eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Vertebrobasilar Stroke

Vladimir Kaye, MD, Consulting Staff, Departments of Neurology and Psychiatry, Hoag Hospital
Murray E Brandstater, MBBS, PhD, Chairman and Program Director, Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine

Updated: Jul 15, 2009

Introduction

Background

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

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

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

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

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

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

Pathophysiology

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

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

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

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

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

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

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

Frequency

United States

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

Related eMedicine topic:
Stroke, Ischemic

Mortality/Morbidity

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

Race

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

Sex

Stroke occurs slightly more commonly in men than in women.

Age

The incidence of stroke increases with age.

Clinical

History

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

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

Related eMedicine topic:
Transient Ischemic Attack

Physical

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

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

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

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

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

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

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

Causes

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

• Increasing age
• Family history
• Race
• Prior history of stroke
• Hypertension
• Coronary artery disease
• Diabetes mellitus
• Cigarette smoking
• Heart disease
• Obesity
• Physical inactivity
• Drug or alcohol abuse

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

Differential Diagnoses

Other Problems to Be Considered

Central pontine myelinolysis
Metastatic disease of the brain
Subarachnoid hemorrhage
Basilar meningitis
Basilar migraine
Cerebellopontine angle tumors
Supratentorial hemispheric mass lesions with mass effect, herniation, and brainstem compression

Workup

Laboratory Studies

• 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, such as the following:
  • Lupus anticoagulant and anticardiolipin antibodies
  • Protein C, protein S, and antithrombin III deficiencies
• Factor V Leiden mutation
• Creatine kinase, cardiac isoenzymes, and troponin level should be tested in the following persons:
  • All symptomatic patients (eg, with chest pain)
  • Patients with evidence of ischemic changes in the electrocardiogram (ECG; because of the high incidence of concomitant coronary artery disease)⁷

Imaging Studies

• Computed tomography (CT) scanning^8,9
  • 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.
  • 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.
  • 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
  • Spiral CT angiography is used further to identify occluded and dolichoectatic vessels.^11,12
• Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA)^8,9,13
  • MRI is more sensitive than CT scanning in the identification of ischemia (since bone does not degrade the image). Newer techniques, 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.^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 a specificity 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 because the production of a vessel's image in MRA is a based on a flow-related phenomenon; hence, the presence of severe stenosis with significant flow compromise may result in poor visualization of a vessel and cause the MRA scan to resemble vascular occlusion.
• Transcranial Doppler (TCD)¹⁹
  • 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.

Related eMedicine topic:
Magnetic Resonance Imaging in Acute Stroke

Other Tests

• Electrocardiography should be performed in all patients on initial evaluation. All patients should be monitored continuously for the first few days. Ischemic changes in the ECG should be investigated further with serum creatine kinase, cardiac isoenzymes, and troponin levels 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, atrial fibrillation) has an impact on long-term patient management related to stroke prevention.
• Echocardiography²⁰ 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, vegetations, intramural or extramural thrombi, ventricular aneurisms, cardiac tumors (myxoma), right-to-left shunts, and poor ejection fraction.

Procedures

• Cerebral (catheter) angiography - While the role of angiography has changed due to the availability of noninvasive imaging modalities (eg, MRI, MRA, TCD), it still is considered the criterion standard for imaging. Catheter cerebral angiography is performed in the following circumstances:
  • In cases when an MRA cannot be carried out because the patient has an absolute contraindication (eg, a pacemaker, metallic implant)
  • When the quality of the noninvasive studies is not satisfactory or when the results of the tests do not explain the clinical findings
  • Angiography should be considered a first-line diagnostic test after a CT scan, once it has been decided that recanalization with thrombolysis should be completed. The most important goal of the workup is to establish the type of vascular lesion and the mechanism of the stroke.

