eMedicine Specialties > Neurology > Neuro-vascular Diseases

Posterior Cerebral Artery Stroke: Treatment & Medication

Author: Michael D Hill, MD, Medical Director, Stroke Unit, Associate Professor of Neurology, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Canada
Coauthor(s): Alastair M Buchan, DSc, MB, BCh, Professor, Head of Medical Sciences Division, University of Oxford, UK
Contributor Information and Disclosures

Updated: Nov 10, 2009

Treatment

Medical Care

The treatment of stroke necessitates an understanding of the mechanism of stroke. The approach to stroke is defined by localization of the problem to determine the vascular territory involved and subsequently by using the history, stroke subtype, and investigational tools to define the stroke mechanism. Establishing a probable mechanism is at times straightforward; for example, the ECG demonstrates atrial fibrillation. At times, however, it is more difficult—for example, TEE with a bubble study demonstrates a patent foramen ovale. The medical treatment of stroke can be divided into acute, subacute, and chronic phases.

  • Acute therapy - Within 3 hours of stroke onset
    • The National Institutes of Neurological Diseases and Stroke (NINDS) trial of recombinant tissue-type plasminogen activator (rtPA), published in 1995, included all types of ischemic stroke.3 However, recent studies have provided new data on rtPA treatment in the 3- to 4.5–hour window in carefully selected patients.4,5 In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the administration of rt-PA following acute stroke were revised to expand the window of treatment from 3 to 4.5 hours to provide more patients with an opportunity to receive benefit from this effective therapy.6 This has not yet been FDA approved.
    • If a clear time of onset can be established, stroke in the PCA territory may be treated with intravenous rtPA. However, because hemianopia may not be recognized immediately, particularly left hemianopia, the risk that patients will mistake the time of stroke onset is significant. Postmarketing analysis of rtPA in acute stroke has warned that failure to follow strict guidelines, including time of onset, of the NINDs rtPA protocol dramatically increases the risk of intracranial hemorrhage.
  • Subacute and chronic therapy - More than 3 hours from stroke onset
    • Even if thrombolytic therapy is contraindicated, the choice of acute or subacute therapy is dependent on the physician's understanding of the stroke mechanism. If possible, patients with acute stroke should be cared for in a stroke unit by staff who are familiar with stroke and its complications.
    • Anticoagulation with heparin often is used, although no strong evidence exists among any stroke type that heparin is useful. The trial of ORG 10172 (danaparoid, a heparinlike drug) in acute stroke treatment (ie, TOAST) has suggested that anticoagulation may be beneficial in stroke due to large artery atherosclerotic disease with major stenosis, although the principal endpoints of the study did not confirm any benefit of anticoagulation.7 Although long-term anticoagulation has been advocated for posterior circulation disease, the decision to use heparin in PCA stroke should be made on an individual basis.
    • Aspirin has been shown to be effective in reducing recurrence of acute stroke in the first 14 days and should be started at admission (assuming anticoagulation is not begun).
    • Although deep vein thrombosis (DVT) is unusual in patients with PCA stroke, any patient who is bedridden should receive prophylactic therapy for DVT.
    • The usual care of patients with stroke includes close attention to swallowing to prevent aspiration pneumonia.
    • Once the stroke mechanism has been determined, long-term secondary preventive treatment can be started. This would include anticoagulation for a cardioembolic source (eg, atrial fibrillation), intrinsic vertebrobasilar disease, or vertebral dissection. When the mechanism is cryptogenic, antiplatelet therapy generally is used.
    • When the ICA is the source of the stroke, surgical endarterectomy may be appropriate. New procedures such as vertebral artery stenting are being tested and may replace the medical-treatment-only approach to intrinsic vertebral artery disease. In unusual circumstances, vertebral artery bypass may be considered; however, this surgical procedure remains an unproved therapy.
    • Finally, attention to rehabilitation should begin early. Involvement of a speech language therapist may be required if alexia if present, with or without aphasia. The occupational therapist should be able to help with teaching patients to turn to look in the blank visual hemifield. Patients often have to relinquish their driver's license because of the visual field loss. This may result in considerable loss of independence and provoke anger and grief in the patient for which counseling may be required.

