AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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

INTRODUCTION

Section 2 of 11  

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

Background

Posterior cerebral artery (PCA) stroke is less common than stroke involving the anterior circulation. An understanding of PCA stroke phenomenology and mechanisms requires knowledge of neurovascular anatomy and of the structure-function relationships of this region of the brain. This article provides an overview of PCA stroke and focuses exclusively on stroke of arterial origin involving the PCA territory.

Anatomy

The PCAs are paired, branching off the top of the basilar artery and curving posterosuperiorly around the midbrain. The PCA supplies parts of the midbrain, the subthalamic nucleus, the basal nucleus, the thalamus, the mesial inferior temporal lobe, and the occipital and occipitoparietal cortices. In addition, the PCAs, via the posterior communicating arteries, may become important sources of collateral circulation for the middle cerebral artery (MCA) territory.

The PCA is divided angiographically into P1 and P2 segments by the posterior communicating artery. Penetrating branches to the mesencephalon, subthalamic and basal structures, and thalamus arise primarily from the P1 segment and the posterior communicating artery. These penetrating arteries include the thalamogeniculate (which may arise independently or more commonly as a branch of the medial posterior choroidal artery), the splenial (posterior paricallosal artery), and the lateral and medial posterior choroidal arteries. The P2 segment bifurcates into the posterior temporal artery (anterior division) and the internal occipital artery (posterior division).

The posterior temporal artery further divides into anterior and posterior temporal branches supplying the inferomedial temporal lobe and the lingual and occipitotemporal gyri, respectively. The internal occipital artery supplies 3 end arteries: 1) the calcarine artery, which supplies the calcarine cortex on the medial surface of the occipital lobe; 2) the occipitotemporal artery, which supplies the orbital surface of the temporal and occipital lobes; and 3) the occipitoparietal artery, which supplies the precuneus and surrounding cortex.

Normal variants of neurovascular anatomy

In approximately 30% of people, one or both PCAs take origin from the internal carotid artery (ICA) directly or via the posterior communicating artery. Direct origin from the ICA is termed "fetal PCA" (when the ipsilateral P1 segment is congenitally absent). This may have important consequences, in that stroke in the PCA territory may be caused by occlusive disease of the anterior circulation.

The central artery of Percheron arises from one P1, then gives rise to bilateral medial thalamic perforators. Occlusion results in bilateral paramedian thalamic infarction. This is one of the few examples in which a cerebral vessel supplies structures on both sides of the midline.

Pathophysiology

Ischemic stroke occurs when local blood flow is suddenly limited by vessel occlusion. The rate of neuronal death varies with blood flow. If blood flow falls to less than 15 mL/100 g/min, energy failure and subsequent cell death occur within minutes. Even suboptimal flow for longer periods may cause the cells to die by an apoptotic mechanism over days to weeks. Rapid restoration of blood flow is essential to save brain tissue.

The mechanism of stroke involving the PCA territory is variable. It is commonly due to embolization from the heart, the aortic arch, the vertebral artery, or the basilar artery. Other mechanisms include intrinsic atherosclerotic disease and vasospasm. Migrainous strokes tend to involve PCAs preferentially. Less commonly, the anterior circulation is to blame (eg, internal carotid stenosis), when a fetal PCA is present. Rare causes of stroke may be considered when usual culprits such as coagulation abnormalities, vasculitis, sympathomimetic drugs, and metabolic disorders are not present.

Frequency

United States

Approximately 5% of ischemic strokes involve the PCA or its branches.

Mortality/Morbidity

• Death from PCA stroke is uncommon. Concomitant basilar occlusion and infarction of the brain stem may cause death.
• Rate of morbidity from PCA stroke is high. Recovery of visual field deficits is very limited. Patients may be unable to drive or read, resulting in major limitations in their quality of life, despite normal motor function.
• Other neuropsychological deficits may include prosopagnosia (inability to recognize faces), visual agnosia, amnesia, and alexia without agraphia. Rarely, PCA stroke results in infarction of the ipsilateral cerebral peduncle with resultant hemiplegia. Thalamic involvement can also produce contralateral sensory loss.