Treatment

Rehabilitation Program

Physical Therapy

Rehabilitation services have been shown to play a critical role in recovery from acute stroke. Physicians and nurses play crucial roles on the rehabilitation team; nurses often are the first to suggest initiation of therapy services, because they have the most extensive involvement with the patient. Prior to a discussion of the specific therapy 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. Initial nursing intervention involves maintaining skin integrity, establishing a bowel and bladder program, maintaining nutrition, and ensuring the person's safety from injury.
  • Other important nursing issues include communication with the treating clinician in order to initiate therapy services for the assessment of ambulation, transfers, swallowing function, and the performance of activities of daily living (ADL). In some patients, the severity of the deficits makes ambulation impossible; however, patients should be 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. If the upper extremity is flaccid or paretic, positioning is critical to the prevention of shoulder subluxation and pain from shoulder-hand syndrome.
  • Nursing staff members always should involve family members in the care of a person who has sustained a stroke. The patient and family members may be unfamiliar with stroke and its effects. Education must be provided to make the patient and his/her family members aware of the importance of continuing with activities, of appropriate precautions, and of continuing therapy upon discharge to home.
• Activity
  • Some patients have fluctuating symptoms and signs, which often are related to position. Because of this possibility, 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 the condition of the patient. Once the symptoms have stabilized, the patient should be mobilized out of bed, which will allow him/her to participate in full PT and OT activities.
• PT 
  • PT is responsible for retraining of gross motor skills, such as gait, balance, transfers, bed mobility, and wheelchair mobility. The physical or occupational therapist may be involved with assessing the patient for the proper wheelchair and seating system.
  • The physical therapist also develops a PT program and instructs the patient in general strengthening and range of motion. Training of the patient and family members in the use of lower extremity orthotics may be necessary to provide for functional mobility.
  • Vestibular evaluation and training are very important, due to a high prevalence of vestibular and cerebellar involvement 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 importance, because dizziness is the third most frequent complaint during physicians' visits from patients aged 65 years 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 pursuit movement, spontaneous and gaze-evoked nystagmus, static/dynamic visual acuity, and vestibulo-ocular reflex (VOR)
    • Positional testing - Hallpike-Dix maneuver
    • Static balance - Romberg, sharpened Romberg, and single leg stance (each test is performed on even and uneven 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 possible mechanisms.
    • 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 training strategy includes focusing on a stationary or moving target while rotating the head, resulting in a retinal slip that facilitates adaptation.
    • Substitution for the loss of function by the remaining intact visual and somatosensory systems - This substitution is used in treating patients with bilateral vestibular lesions (complete or partial loss of both labyrinths).
    • Habituation for postural vertigo, resulting in decreased response to repeated provoking stimuli - Patients move into the provoking position 2-3 times, with this repeated 3-5 times per day.
    • Repositioning maneuvers (eg, Epley maneuver) - These maneuvers are used for positional vertigo, based on the mechanical displacement of the debris from the affected canal(s) by a series of head movements. Alternating eye patches or prisms can help diplopia.
  • General conditioning also is incorporated into the overall rehabilitation plan, encouraging an increase in the performance of ADL as tolerated.

Related eMedicine topic:
Motor Recovery In Stroke
Stroke Team Creation and Management

Occupational Therapy

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

Speech Therapy

Speech therapy (ST) is used for cognitive retraining, speech and language skills, safety skills, swallowing assessment, and family training. Patients with dysphagia present with increased pooling of a bolus in the vallecula and/or pyriform sinuses, which spills into the airway, posing a significant risk for aspiration and pneumonia. Evaluation of these patients should be thorough and should include a videofluoroscopy with a modified barium swallow to assess for silent aspiration. 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.

The patient's vocalization and possible reading, writing, and processing deficits also are addressed. Interventions for the prevention of aspiration include compensatory strategies, such as oromotor exercises and postural changes while swallowing, as well as facilitative strategies (eg, modification of bolus consistency, volume, delivery). With brainstem lesions, the cricopharyngeus muscle may fail to open sufficiently, resulting in an impaired passage of the bolus from the pharynx to the esophagus and a much increased risk of aspiration.