Surgical Care

Surgical and endovascular therapies aimed at the posterior circulation are largely experimental and should be considered only as research protocols or in unusual circumstances. At present, little evidence exists to support medical therapy or surgical/endovascular therapy beyond case series and retrospective reports. Nevertheless, several procedures have been described.

  • Vertebral artery bypass and occlusion
    • Extracranial (EC)-to-intracranial (IC) vertebral artery bypass may be undertaken by connection of the occipital artery to the vertebral, superior cerebellar, anterior ICA, or posterior ICA. The superficial temporal artery also has been used as a donor artery. Shunting to the PCA may be accomplished by using veins or synthetic grafts. In general, EC-to-IC circulation shunting has been relegated to use in extenuating circumstances since publication of the negative EC-IC bypass trial.
    • Atherosclerotic disease of the vertebral artery orifice has been treated with bypass (usually a common carotid to vertebral graft) and by subclavian artery reconstruction. Although endarterectomy is possible, it is done rarely. The proximal vertebral artery may be amenable to angioplasty and stenting.
    • Occlusion of the vertebral artery may be undertaken to exclude an aneurysm, dissecting aneurysm, or pseudoaneurysm from circulation. Rarely, dissection of the vertebral artery extends into the intracranial segment, ruptures, and causes subarachnoid hemorrhage. Similarly, vertebral artery dissection may fail to heal completely, leaving a proximal pseudoaneurysm as a source of future emboli. The traditional solution to these problems is to sacrifice the vertebral artery with proximal occlusion.
  • Angioplasty and stenting
    • Angioplasty and stenting of the vertebrobasilar circulation are increasingly being reported. Most neurologists and neurosurgeons are highly suspicious of the possibility of ruptured plaque material embolizing distally after angioplasty. Nevertheless, where medical therapy has failed to control symptoms, accumulating reports of successful vertebral and even basilar angioplasty and stenting demonstrate the potential of this procedure.
    • Much refinement is required before this procedure becomes a mainstream approach to atherosclerotic disease of the vertebrobasilar system.

Consultations

  • Stroke care is a multidisciplinary process. A stroke nurse specialist, physical therapist, occupational therapist, speech therapist, and physiatrist or neurologist involved in rehabilitation should all be involved early (usually in the first 48 hours after stroke).
  • Early attention to rehabilitation and eventual reintegration into the community speeds recovery and shortens the length of hospital stay.
  • When indicated, involvement of the cardiologist and hematologist may be important in understanding the stroke mechanism.
  • Neurosurgical expertise is needed only in unusual cases of posterior circulation stroke as detailed already.

Diet

  • A speech pathologist and dietitian may provide advice on diet both immediately and in the long term.
  • Usually, dysphagia is not an issue with this type of stroke. However, patients may not be able to see one side of the plate and may neglect some of their food; they need to have the plate turned and eventually be taught to turn their head to see the blind hemifield.
  • A "heart-healthy" diet is really an anti-atherosclerosis diet and may be applicable depending on stroke mechanism and underlying risk factors. This prescription should be based on follow-up testing and investigation.

Activity

  • Activity varies depending on the patient's deficits.
  • The patient should be encouraged to remain mobile if possible.
  • At discharge, activities may be limited by neurological deficits.
  • The patient may be required to give up driving.

Medication

Thrombolytic therapy may be used for treatment of acute stroke within the first 3 hours when appropriate criteria are met. When thrombolysis is inappropriate, many patients are administered heparin intravenously (IV) despite a lack of convincing evidence of its efficacy. The rationale for the acute use of anticoagulant therapy lies in preventing acute recurrence of stroke. Trials have shown both that this risk is low, in the order of 1-3% in the first 3 months, and that heparin does not provide any functional or survival advantage. This is still a controversial area, however, in which some stroke experts have strong opinions about anticoagulation. In general, the stroke mechanism should be identified so that a better informed decision can be made before long-term anticoagulation is chosen.

