27, 28] but the AHA/ASA stated that, despite itsrecommendation, the effectiveness of tPA administration in comparison with other treatments for thrombosis,within that time period, is not yet known.

The eligibility criteria for treatment between 3 and 4.5 hours are similar to those employed for treatment prior to 3

hours, as established in the AHA/ASA's 2007 guidelines,[29] but with the exclusion criteria expanded to includeany of the following patient characteristics:

Age greater than 80 yearsUse of oral anticoagulantsBaseline National Institutes of Health (NIH) Stroke Scale score >25A history of both stroke and diabetes

In the early 1980s, Nenci and colleagues reported the first 4 cases of local thrombolysis for vertebrobasilar

occlusion, establishing a trend to treat patients with intra-arterial thrombolysis.[8, 30] To date, several case serieshave been published. The average time to treatment has ranged from 8-48 hours. Overall mortality has decreasedfrom 46-75% to 26-60%. The patient's condition at presentation appears to be the major prognostic factor; patientswith quadriplegia and/or coma have demonstrated the least favorable outcomes. Despite the above efforts, intra-arterial thrombolysis for vertebrobasilar occlusion has not been studied systematically in randomized, controlledtrials.

Of the different agents currently used for thrombolysis (urokinase, prourokinase, streptokinase, tPA), prourokinaseand tPA seem to have more selectivity for thrombi. Streptokinase has not been used for stroke since themulticenter European and Australian trials documented a greater mortality in the treated patients. Because ofconcerns with its production, urokinase is not currently available in the United States.

Prourokinase was tested in a prospective, randomized fashion, including only patients with middle cerebral arterystem occlusion. Results showed a better outcome in treated patients, but prourokinase has not been approved foruse in acute stroke.

At this time, the only viable option for thrombolysis in the United States continues to be tPA. This drug has beenstudied prospectively in trials involving combined intravenous and intra-arterial therapy, in doses of 0.3 mg/kg, witha maximum of 10-20 mg. Limited experience with the use of GPIIb/IIIa inhibitors, such as abciximab, to block theplatelet function and rethrombosis has shown an overall reocclusion rate of approximately 30%.

Anticoagulation

Anticoagulation therapy with heparin has been used, but there is no evidence that it has an impact on outcome.Results from a trial using low–molecular weight heparin intravenously in patients with acute stroke, althoughnegative overall, did show a better outcome at 7 days for patients with large vessel disease.

Angioplasty

Angioplasty has been performed to treat patients with atherosclerotic basilar artery stenosis. The use ofangioplasty is based on the tendency of thrombosis to occur in stenosed arterial segments. Reports describeangioplasty performed in patients with acute vertebrobasilar occlusion, as well as electively. The published caseseries report a morbidity rate of 0-16% and a mortality rate of up to 33%; however, the role of angioplasty in thetreatment of vertebrobasilar occlusion is not well defined.

Other Treatment

Other aspects of treatment for vertebrobasilar stroke should include the following:

Aggressive pulmonary toilet to prevent mucous congestion and pneumoniaPrevention of aspiration pneumonitisEarly establishment of bowel and bladder programs

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Monitoring of skin and all indwelling catheters for signs of infectionControl of body temperature (fever may worsen the outcome in stroke patients)Tight blood glucose controlHeel protectors or L'Nard Multi Podus boots with regular skin inspection for breakdown/decubitusDeep vein thrombosis prophylaxis with sequential compression devices or arteriovenous pumps and/oranticoagulants (eg, low–molecular weight heparin; adjusted-dose, subcutaneous heparin; warfarin), providedthat there are no contraindications

Further inpatient care

Most patients with vertebrobasilar stroke have a significant degree of disability, due to involvement of the brainstemand cerebellum, with resultant multisystem dysfunction (eg, quadriplegia or hemiplegia, ataxia, dysphagia,dysarthria, gaze abnormalities, cranial neuropathies). They often require ongoing, acute rehabilitation, withattention paid to specific patient issues and the formulation of short-term and long-term care plans. Therehabilitation and planning are performed best in a multidisciplinary and interdisciplinary setting.

Rehabilitation After Vertebrobasilar Artery Stroke

Rehabilitation services have been shown to play a critical role in recovery from acute stroke. Physicians andnurses play crucial roles on the rehabilitation team; nurses often are the first to suggest initiation of therapyservices, because they have the most extensive involvement with the patient. Prior to a discussion of the specifictherapy disciplines, address nursing issues in the care of patients with vertebrobasilar stroke.

Nursing issues

A wide variation in symptoms may be seen with stroke, depending on the severity of the brain damage. Initialnursing intervention involves maintaining skin integrity, establishing a bowel and bladder program, maintainingnutrition, and ensuring the person's safety from injury.

Other important nursing issues include communication with the treating clinician in order to initiate therapyservices for the assessment of ambulation, transfers, swallowing function, and the performance of activities of dailyliving (ADL). In some patients, the severity of the deficits makes ambulation impossible; however, patients shouldbe mobilized out of bed and should be actively involved in physical and occupational therapy.