Surface electromyography biofeedback for dysphagia has shown promising results. Surface electromyography is used 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 passage of the food bolus through to the esophagus. The patient observes the plateau (as opposed to the peak) of the generated waveform on the screen, reinforcing the concept of muscle activation in the desired position (thyroid cartilage elevation).

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. If there is a high risk of aspiration, a nasogastric or nasoduodenal tube should be placed, although neither completely eliminates the aspiration risk. If the swallowing abnormalities are so severe that recovery is expected to take weeks or months, then a gastrostomy tube should be placed either surgically or percutaneously.

Recreational Therapy

The recreational therapist should concentrate on finding alternative recreational activities for the patient who is unable to perform at his/her premorbid level. Engaging in these activities provides a creative outlet and a positive emotional gain that potentially enhance the patient's psychological recovery.

Medical Issues/Complications

Ideally, all patients who have suffered a vertebrobasilar stroke should be admitted to a unit specializing in the care of stroke patients. Patients demonstrating unstable or fluctuating neurologic symptoms, a decreased level of consciousness, hemodynamic instability, or active cardiac or respiratory problems or those who are candidates for interventional therapies, such as thrombolysis, must be admitted to a neurologic intensive care unit (ICU).²¹

• Hemodynamic management
  • This approach should be aimed at minimizing the ischemic injury. Cerebral ischemia results in impaired autoregulation. Mechanisms underlying the autoregulatory response of the brain involve vasoconstriction and vasodilatation. Therefore, under ischemic conditions, the cerebral blood flow becomes blood pressure–dependent.²² An increase in the mean arterial pressure (MAP) results in vasoconstriction. This response limits the perfusion pressure and the blood volume. A 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 chronic hypertensive patients, the curve of autoregulation is shifted upward. In the patients with severe cerebral vascular occlusive disease, the MAP and the cerebral perfusion pressure (CPP) become critical in maintaining the cerebral blood flow. CPP is equal to MAP less intracranial pressure (ICP) (ie, CPP = MAP-ICP). Therefore, overzealous treatment of hypertension should be avoided, because it can decrease the cerebral perfusion pressure and exacerbate 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 be treated 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 systolic blood pressure is over 200 mm Hg. Otherwise, when thrombolysis is a strong consideration, the treatment parameters become 110 mm Hg or more for diastolic blood pressure or greater than 180 mm Hg for systolic blood pressure.
  • Commonly used antihypertensives are labetalol and nitroprusside. When diastolic blood pressure is greater than 140 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 using isotonic 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 failure and pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary wedge pressure. This approach would improve monitoring of the intravascular volume to avoid overload.
• 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. Assessment of the respiratory drive, 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 Glasgow coma score of less than 8 to maintain the airway and normal ventilation. Of the mechanical ventilation modes, pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation are used most often. For patients with good respiratory drive, the most comfortable mode is PSV. In this mode, the ventilator does not deliver a set of breaths but provides enough pressure support to maintain the desired tidal volume, usually in the range of 5-8 mL/kg. Most patients with no pulmonary 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 the patient's inspiratory effort while allowing the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort when taking them. Sedation and paralysis should be avoided, because they may obscure the neurologic assessment. Circumstances may exist that require the use of sedation and paralysis (eg, neurogenic hyperventilation) to avoid hypocarbia and worsening of the ischemic process.
• Thrombolysis
  • Based on data from the National Institute of Neurological Disorders and Stroke trial, in 1996 the Food and Drug Administration (FDA) approved tissue plasminogen activator (tPA)⁸ for the treatment of acute ischemic stroke within the first 3 hours of onset. The trial showed an overall benefit for the treated group versus the untreated group. A higher number of treated patients had minimal deficit and minimal or no disability. The results applied to all of the subgroups, regardless of the etiology. This trial did not include patients in stupor or coma. This selection probably excluded patients who suffered a basilar artery occlusion. Moreover, the trial did not study the vascular anatomy systematically in all 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 advisory recommending 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 its recommendation, 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 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, 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 series have been published. The average time to treatment has ranged from 8-48 hours. Overall mortality has decreased from 46-75% to 26-60%. The patient's condition at presentation appears to be the major prognostic factor; patients with 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, controlled trials.
  • Of the different agents currently used for thrombolysis (urokinase, prourokinase, streptokinase, tPA), prourokinase and tPA seem to have more selectivity for thrombi. Streptokinase has not been used for stroke after the multicenter European and Australian trials documented a greater mortality in the treated patients. Because of concerns 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 artery stem occlusion. Results showed a better outcome in treated patients, but prourokinase has not been approved for use in acute stroke.
  • At this time, the only viable option for thrombolysis in the United States continues to be tPA. This drug has been studied prospectively in trials involving combined intravenous and intra-arterial therapy, in doses of 0.3 mg/kg, with a maximum of 10-20 mg. Limited experience with the use of GPIIb/IIIa inhibitors, such as abciximab, to block the platelet function and rethrombosis has shown an overall reocclusion rate of approximately 30%.
• Other therapies
  • 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, although negative overall, did show a better outcome at 7 days for patients with large vessel disease.
  • Angioplasty has been performed to treat patients with atherosclerotic basilar artery stenosis. The use of angioplasty is based on the tendency of thrombosis to occur in stenosed arterial segments. Reports describe angioplasty performed in patients with acute vertebrobasilar occlusion, as well as electively. The published case series report a morbidity rate of 0-16% and a mortality rate of up to 33%; however, the role of angioplasty in the treatment of vertebrobasilar occlusion is not well defined.