One subgroup that may benefit from urgent anticoagulation is the group of patients with stroke due to carotid or other large artery atherosclerotic stenosis. Analysis of the recent TOAST trial results demonstrated that patients who had large-artery stenosis identified as the causative lesion and received danaparoid had better outcomes than those who did not receive the drug.8 Heparin and low-molecular-weight heparin (LMWH) should be titrated individually on the basis of aPTT. Weight-based nomograms are available. Because these nomograms have been designed for rapid anticoagulation in the setting of pulmonary embolism, DVT, or unstable angina, they may not be suitable for acute stroke.

Many neurologists, fearful of overshooting a target aPTT of 2 times the normal, opt not to give an upfront bolus of heparin and adopt a less aggressive dosing regimen. This approach may be justifiable given recent evidence that heparin does not provide an acute advantage in nonselective use in ischemic stroke. The optimal dosing regimen for heparin in stroke has not been established. A weight-based dosing approach is used in children. Fractionated heparins, or LMWH, have become available in the last few years and have revolutionized therapy of venous thrombosis and acute coronary syndromes. Few neurologists have adopted LMWH therapy in the acute setting because no antidote is available for quick reversal of anticoagulation in the event of intracerebral hemorrhage. In the subacute setting, LMWH may be used as a prelude to long-term anticoagulation with warfarin. Long-term warfarin may be used, particularly for secondary prevention in a defined cardioembolic source such as atrial fibrillation.

Several new oral anticoagulant medications 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.

Antiplatelet agents have demonstrated efficacy in reducing the risk of recurrent stroke. Acetylsalicylic acid (aspirin, or ASA), 325 mg qd, has been shown to reduce the rate of acute recurrence of stroke (ie, in the first 14 days after first stroke) when administered within 48 hours of the first stroke. Ticlopidine, clopidogrel, and Aggrenox (aspirin plus extended-release dipyridamole) also prevent recurrent stroke, although ticlopidine is rarely used due to a higher risk of side effects.

Control of stroke risk factors with antihypertensive drugs, cholesterol-lowering medication, and possibly homocysteine-lowering vitamins (ie, folic acid, pyridoxine, cobalamin) also is part of the preventive regimen.

Despite many phase 2 and phase 3 randomized clinical trials of neuroprotective agents, none of these agents have shown efficacy to date. Multiple reasons have been postulated for the disparity between the success of these drugs in the lab and their failure in the clinic. Several trials are ongoing.

Thrombolytic agents

Several thrombolytic agents have been studied for their use in the dissolution of thrombus. In acute ischemic stroke, only single-chain rtPA (alteplase but not reteplase or duteplase), delivered IV, has demonstrated efficacy and safety for all ischemic stroke types. Pro-urokinase, given intra-arterially, recently has been shown to be useful for MCA stroke only, but has not yet been licensed for this indication. This drug is not available; advocates for the somewhat investigational use of intra-arterial thrombolysis use tPA. Thrombosis of the basilar artery is one stroke type in which the prognosis without treatment is poor, and thrombolytic therapy may offer some hope.


Alteplase; rtPA (Activase)

Single-stranded endogenous serine protease that cleaves fibrin and functions as endogenous anticoagulant. Although has short half-life of 6-7 min in vivo, binds relatively specifically to clot-bound fibrin, making its functional half-life longer.

Adult

0.9 mg/kg IV over 1 h, with 10% of total dose given as initial IV bolus over 2 min, remainder over 1 h; not to exceed 90 mg (note that dose for acute ischemic stroke is lower than that for acute MI)
When given intra-arterially, total dose is lower, usually not exceeding 30 mg given in 5-6 mg boluses at clot face

Pediatric

Not established

Drugs that alter platelet function (such as aspirin, dipyridamole, and abciximab) may increase risk of bleeding prior to, during, or after therapy; either heparin or alteplase may cause bleeding complications; no antiplatelet or anticoagulant therapy is given for 24 h after IV tPA

