AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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; however, many 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 neurological 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 following:

• 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 one 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.

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, at the pontomedullary junction, merge 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 (PCA), the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain, and the superior surface of the cerebellum. The cerebellum is supplied by long circumferential arteries, the PICA, and the anterior inferior and the superior cerebellar 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 PCA perfuse the midbrain and thalamus, and the occipital cortex is perfused by the PCA.

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.

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 in atherosclerosis, as the small vessels become occluded by a process called lipohyalinosis that 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 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

Actual 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 these lesions 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% involve the pons.

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%. 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

Incidence of stroke increases with age.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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% 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 following:

• 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

Physical

Common clinical findings observed in more than 70% of patients include abnormal level of consciousness and 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 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 for narrowing down the search, including the following examples:

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

A variety of specific neurologic syndromes have been described based on constellations of findings. Some examples are listed below.

• Lateral medullary (Wallenberg) syndrome
  • Most often, this syndrome is 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 ataxia and dysmetria, due to damage of the inferior cerebellar peduncle and cerebellum; Horner syndrome (eg, ptosis, miosis, hypohidrosis or anhidrosis, enophthalmos), due to the damage to descending sympathetic fibers; facial pain and temperature loss; reduced corneal reflex from damage to the descending spinal tract and nucleus of CNV; nystagmus; hypoacusis (cochlear nucleus); dysarthria; dysphagia; paralysis of the pharynx, palate, and vocal cord; and 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 olive.
  • 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 due to occlusion of a vertebral artery or its branch to the anterior spinal artery, and 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 since 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 results from occlusion of the proximal and middle segments of the basilar artery, or hemorrhage involving that region, and also may be caused by trauma, central pontine myelinolysis, encephalitis, or tumor.
  • Bilateral ventral pontine lesions involving both corticospinal and corticobulbar tracts lead to quadriplegia. The patient is unable to speak, or produce facial movement (damage to the corticobulbar tracts), as well as 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 patients 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: 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. 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 or may not be present.
• Top-of-the-basilar syndrome
  • This syndrome is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery, usually due to 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, hemianopsia, cortical blindness, abnormal color vision/color dysnomia). These patients also can demonstrate oculomotor abnormalities, most commonly of the vertical gaze, such as gaze palsy, skew deviation, convergence spasm resulting in pseudo-abducens 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, resulting 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 since both nuclei of CN III and peripheral innervation of the medial recti muscles are intact.
  • Since horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI (relative to the lesion), disruption of the communication pathway (ie, 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 syndrome
  • 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 (one), and 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+/- CNVI 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 from occlusion of paramedian branches of either the basilar artery, PCA, or both.
• The patient demonstrates ipsilateral oculomotor palsy, ptosis, and mydriasis (like in Weber syndrome), along with the contralateral involuntary movements, such as intention tremor, ataxia, or chorea (due to the involvement of the red nucleus).

• Posterior cerebral artery occlusion

• The most common finding is occipital lobe infarction leading to contralateral hemianopsia 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.

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

DIFFERENTIALS

Section 4 of 10  

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• Medication
• Follow-up
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• References

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

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• Laboratory workup should include the following:
• • CBC count
  • Electrolytes
  • BUN and creatinine
  • Prothrombin time and activated partial thromboplastin time (aPTT)
  • Cholesterol level
  • Lipid profile
• Patients younger than 45 years or patients with 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:
  • All symptomatic patients (eg, with chest pain)
  • Those with evidence of ischemic changes in the ECG (because of the high incidence of concomitant coronary artery disease)