Related eMedicine topics:
Cerebral Revascularization
Mechanical Thrombolysis in Acute Stroke
Neuroprotective Agents in Stroke
Stroke Anticoagulation and Prophylaxis
Thrombolytic Therapy
Thrombolytic Therapy in Stroke

Related Medscape topics:
CME AHA Issues Statement on Ambulatory BP Monitoring in Youths 
CME/CE Challenging Cases in Acute Blood Pressure Management: Putting the Guidelines Into Practice

Consultations

In addition to consultations with physical, occupational, and speech therapists (see Rehabilitation Program), the following specialists may also be required in the management of patients with vertebrobasilar stroke:

• Neuropsychologist - Evaluation is recommended to screen for depression, family dysfunction, coping skills, and subtle cognitive, memory, or processing deficits, all of which may affect future participation and compliance.
• Social services worker - The social services department is responsible for coordinating intake and planning discharge. Depending on the setting, the social services representative may be a licensed social worker or may instead be someone with a more limited background. Home health agencies typically employ licensed social workers, but in nursing homes, the social worker usually is not licensed or certified.

Other Treatment

Other 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
• 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, low – molecular weight heparin; adjusted-dose, subcutaneous heparin; Coumadin), provided that there are no contraindications

Medication

Medications used in the treatment of patients with vertebrobasilar stroke include thrombolytic agents, anticoagulants, and antihypertensive and antiplatelet agents. Patients with severe and/or active comorbidities, such as acute myocardial infarction, may require administration of inotropic agents and vasopressors.

Several oral anticoagulant medications are in various stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke.³¹ Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Related eMedicine topic:
Medical Treatment of Stroke

Antihypertensives

Antihypertensive agents are used to control severe hypertension. Antihypertensives are recommended for patients who are considered candidates for thrombolytic therapy and who have a systolic blood pressure greater than 180 mm Hg and/or a diastolic blood pressure above 110 mm Hg.