Sex

In recently published data from the Tufts New England Medical Center posterior circulation stroke registry, 58% of patients were male and 42% were female.

Age

In recently published data from the Tufts New England Medical Center posterior circulation stroke registry, the mean age of stroke was 61.5 years.

CLINICAL

Section 3 of 11  

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

History

The approach to stroke in the PCA territory is no different from stroke elsewhere in the brain. A simple 3-step algorithm can be applied as follows:

• First, confirm the diagnosis of stroke. If the patient is seen within the 3-hour time window, consider thrombolytic therapy (ie, intravenous tissue plasminogen activator [tPA]).
• Second, confirm the PCA stroke syndrome by localizing the lesion.
• Third, use the stroke syndrome as a guide and perform investigations to determine the stroke mechanism or cause.
• Based on these 3 steps, decide upon appropriate secondary preventive strategies. In practice, these 3 steps are done almost simultaneously.
• The phenomenology of PCA stroke is a function of the neuroanatomy and corresponding vascular supply, as described above.
• PCA syndromes can be divided roughly into those involving the midbrain, thalamus, occipital cortex, medial temporal lobe, occipitoparietal cortex, and combinations of these.
• Historical features are discussed in the Physical section.

Physical

• In general, because of the diversity of PCA syndromes, a complete neurologic examination is necessary.
• When thrombolytic therapy is being considered, an abridged 5- to 10-minute examination focusing on the major areas of neurological dysfunction is appropriate, for example, level of consciousness, language, hemi-inattention, visual fields, eye movements, lower cranial nerves, crude motor function, sensory loss, and ataxia. The NIH Stroke Scale is recommended as a guide to patient selection for thrombolytic therapy.
• The physical examination also should encompass a cardiologic and atherosclerosis examination, searching for arterial bruits, murmurs that suggest valvular heart disease, signs of atrial fibrillation, and signs of hyperlipidemia (eg, corneal arcus, tendinous xanthomata).
• The major PCA stroke syndromes are described here. Often, many of the features occur concomitantly.
• • Paramedian thalamic infarction
    • This syndrome, resulting from bilateral medial thalamic infarction, is part of the differential diagnosis of delirium and coma. Patients often are obtunded to comatose or agitated, and they may or may not have associated hemiplegia or hemisensory loss. Occasionally, the cranial nerve III nucleus is involved, with resultant ophthalmoplegia.
    • Patients may take days to weeks to recover and seem to be in a sleeplike state. Although alertness generally returns, prognosis for good functional recovery is poor because of severe memory dysfunction.
    • The syndrome may result from a "top of the basilar" artery embolus. The artery of Percheron, referred to earlier, may be involved. This has been referred to as a posterior variant of the syndrome of akinetic mutism.
  • Pure hemisensory loss
    • Infarction of the ventral posterolateral nucleus of the thalamus results in hemisensory loss. This is one of the well-described lacunar syndromes. Usually, the vessel involved is the thalamogeniculate branch.
    • A related disorder is Dejerine-Roussy syndrome, in which quickly resolving hemiparesis and hemiataxia leave the patient with delayed, persistent, hemisensory disturbance with paroxysmal pain on the affected side.
  • Visual field loss
    • A general rule of visual field examination is that the further posterior the lesion, the more congruous is the visual field loss.
    • Bilateral infarctions of the occipital lobes produce varying degrees of cortical blindness depending upon the extent of the lesion. Patients often exhibit Anton syndrome, a state in which they fervently believe they can see when they cannot. Patients may describe objects that they have not seen previously in exquisite detail, completely in error and oblivious to that error. Another intriguing phenomenon is blindsight—although cortically blind, patients can respond to movement or sudden lightening or darkening of environment.
    • Unilateral infarction produces homonymous hemianopia. Sparing of the macula is encountered frequently in infarction of the occipital lobes due to PCA occlusion. Macular sparing probably is caused by collateral vascular supply to the occipital pole from posterior branches of the MCA and preservation of the optic radiations, though bilateral representation of macular vision also has been suspected.
    • Infarction of the lateral geniculate nucleus may produce hemianopia, quadrantanopia, or sectoranopia. The vascular supply is dual; the anterior choroidal artery supplies the anterior hilum and anterolateral areas, and the posterior choroidal artery supplies the rest. Occlusion of the posterior choroidal artery may produce a distinct syndrome of hemianopia, hemidysesthesia, and memory disturbance due to infarction of the lateral geniculate, fornix, dorsomedial thalamic nucleus, and posterior pulvinar.
  • Visual agnosia
    • This refers to a lack of recognition or understanding of visual objects or constructs. It is a disorder of higher cortical function.