Positioning in bed and in a chair assures the patient's comfort and prevents complications from skin breakdown. Ifthe upper extremity is flaccid or paretic, positioning is critical to the prevention of shoulder subluxation and painfrom shoulder-hand syndrome.

Nursing staff always should involve family members in the care of a person who has sustained a stroke. Thepatient and family members may be unfamiliar with stroke and its effects. Education must be provided to make thepatient and his/her family members aware of the importance of continuing with activities, of appropriateprecautions, and of continuing therapy upon discharge to home.

Some patients have fluctuating symptoms and signs, which often are related to position. Because of thispossibility, precautions are necessary with activities that can be undertaken until the symptoms have stabilized.

Physical therapy (PT) and occupational therapy (OT) should be initiated soon after admission, depending on thecondition of the patient. Once the symptoms have stabilized, patients should be mobilized out of bed, which willallow them to participate in full PT and OT activities.

Physical therapy

The physical therapist is responsible for retraining of gross motor skills, such as gait, balance, transfers, bedmobility, and wheelchair mobility. The physical or occupational therapist may be involved with assessing thepatient for the proper wheelchair and seating system.

The physical therapist also develops a PT program and instructs the patient in general strengthening and range ofmotion. Training of the patient and family members in the use of lower extremity orthotics may be necessary toprovide for functional mobility.

Vestibular evaluation and training are very important, due to a high prevalence of vestibular and cerebellarinvolvement in vertebrobasilar strokes. Patients often need extensive balance and gait training. Evaluation always

should begin with a detailed and focused history. A premorbid vestibular status determination is of great

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should begin with a detailed and focused history. A premorbid vestibular status determination is of great

importance, because dizziness is the third most frequent complaint during physician visits from patients aged 65years and the most frequent complaint from patients aged 75 years and older.

Further clinical testing may include the following:

Oculomotor examination - Visual tracking, convergence/divergence, saccades and smooth pursuitmovement, spontaneous and gaze-evoked nystagmus, static/dynamic visual acuity, and vestibulo-ocularreflex (VOR)Positional testing - Hallpike-Dix maneuverStatic balance - Romberg, sharpened Romberg, and single leg stance (each test is performed on even anduneven surfaces, with eyes open and closed)Dynamic balance - Thorough gait assessment, including head turning, tandem gait, retro walking,negotiating obstacles, and turning

An exercise-based approach has been successful in the treatment of vestibular disorders, due to several possiblemechanisms. These include adaptation, substitution, habituation, and repositioning.

With adaptation by the central vestibular system, the brain modulates the gain of the vestibular response,attempting to correct for a retinal slip (error signal) caused by the decreased gain of the VOR. The VOR trainingstrategy includes focusing on a stationary or moving target while rotating the head, resulting in a retinal slip thatfacilitates adaptation.

Substitution for the loss of function by the remaining intact visual and somatosensory systems is used in treatingpatients with bilateral vestibular lesions (complete or partial loss of both labyrinths).

Habituation for postural vertigo results in decreased response to repeated provoking stimuli. Patients move into theprovoking position 2-3 times during each session, and repeat these sessions 3-5 times per day.

Repositioning maneuvers (eg, Epley maneuver) are used for positional vertigo, based on the mechanicaldisplacement of the debris from the affected canal(s) by a series of head movements. Alternating eye patches orprisms can help diplopia.

General conditioning also is incorporated into the overall rehabilitation plan, encouraging an increase in theperformance of ADL as tolerated.

Occupational therapy

OT is used for retraining fine motor skills that are needed to perform ADL (eg, dressing, bathing, grooming), as wellas for improving hand and arm function. OT also is involved in general strengthening, wheelchair mobility, upperextremity orthotics, and the evaluation of needs for adaptive equipment, as well as in family training and cognitiveretraining for safety and ADL.

Speech therapy

Speech therapy (ST) is used for cognitive retraining, speech and language skills, safety skills, swallowingassessment, and family training. In patients with dysphagia from brainstem lesions, the cricopharyngeus musclemay fail to open sufficiently, resulting in an impaired passage of the bolus from the pharynx to the esophagus.Increased pooling of a bolus in the vallecula and/or pyriform sinuses, which spills into the airway, poses asignificant risk for aspiration and pneumonia.

Evaluation of these patients should be thorough and should include a videofluoroscopy with a modified bariumswallow to assess for silent aspiration. The speech and language therapist often performs the initial swallowingevaluation and determines the risk for aspiration and the consistency of the patient's diet.

The patient's vocalization and possible reading, writing, and processing deficits also are addressed. Interventionsfor the prevention of aspiration include compensatory strategies, such as oromotor exercises and posturalchanges while swallowing, as well as facilitative strategies (eg, modification of bolus consistency, volume,delivery).

Surface electromyography biofeedback for dysphagia has shown promising results. Surface electromyography isused in training a patient to perform maneuvers that compensate for the weak swallow.