Nitroprusside sodium (Nitropress)

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

Dosing

Adult

0.5-10 mcg/kg/min IV until blood pressure is controlled

Pediatric

Not established

Interactions

May increase toxicity of other antihypertensives

Contraindications

Documented hypersensitivity, compensatory hypertension, aortic coarctation, heart failure, and congenital optic atrophy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with increased intracranial pressure, renal or hepatic failure, and hyponatremia; rapid or long-term use can cause cyanide toxicity

Labetalol (Normodyne, Trandate)

Functions to block beta 1 –, beta 2 –, and alpha-adrenergic receptor sites, decreasing blood pressure.

Dosing

Adult

Initial dose: 20 mg IV bolus over 2 min; repeat doses of 40-80 mg can be given at 10 min intervals until the desired blood pressure has been achieved or a total dose of 300 mg has been reached; alternatively, a labetalol drip at a rate of 2 mg/min may be administered

Pediatric

Not established

Interactions

Coadministration with tricyclic antidepressants may cause tremor; blocks the bronchodilator effect of beta-receptor agonists; interacts with antihypertensives, cimetidine, halothane, and nitroglycerine

Contraindications

Documented hypersensitivity, heart failure, chronic obstructive pulmonary disease, bronchial asthma, heart block greater than first degree, cardiogenic shock, severe bradycardia, and hepatic failure

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in patients with overt congestive heart failure; abrupt cessation of therapy may precipitate angina; hepatocellular injury may occur (usually reversible); therefore, discontinue in case of persistent LFT elevation; may block the sympathetic response triggered by hypoglycemia; symptomatic postural hypotension may occur

Enalapril (Vasotec)

Competitive inhibitor of angiotensin-converting enzyme. Enalapril reduces angiotensin II levels, decreasing aldosterone secretion.

Dosing

Adult

0.650-1.25 mg IV q6h

Pediatric

Not established

Interactions

Hypotension in patients receiving other antihypertensive agents may occur; hyperkalemia may occur in patients receiving potassium-sparing agents, such as spironolactone and triamterene

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure

Anticoagulants

These agents are used to prevent recurrent embolism or extension of the thrombosis.

Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K – dependent coagulation factors. Warfarin is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. It is employed for long-term stroke prophylaxis.

Dosing

Adult

Adjust dose to maintain INR between 2 and 3 for most indications and between 2.5 and 3.5 for patients with prosthetic heart valves; tailor dose to maintain an INR of 2-3

Pediatric

Not established

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; pregnancy, hemorrhage, and blood dyscrasias; unsupervised elderly patients; alcoholism

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Heparin (Hep-Lock)

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

Dosing

Adult

Use a nomogram and administer IV bolus or start an IV drip at approximately 1000 U/h or 18 U/g/h; aPTT is checked at 4 h, and the infusion is adjusted accordingly until reaching the target aPTT of 1.5-2 times control; for prophylaxis of DVT the dose is 5000 U SC q12h

Pediatric

Not established

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Contraindications

Documented hypersensitivity; active systemic or intracranial bleeding; severe thrombocytopenia and blood dyscrasias; brain, spinal cord, or eye surgery

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock; monitor for bleeding in peptic ulcer disease, menstruation, increased capillary permeability, and when giving IM injections

Antiplatelet agents

These drugs inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of strokes.

Aspirin (Bayer Aspirin, Ascriptin, Anacin)

Inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. Aspirin may be used in low dose to inhibit platelet aggregation and to improve complications of venous stasis and thrombosis.

Dosing

Adult

81-1300 mg PO qd

Pediatric

Not established

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye syndrome, do not use in children (<16 y) with flu

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

Thrombolytics

Potential benefits of thrombolytic therapy for the treatment of strokes include the fast dissolution of physiologically compromising emboli, faster recovery, the prevention of recurrent thrombus formation, and the rapid resolution of hemodynamic disturbances.

Alteplase; tPA (Activase)

TPA is used in the management of acute ischemic stroke.
The safety and efficacy with concomitant administration of heparin or aspirin during the first 24 h after symptom onset have not been investigated.
Currently, tPA is the only drug approved for use in patients with acute ischemic stroke, within 3 hours of the onset of symptoms.