    • The strict diagnosis of visual agnosia requires intact visual acuity and language function. Most patients have bilateral lesions, sparing the visual cortex but disrupting or disconnecting visual information from reaching parts of the visual association cortex for reference to visual memories. The patient with visual agnosia can recognize objects presented in another modality; for example, the patient can identify keys by palpating them or hearing them jingle, but not by seeing them.
    • True visual agnosia has been divided into apperceptive and associative subtypes.
    • In apperceptive visual agnosia, patients cannot name objects presented to them, draw objects from memory, or identify or match objects. Yet, they can see and avoid obstacles when ambulating and detect subtle changes in light intensity.
    • In associative agnosia, patients can draw objects to command and match them or point to them but cannot name them. They can see shapes and reproduce them in drawing, yet not recognize the identity of objects.
  • Balint syndrome
    • This typically occurs in degenerative diseases but also may occur with bilateral parieto-occipital infarction, most often in the watershed between the PCA and MCA territories. It is a triad of visual simultanagnosia, optic ataxia, and apraxia of gaze.
    • Visual simultanagnosia implies an inability to examine a scene and integrate its parts into a cohesive interpretation. A patient can identify specific parts of a scene but cannot describe the entire picture.
    • Optic ataxia implies a loss of hand-eye coordination such that reaching or performing a motor task under visual guidance is clumsy and uncoordinated.
    • Finally, apraxia of gaze is a misnomer describing a supranuclear deficit in the ability to initiate a saccade on command.
  • Disorders of face recognition
    • Prosopagnosia refers to an inability to recognize faces. Typically, this deficit results from bilateral lesions of the lingual and fusiform gyri; however, cases of unilateral nondominant hemisphere lesions resulting in prosopagnosia have been reported.
    • Usually, it does not occur in isolation and other object agnosias coexist. Autoprosopagnosia, or inability to recognize one's own face in a picture or mirror, may occur as a subset of this syndrome.
  • Palinopsia, micropsia, and macropsia
    • These are illusory phenomena that are of uncertain pathophysiology. They may represent seizure activity and traditionally are treated with anticonvulsants.
    • Palinopsia describes the persistence of a visual image for several seconds to days in a partially blind hemifield.
    • Micropsia and macropsia describe situations where objects appear smaller or larger than expected.
  • Disorders of reading (alexia, dyslexia)
    • Pure alexia may result from infarction of the dominant occipital cortex. Words are treated as if they were from a foreign language. Patients may retain the ability to formulate a word and its meaning if spelled out to them orally or if they trace the letters with their hand. Patients may then learn to read, albeit terribly slowly, in a letter-by-letter fashion, being unable to integrate multiple letter groups.
    • Classic alexia without agraphia was described by Dejerine in the late 19^th century. In his case study, he emphasized a left occipital cortex lesion and also infarction of the splenium of the corpus callosum, which disconnected fibers from the right occipital lobe from reaching the angular gyrus.
    • Rarely, the dominant-hemisphere, posterior temporal lobe is supplied by PCA. Damage to this area results in a Wernicke-type aphasia with associated dyslexia and right hemianopia due to concomitant left occipital infarction.
  • Disorders of color vision (achromatopsia, dyschromatopsia)
    • Lesions of the lingual gyrus in the inferior occipital lobe may produce disorders of color perception. Testing with Ishihara plates reveals a deficit. Colors may be described as washed out or gray. This deficit usually occurs only in the contralateral visual field and is called "hemiachromatopsia."
    • A related problem is color anomia, also called color agnosia, in which patients can perceive and match colors but cannot associate them with the proper color names. This deficit also has been explained by a disconnection model.
  • Memory (amnesia)
    • Infarction of the medial temporal lobe, fornices, or medial thalamic nuclei may result in permanent anterograde amnesia.
    • Although traditionally bilateral infarction has been thought to be required for amnesia, memory functions may be lateralized such that infarction of left-sided structures may have a more lasting impact on verbal function.
    • Older patients frequently have lasting short-term memory impairment from unilateral PCA territory infarction.
    • Recent imaging in patients with transient global amnesia has demonstrated diffusion-weighted lesions in unilateral temporal lobes resulting in temporary amnesia.
  • Motor dysfunction
    • When the blood supply to the cerebral peduncles arises from perforators of P1 segment, infarction may occur, resulting in hemiplegia or hemiparesis.
    • The clinical syndrome is no different from capsular infarction but often includes concomitant hemianopia because of occipital lobe involvement.
    • The syndrome may mimic a large MCA infarction.