The Mendelsohn maneuver, for example, requires voluntary maintenance of the thyroid cartilage in an elevated

position for a few seconds, resulting in further widening of the opening of the cricopharyngeus muscle and easier

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position for a few seconds, resulting in further widening of the opening of the cricopharyngeus muscle and easierpassage of the food bolus through to the esophagus. The patient observes the plateau (as opposed to the peak) ofthe generated waveform on the screen, reinforcing the concept of muscle activation in the desired position (thyroidcartilage elevation).

The patient should be on a nothing-by-mouth restriction until the swallowing mechanism has been assessed andcleared and the airway has been protected. If there is a high risk of aspiration, a nasogastric or nasoduodenal tubeshould be placed, although neither completely eliminates the aspiration risk. If the swallowing abnormalities are sosevere that recovery is expected to take weeks or months, then a gastrostomy tube should be placed eithersurgically or percutaneously.

Recreational therapy

The recreational therapist should concentrate on finding alternative recreational activities for patients who areunable to perform at their premorbid level. Engaging in these activities provides a creative outlet and a positiveemotional gain that potentially enhance the patient's psychological recovery.

Other consultations

In addition to consultations with physical, occupational, and speech therapists, consultation with aneuropsychologist and a social services worker may also be required in the management of patients withvertebrobasilar stroke.

Evaluation by a neuropsychologist is recommended to screen for depression, family dysfunction, coping skills,and subtle cognitive, memory, or processing deficits. All of these may affect future participation in and compliancewith rehabilitation.

The social services department is responsible for coordinating intake and planning discharge. Depending on thesetting, the social services representative may be a licensed social worker or may instead be someone with amore limited background. Home health agencies typically employ licensed social workers, but in nursing homes,the social worker usually is not licensed or certified.

Follow-up After Vertebrobasilar Stroke

Patients should follow up with the primary care provider, neurologist, and other specialists, including thephysiatrist, and continue with the outpatient rehabilitation program. The patient requires continued reassessmentof various factors (eg, functional gains, psychological status, mood, the need for further equipment, home andother modifications, skin care, bowel and bladder function, spasticity management, pain, vocational needs, andsocial issues).

Prevention of recurrent stroke

Strict risk factor control is important to decrease the risk of stroke recurrence.[31] Prevention strategies depend onthe primary cause of the stroke. Patients with a definite cardioembolic source, such as atrial fibrillation, should betreated with warfarin to maintain an international normalized ratio of 2-3.

Treatment of patients with basilar artery stenosis and, for that matter, vertebral artery stenosis is less clear.Retrospective evidence suggests that warfarin is better than aspirin for the prevention of stroke recurrence inpatients with greater than 50% basilar artery stenosis. The ongoing warfarin-aspirin trial for symptomaticintracranial disease will provide valuable information in that regard.

Several oral anticoagulant medications are in various stages of clinical trials for the prophylaxis of ischemic

thromboembolic stroke.[32] If approved for use, the potential of such drugs in the arena of stroke treatment issignificant.

Prognosis

Patients with acute basilar artery occlusion have a mortality rate of more than 85%. Survivors usually are left withsignificant neurologic deficit. For symptomatic patients who survive, the risk of recurrent stroke is 10-15%.

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Patient Education

For patient education information, see the Stroke Center, as well as Stroke.

Contributor Information and DisclosuresAuthorVladimir Kaye, MD Consulting Staff, Departments of Neurology and Psychiatry, Hoag Hospital

Vladimir Kaye, MD is a member of the following medical societies: American Academy of Anti-Aging Medicine,American Academy of Physical Medicine and Rehabilitation, and North American Spine Society

Disclosure: Nothing to disclose.

Coauthor(s)Murray E Brandstater, MBBS, PhD Chairman and Program Director, Professor, Department of PhysicalMedicine and Rehabilitation, Loma Linda University School of Medicine

Murray E Brandstater, MBBS, PhD is a member of the following medical societies: American Academy ofPhysical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine,American Congress of Rehabilitation Medicine, American Medical Association, Association for AcademicPsychiatry, California Society of Physical Medicine and Rehabilitation, Canadian Association of PhysicalMedicine and Rehabilitation, Canadian Medical Association, Canadian Society of Clinical Neurophysiologists,Catholic Medical Association, National Stroke Association, Ontario Medical Association, Royal College ofPhysicians and Surgeons of Canada, and Royal College of Physicians and Surgeons of the United States

Disclosure: Nothing to disclose.

Specialty Editor BoardMilton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and OhioValley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of DisabilityEvaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy,American Academy of Physical Medicine and Rehabilitation, American Medical Association, AmericanOsteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, AmericanPain Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine andRehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine,American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives,American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Chief EditorDenise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, BarrowNeurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director,NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, AmericanAssociation of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association ofAcademic Physiatrists, and Consortium of Multiple Sclerosis Centers

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Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking andteaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research fundsinvestigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research fundsinvestigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology CorpGrant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

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