Absolute: Hemorrhage on CT scan; active internal bleeding or bleeding at noncompressible site; rapidly resolving deficit; BP >185/110 mm Hg after 2 attempts to reduce BP to or below this level
Relative: Decreased level of consciousness; CT scan showing large areas of early infarct changes; platelet count <100 x 109/L, INR >1.4, or PT >15, aPTT >40; intracranial or intraspinal surgery in past 2 mo; stroke or head injury in last 3 mo; GI or GU bleeding in last 21 d; recent surgery or trauma within last 21 d; previous intracerebral hemorrhage; glucose <2.7 mmol/L or >22.2 mmol/L; seizure at stroke onset; pregnancy; endocarditis; acute pericarditis; serious underlying medical illness

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

Rarely may be associated with angioedema and anaphylaxis; risk factors for this complication include use of ACE inhibitors; monitor for bleeding, especially at arterial puncture sites, or with coadministration of vitamin K antagonists; control and monitor BP frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause intracranial hemorrhage

Antiplatelet agents

These agents inhibit cyclooxygenase system, decreasing level of thromboxane A2, which is a potent platelet activator.


Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Adult

30-1300 mg/d PO qd or divided (larger doses); most prescribers now accept that 50-325 mg/d provides same risk reduction as lower or higher doses; theoretical group of patients, called "aspirin nonresponders" are resistant, or may develop resistance, to aspirin; some aspirin nonresponders respond to higher doses (1300 mg/d); paradoxically, aspirin dose has never been major issue in cardiology literature

Pediatric

Not established

Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease 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
Because of association with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

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


Ticlopidine (Ticlid)

Inhibits platelet function by blocking platelet ADP receptor. (For review, see Sharis et al, 1998.)

Adult

250 mg PO bid

Pediatric

Not recommended

Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDS increase toxicity

Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage; active bleeding disorders

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause granulocytopenia in as many as 1% of patients newly exposed to drug; blood counts should be performed every 2 wk for first 3 mo; may cause thrombotic thrombocytopenic purpura


Clopidogrel (Plavix)

Inhibits platelet function by blocking platelet ADP receptor.

Adult

75 mg PO qd

Pediatric

Not recommended

Naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established

Documented hypersensitivity; active pathological bleeding, such as peptic ulcer or intracranial hemorrhage

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (such as ulcers); rarely has been associated with thrombotic thrombocytopenic purpura (risk probably lower than with ticlopidine)


Aspirin plus slow-release dipyridamole (Aggrenox)

Aspirin inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stasis and thrombosis.
Dipyridamole is platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-AMP within platelets and formation of potent platelet activator thromboxane A2.
European Stroke Prevention Trial 2 demonstrated that combination therapy was better than aspirin alone for prevention of recurrent stroke or TIA.

Adult

25 mg aspirin + 200 mg dipyridamole SR PO bid (1 tab bid)

Pediatric

Not established

Antacids and urinary alkalinizers may decrease aspirin effects; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of aspirin or anticoagulants; aspirin may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; aspirin doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Theophylline may decrease hypotensive effects of dipyridamole; antiplatelet activity of dipyridamole may increase heparin toxicity

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

Pregnancy

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

Precautions

Aspirin 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
Caution in hypotension when using dipyridamole; dipyridamole has peripheral vasodilating effects

HMG-CoA reductase inhibitors

Elevated cholesterol is a potential risk factor for stroke; sustained reduction in cholesterol levels may reduce the chances of stroke. Risk of stroke is reduced by the "statin" class of medications after treatment for coronary artery disease. Several statins (eg, lovastatin, simvastatin, pravastatin, atorvastatin) are available. Simvastatin and pravastatin are approved by the US Food and Drug Administration (FDA) for stroke prevention in patients with coronary artery disease. All inhibit enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in anabolism of cholesterol. These drugs are very effective in reducing levels of low-density lipoprotein (LDL) cholesterol but have less effect on high-density lipoprotein (HDL) and triglycerides. They may have other effects in stroke prevention such as plaque stabilization, reduction of free radical formation, and antiplatelet effects.


Atorvastatin (Lipitor)

Inhibits HMG-CoA reductase, which in turn inhibits cholesterol synthesis and increases cholesterol metabolism.

