eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Vertebrobasilar Stroke: Treatment & Medication

Author: Vladimir Kaye, MD, Consulting Staff, Departments of Neurology and Psychiatry, Hoag Hospital
Coauthor(s): Murray E Brandstater, MBBS, PhD, Chairman and Program Director, Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine
Contributor Information and Disclosures

Updated: Jul 15, 2009

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.

Adult

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

Pediatric

Not established

May increase toxicity of other antihypertensives

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

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.

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

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

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

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.

Adult

0.650-1.25 mg IV q6h

Pediatric

Not established

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

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.

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

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

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

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.

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

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

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

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.

Adult

81-1300 mg PO qd

Pediatric

Not established

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

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

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.

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

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

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

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

More on Vertebrobasilar Stroke

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Multimedia: Vertebrobasilar Stroke
References
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Further Reading

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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

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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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