Causes

After an assessment of PCA stroke syndrome, the next step is to determine the mechanism of stroke. One approach is to start with the heart and proceed rostrally.

• Cardioembolism
• • Cardioembolism is the most common cause of PCA stroke.
  • Emboli may form in the heart from multiple underlying diseases. The most common cause is atrial fibrillation. Stroke from atrial fibrillation is preventable with long-term anticoagulation.
  • Other possibilities include a mural thrombus on a hypokinetic segment (eg, post-myocardial infarction [MI], dilated cardiomyopathy, atrial septal aneurysm), bacterial endocarditis, Libman-Sachs endocarditis, prosthetic heart valves, paradoxical embolism via a patent foramen ovale, and atrial septal defect.
  • Mitral valve prolapse and mitral valve strands are probably only weak risk factors for stroke.
  • Embolism from aortic arch atheroma
    • With the advent of transesophageal echocardiography, examination and quantitation of atheromatous disease of the aortic arch has been possible.
    • Thickness of plaque greater than 4 mm and/or presence of mobile thrombus are highly predictive of stroke.
  • Proximal vertebral artery disease
    • Stenosis of a vertebral artery origin often is found in patients with posterior circulation ischemia.
    • Analogous to the narrowed ICA, stenosis may lead to artery-to-artery embolism.
  • Dissection
    • The vertebral arteries are uniquely prone to dissection in the distal or V3 segment as they pass over the arch of C1, pierce the dura, and enter the foramen magnum.
    • Dissection may be spontaneous or related to minor or major trauma.
    • The mechanisms of PCA stroke secondary to vertebral artery dissection are believed to be due to formation of embolism or thrombus around an intimal tear.
    • The usual treatment of stroke secondary to dissection is anticoagulation; however, no solid evidence exists to support this practice.
  • Vertebral atherosclerotic disease
    • Caplan studied 10 cases of stroke due to arterioembolism from atherosclerotic vertebral arteries.
    • Most commonly, the cerebellum was affected, but PCA territory infarction also was reported.
  • Basilar artery disease: Emboli traveling up the posterior circulation may arrest at the top of the basilar, producing ischemia of both PCA territories, the thalamus, and midbrain.
  • Posterior cerebral artery disease: Intrinsic PCA stenosis from atherosclerosis is quite rare. Nevertheless, it is a recognized cause of stroke.
  • Vasospasm and migraine
    • Migraine typically affects the posterior circulation.
    • The clinical manifestations of an aura such as scintillating scotomata may represent spreading depression of Leão across the occipital cortex.
    • Angiography of patients with migraine shows a beaded pattern of vasospasm.
    • Migrainous stroke is said to occur most commonly in the occipital lobes.
• Other diagnostic considerations
• • Diagnosis of stroke is usually not difficult. Suddenness of onset should alert the clinician to the vascular nature of the insult. The usual differential diagnosis includes other vascular diseases such as intracerebral hemorrhage, vascular malformations, venous infarction, subarachnoid hemorrhage, and subdural hemorrhage. Rarely, space-occupying lesions (eg, glioma) present with sudden onset of deficit. One to two percent of patients in the large British TIA trial were found to have neoplastic lesions.
  • Demyelinating lesions (eg, multiple sclerosis) rarely present with hemianopia, but this does occur in a few patients. Migraine is usually evident by the accompanying headache and nausea and may ultimately (but rarely) progress to infarction. Hypoglycemia should be ruled out with simple laboratory studies.