Dosing

Adult

0.9 mg/kg IV; not to exceed 90 mg; 10% of the dose to be administered over 2-3 min and the rest over 1 h
Alternatively, 0.3 mg/kg IV; not to exceed 10-20 mg

Pediatric

Not established

Interactions

Drugs that alter platelet function (aspirin, dipyridamole, and abciximab) may increase risk of bleeding prior to, during, or after alteplase therapy; may give heparin with and after alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications

Contraindications

Documented hypersensitivity; patients with active systemic or intracranial bleeding, intracranial neoplasm, arteriovenous malformation, patients on heparin or those with aPTT >1.5 times control; patients on warfarin or with INR >1.6; patients with coagulopathies, recent major surgery, head injury or stroke in the previous 3 mo, and history of intracranial hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when treating acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH

Follow-up

Further Inpatient Care

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

Further Outpatient Care

• Patients should follow up with the primary care provider, neurologist, and other specialists, including the physiatrist, and continue with the outpatient rehabilitation program. The patient needs strict risk factor control to decrease the risk of stroke recurrence³² and requires continued reassessment of various factors (eg, functional gains, psychological status, mood, the need for further equipment, home and other modifications, skin care, bowel and bladder function, spasticity management, pain, vocational needs, and social issues).

Inpatient & Outpatient Medications

• Continual monitoring of patients who have suffered a vertebrobasilar stroke (by all members of the rehabilitation team and by involved family members) for the possible adverse effects and interactions associated with polypharmacy is important.

Deterrence

• Prevention strategies depend on the primary cause of the stroke.
  • Patients with a definite cardioembolic source, such as atrial fibrillation, should be treated 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 in patients with greater than 50% basilar artery stenosis. The ongoing warfarin-aspirin trial for symptomatic intracranial disease will provide valuable information in that regard.

Complications

• Aspiration pneumonia
• Deep venous thrombosis
• Pulmonary embolism
• Myocardial infarction

Prognosis

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

Patient Education

• See the Rehabilitation Program section.
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Multimedia

Media file 1: Lesion of the medial longitudinal fasciculus (MLF) resulting in internuclear ophthalmoplegia (INO). (Courtesy of BC Decker Inc.)

Media file 2: Center for vertical gaze and pathways involved in vertical eye movement (Courtesy of Cranial Nerves--Anatomy and Clinical Comments. BC Decker Inc; Toronto. 1988)

Media file 3: Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex. (Courtesy of BC Decker Inc.)

Media file 4: Vestibular reflex illustrating horizontal eye movements only. (Courtesy of BC Decker Inc.)

Media file 5: Visceral motor component of CN III and pathways involved in pupillary constriction. (Courtesy of BC Decker Inc.)

Media file 6: Connections of the primary visual cortex. (Courtesy of BC Decker Inc.)

Media file 7: LMN Lesion of the hypoglossal nerve producing tongue deviation to the side of the lesion. (Courtesy of BC Decker Inc.)

Media file 8: Note the horizontal eye movement. Also note a topographic relationship of the center for vertical gaze. (Courtesy of BC Decker Inc.)

Media file 9: Vestibular nuclei and their connections. (Courtesy of BC Decker Inc.)

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32. Ois A, Gomis M, Rodríguez-Campello A, et al. Factors associated with a high risk of recurrence in patients with transient ischemic attack or minor stroke. Stroke. Jun 2008;39(6):1717-21. [Medline].

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124. Whisnant JP, Cartlidge NE, Elveback LR. Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. Ann Neurol. Feb 1978;3(2):107-15. [Medline].

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

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

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

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

Keywords

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

Contributor Information and Disclosures

Author

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

Coauthor(s)

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

Medical Editor

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

Pharmacy Editor

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

Managing Editor

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

CME Editor

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

Chief Editor

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

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