Imaging Studies

• Computed tomography
• • Computed tomography (CT) usually is the first imaging study performed, as it has a sensitivity of more than 95% to identify intra-axial or extra-axial hemorrhage within the first 24 hours of onset.
  • The disadvantages of CT scan 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 of the presence of a hyperdense basilar artery, suggesting a probable occlusion.
  • Spiral CT angiography is used further to identify occluded and dolichoectatic vessels.
• Magnetic resonance imaging and magnetic resonance angiography
• • Magnetic resonance imaging (MRI) is superior to CT scan in its sensitivity to identify ischemia (since bone does not degrade the image). Newer techniques, including flow suppression, diffusion, and perfusion-weighted images, make it a very powerful tool to exclude intraparenchymal hemorrhage or edema and to identify early and potentially reversible ischemia.
  • MRI and magnetic resonance angiography (MRA) are very helpful in finding occult lesions such as demyelinating plaques, tumors, vertebrobasilar dolichoectasia, or dissection. MRA can identify vertebrobasilar occlusion with sensitivity up to 97% and specificity up to 98%. A limitation of the MRA is a tendency to overestimate the degree of stenosis. This overestimation occurs because the image of the vessel in MRA is a flow-related phenomenon; hence, severe stenosis with significant flow compromise may result in poor visualization of the vessel and may resemble vascular occlusion.
• Transcranial Doppler
• Transcranial Doppler (TCD) is used in 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 sensitivity of 72% and specificity of 94% in patients with basilar artery disease.

Other Tests

• ECG 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 the long-term management for stroke prevention.
• Echocardiography should be considered in the following patients:
• • Those younger than 45 years
  • Those with explained basilar artery occlusion

    Findings that may affect the 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. 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

Section 6 of 10  

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Rehabilitation Program

Physical Therapy

Rehabilitation services have been shown to play a critical role in recovery from acute stroke. In addition to the physicians, nurses play a crucial role on the rehabilitation team and often are first to suggest initiation of therapy services as they have the most extensive involvement with the patient. Prior to 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 maintenance of 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 physician to initiate therapy services for assessment of ambulation, transfers, swallowing function, and 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 involved actively with 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 prevent 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 family members aware of the importance of continuing with activities, appropriate precautions, and continuation of 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, allowing full physical and occupational therapy activities.
• Physical therapy
  • PT is responsible for retraining of gross motor skills, such as gait, balance, transfers, bed mobility, and wheelchair mobility. Either the physical or occupational therapist may be involved with assessing the patient for 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 with 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 since, statistically, dizziness is the third most frequent complaint during physicians' visits in patients aged 65 years and the most frequent complaint in 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, 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 performance of ADL as tolerated.

Occupational Therapy

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

Speech Therapy

Speech therapy (ST) is responsible 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 determine the risk for aspiration and consistency of the diet.

The vocalization and possible reading, writing, and processing deficits also are addressed. Interventions for prevention of aspiration include compensatory strategies, such as oromotor exercises and postural changes while swallowing, and facilitative strategies (eg, modification of bolus consistency, volume, delivery). With the 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 compensating for the weak swallow, such as the Mendelsohn maneuver. This technique 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 protected. If there is a high risk of aspiration, a nasogastric or a nasoduodenal tube should be placed. 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 not able to perform at his/her premorbid level. Engaging in these activities provides a creative outlet and positive emotional gain that potentially enhances psychological recovery.

Medical Issues/Complications

Ideally, all patients should be admitted to a unit specializing in the care of stroke patients. Patients demonstrating unstable or fluctuating neurologic symptoms, 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 ICU.