DIFFERENTIALS

Section 4 of 11  

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

Other Problems to be Considered

Hypoglycemia
Venous infarction
Carotid disease and stroke

WORKUP

Section 5 of 11  

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

Lab Studies

• In the acute phase, routine blood tests are all that is needed. These include a complete blood count (with platelet count), prothrombin time (PT)/activated partial thromboplastin time (aPTT)/international normalized ratio (INR), electrolytes, creatinine, serum creatine kinase (CK), and serum glucose. These tests are required to assess whether the patient is a candidate for thrombolysis and are a part of the stroke mechanism workup.
• If the stroke mechanism is not evident on the basis of imaging studies, then special hematologic and serologic examinations should be ordered. A full coagulation workup typically might include assays for antiphospholipid antibodies and lupus anticoagulant. Hypercoagulable factors usually associated with venous infarction, such as protein C, protein S, factor V Leiden-activated protein C resistance, antithrombin III, and prothrombin gene polymorphism, may be appropriate if the stroke mechanism is thought to involve either venous thrombosis or paradoxical embolism. These tests are better done 2-3 weeks after the acute event. Blood smear examination, platelet aggregation studies, sucrose lysis test for paroxysmal nocturnal hemoglobinuria, and Venereal Disease Research Laboratory test (VDRL) also should be considered. Abnormalities in any of these blood tests are rare causes of stroke. Nevertheless, particularly in a young patient, a full workup should be considered.
• When the mechanism of stroke is atherosclerotic disease, follow-up blood tests should be done to assess atherosclerotic risk factors. Diabetes should be considered and screened for. A fasting serum cholesterol profile may be artifactually low in the acute setting and should therefore be conducted 8-12 weeks after the stroke. High cholesterol is a definite risk factor for stroke and is amenable to treatment.
• In selected patients, assessing fasting serum homocysteine levels is reasonable. High serum homocysteine level is an independent risk factor for all atherosclerotic disease and may be treated with simple B complex vitamins—pyridoxine, folic acid, and vitamin B-12. A large, randomized trial of vitamin supplementation for stroke prevention is currently underway. This study is entitled Vitamin Intervention in Stroke Prevention or VISP.

Imaging Studies

• Neuroimaging: All patients with stroke should undergo neuroimaging, either with the traditional brain CT scan or MRI with diffusion and perfusion imaging (see Image 1).
• An emergent CT scan is required prior to considering thrombolysis. CT is less sensitive for the posterior fossa strokes because of bone artifact and decreased tissue detail. MRI is a better choice.
• MRI defines multiple lesions and allows a much better examination of midbrain, subthalamic, and thalamic structures than CT scan. With the use of diffusion- and perfusion-weighted imaging, a much more complete assessment of the infarcted tissue and tissue at risk is available.
• Other possible brain imaging procedures include single-photon emission computed tomography (SPECT) and positron emission tomography (PET).
• • SPECT is a nuclear medicine study using radioisotopes of technetium. It provides an analysis of relative blood flow by region, usually in the resting state. It is rarely useful in the clinical setting in acute stroke and can be considered a research tool.
  • PET can be used to analyze neurometabolism in vivo; it is at present a research tool.
• Rarely, plain skull films demonstrate an unexpected tumor or calcification in an aneurysm.
• Transcranial Doppler ultrasonography (TCD) is not yet widely used and remains largely a research tool; however, that it is a highly useful adjunct in the emergent evaluation of patients with stroke is becoming increasingly apparent. TCD is dependent upon the skill and experience of the operator. In skilled hands, both the distal basilar and P1 and P2 segments can be assessed. Much more information is available about the MCA than the PCA. However, TCD may detect acute clot in the PCA.
• Carotid duplex ultrasonography is used widely and should not be overlooked in PCA stroke. When a fetal origin PCA is present, the cause of stroke still may be significant carotid artery atherosclerotic disease. The appropriate treatment for secondary prevention will then be carotid endarterectomy rather than medical therapy.
• Selective catheter cerebral angiography remains the criterion standard to evaluate the vascular anatomy. However, it is invasive and does carry a small risk of procedure-related morbidity. Increasingly, noninvasive methods of viewing the arterial anatomy are being developed—magnetic resonance angiography, CT angiography (CTA), and TCD. Currently these tests are reasonably good for assessment of the proximal circulation. When these are doubtful or more information is needed about the distal circulation, angiography is required. Angiography is needed to diagnose small aneurysms or vasculitis. In addition, angiography is required as a precursor to endovascular therapeutic techniques. Angioplasty and angioplasty with stenting are being adapted to the cerebral circulation. Presently, these techniques should be considered experimental.
• Echocardiography: Standard transthoracic echocardiography (TTE) is used in investigation of possible cardiac sources of embolus. This noninvasive test is done routinely in most tertiary care centers. Transesophageal echocardiography (TEE) is a more detailed test and is used to examine the aortic arch as well as cardiac sources of emboli. It is about 3 times more sensitive than TTE in detecting possible sources of emboli. A recent study suggested that it is cost-effective in acute stroke, whereas the TTE is not, despite the greater cost of TEE.