Adult

10 mg PO qd; titrate to maximum 80 mg/d as necessary

Pediatric

Not established

Triazole antifungals, CNS depressants, macrolide antibiotics, and mibefradil increase toxicity

Documented hypersensitivity; significant hepatic impairment; myositis, myotonia, or other disorders of muscle

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause myonecrosis in susceptible individuals (incidence <1%); serum CK may increase asymptomatically while on statins; cramps and/or muscle pain or weakness are an indication to discontinue drug
May elevate serum transaminases; perform LFTs before therapy and 12 weeks following both initiation of therapy and any elevation of dose.


Lovastatin (Mevacor)

Competitively inhibits HMG-CoA reductase, which catalyzes rate-limiting step in cholesterol synthesis.
Before initiating therapy, patients should be placed on cholesterol-lowering diet for 3-6 mo and the diet continued indefinitely.

Adult

30 mg PO with evening meal; adjust dose every 4 wk; not to exceed 80 mg/d

Pediatric

Not established

Increases toxicity of gemfibrozil, clofibrate, niacin, cyclosporine, and oral anticoagulants; itraconazole and ketoconazole increase toxicity; erythromycin may increase risk of rhabdomyolysis

Documented hypersensitivity; active liver disease

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May elevate aminotransferases; perform LFTs before therapy and every 4-6 wk for 12-15 mo, periodically thereafter


Pravastatin (Pravachol)

Competitively inhibits HMG-CoA reductase, which catalyzes rate-limiting step in cholesterol synthesis.
Before initiating therapy, patients should be placed on cholesterol-lowering diet for 3-6 mo and the diet continued indefinitely.

Adult

10-20 mg PO hs; may increase to 40 mg hs

Pediatric

Not established

Cholestyramine increases effects; increases toxicity of gemfibrozil, clofibrate, niacin, cyclosporine, and oral anticoagulants; itraconazole and ketoconazole increase toxicity; erythromycin may increase risk of rhabdomyolysis

Documented hypersensitivity; active liver disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May elevate aminotransferases; perform LFTs before therapy and every 4-6 wk for 12-15 mo, periodically thereafter

Vitamins

These agents are essential for normal metabolic processes and DNA synthesis.


Folic acid (Folvite)

Important cofactor for enzymes used in production of red blood cells. Folic acid, pyridoxine (vitamin B-6), and cobalamin (vitamin B-12) may help to reduce levels of serum homocysteine.

Adult

0.5-5 mg/d PO; may need to be taken with both pyridoxine and vitamin B-12

Pediatric

Not established

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Megadoses of pyridoxine may cause a subacute sensory neuronopathy, which may not be reversible on discontinuation of drug; vitamin B-12 deficiency may be masked by exogenous folate

Defibrinogenating agents

This agent is used to establish and maintain anticoagulation in heparin-intolerant patients.


Malayan pit viper venom (Ancrod, Viprinex)

This purified venom is defibrinogenating agent. Enzyme catalyzes destruction of free fibrinogen, inhibiting clot formation and reducing viscosity of blood. Used in past for heparin-associated thrombocytopenia/thrombosis. After small trial conducted in early 1980s, in which acutely administered, a recent, large randomized trial has been reported, suggesting benefit for patients treated acutely with Ancrod. The drug has not been approved for use in acute stroke and is not available in the United States.

Adult

Dose by weight and titrate according to fibrinogen levels; analogous to heparin, degree of defibrinogenation must be monitored quite closely

Pediatric

Not established

May increase effects of warfarin, heparin, and aspirin

Documented hypersensitivity; uncontrolled hypertension; recent intracranial surgery; malformation or aneurysm; bleeding diathesis

Pregnancy

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

Precautions

Use of Ancrod is precarious, since overshooting target level of fibrinogen is easy
Very low levels of fibrinogen are associated with significantly increased risk of bleeding, both extracranial and intracranial

More on Posterior Cerebral Artery Stroke

Overview: Posterior Cerebral Artery Stroke
Differential Diagnoses & Workup: Posterior Cerebral Artery Stroke
Treatment & Medication: Posterior Cerebral Artery Stroke
Follow-up: Posterior Cerebral Artery Stroke
Multimedia: Posterior Cerebral Artery Stroke
References
[ CLOSE WINDOW ]

References

  1. Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol. Jul 1999;56(7):824-32. [Medline].