• 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. 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, as 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 the evidence from experimental models and 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 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 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 decreased level of consciousness and 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 during the extra breaths. Sedation and paralysis should be avoided because they may obscure the neurologic assessment. Circumstances may exist that require use of sedation and paralysis (eg, neurogenic hyperventilation) to avoid hypocarbia and worsening of the ischemic process.
• Thrombolysis
  • In 1996, the Food and Drug Administration approved tissue plasminogen activator (tPA) for the treatment of acute ischemic stroke within the first 3 hours of onset, based on the data from the National Institute of Neurological Disorders and Stroke trial. The trial showed an overall benefit for the treated versus the untreated group. A higher number of treated patients had minimal or no disability and minimal deficit. Results applied to all 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.
  • In the early 1980s, Nenci et al reported the first 4 cases of local thrombolysis for vertebrobasilar occlusion, establishing a trend to treat patients with intra-arterial thrombolysis. To date, several case series have been published. 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, as patients with quadriplegia and/or coma have demonstrated the least favorable outcomes. Despite these efforts, intra-arterial thrombolysis for vertebrobasilar occlusion has not been studied systematically yet in randomized controlled trials.
  • Of the different agents used for thrombolysis today (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. Urokinase is not available currently in the United States, due to concerns with its production. Prourokinase was tested in a prospective randomized fashion, including only the patients with middle cerebral artery stem occlusion. Results showed a better outcome in treated patients, but it 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. A limited experience with the use of GPIIb/IIIa inhibitors, such as abciximab, to block the platelet function and rethrombosis showed the overall reocclusion rate of approximately 30%.
• Other therapies
• • Anticoagulation therapy with heparin has been used, but there is no evidence showing 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 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 up to 33%; however, the role of angioplasty in the treatment of vertebrobasilar occlusion is not well defined.

Consultations

In addition to the therapy (physical, occupational, and speech therapists) consultations that have been discussed in the rehabilitation section, the physician also may recommend the following:

• 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 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 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 all indwelling catheters and skin for signs of infection
• Control of body temperature (fever may worsen outcome in stroke patients)
• Tight blood glucose control
  • Heel protectors or L'Nard Multi Podus boots with regular skin inspection for breakdown/decubiti
  • 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 there are no contraindications

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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

Drug Category: Antihypertensives

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

Drug Category: Anticoagulants

Used to prevent recurrent embolism or extension of the thrombosis.

Drug Category: Antiplatelet agents

Inhibit platelet function by blocking cyclo-oxygenase 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.

Drug Category: Thrombolytics

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

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Further Inpatient Care

• Most patients with 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). They often require ongoing acute rehabilitation, with attention to specific patient issues and formulation of both 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 physician, 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 recurrence and continued reassessment of various factors (eg, functional gains, psychological status, mood, need for further equipment, home and other modifications, skin care, bowel and bladder function, spasticity management, pain, vocational needs, and social issues).

In/Out Patient Meds

• Monitoring for possible adverse effects and interactions of polypharmacy is important on a continued basis by all members of the rehabilitation team and family members involved.

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 in 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

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Vertebrobasilar stroke. Lesion of the medial longitudinal fasciculus (MLF) resulting in internuclear ophthalmoplegia (INO). Courtesy of BC Decker Inc.
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Media file 2:  Vertebrobasilar stroke. Center for vertical gaze and pathways involved in vertical eye movement (Courtesy of Cranial Nerves--Anatomy and Clinical Comments. BC Decker Inc; Toronto. 1988)
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Media file 3:  Vertebrobasilar stroke. Illustration of afferent (CN V) and efferent (CN VII) limbs of the blink reflex. Courtesy of BC Decker Inc.
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Media file 4:  Vertebrobasilar stroke. Vestibular reflex illustrating horizontal eye movements only. Courtesy of BC Decker Inc.
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Media file 5:  Vertebrobasilar stroke. Visceral motor component of CN III and pathways involved in pupillary constriction. Courtesy of BC Decker Inc.
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Media file 6:  Vertebrobasilar stroke. Connections of the primary visual cortex. Courtesy of BC Decker Inc.
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Media file 7:  Vertebrobasilar stroke. LMN Lesion of the hypoglossal nerve producing tongue deviation to the side of the lesion. Courtesy BC Decker Inc.
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Media file 8:  Vertebrobasilar stroke. Note the horizontal eye movement. Also note a topographic relationship of the center for vertical gaze. Courtesy of BC Decker Inc.
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Media file 9:  Vertebrobasilar stroke. Vestibular nuclei and their connections. Courtesy of BC Decker Inc.
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REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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