Other Tests

• All patients with stroke should have immediate ECG.

TREATMENT

Section 6 of 11  

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

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 tPA (rtPA), published in 1995, included all types of ischemic stroke. 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. 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

Section 7 of 11  

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

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. Recent 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. 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 recently 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 these agents have not been compared directly in clinical trials, the combination of aspirin and extended-release dipyridamole may be more effective than clopidogrel in prevention of stroke.

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.

Drug Category: 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.

Drug Category: Antiplatelet agents

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

Drug Name	Ticlopidine (Ticlid)
Description	Inhibits platelet function by blocking platelet ADP receptor. (For review, see Sharis et al, 1998.)
Adult Dose	250 mg PO bid
Pediatric Dose	Not recommended
Contraindications	Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage; active bleeding disorders
Interactions	Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDS increase toxicity
Pregnancy	X - Contraindicated in pregnancy
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

Drug Name	Clopidogrel (Plavix)
Description	Inhibits platelet function by blocking platelet ADP receptor.
Adult Dose	75 mg PO qd
Pediatric Dose	Not recommended
Contraindications	Documented hypersensitivity; active pathological bleeding, such as peptic ulcer or intracranial hemorrhage
Interactions	Naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established
Pregnancy	X - Contraindicated in pregnancy
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)

Drug Name	Aspirin plus slow-release dipyridamole (Aggrenox)
Description	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 Dose	25 mg aspirin + 200 mg dipyridamole SR PO bid (1 tab bid)
Pediatric Dose	Not established
Contraindications	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
Interactions	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
Pregnancy	D - Unsafe in pregnancy
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

Drug Category: 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.

Drug Name	Lovastatin (Mevacor)
Description	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 Dose	30 mg PO with evening meal; adjust dose every 4 wk; not to exceed 80 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; active liver disease
Interactions	Increases toxicity of gemfibrozil, clofibrate, niacin, cyclosporine, and oral anticoagulants; itraconazole and ketoconazole increase toxicity; erythromycin may increase risk of rhabdomyolysis
Pregnancy	A - Safe in pregnancy
Precautions	May elevate aminotransferases; perform LFTs before therapy and every 4-6 wk for 12-15 mo, periodically thereafter

Drug Name	Pravastatin (Pravachol)
Description	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 Dose	10-20 mg PO hs; may increase to 40 mg hs
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; active liver disease
Interactions	Cholestyramine increases effects; increases toxicity of gemfibrozil, clofibrate, niacin, cyclosporine, and oral anticoagulants; itraconazole and ketoconazole increase toxicity; erythromycin may increase risk of rhabdomyolysis
Pregnancy	X - Contraindicated in pregnancy
Precautions	May elevate aminotransferases; perform LFTs before therapy and every 4-6 wk for 12-15 mo, periodically thereafter

Drug Category: Vitamins

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

Drug Category: Defibrinogenating agents

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

FOLLOW-UP

Section 8 of 11  

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

Prognosis

• The prognosis for recovery largely depends upon the location of ischemic damage.
• Visual field deficits are unlikely to resolve.
• Some neuropsychological deficits may improve with rehabilitation and time.