  2. Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology. Aug 1992;42(8):1505-12. [Medline].

  3. NINDS and Stroke rt-PA Stroke Study Group. 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].

  4. Hacke W, Kaste M, Bluhmki E, Brozman M, Davalos A, Guidetti D, 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].

  5. Wahlgren N, Ahmed N, Davalos A, Hacke W, Millan M, Muir K, 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].

  6. Del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr. 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. Aug 2009;40(8):2945-8. [Medline]. [Full Text].

  7. TOAST Investigators. Low molecular weight heparinoid, ORG 10172 (danaparoid), and outcome after acute ischemic stroke: a randomized controlled trial. The Publications Committee for the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. JAMA. Apr 22-29 1998;279(16):1265-72. [Medline].

  8. Adams HP, Bendixen BH, Leira E, et al. Antithrombotic treatment of ischemic stroke among patients with occlusion or severe stenosis of the internal carotid artery: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology. Jul 13 1999;53(1):122-5. [Medline].

  9. Amarenco P, Cohen A, Tzourio C, et al. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med. Dec 1 1994;331(22):1474-9. [Medline].

  10. 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].

  11. Ausman JI, Diaz FG, de los Reyes RA, et al. Anastomosis of occipital artery to anterior inferior cerebellar artery for vertebrobasilar junction stenosis. Surg Neurol. Aug 1981;16(2):99-102. [Medline].

  12. Ausman JI, Lee MC, Chater N, Latchaw RE. Superficial temporal artery to superior cerebellar artery anastomosis for distal basilar artery stenosis. Surg Neurol. Oct 1979;12(4):277-82. [Medline].

  13. Ausman JI, Nicoloff DM, Chou SN. Posterior fossa revascularization: anastomosis of vertebral artery to PICA with interposed radial artery graft. Surg Neurol. May 1978;9(5):281-6. [Medline].

  14. Barnett HJM, Mohr JP, Stein BM. Stroke. 3rd ed. New York: Churchill Livingstone;1998.

  15. Bennett CL, Davidson CJ, Raisch DW, et al. Thrombotic thrombocytopenic purpura associated with ticlopidine in the setting of coronary artery stents and stroke prevention. Arch Intern Med. Nov 22 1999;159(21):2524-8. [Medline].

  16. Bennett CL, Weinberg PD, Rozenberg-Ben-Dror K, et al. Thrombotic thrombocytopenic purpura associated with ticlopidine. A review of 60 cases. Ann Intern Med. Apr 1 1998;128(7):541-4. [Medline].

  17. Broderick JP, Swanson JW. Migraine-related strokes. Clinical profile and prognosis in 20 patients. Arch Neurol. Aug 1987;44(8):868-71. [Medline].

  18. Buchan AM, Barber PA, Newcommon N, et al. Effectiveness of t-PA in acute ischemic stroke: outcome relates to appropriateness. Neurology. Feb 8 2000;54(3):679-84. [Medline].

  19. Caplan LR, DeWitt LD, Pessin MS, et al. Lateral thalamic infarcts. Arch Neurol. Sep 1988;45(9):959-64. [Medline].

  20. Carpenter MB. Core Text of Neuroanatomy. 4th ed. Baltimore, Md: Williams and Wilkins;1991.

  21. Chambers BR, Brooder RJ, Donnan GA. Proximal posterior cerebral artery occlusion simulating middle cerebral artery occlusion. Neurology. Mar 1991;41(3):385-90. [Medline].

  22. Clark WM, Wissman S, Albers GW, et al. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset. The ATLANTIS Study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA. Dec 1 1999;282(21):2019-26. [Medline].

  23. Devinsky O, Bear D, Volpe BT. Confusional states following posterior cerebral artery infarction. Arch Neurol. Feb 1988;45(2):160-3. [Medline].

  24. Dorfman LJ, Marshall WH, Enzmann DR. Cerebral infarction and migraine: clinical and radiologic correlations. Neurology. Mar 1979;29(3):317-22. [Medline].