Patient Education

• At discharge, all patients who have had a stroke should be counseled about the symptoms and signs of acute stroke.
• Since a delay in receiving emergency care is the major reason why patients cannot be treated with thrombolytic therapy, patients must be taught what to do if a stroke occurs.
• The major symptoms of stroke are (1) sudden loss of vision, (2) sudden loss of ability to speak or understand speech, (3) sudden weakness on one side of the body, (4) sudden loss of sensation on one side of body, and (5) sudden onset of incoordination.
• Patients should be instructed to call an ambulance (ie, call 911) if they or their friends/relatives suffer from any of these symptoms.
• For excellent patient education resources, visit eMedicine's Stroke Center, Cholesterol Center, and Statins Center. Also, see eMedicine's patient education article Stroke, High Cholesterol, Cholesterol FAQs, and Atorvastatin (Lipitor).

MISCELLANEOUS

Section 9 of 11  

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

Medical/Legal Pitfalls

• Medicolegal cases involving PCA stroke are rare.
• • However, one issue that inevitably arises with infarction of the visual cortex or its afferent fibers is competency to drive a vehicle.
  • Each physician must be aware of local laws governing the right to drive. Patients with infarction in the territory of the left PCA may have preserved macular vision but severe restriction of peripheral vision as well as inability to read in any visual field.
  • Patients with infarction in the territory of right PCA may have significant visual hemineglect.
• Careful examination and knowledge of local legal requirements is a necessity.

MULTIMEDIA

Section 10 of 11  

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

Media file 1:  Posterior cerebral artery (PCA) stroke. Subacute (36 hour) infarction of the left PCA territory.
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

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

• 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].
• 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].
• 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].
• 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].
• 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].
• 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].
• Barnett HJM, Mohr JP, Stein BM. Stroke. 3rd ed. New York: Churchill Livingstone;1998.
• 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].
• 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].
• Broderick JP, Swanson JW. Migraine-related strokes. Clinical profile and prognosis in 20 patients. Arch Neurol. Aug 1987;44(8):868-71. [Medline].
• 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].
• Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology. Aug 1992;42(8):1505-12. [Medline].
• Caplan LR, DeWitt LD, Pessin MS, et al. Lateral thalamic infarcts. Arch Neurol. Sep 1988;45(9):959-64. [Medline].
• Carpenter MB. Core Text of Neuroanatomy. 4th ed. Baltimore, Md: Williams and Wilkins;1991.
• Chambers BR, Brooder RJ, Donnan GA. Proximal posterior cerebral artery occlusion simulating middle cerebral artery occlusion. Neurology. Mar 1991;41(3):385-90. [Medline].
• 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].
• Devinsky O, Bear D, Volpe BT. Confusional states following posterior cerebral artery infarction. Arch Neurol. Feb 1988;45(2):160-3. [Medline].
• Dorfman LJ, Marshall WH, Enzmann DR. Cerebral infarction and migraine: clinical and radiologic correlations. Neurology. Mar 1979;29(3):317-22. [Medline].
• Duncan GW, Weindling SM. Posterior cerebral artery stenosis with midbrain infarction. Stroke. May 1995;26(5):900-2. [Medline].
• 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].
• 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].
• Gomori AJ, Hawryluk GA. Visual agnosia without alexia. Neurology. Jul 1984;34(7):947-50. [Medline].
• 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].
• Grotta J, Bratina P. Subjective experiences of 24 patients dramatically recovering from stroke. Stroke. Jul 1995;26(7):1285-8. [Medline].
• 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].
• 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].
• Hill MD, Hachinski V. Stroke treatment: time is brain. Lancet. Oct 1998;352 Suppl 3:SIII10-4. [Medline].
• Hill MD, Barber PA, Takahashi J, et al. Anaphylac