  25. Duncan GW, Weindling SM. Posterior cerebral artery stenosis with midbrain infarction. Stroke. May 1995;26(5):900-2. [Medline].

  26. Furlan A, Higashida R, Wechsler L, et al. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. Dec 1 1999;282(21):2003-11. [Medline].

  27. Georgiadis AL, Yamamoto Y, Kwan ES, et al. Anatomy of sensory findings in patients with posterior cerebral artery territory infarction. Arch Neurol. Jul 1999;56(7):835-8. [Medline].

  28. Gomori AJ, Hawryluk GA. Visual agnosia without alexia. Neurology. Jul 1984;34(7):947-50. [Medline].

  29. Grond M, Stenzel C, Schmulling S, et al. Early intravenous thrombolysis for acute ischemic stroke in a community-based approach. Stroke. Aug 1998;29(8):1544-9. [Medline].

  30. Grotta J, Bratina P. Subjective experiences of 24 patients dramatically recovering from stroke. Stroke. Jul 1995;26(7):1285-8. [Medline].

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

  32. Hacke W, Kaste M, Fieschi C, et al. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Second European-Australasian Acute Stroke Study Investigators. Lancet. Oct 17 1998;352(9136):1245-51. [Medline].

  33. Hill MD, Barber PA, Takahashi J, et al. Anaphylactoid reactions and angioedema during alteplase treatment of acute ischemic stroke. CMAJ. May 2 2000;162(9):1281-4. [Medline].

  34. Hill MD, Hachinski V. Stroke treatment: time is brain. Lancet. Oct 1998;352 Suppl 3:SIII10-4. [Medline].

  35. Hommel M, Besson G, Pollak P, et al. Hemiplegia in posterior cerebral artery occlusion. Neurology. Oct 1990;40(10):1496-9. [Medline].

  36. Hommel M, Moreaud O, Besson G, Perret J. Site of arterial occlusion in the hemiplegic posterior cerebral artery syndrome. Neurology. Apr 1991;41(4):604-5. [Medline].

  37. International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet. May 31 1997;349(9065):1569-81. [Medline].

  38. Johansson T, Fahlgren H. Alexia without agraphia: lateral and medial infarction of left occipital lobe. Neurology. Mar 1979;29(3):390-3. [Medline].

  39. Klinkel WR, Newman RP, Jacobs L. Posterior cerebral artery branch occlusions: CT and anatomic considerations. In: Berguer R, Bauer RB, eds. Vertebrobasilar Arterial Occlusive Disease: Medical and Surgical Management. Proceedings of the First International Conference on Vertebrobasilar. New York: Raven Press;. 1984.

  40. Koroshetz WJ, Ropper AH. Artery-to-artery embolism causing stroke in the posterior circulation. Neurology. Feb 1987;37(2):292-5. [Medline].

  41. Kumral E, Bayulkem G, Atac C, Alper Y. Spectrum of superficial posterior cerebral artery territory infarcts. Eur J Neurol. Apr 2004;11(4):237-46. [Medline].

  42. Levine DN, Rinn WE. Opticosensory ataxia and alien hand syndrome after posterior cerebral artery territory infarction. Neurology. Aug 1986;36(8):1094-7. [Medline].

  43. Marinkovic SV, Milisavljevic MM, Kovacevic MS. Anastomoses among the thalamoperforating branches of the posterior cerebral artery. Arch Neurol. Aug 1986;43(8):811-4. [Medline].

  44. Moen M, Levine SR, Newman DS. Bilateral posterior cerebral artery strokes in a young migraine sufferer. Stroke. Apr 1988;19(4):525-8. [Medline].

  45. Mohr JP, Leicester J, Stoddard LT, Sidman M. Right hemianopia with memory and color deficits in circumscribed left posterior cerebral artery territory infarction. Neurology. Nov 1971;21(11):1104-13. [Medline].

  46. Mohr JP, Pessin MS. Posterior Cerebral Artery Disease. 3rd ed. New York: Churchill Livingstone;1998.

  47. Neau JP, Bogousslavsky J. The syndrome of posterior choroidal artery territory infarction. Ann Neurol. Jun 1996;39(6):779-88. [Medline].

  48. North K, Kan A, de Silva M, Ouvrier R. Hemiplegia due to posterior cerebral artery occlusion. Stroke. Nov 1993;24(11):1757-60. [Medline].

  49. Percheron G. [Arteries of the human thalamus. I. Artery and polar thalamic territory of the posterior communicating artery]. Rev Neurol (Paris). May 1976;132(5):297-307. [Medline].

  50. Percheron G. [Arteries of the human thalamus. II. Arteries and paramedian thalamic territory of the communicating basilar artery]. Rev Neurol (Paris). May 1976;132(5):309-24. [Medline].

  51. Pessin MS, Kwan ES, DeWitt LD, Hedges TR 3rd. Posterior cerebral artery stenosis. Ann Neurol. Jan 1987;21(1):85-9. [Medline].

  52. Pessin MS, Kwan ES, Scott RM, Hedges TR 3rd. Occipital infarction with hemianopsia from carotid occlusive disease. Stroke. Mar 1989;20(3):409-11. [Medline].

  53. Pessin MS, Lathi ES, Cohen MB, et al. Clinical features and mechanism of occipital infarction. Ann Neurol. Mar 1987;21(3):290-9. [Medline].

  54. Piechowski-Jozwiak B, Bogousslavsky J. Basilar occlusive disease: the descent of the feared foe?. Arch Neurol. Apr 2004;61(4):471-2. [Medline].

  55. Pillon B, Bakchine S, Lhermitte F. Alexia without agraphia in a left-handed patient with a right occipital lesion. Arch Neurol. Dec 1987;44(12):1257-62. [Medline].

  56. Sharis PJ, Cannon CP, Loscalzo J. The antiplatelet effects of ticlopidine and clopidogrel. Ann Intern Med. Sep 1 1998;129(5):394-405. [Medline].

  57. Sherman DG, Atkinson RP, Chippendale T, et al. Intravenous ancrod for treatment of acute ischemic stroke: the STAT study: a randomized controlled trial. Stroke Treatment with Ancrod Trial. JAMA. May 10 2000;283(18):2395-403. [Medline].

  58. Stommel EW, Friedman RJ, Reeves AG. Alexia without agraphia associated with spleniogeniculate infarction. Neurology. Apr 1991;41(4):587-8. [Medline].

  59. Stroke Unit Trialists' Collaboration. Collaborative systematic review of the randomised trials of organised inpatient (stroke unit) care after stroke. Stroke Unit Trialists' Collaboration. BMJ. Apr 19 1997;314(7088):1151-9. [Medline].

  60. Tanne D, Bates VE, Verro P, et al. Initial clinical experience with IV tissue plasminogen activator for acute ischemic stroke: a multicenter survey. The t-PA Stroke Survey Group. Neurology. Jul 22 1999;53(2):424-7. [Medline].

  61. Tatemichi TK, Steinke W, Duncan C, et al. Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging. Ann Neurol. Aug 1992;32(2):162-71. [Medline].

  62. The EC/IC Bypass Study Group. 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].

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

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

stroke, posterior cerebral artery stroke, vertebrobasilar insufficiency, posterior circulation stroke, PCA, PCA stroke, ischemic stroke, embolization, intrinsic atherosclerotic disease and vasospasm, migrainous strokes, PCA syndromes, paramedian thalamic infarction, cardioembolism

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Michael D Hill, MD, Medical Director, Stroke Unit, Associate Professor of Neurology, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Canada
Michael D Hill, MD is a member of the following medical societies: Alberta Medical Association, American Academy of Neurology, American College of Physicians, American Stroke Association, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Hoffmann La Roche Canada Ltd Honoraria Speaking and teaching

Coauthor(s)

Alastair M Buchan, DSc, MB, BCh, Professor, Head of Medical Sciences Division, University of Oxford, UK
Disclosure: Nothing to disclose.

Medical Editor

Thomas A Kent, MD, Professor, Department of Neurology, Baylor College of Medicine; Neurology Care Line Executive, Michael E DeBakey Veterans Affairs Medical Center
Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.